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:';-~
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•1 •
A 40-year-old man comes to the emergency department because of right upper quadrant pain and fever. During the abdominal examination, the
.2 patient Is instructed to breathe out while the examiner applies gentle pressure In the patient's right upper quadrant below the costal margin at the
mldclavlcular line. The patient is then instructed to breathe in. At this point, he winces and abruptly stops his inhalation.
•3

·4 What Is the function of the organ that likely needs to be removed?

•5
:
•6 A. Conjugation of bil e
.7
B. Production of bil e
·8
c. Production of coagulation factors
.9
• 10 D. Secretion of digestive enzymes

• 11 E. Storage of bile
• 12
• 13
• 14
• 15
• 16
• 17
. 18

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1 •
Th e co rrect an sw er i s E. 880/o chose this.
.2
The patient is suffering from acute cholecystitis, which is supported by his clinical presentation and positive Murphy sign on abdominal exam. The Inflamed
•3 gallbladder comes in contact with the examiner's hand on inspiration and elicits tenderness. Murphy sign is detected by first finding the exact location of
the gallbladder with the use of ultrasound imaging and then eliciting maximal point tenderness beneath the ultrasound probe with the application of
·4 pressure to the gallbladder. This patient will likely undergo cholecystectomy. The primary function of the gallbladder is the storage and concentration of
•5 bile, though there are minimal changes in digestion following cholecystectomy.
Cholecyste<tomy Cholecystitis Gallbladder Ultrasound Medical ultrasound B le '1u phy s sogn Digestion
•6
A i s not correct. 3% chose t his.
.7 Conjugation of bile occurs in the liver, where bile is conjugated with taurine or glycine to form bile salts, which are water-soluble and able to emulsify
·8 lipids. Since obstruction of cystic ducts by gallstones results in inflammation of the gallbladder in cholecystitis, removal of the liver is not necessary.
Cholecystitis Glycine Taurine Gallbladder Bile Liver Bile acid Gallstone Emo •s on Upod Inflammatoon Conjugated system
.9
B i s not co rrect. 5% chose th is .
• 10 Bile Is produced in liver hepatocytes, where primary bile acids are synthesized. They are then conjugated with taurine or glycine to form bile salts. In the
• 11 gallbladder, bile is concentrated as solutes and water are reabsorbed .
Taurine Glycine Gallbladder Bile acid Liver Bile Hepatocyte Conjugated system
• 12
C is no t co rrect . 20/o chose this •
• 13 Production of coagulation factors occurs in the liver, not the gallbladder. Liver Is not affected in the pathophysiology of cholecystitis and hence Its removal
• 14 Is not surgically necessary.
Cholecystitis Gallbladder Liver Coagulation Pathophysiology
• 15
D is no t co rrect. 20/o ch ose this .
• 16 The pancreas Is responsible for secreting enzymes, including trypsin, pancreatic lipase, pancreatic amylase, and chymotrypsin, to help with the digestion
• 17 of carbohydrates, protein, and fat .
Chymotrypsin Trypsin Pancreatic lipase Amylase Pancreas Carbohydrate Lipase Protein Digestion Enzyme
. 18

Bottom Line:
The gallbladder is responsible for the storage of bile. A positive Murphy sign supports a diagnosis of acute cholecystitis, which will require remova l of the
gallbladder.

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... w... .. w ... ..

1 Chymotrypsin Trypsin Pancreatic lipase Amylase Pancreas Carbohydrate lipase Protein Digestion Enzyme
. 2
•3
Bottom Line:
.4 The gallbladder is responsible for the storage of bile. A positive Murphy sign supports a diagnosis of acute cholecystitis, which will require removal of the
•5 gallbladder.
Cholecystitis Gallbladder Cholecystectomy Bile Murphy' s sign
•6
.7
•8
I iii I;fi 1!1 I•J for year:l 2017 ..
FI RST AI D FA CT S
•9
• 10
FA17 p 379.1
· 11
Gallstones t cholesterol and/or bil irubin, ~
bile salts, and Risk fa ctors (4 F's):
• 12
(cholelithiasis) gallbladder stasis all cause stones. L Female
• 13
2 types of stones: 2. Fat
• 14 • Cholesterol stones (radiolucent with 10- 20% 3. Fertile (pregnant)
• 15 opaque due to calcifications) - 80% of stones. 4. Forty
• 16 Associated with obesity, Crohn disease, Diagnose with ultrasound 11). Treat with elective
• 17
advanced age, estrogen therapy, multiparity, cholecystectomy if symptomatic.
rapid weight loss, ative American origin . Can cause fi stula between gallbladder and
• 18
Pigment stones rJ (black = radiopaque, Ca 2+ Gl tract - air in biliary tree (pneumobilia)
bilirubinate, hemolysis; brown= radiolucent, - passage of ga llstones into intestinal tract
infection). Associated with Crohn disease, - obstruction of ileocecal valve (gallstone
ileus).
..
chronic hemolysis, alcoholic cirrhosis,
'. . r . , .. '

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1 Altered mental status •

.2 Shock (hypotension)
•3
FA17 p 358.5
·4
•5 Bile Composed of bile salts (bile acids conjugated to glycine or taurine, making them water soluble),
•6 phospholipids, cholesterol, bilirubin, water, and ions. Cholesterol ?a-hydroxylase catalrzes
rate-limiting step of bile acid S}'nthe~is.
.7
Functions:
·8 Digestion and absorption of lipids and fat-soluble vitamins
.9 Cholesterol excretion (body's 1° means of eliminating cholesterol)
• 10 Antimicrobial activity (via membrane disruption)
• 11

• 12 FA17 p 353.1

• 13 Biliary structures Gallstones (Fill ing defects in gallbladder and cystic duct, red arrows in fJ) that reach the con Auencc
• 14 of the common bi le and pancreatic ducts at lhe ampulla of aler can block both the common bile
• 15 and pancreatic ducts (double duct sign), causing both cholangitis and pancreatitis, respectively.
• 16
Tumors that arise in head of pa ncreas (usuall)' ductal adenocarcinoma) can cause obstruction of
common bile duel-+ enlarged gallbladder with painless jaundice (Courvoisier sign).
• 17
. 18
Cystic duct ~
lJVer
Gallbladder-......_
- Common hepatic duct
-
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1 •
A 3-week-old boy is brought to the emergency department by his parents after a 1-week history of nonbilious vomiting . His parents report that the
.2 child spits up after meals much more frequently than his older brother did at this age and that the vomiting sometimes seems forceful.

