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Flashcards in Exam Review Quick Facts Deck (50)

Where do you see squamous cells, columnar, squamous mesothelial?

squamous-esophageal epithelium

columnar- intestinal epithelium, lining of stomach, colon (also has Goblet cells)

squamous mesothelial- serosa (outermost layer of GI tract)


Almost all contractile tissue of GI tract is smooth muscles. What is the exception?

Those in pharynx, the upper 1/3rd of esophagus, the external anal sphincter are striated muscle.


Where do you see tight junctions in GI tract? Gap junctions?

Smooth muscle of GI tract forms gap junctions (low resistance) with interstitial cells of Cajal (ICCs) – permits rapid cell-to-cell spread of action potentials.

is a single continuous layer of specialized cells lining the lumen of entire GI tract and interconnected via tight junctions.


Where are phasic contractions found? Where are tonic contractions found?

Phasic contractions – periodic contractions followed by relaxation – found in esophagus, gastric antrum, small intestine – involved in mixing and propulsion.

Tonic contractions – a constant level of contraction or tone without regular periods of relaxation – found in orad (upper) region of stomach and lower esophagheal, ileocecal and internal anal sphincters.


What are interstitial cells of Cajal?

The slow waves originate in the interstitial cells of Cajal (ICCs), located between the longitudinal and circular layers of muscularis externa – they are called the pacemaker cells for GI smooth muscle.


Describe the allosteric effects of AMP, glucose and ATP on glycogen phosphorylase.

Under certain circumstances, when AMP level is high (during muscle exercise), AMP directly binds to “b” form (dephosphorylated inactive), resulting protein conformational change to become an active form (irrespective of phosphorylation status), overriding the negative effect of ATP.

Similarly, when Glucose and ATP level are high (necrosis, trigger inflammatory and liver injury), they could directly bind to the active “a” form (phosphorylated active) to cause inactivity.


What effect will too much G6P have? (Allosteric effect on an enzyme)

Under certain circumstances (pathological situations such as GSDs), when glucose 6-phosphate is high, it directly binds to “b” form of glycogen synthase, cause conformational change to allosterically activate its activity.


How does cAMP affect liver and muscle differently?

will promote glycogen degradation in BOTH

will INHIBIT glycolysis in liver

will ACTIVATE glycolysis in muscle


Where do you see short pits and long glands? Long pits and short glands?

Describe sm. intestine.
Describe colon

gastric fundus/body- shallow pits and long branched tubular glands

in pylorus: long pits and short glands Upper glands-mostly parietal cells)

Small intestine (long villi; short crypts)

Colon- no villi but simple columnar absorptive cells with short microvilli. Lots of goblet cells. Crypts of Lieberkuhn

Slide 9/10 GI 5/6


What does alkaline tide refer to?

(cellular mech of gastric acid secretion)

In the basolateral membrane: HCO3- is absorbed into the blood via Cl- - HCO3- exchanger. This absorbed HCO3- is the reason for the “alkaline tide” (high pH) in gastric venous blood after a meal. This HCO3- is eventually secreted back in the GI tract by the pancreas.

Slide 21, GI 5/6


What does atropine, cimetidine, and omeprazole do?

Atropine (inhibits muscarinic receptors) blocks Ach effects on parietal cells.

Cimetidine blocks H2 receptors – blocks histamine effect.

omeprazole blocks H/K ATPase on apical membrane

GI5/6 slide 30



Brunner glands
Lieberkuhn glands
Paneth cells

Histological features of sm. intestine:

Brunner glands: cells secreting mucus and Bicarbonate. Its main physiological function is the secretion of alkaline-based mucus to protect the duodenal lining from the acid secreted in the stomach.

Lieberkühn glands: also Lieberkühn crypts,
secrete peptidases and enzymes that
digest carbohydrates.

Paneth cells reside at the bottom of villi and secrete antimicrobial peptides and enzymes (ribonuclease, esterases, etc.)


What's the significance of enterokinase?

activates trypsinogen to trypsin in the small intestine


Describe cystinuria.

transporter for dibasic amino acids (cystine, lysine, arginine, ornithine) is absent in small intestine and kidney - low or no absorption of these in intestine or kidney. The intestinal defect results in failure to absorb amino acids – excreted in feces. The renal defect results in increased excretion – thus called cystinuria.


What are the emulsifying agents in the stomach and small intestine?

In the stomach, lipid droplets are emulsified by dietary proteins.

In the small intestine, the primary emulsifying agents are bile acids


Pancreatic juice contains three important lipolytic enzymes that can work at neutral pH. Describe.

Pancreatic lipase
Phospholipase A2
Cholesterol ester hydrolase


What does cofactor colipase do?