•3
The section of the gastrointestinal tract affected in this condition typically plays a role in regulating which of the following parts of digestion?
·4
•5 :
A. Gastric aod production
•6
.7 B. Gastric emptying

·8 c. Prevention of food backflow into the esophagus

.9
D. Propulsion of food into the stomach
• 10
E. Swallowing
• 11

• 12
• 13
• 14
• 15
• 16
• 17
. 18

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1 Th e co rrect a nsw er i s B. 63% ch ose this. •

2 This patient presents with a history of classic pyloric stenosis, which Involves the pyloric sphincter, which controls passage of gastric contents Into the
duodenal bulb. This condition is much more common in male than in female Infants and usually develops between 3 and s weeks of age, and very rarely
•3 after 12 weeks. The patient presents with regurgitation and relentless projectile, nonbilious vomiting. On physical examination, visible peristalsis generally
can be seen, and a mass (commonly described as "olive" -like) usually can be palpated in the epigastric region. The normal role of the pylorus Is to limit
·4 the rate of gastriC emptying. This is accomplished by contracting in response to each peristaltic wave.
•5 Duodena ulb Peristalsis Pylorus Pyloric sphincter Pyloric stenosis Duodenum Steno~ s Epigastrium Regurgitation (digestion) Sphincter vomiting Palpation
Physica e· ami nation Stomach
•6
A i s not correct. 4% chose this.
.7
Gastric acid is secreted by parietal cells located in the gastric glands of the body and fundus of the stomach. Gastrin -induced histamine release Is the
·8 primary stimulus for acid production, but acetylcholine from the parasympathetic nervous system also plays a role. Add production is inhibited by the
hormone somatostatin. Dysfunctional add production would lead to impaired ability to break up food particles but does not lead to the projectile
.9 vomiting.
• 10 Somatostatin Gastric acid Histamine Acetylcholine Parasympathetic nervous system Parietal cell Gastric glands Hormone Vomiting Fundus (stomach) Parietal lobe
Stomach
• 11
C is not co rrect. 1 7 % chose t his •
• 12
The lower esophageal sphincter, located at the gastroesophageal junction, Is responsible for preventing backflow of food and acid from the stomach Into
• 13 the esophagus. If this sphincter fails to constrict completely, the patient may experience acid reflux accompanied by an epigastric burning sensation. In
Infants, If the lower esophageal sphincter does not form properly, it Is possible for stomach contents to back up into the esophagus and vomiting to
• 14 occur; however, this action is not projectile, as seen in classic pyloric stenosis.
• 15 Esophagus Gastroesophageal junction Gastroesophageal reflux disease Lower esophageal sphincter Pyloric stenosis Stenosis Sphincter Epigastrium vomiting
Cardia Pylorus Esophageal cancer Stomach
• 16
D is not co rrect. 120/o ch ose this .
• 17
The Inner circular and outer longitudinal muscle layers of the esophagus aid In esophageal motility. The peristaltic contractions of the esophagus help
. 18 propel food into the stomach. Dysregulation of this process can result In diffuse esophageal spasm, which can cause chest pain and dysphagia .
Dysphagia Esophagus Peristalsis Esophageal spasm Chest pain Motility Esophageal cancer Diffuse esophageal spasm Stomach Muscle

E i s not correct. 40/o chose this.

The process of swa llowing is initiated when touch receptors near the pharyngea l opening are stimulated, sending a signal to the swallowing center In the
medulla and lower pons. This center sends impulses to the muscles of the pharynx and esophagus, which then enact swallowing.

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1 The inner circular and outer longitudinal muscle layers of the esophagus aid in esophagea l motility. The peristaltic contractions of the esophagus help
propel food into the stomach. Dysregulation of this process can result in diffuse esophagea l spasm, which can cause chest pain and dysphagia .
2
Dysphagia Esophagus Peristalsis Esophageal spasm Chest pain Motility Esophageal cancer Diffuse esophageal spasm Stomach Muscle
•3
E is not correct. 4 % chose this .
.4 The process of swallowing is initiated when touch receptors nea r the pharyngeal opening are stimulated, sending a signal to the swallowing center in the
•5 m edulla and lower pons. This center sends impulses to the muscles of the pharynx and esophagus, which then enact swallowing.
Esophagus Pharynx Pons Medulla oblongata Somatosensory system Pharyngeal opening of auditory tube Receptor (biochemistry)
•6
.7
Bottom Line:
•8
Pyloric stenosis in infants presents with regurgitation and relentless projectile, nonbilious vomiting . On physical exa mination, peristalsis generally can be
•9 seen, and a m ass (commonly described as "olive" -like ) usually can be palpated in the epigastric region.
Peristalsis Pyloric stenosis Stenosis Regurgitation {digestion) Vomiting Epigastrium Palpation Pylorus Physical examination Regurgitation (circulation)
• 10

· 11
• 12
lijj ;fi IJ l•l for year:l 2017 ..
• 13 FIRST AID FAC T S

• 14
• 15 FA11 p 345.1

• 16 Hypertrophic pyloric Most common cause of gastric outlet obstruction in infants (1:600). Palpable olive-shaped mass in
• 17
stenosis epigastric region, visible peristaltic wm·es, and nonbilious projectile vomiting at - 2-6 weeks old.
More common in firstborn males; associated with exposure to macrolides. Results in hypokalemic
• 18
hypochloremic metabolic alkalosis (2° to vomiting of gastric acid and subsequent volume
contraction). Treatment is surgical incision (pyloromyotomy).

FA17 n !i61?

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1 •
FA17 p 345.1
2
•3 Hypertrophic pyloric f\1ost common cause of gastric outlet obstruction in infants (1:600). Palpable olive-shaped mass in
·4
stenosis epigastric region, visible peristaltic \\<1\ C~. and nonbilious projectile \'Omiting at - 2-6 \\ Ceks old.
.\tlore common in firstborn males; associated '' ith ex po~ure to macrolides. Results in h) pokalcmic
•5
hypochloremic metabolic alkalosis (2° to vomiting of gastric acid and subsequent ,·olume
•6
contraction). Treatment is surgical incision (p) loromyotomy).
.7
·8
FA17 p 561.2
.9
Acidosis and alkalosis
• 10
• 11 Check arterial pH
• 12 pH < 7.35 pH > 745
• 13 ( '\
Acidemia Alkalemia
• 14
• 15 Pco2 > 44 mm Hg HC03- < 20 mEq/L Pco2 < 36 mm H~o3- > 28 mEq/L
• 16
• 17 Respiratory
1
Metabolic acidosis
Respiratory
l
Metabolic alkalosis
acidosis alkalosis
. 18

Hypoventilation Check anion gap Hyperventilation H• lossiHCO,- excess

= Na• - (CJ +HC01 )
Airway obstruction Hysteria loop diuretics
Acute lung disease
........ _ . _ ... ___ .-.t...____
I -.. . .
Hypoxemia (eg. high altitude)
. .. Vomiting
~
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1 •
A 2-year-old boy is brought to the emergency department because of a fever of 40°C (104°F). He is m aking poor eye contact, displays limited
2 Interaction with his surroundings, and appea rs ill. Blood culture is positive for Streptococcus pneumoniae .

•3
Which of the following are cells in the liver that would help to clear this organism?
·4
•5 :
A. Alveolar macrophages
•6
.7 B. Kupffer cells

·8 c. Langerhans cells
.9
D. Mesangial cells
• 10
E. Microglia
• 11

• 12
• 13
• 14
• 15
• 16
• 17
. 18

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1 The co rrect a nswer is B. 84% cho se this.

2 The child has bacteremia. Ba cteremia, which is defined by presence of viable bacteria in the circulating blood, may result from simple daily activities such
as tooth brushing or from more complicat ed causes such as indwelling cathet ers, dental procedures, intravenous drug use or infections. Streptococcus
3 pneumoniae is a gram-positive, a-hemolytic diplococcus that may cause pneumonia, bacteremia, meningitis, and cellulitis. Ba cteria in the bloodstream
are typically destroyed by the reticuloendothelial system . Kupffer cells are reticuloendothelial cells found in the liver that would help to clear this organism
.4 from the bloodstream .
Streptococcus pneumoniae Bacteremia Meningitis Cellulitis Gram-positive bacteria Pneumonia Kupffer cell Streptococcus Intravenous therapy Bacteria
•5
Drug injection liver Mononuclear phagocyte system Catheter Circulatory system Diplococcus
•6
A is no t co rrect. 6 % cho se this.
.7
Alveolar macrophages are part of the reticuloendothelial system found in the lung. They are phagocytic cells and clear microorganisms from the
•8 circulation .
Alveolar macrophage Mononuclear phagocyte system Phagocyte Macrophage Phagocytosis Microorganism Pulmonary alveolus lung
•9
• 10
c is no t co rrect. 5 % cho se this •
Langerhans cells are involved in antigen uptake in the skin and travel to lymph nodes to present antigen to T-lymphocytes.
· 11 Antigen T cell langerhans cell lymph node lymph

• 12 D is no t co rrect. 3 % cho se this.

• 13 Mesangial cells are part of the reticuloendothelial system found in the spleen and kidney. They are phagocytic cells and clear microorganisms from the
circulation .
• 14 Spleen Phagocyte Mononuclear phagocyte system Phagocytosis Kidney Mesangial cell Microorganism

• 15 E is no t co rrect. 2 % cho se this.

• 16 Microglia cells are part of the reticuloendothelial system found in the brain. They are phagocytic cells and clear microorganisms from the circulation .
Microglia Mononuclear phagocyte system Phagocyte Phagocytosis Microorganism Human brain Brain
• 17

• 18
Botto m Li ne:
In bacteremia, Kupffer cells (reticuloendothelial cells found in the liver) help to clear pathogens from the bloodstream .
Bacteremia Kupffer cell liver Mononuclear phagocyte system Pathogen Circulatory system

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2
Bottom Line:
3
In bacteremia, Kupffer cells (reticuloendothelial cells found in the liver ) help to clear pathogens from the bloodstream .
.4 Bacteremia Kupffer cell liver Mononuclear phagocyte system Pathogen Circulatory system

•5
•6
.7 lijl;fiiJI•l foryear:[2017 • ]
FIRST AID FACTS
•8
•9 FA17 p 352.1

• 10 Liver tissue Apical surface of hcpatocytes faces bile Zone I- periportal zone:
· 11 architecture canaliculi. Basolateral surface faces sinusoids. • Affected 1st by viral hepatitis
• 12 Kupffer cells, wh ich are specialized • Ingested toxins (eg, cocaine)
macrophages, form the lining of these Zone TJ - intermed iate zone:
• 13
sinusoids (black arrows in t'J; 2 yellow arrows • Yellow fever
• 14
show hepatic venule). Zone 111-pericentral vein (centrilobular) zone:
• 15 Hepatic stellate (Ito) cells in space of Disse • Affected 1st by ischemia
• 16 store vitam in A (when qu iescent) and produce • Contains cytochrome P-450 system
• 17 extracellular matrix (when activated). • Most sensitive to metabolic toxins
• Site of alcoholic hepatitis
• 18
Sinusoids draining
to central vein ---~

Bile canaliculus
Kupffer cell
-< .............. ,..,, n:.-~...

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1 •
A 22-year-old college student presents to the emergency department with sudden-onset severe epigastric pain that radiates to the back. He has a
2 history of heavy alcohol abuse.