Pancreatic lipase
Hydrolyzes triglycerides to monoglycerides and fatty acids.

Bile acids inactivate pancreatic lipase- which is overcome by an important cofactor colipase.

Colipase binds to both bile acids and lipase – anchors lipase to the fat droplet even in the presence of bile acids.


Descriibe lysolecithin.

Bile acids together with lysolecithin and products of lipid digestion surround and emulsify dietary lipids.

phospholipase A2 hydrolyzes phospholipids such as those present in cell membranes to lysolecithin and fatty acids.


What is the major site of Na absorption in the small intestine?

The jejunum is the major site of Na+ absorption in the small intestine.


Describe the differences between absorption in apical/basolateral membranes of ileum/jejunum.

The ileum contains the same transport mechanisms as jejunum.

It also has a Cl- - HCO3- exchange mechanism in the apical membrane.

It has a Cl- transporter (instead of HCO3- transporter) in the basolateral membrane.

Thus on the apical side, both H+ and HCO3- are secreted.

Thus on the apical side there is net movement of NaCl into the cell, which is then absorbed.

So in ileum, there is net absorption of NaCl and in the jejunum there is net absorption of NaHCO3.


What happens in cholera?

In diseases like Cholera, adenylyl cyclase is highly activated - fluid secretion by the crypt overwhelms the absorptive capacity of villus cells causing life-threatening diarrhea.

Secretory Diarrhea:

Secretory diarrhea (example in Cholera) is caused by excessive secretion of fluid by crypt cells.

The major cause of secretory diarrhea is overgrowth of enterohepatic bacteria – e.g. Vibrio cholerae or Escherichia coli.


Describe the absorption of B12.

-Vitamin B12 is released from food by pepsin in the stomach – binds to R proteins.
-In the duodenum, pancreatic proteases degrade R proteins – vitamin B12 transferred to intrinsic factor (IF), secreted by gastric parietal cells.
-Vitamin B12 -IF complex absorbed by a specific transport mechanism in the ileum.
-In gastrectomy, parietal cells are lost - IF is not released – no vitamin B12 absorption – can lead to pernicious anemia - vitamin B12 injection can prevent this.


What is Hirschsprung's disease?

Condition where a segment of the colon is permanently contracted –causing obstruction (usually diagnosed in infants).

Failure of enteric nervous system to develop properly – the effected area completely lacks the plexuses of enteric nervous system and associated ganglia.

Mutations in glial-derived neurotrophic factor, endothelin III and their receptors have been shown in these patients.

Surgical excision of the affected segment alleviates the symptoms.



classic hepatic lobule
portal lobule
portal acinus

Classic Hepatic Lobule- drains blood from portal vein and hepatic artery to the hepatic or central vein

Portal Lobule- drains bile from hepatocytes to the bile duct

Portal Acinus- supplies oxygenated blood to hepatocytes


When does jaundice become clinically manifest?

Jaundice becomes clinically manifest when total plasma bilirubin is >2 mg/dl (> 34 µM)


How could hemolytic anemia lead to jaundice?

heme degradation

Excess production of bilirubin (e.g. hemolytic anemia)

(Causes of hyperbilirubinemia)


What is another name for serotonin?

Where is it released from (what type of cells)?

What role does it play?

Serotonin (5-hydroxytryptamine or 5-HT)

released from enteric neurons, mucosal mast cells and specialized EECs called enterochromaffin cells regulate the contractile activity of smooth muscle cells in the GI system.


At what level must fasting blood glucose levels be maintained?

above 60mg/100mL (acute hypoglycemia causes neurological problems, coma and death)


In glycolysis which enzymes catalyze steps in which ATP is used? Which catalyze steps in which ATP is generated ?

It is important to note that the
first two enzymes (Hexokinase/glucokinase and PFK-1) utilize ATP, and the last two (Pyruvate
Kinase and Phosphoglycerate kinase) generate ATP.


Describe the role of alanine.

PK is inhibited by ATP and alanine.

- Alanine is an amino acid that increases in fasting mode.
- Alanine serves as a significant precursor for gluconeogenesis.


What can lead to hemolytic anemia?

The deficiency of glycolytic enzymes can lead to hemolytic anemia. Red blood cells burst, lose
hemoglobin, and you become anemic.

- A genetic deficiency of pyruvate kinase can lead to hemolytic anemia.


Why must NAD+ be regenerated? How? 3 ways.

NAD+ must be regenerated for glycolysis to continue

Lactate dehydrogenase (Cytosolic reaction)

Malate-aspartate shuttle (Cytosol and mitochondria)

Glycerol-phosphate shuttle (Cytosol and mitochondria)

This is because the mitochondrial inner membrane is impermeable to NADH.