3 The organ involved in this patient's pathology plays a key role in normal gastrointestinal physiology. Under normal physiologic conditions, the organ Is
stimulated by a hormone secreted by the duodenum in response to acidic chyme present in the lumen.
.4
•5
What effect does this hormone have when it stimulates the organ of interest?
•6
.7 :
A. Insulin secretion
·8
B. Secretion of acid
.9
• 10 c. Secretion of bicarbonate

• 11 o. Secretion of bile
• 12
E. Secretion of intrinsic factor
• 13
• 14
• 15
• 16
• 17
. 18

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1 •

3 The correct an swer i s c. 73% chose this.

Secretin Is released from duodenal s -cells when acidic chyme from the stomach is present
4
In the duodenal lumen. Secretin acts on pancreatic duct cells to stimulate bicarbonate

--
•5 secretion. The diagram is an overview of the locations of GI secretory cells. GAP • ~·'"' 111 . . 19 pepll:il!t
AJ::'At =aoe.trUKAne

-----
Chyme S '< etin Pancreatic duct Secretin receptor Bicarbonate Duodenum Lumen anatomy1
GIP ·~----

--
-·
•6
Acid Secretion Stomach
.7 Stocnoch

·8 --·
GfOCIIIt•

•fOIWt••...a.
-.n.
.9
• 10 ........,.
• 11
GasiMIIO craAIIIOnl)
• 12 '--ecLcllt
• 13
A is not co rrect. so;o chose t his •
• 14
Insulin secretion is regulated by glucose levels in the blood. A rise in blood glucose results in glucose uptake into pancreatic j3 cells, facilitated by the
• 15 GLUT-2 glucose transporter. Metabolism of glucose generates ATP, increasing the Intracellular ATP/ADP ratio. This inhibits the activity of the ATP-sensltlve
K+ channel on the 13-cell membrane, leading to membrane depolarization and the Influx of Ca 2 + through voltage -dependent ca 2 + channels. Increased
• 16 Intracellular ca 2+ stimulates secretion of insulin .
Glucose transporter Glucose Depolarization Insulin signal transduction pathway Pulsatile insulin Adenosine triphosphate Insulin Blood sugar Metabolism
• 17
Intracellular Secretion
. 18
B i s n ot co rrect. JOfo ch ose this.
Parietal cells of the gastric fundus secrete acid in response to gastrin, histamine, and vagal acetylcholine release. Acid is not produced by the pancreas.
Gastric fundus Gastrin Histamine Acetylcholine Pancreas Parietal cell Vagus nerve Par'etal lobe Fundus (stomach)

D is not correct. 14% ch ose this.

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I
1
D is not correct. 14% chose this.
2 Cholecystokinin (CCK ) is produced and secreted by the I cells of the duodenum in response to small peptides and fatty acids from the stomach. CCK acts
3 to stimulate contraction of the gallbladder while simultaneously relaxing the sphincter of Oddi. This results in bile secretion. CCK is not released in
responsed to high acid levels and is therefore not correct.
4 Sphincter of Oddi Cholecystokinin Duodenum Gallbladder Bile Sphincter Fatty acid Peptide Cholecystokinin receptor Secretion Stomach

•5 E is not correct. 2 % chose this.

•6 Intrinsic factor is produced by parietal cells of the gastric fundus and not by the pancreas. It is important for vitamin B 12 absorbtion in the gut .
Intrinsic factor Gastric fundus Vitamin B12 Pancreas Parietal cell B vitamins Vitamin Fundus (stomach) Gastrointestinal tract
.7
•8
Bottom Line:
•9
Secretin primarily acts on the pancreas to stimulate secretion of bicarbonate .
• 10 Secretin Pancreas Bicarbonate

· 11
• 12
• 13 lijj ;fi IJ l•l for year: 2017 •
FI RST AI D FA CTS
• 14
• 15
FA17 p 357.1
• 16 Gastrointestinal secretory products
• 17 PRODUCT SOURCE ACTION REGULATION NOTES

• 18 Intrinsic fact or Parietal cel ls Vitamin B1rbincling Autoimmune destruction

(stomach) protein (required for B12 of parietal cells .... chronic
uptake in terminal ileum) gastritis and pern icious
anemia.
I ... t.,... .~.... ,..,...h .... u

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1 •

2 FA17 p 357.1
3 Gastrointestinal secretory products
4 PRODUCT SOURCE ACTION REGULATION NOTES

•5 Intrinsic factor Parietal cel ls Vitamin B1rbinding Autoimmune destruction

•6 (stomach) protein (required for B12 of parietal cells .... chronic
uptake in terminal ileum) gastritis and pernicious
•7
anemia.
•8
Gastric acid Parietal cells l stomach pH t by histamine,
•9
(stomach) ACh, gastrin
• 10 l by somatostatin,
· 11 GIP,
• 12 prostaglandin,
• 13
secretin
• 14 Pepsin Chief cells Protein digestion t by vagal Pepsinogen (inactive) is
(stomach) stimulation, converted to pepsin (active) in
• 15
local acid the presence of H+.
• 16
Bicarbonate Mucosal cells eutralizes acid t by pancreatic Trapped in mucus that covers
• 17
(stomach, and bilia ry the gastric epithelium.
• 18 duodenum, secretion with
sal ivary glands, secretin
pancreas) and
Brunner glands
(..J •• ,.. ..l .... .., ...- ' •

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1 •
FA17 p 357.2
2
locations of gastrointestinal secretory cells
3
4
Vagus nerve --<c-.:>">
•5 fundus

•6
.7 ACh
HC' - t
·8 Body
.9 Intrinsic-
factor
• 10
Pyl()(iC ~
• 11 sphincter ".
Pepsinogen H1stam1ne
~
• 12 CCK Somalo· Antrum .... .
• 13
!eels t J statm
Mucus
J
• 14
• 15
• 16
Scells '\
Secretm Ju de ~um
'•
Mt.:cous
cells
GRP
•
G tc 15
......_ Gastrin
(to Circulation)
/
__.1¥
. ~ ECL cells

. _GIP
• 17 Kcells
. 18

Gastrin t acid secretion primarily through its effects on enterochromaffin-like (ECL) cells (leading
to histamine release) rather than through its direct effect on parietal cells.

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2
A 42-year-old mother of five comes to a primary care physician complaining of acute pain in her abdomen for 3 days that is most pronounced after
meals. She is afebrile, her vital signs are stable, and her body mass index Is 34 kg/m• . On physical examination she has tenderness to palpation with
lA• A] •
voluntary guarding under the rib cage on the right side. Ultrasound confirms the diagnosis. The patient is counseled on surgical options as well as
3 lifestyle modifications.
4
•5 Which pair correctly matches the type of food the patient should avoid with the function of the hormone that is causing her abdominal pain?

•6 :
A. High-carbohydrate foods; inhibits gastric add secretion
.7
·8 B. High-carbohydrate foods; stimulates gastric add secretion

.9 c. High-fat foods; increases gastric motility

• 10
o. High-fat foods; stimulates gallbladder contraction
• 11
E. High-fat foods; stimulates pancreatic bicarbonate secretion
• 12
• 13 F. High-protein foods; inhibits gastric emptying

• 14
• 15
• 16
• 17
. 18

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3
The co rrect a nswer is D. 8 5 % cho se this.
4 The patient has gallstones (cholelithiasis), as supported by her clinical presentation, ultrasound diagnosis, and risk factors (the " 4 F's": Female, Fat,
5 Fertile, and Forty years old or older ). The gallbladder typically holds bile acids and lecithin, used to solubilize cholesterol and/or bilirubin. When these
solubilizing substances are overwhelmed by high concentrations of either cholesterol and/or bilirubin, precipitants form and eventually make gallstones.
•6 Ea ting high-fat foods stimulat es the relea se of cholecystokinin (CCK ) by I cells of the duodenum and j ejunum. CCK has multiple functions in the
gastrointestinal tract including stimulation of gallbladder contraction . This can cause increa sed pain in gallstone sufferers. CCK also stimulat es pancrea tic
.7 enzyme secretion and inhibits gastric emptying.
•8 Gallstone Bilirubin Jejunum Cholecystokinin Duodenum Gallbladder lecithin Enzyme Human gastrointestinal tract Cholesterol Gastrointestinal tract Bile Bile acid

Ultrasound Pancreas Medical ultrasound Secretion Stomach

•9
A is no t co rrect. 2% cho se this •
• 10
Secretin, which inhibits gastric acid secretion, does not have a direct effect on the gallbladder like cholecystokinin does. It is stimulat ed by an increa se in
· 11 acid or fatty acids in the lumen of the duodenum, and is not stimulat ed by high-carbohydrat e foods.
Secretin Cholecystokinin Duodenum Gastric acid Gallbladder lumen (anatomy) Fatty acid Secretion
• 12
B is no t co rrect. 4 % cho se this •
• 13
Ga strin does not directly affect the gallbladder. Its relea se is stimulat ed by gastric distention, amino acids, peptides, and the vagus nerve, so high-
• 14 carbohydrat e foods would not be expected to significantly stimulat e its relea se.
Gastrin Gallbladder Vagus nerve Amino acid Peptide
• 15
• 16
c is no t co rrect. 4 % cho se this •
Ga strin secretion by the G cells of the antrum of the stomach stimulat es the secretion of stomach acids as well as increa ses gastric motility. Unlike
• 17 cholecystokinin, gastrin does not have a direct effect on the gallbladder.
Cholecystokinin Gastrin Gallbladder G cell Pyloric antrum Antrum Secretion Stomach
• 18
E is no t co rrect. 3 % cho se this.
High-fat foods are to be avoided in gallstone sufferers, but to prevent the relea se of cholecystokinin, not secretin . Secretin is stimulat ed by acid and fatty
acids in the duodenum and is secret ed by s cells of the duodenum. It stimulat es pancrea tic bicarbonat e secretion to neutralize stomach acids and inhibits
gastric acid secretion .
Gallstone Secretin Cholecystokinin Duodenum Gastric acid Bicarbonate Fatty acid Secretion Stomach

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cholecystokinin, gastrin does not have a direct effect on the gallbladder.

1
Cholecystokinin Gastrin Gallbladder G cell Pyloric antrum Antrum Secretion Stomach
2
E is not correct. 3% chose this.
3 High-fat foods are to be avoided in gallstone sufferers, but to prevent the relea se of cholecystokinin, not secretin . Secretin is stimulat ed by acid and fatty
4 acids in the duodenum and is secret ed by s cells of the duodenum. It stimulat es pancrea tic bicarbonat e secretion to neutralize stomach acids and inhibits
gastric acid secretion .
5 Gallstone Secretin Cholecystokinin Duodenum Gastric acid Bicarbonate Fatty acid Secretion Stomach

•6 F is not correct. 2 % chose this.

.7 High-fat, not high-protein, foods should be avoided to decrea se cholecystokinin (CCK ) relea se. Although amino acids also regulat e CCK secretion, fatty
foods have a grea t er effect on its relea se. CCK inhibits gastric emptying.
•8 Cholecystokinin Amino acid Stomach CCK Secretion

•9
• 10 Bottom Line:
· 11 Gallstone risk factors include the " 4 F's." Cholecystokinin, which stimulat es gallbladder contraction, causes increa sed pain in patients with gallstones.
Gallstone Cholecystokinin Gallbladder
• 12
• 13
• 14
I ill ;fi 1!1 I•J for year:[ 2017 ..
• 15 FI RST AI D FA CTS

• 16
• 17 FA17 p356.1
Gastrointestinal regulatory substances
• 18
REGULATORY SUBSTANCE SOURCE ACTION REGULATION NOTES

Gastrin G cells (antrum t gastric H+ secretion t by stomach t by chronic PPl use.

of stomach, t growth of gastric mucosa distention/ t in ch ronic atrophic gastritis
duodenum) t gastric motil ity alkalinization, (cg, H pylori).

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•
1
2
I ill ;fi 1!1 I•J for year:[ 2017
FI RST AID FAC TS
•I
3
4 FA17 p356.1
Gastrointestinal regulatory substances
5
REGULATORY SUBSTANCE SOURCE ACTION REGULATION NOTES
•6
Gastrin G cells (antrum t gastric H+ secretion t by stomach t by chronic PPl use.
•7
of stomach, t growth of gastric mucosa distention/ t in chronic atroph ic gastritis
•8 duodenum) t gastric motility alkalinization, (cg, H pylori).
•9 amino acids, t t in Zollinger-Eilison
0 10
peptides, vagal syndrome (gastrinoma).
stimulation via
· 11 gastrin-releasing
• 12 peptide (GRP)
• 13 ~ by pH< 1.5
• 14 Somatostatin D cells ~ gastric acid and t by acid Jn h ibits secretion of various
(pancreatic islets, pepsinogen secretion ~ by vagal hormones (encourages
0 15
Gl mucosa) ~ pancreatic and small stimulation somato-stasis). Octreotide
• 16
intestine Auid secretion is an analog used to treat
• 17 ~ gallbladder contraction acromegaly, carcinoid
• 18 ~ insuli n and glucagon syndrome, and variceal
release bleeding.
Cholecystokinin J cells (duodenum, t pancreatic secretion t by fatty acids, Acts on neural muscarinic
jejunum) t gallbladder contraction amino acids pathways to cause pancreatic
~ gastric emotving secretion. •