How will low levels of cellular NADH affect lactate formation?

decrease lactate formation


Describe how a LDH deficiency will affect patients.

These patients cannot maintain moderate levels of exercise due to an inability to utilize glycolysis to produce ATP needed for muscle contraction under anaerobic conditions.

When lactate dehydrogenase levels are insufficient, the level of NAD+ becomes limiting during exercise and flux through the glyceraldehyde-3-P dehydrogenase reaction is inhibited.


What is the most common form of PDH deficiency? How is it inherited? How are other forms inherited?

What do children with PDH deficiency exhibit in serum levels? What is produced?

What does treatment include?

The most common form of pyruvate dehydrogenase deficiency is caused by mutations in the E1 alpha gene, and is inherited in an X-linked dominant manner

All other forms are caused by various genes and are inherited in an autosomal recessive manner.

Children with pyruvate dehydrogenase deficiency exhibit elevated serum levels of lactate, pyruvate and alanine, which produce a chronic lactic acidosis.

Treatment typically includes dietary supplementation with thiamine, carnitine, and lipoic acids.

Some patients have been treated with dichloroacetate, an inhibitor of the protein kinase subunit of pyruvate dehydrogenase complex.


Compare endocrine/exocrine pancreas.

Endocrine pancreas – islets of Langerhans (2% of pancreatic volume): insulin, glucagon, somatostatin (inhibitor of G stomach cells), pancreatic polypeptide;

Exocrine pancreas – (90% of pancreatic volume) - Secretion of enzymatic and aqueous components.


If gastrin increased after giving a secretin injection to assess for normal pancreatic function, what would this indicate?

normally gastric cells don't respond to secretin (bc secretin receptors in ductal cells) but bc these cells in pancreas they may have secretin receptors. and these cells v sensitive to secretin test. if gastrinoma and do secretin test gastrin goes way higher than normal.


What is the allosteric activator and inhibitor of Acetyl CoA Carboxylase?

Allosteric Activator: Citrate

Allosteric Inhibitor: Palmitoyl-CoA [long chain (C16-C18) fatty acyl CoA]


For transaminase reactions, (alpha-ketoglutarate as acceptor to form glutamate in urea reaction), what cofactor is necessary?

pyridoxal phosphate

(active derivative of Vit. B6


Urea is synthesized in the liver. However, amino acid metabolism also occurs in
tissues other than liver (e.g., muscle). Therefore, the nitrogen must be transferred to liver for conversion to urea. What are the main carriers of nitrogen to the liver?

Alanine (via the alanine-glucose cycle) and glutamine are the main carriers of nitrogen to the liver. These two are present in blood at higher
concentrations than other amino acids.


What does leflunomide treat and how?

Leflunomide, an immunosuppressive drug used to treat rheumatoid arthritis,
blocks pyrimidine biosynthesis by inhibiting dihydroorotate dehydrogenase.


What is kernicterus?

toxic encephalopathy when unconjugated bilirubin builds up beyond capacity of albumin to carry it (25mg/dL)


What initiates contractile activity in the small intestine?

initiated in response to distension of the bowel wall.

(peristalsis, segmentation, tonic contractions)


How can bacterial toxins cause diarrhea?

bacterial toxins specifically inhibit neutral NaCl absorption.

Toxins augment diarrhea by increasing salt and water secretion by intestinal crypt cells

(Oral rehydration involves utilizing the sodium glucose coupled co-transport pathway)


What is primary and secondary peristalsis in esophagus controlled by?

A primary peristaltic contraction (coordinated by swallowing reflex) occurs, involves a series of coordinated sequential contractions (peristaltic wave) - propels food down the esophagus.

Distension of the esophagus by the moving bolus initiates another wave called secondary peristalsis – (mediated by enteric nervous system) – repetitive secondary peristalsis clears the esophagus of the bolus.


What deficiencies are associated with microcytic anemia?

glucose-6-phosphatase deficiency is most common metabolic disorder of RBC and associated with microcytic anemia

result of reduced stores of iron


Where are iron, Ca, and folate primarily absorbed? amino acids?
most water and electrolyte absorption?


amino acids-jejunum

most water and electrolyte absorption occurs in jejunum


How will resection of the fundus affect rate of gastric emptying?

lessens vagal input (receptive relaxation/vago-vagal reflex) so increase in intragastric pressure in response to increase in intragastric volume

(intragastric pressure is primary det. of rate of liquid emptying of stomach) so there will be an increase in gastric emptying of liquids


Where does gas in colon come from?

gas in colon is derived primarily from fermentation of undigested material by intestinal bacteria to produce CO2, H2, and methane


Nearly all binding of cobalamin (vitamin B12) to intrinsic factor
occurs in which organ?