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1 •
Ghrelin Stomach t appetite f in fasting slate f in Prader-Willi syndrome.
2 l by food l after gastric bypass surgery.
3
4 FA17 p 358.1
5
Pancreatic secretions Isotonic Auid; lo\\' Aow - high Cl-, high Oo" - high I IC0 3-.
•6
ENZYME ROLE NOTES
.7
a -amylase Starch digestion Secreted in acti,·e form
·8
lipases Fat digestion
.9
Proteases Protein digestion Includes trypsin, chymotrypsin, elastase,
• 10
carbox} peptidascs
• 11
Secreted as proenzymes also known as
• 12 zymogens
• 13 Trypsinogen Converted to active enzyme trypsin Converted to trypsin by enterokinase/
• 14 - <•ctivation of other procnzpn cs and clcaving cnteropcptidasc, a brush-border enzyme on
• 15 of additional trypsinogen molecules into active duodenal and jejunal mucosa
• 16
trypsin (positive feedback loop)

• 17
. 18 FA17p379.1

Gallstones f cholesterol and/or bil irubin, l bile salts, and Risk factors (4 F's):
(cholelithiasis) gallbladder stasis all cause stones. 1. Female
2 types of stones: 2. Fat
r.hf\lPd Prf\1 df\nP< fr<ll'l i" l""""' "'ilh IO_JOCZ. ~ I"PrtilP fnrPun 01 nt\

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1 •
FA17p379.1
2
Gallstones t cholesterol and/or bil irubin, ! bile salts, and Risk factors (4 F's):
3
(cholelithiasis) gallbladder stasis all cause stones. 1. Female
4
2 trpes of stones: 2. Fat
5 • C holesterol stones (radiolucent with 10-20% 3. Fertile (pregnant)
•6 opaque due to calcificat ions)-80% of stones. 4. Forh
.7 Associated with obesitv,
•
Crohn disease. Diagnose with ultrasound rn.Treat\\ ith electi\ e
·8
ad,·anced age, estrogen thcrapr. multiparitr. cholecystectomr if srmptomatic.
rapid weight loss, 'ativc mcricm1 origin. Can cause fistula between gallbladder and
.9
Pigment stones fJ (black = radiopaque, Ca 2+ Gl tract - air in biliary tree (pneumobilia)
• 10
bilirubinate, hemolysis; brown= radiolucent, - passage of gallstones into intestinal tract
• 11 infection). Associated with Crohn disease, - obstruction of ileocecal vah-e (gallstone
• 12 chronic hemolysis, alcoholic cirrhosis, ileus).
• 13
advanced age, biliary infections, total
parenteral nutrition (TP1 ).
• 14
I\ lost common compli ct~ti on is cholecystitis;
• 15
can also cause acute pancreatitis, ascending
• 16 cholangitis.
• 17
RELAlED PATHOLOGIES CHARACTERISTICS
. 18 Biliary colic Associated with nausea/vomiting and dull RUQ pain. 1 eurohormonal activation (eg, by CCK after
a fatty meal) triggers contraction of gallbladder, fo rcing stone into cystic duct. Labs arc normal,
ultrasound shows cholelith iasis.
Choledocholithiasis Presence of gallstonc(s) in common bile duct, often leading to eb ·ated ALP, GGT, direct bilirubin,

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1
A 34-year-old man comes to his physician complaining of worsening heartburn and reflux . He has been t aking over-the-counter ranitidine but feels he
needs a stronger prescription.
IA•A] •
2

3
What Is the mechanism of action of ra nitidine?
4
5 :
A. Binds to the gastrin receptor on parietal cells
•6
.7 B. Binds to the M3 -receptor

·8 C. Binds to the prostag land in receptor

.9
D. Binds to the somatostatin receptor
• 10
E. Inhibition of a G5 -coupled receptor
• 11

• 12
• 13
• 14
• 15
• 16
• 17
. 18

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1 The co rrect a nswer is E. 56 % cho se this.

2 Ranitidine belongs to the class of drugs t ermed H2 -receptor antagonists. Other H2 -receptor antagonists include famotidine and cimetidine. They bind to
H 2 -receptors on pariet al cells to block the receptors' interaction with histamine. This lea ds to an inhibition of G 5 -coupled receptor; resulting in decrea sed
3 downstream cAMP and acid production.
Cimetidine Ranitidine Famotidine Histamine Parietal cell Cyclic adenosine monophosphate
4
A is no t co rrect. 20 % cho se this.
5
There is no known inhibitor for the gastrin receptor.
6 Gastrin Receptor (biochemistry)

.7 B is no t co rrect. 11% cho se this.

•8 Anticholinergics such as atropine bind to the M3 -receptor to block its interaction with acetylcholine, which stimulat es acid secretion .
Atropine Acetylcholine Anticholinergic Secretion
•9
c is no t co rrect. 7 % cho se this •
• 10 Prostaglandins bind to the prostaglandin receptor on pariet al cells and decrea se acid secretion .
· 11 Prostaglandin receptor Prostaglandin Parietal cell Receptor (biochemistry) Secretion

• 12 D is no t co rrect. 6 % cho se this •

There are no known inhibitors of the somatostatin receptor.
• 13
Somatostatin Somatostatin receptor Receptor (biochemistry)
• 14
• 15
Botto m Li ne:
• 16
Ranitidine is an H2 -blocker that reversibly blocks histamine H2 -receptors to decrea se hydrogen ion secretion by pariet al cells, and thereby relieves
• 17 symptoms of heartburn and reflux .
Ranitidine Histamine Heartburn Parietal cell Gastroesophageal reflux disease Hydrogen Secretion
• 18

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FI RST AI D FA CTS

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2
Bottom Line:
3
Ranitidine is an H2 -blocker that reversibly blocks histamine H2 -receptors to decrease hydrogen ion secretion by parietal cells, and thereby relieves
4 symptoms of heartburn and reflux.
Ranitidine Histamine Heartburn Parietal cell Gastroesophageal reflux disease Hydrogen Secretion
5
6
.7
I iii I;fi 1!1 I•J for year:l 2017 ..
•8 FI RST AI D FA CTS

•9
FA17 p 381 .2
• 10

· 11 H2 blockers C imetidine, ranitidinc, famotidinc, nizatidinc. Take Hz blockers before you dine. Think "table
for 2" to remember 112 .
• 12
• 13
MECHANISM Reversible block of histamine l-Iz-receptors - l l-J+ secretion by parietal cells.
• 14 CLINICALUSE Peptic ulcer, gastritis, mild esophageal reflux.
• 15 ADVERSE EFFECTS Cimetidine is a potent inh ibitor of cytochrome P-450 (multiple drug interactions); it also has
• 16
antiandrogenic effects (prolactin release, gynecomastia, impotence, l libido in males); can
cross blood-brain barrier (confusion, dizzi ness, headaches) and placenta. Both cimetidine and
• 17
ranitidine l renal excretion of creatinine. Other Hz blockers are relati,·ely free of these effects .
• 18

FA17 p 357.1
Gastrointestinal secretory products
PROOUCT SOURCE ACTION REGULATION NOTES

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1 ran itidine l renal excretion of creatinine. Other 11 1 blockers are relati,·elr free of these effects. •

3 FA17p357.1
4 Gastrointestinal secretory products
5 PRODUCT SOURCE ACTION REGULATION NOTES

6 Intrinsic factor Parietal cells itamin B12-binding Autoimmune destruction

0 7 (stomach) protein (required for B12 of parietal cells .... chronic
uptake in terminal ileum) gastritis and pernicious
o8
anem1a.
.9
Gastric acid Parietal cells l stomach pll I by histamine,
• 10
(stomach) ACh, gastrin
• 11 l by somatostatin,
• 12 C IP,
• 13 prostaglandin,
0 14
secretin
• 15
Pepsin Chief cells Protein digestion I by vagal Pepsinogen (inactive) is
(stomach) stimulation, converted to pepsin (active) in
0
16
loca I acid the presence of H+.
0
17 1
Bicarbonate Mucosal cells eutral izcs acid I by pancreatic Trapped in mucus that covers
. 18
(stomach, and biliary the gastric epithel ium.
duodenum, secretion with
saJi,·ary glands, secretin
pancreas) and
n

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1 •
An 8-year-old boy presents to the emergency department because of 18 hours of severe vomiting . Arterial blood gas analysis reveals a pH of 7.48, a
2 HCo 3 - level of 35 mEq/L, and a partial carbon dioxide pressure (Pco 2 ) of 48 mm Hg.

3
What Is the type of acid-base disturbance occurring in this patient?
4
5 :
A. Metabolic alkalosis and metabolic addosis
6
0 7 B. Metabolic alka losis and respiratory addosis

o8 c. Metabolic alka losis and respiratory alka losis

.9
D. Metabolic alka losis w ith respiratory compensation
• 10
E. Respiratory al kalosis
• 11

• 12 F. Respiratory alkalosis with metabolic compensation

• 13
0 14
• 15
0
16
0
17
. 18

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1 •

2
Th e correct a n sw er i s D. 650/o chose this.
3 This patient is presenting with alkalosis (normal arterial pH is 7.35-7.45). The Hco3- level is substantially elevat ed(> 11 m Eq/L above normal), which
suggests that the patient is experiencing m et abolic alka losis. This alkalosis Is caused by the patient's recent history of severe vomiting. The vomiting
4
causes a loss of hydrochloric acid from the gastrointestinal tract; this acid must be replaced, which triggers a respiratory compensation. Through
5 hypoventilatlon, the Pco 2 rises and generates carbonic acid, which aids In lowering and normalizing the pH. This expected Pco 2 can be quantified with the
formula (expected Pco 2 = (0.7 x HCo 3 - ) + 20 ± 5). The patient's Pco 2 is 48, which 1s w1thin the predicted range (39.5- 49.5).
6 Hyd ochlo••c ac•d Metabolic alkalosis carbonic acid PH Respiratory compensation Hy• >011ent 1ation Gastrointestinal tract Alkalosis Vomiting
7 H •man ga ointestinal tract Metabolism

·8 A i s not correct. 3% chose this.

.9 Vomiting typically induces a metabolic alkalosis due to a loss of H+ from the stomach, leading to an increase in pH. This leaves an increased Hco3-
concentratlon (generally >24 m Eq/ L) in the bloodstream; therefore, this patient does indeed have a metabolic alkalosis. However, some patients present
• 10 with more than one condition causing an acid -base imbalance, which Is known as a complicated, or mixed, condition. If a metabolic acidosis were
occurring simultaneously (such as in ketoacidosis or diarrhea), the HCo3- level would be closer to normal because the two processes would have opposing
• 11 effects on HCo3- levels and effectively cancel each other out. Therefore, there Is no evidence of a concomitant m etabolic acidosis in this vignette.
• 12 Metabolic alkalosis Metabolic acidosis Diarrhea Ketoacidosis Vomiting Alkalosis Acidosis Stomach Circulatory system Metabolism

• 13 B is not co rrect. 2 1 Ofo chose this •

This patient has a metabolic alkalosis, as evidenced by the increased pH with Increased HC0 3 -level. Pco 2 is elevat ed as well, indicating that appropriate
• 14 respiratory compensation is occurring. If a simultaneous respiratory acidosis were occurring, the Pco 2 would be even higher than anticipated, based on
• 15 normal compensatory mechanisms. Therefore, there is no evidence of a concomitant respiratory acidosis in this vignette. Generally, Pco 2 should rise by
0. 7 mm Hg for every 1-m Eq/l increa se in HC03- level. So if C02 levels Increase by more than that, a coexistent respiratory acidosis should be suspected .
• 16 Respiratory acidosis Metabolic alkalosis Respiratory compensation PH Alkalosis Acidosis Metabolism
• 17 C is not co rrect. aoto ch ose this.
. 18 This patient has an alkalosis, as evidenced by the elevated pH with increased HCo3- . Pco 2 is elevated as well, indicating that there is appropriate
respiratory compensation occurring. I f a simultaneous respiratory alkalosis were occurring, the Pco 2would be normal (mea ning there is a failure of
respiratory compensatory mechanisms) or it would be decreased. Therefore, there is no evidence of a concomitant respiratory alkalosis in this vignette. In
an Isolated metabolic alkalosis, respiratory compensation should occur. If It does not or if Pco 2 is low, a concurrent respiratory alkalosis should be
suspected.
Respiratory alkalosis Metabolic alkalosis Respiratory compensation PH Alkalosis Metabol•sm Bicarbonate

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1 C is not co rrect . aoto ch ose this. •

This patient has an alkalosis, as evidenced by the elevated pH with Increased HCo3-. Pco 2 is elevated as well, indicating that there is appropriate
2 respiratory compensation occurring. If a simultaneous respiratory alkalosis were occurring, the Pco 2 would be normal (meaning there is a failure of
3 respiratory compensatory mechanisms) or it would be decreased. Therefore, there is no evidence of a concomitant respiratory alkalosis in this vignette. In
an Isolated metabolic alkalosis, respiratory compensation should occur. If It does not or if Pco 2 is low, a concurrent respiratory alkalosis should be
4 suspected.
Respiratory al alosis "'etabol c alkalosis Respiratory compensation PH Alkalosis Metaool.sm Bicarbonate
5
E i s not correct. 1% chose t his.
6
Respiratory alkalosis results from increased respiration or hyperventilation, which Incr eases the blood pH. However, the patient's Pco 2 is >40 mm Hg,
7 suggesting that his symptoms are not caused by hyperventil ation.
Resp•ratory a• alosis Hyperventilation Alkalosis Cellular respiration Respiration 1phys1ologYJ
·8
F i s not correct. 2 % chose this.
.9
Respiratory alkalosis would result in the elevated pH seen in this patient, but would also cause a decreased Pco 2 of <40 mm Hg. Metabolic compensat ion
• 10 occurs to lower the blood Hco3 - levels by having the kidney excrete more HCo3 -.
Respiratory alkalosis PH Alkalosis Kidney
• 11

• 12
• 13 Bottom Li ne:

• 14 Severe vomiting can cause metabolic alkalosis because of loss of hydrochloric acid from the gastrointestinal tract . This increa se in p H will generally be
counteracted by a decrease in respiratory rat e, which will serve to decrease pH In the form of carbonic acid . A structured way to address acid-base
• 15 questions Is to look at the p H first to cat egorize the disorder as alkalosis or acidosis, and then to examine the Pco 2 levels to see if there Is
compensation .
• 16 Metabolic alkalosis Hydrochloric acid Carbonic acid PH Gastrointestinal tract Alkalosis Human gastrointestinal tract Vomiting Acidosis Respiratory rate Metabolism
• 17
. 18
ljl;fil!1j•J f o r yea r : 2017 •
FIRST A I 0 FAC T S

FA17o 561 .1

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1 •

2 FA17p561 .1
Acid-base physiology
3
pH P<Oz IHC01 I COMPENSATORY RESPONSE
4
5
Metabolic acidosis J J J llyper.·entilation (immediate)
6 Metabolic alkalosis t t t I lypo,entilation (immediate)
7 Respiratory acidosis J t t t renal (I-IC03-J reabsorption (delayed)
·8 Respiratory alkalosis f J J l renal [HC03-Jreabsorption (delayed)
.9 Ke): t l = I" disturbance; l t =compensatory response.
• 10
. [IICO -]
• 11 Henderson-Hasselbalch eqtwhon: pi I = 6. 1 +log _ P~Oz
0 03
• 12
• 13 Predicted respiratory compensation for a simple metabolic acidosis can be calculated using the
Winters formula. If measured Pco2 > predicted Pco2 - concomitant respirator)' acidosis; if
• 14
measured Pco2 < predicted Pco2 - concom itant respiratory alkalosis:
• 15
Pco2 = 1.5 IHC03-J+ 8 :!: 2
• 16
• 17
. 18 FA17 p 561 .2

Acidosis and alkalosis

Check arterial pH
nH<H~ nH > 74~

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Cal culat o r

1 •
FA17 p 561 .2
2
Acidosis and alkalosis
3
4 Check arterial pH
5 pH< 7.35 pH > 745
6
Ac.idemia Alkalemia
7
·8
.9
• 10 RespiratOf}' Respiratory
MetaboUc acidos1s Metabolic alkalOSIS
• 11
acidosis alkalosis

• 12
Hypowntilation Check anion gap Hyperventilation H• loss/HC0 1- excess
• 13 =Na • - (CI- t HCO; l
Airway obstruction Hysteria loop diuretics
• 14 Acute lung disease Hypoxemia (eg, high altitude) Vomiting
Chronic lung disease Salicylates (early) Antacid use
• 15
Opioids, sedatives Tumor Hyperaldosteronism
• 16 Weakening of respiratory Pulmonary embolism
muscles
• 17
. 18
> 12 mEq/L 8-12 mEq/l
Pco •
I 45 40 mm Hg
40 Resporatory
Nonnal anion gap acidosis

-
I Anion gap
U lli\OU I:C· UAonacc. ~ 35

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1 •
A 10-year-old boy stayed home from school today because he is extremely nauseated and vomited six times overnight.
2

3 Choice pH Pco HCOt.

2
4
5 A <7.4 low low
6
B <7.4 high high
7
·8 c >7.4 low low
.9
D >7.4 low high
• 10
E >7.4 high high
• 11

• 12
• 13 Which of the following set of laboratory values would most likely be found In this patient?

• 14 :
A
• 15
• 16 B
• 17
c
. 18
0

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1 •
Th e co rrect a n swer i s E. 530/o chose this.
2 Metabolic alkalosis is characterized by a pH > 7.4 and high [HC03-) due to loss of hydrogen ions in gastric acid, or a direct increa se in [HC0 3T Excessive
vomit ing causes a loss of hydrochloric acid from the stomach and is a common cause of metabolic alkalosis. I n response to the alkalosis, the respiratory
3 system compensates by decreasing vent ilation, which increases the PC02, and lowers the pH. Other causes of m eta bolic alkalosis include diuretic or
4 antacid use and hyperaldosteronism.

5 Notably, vomiting-induced metabolic alkalosis, even if severe enough to cause hypovolemia, is NOT a true contra ction alkalosis. That term refers to the
excessive loss of bicarbonate-poor fluid, such as in overdiuresis, that artifici ally Increases the [Hco 3·] by keeping a simil ar absolute amount of Hco3· In
6 the serum whil e removing free wat er. Vomit ing -induced metabolic alkalosis as In this case results from foss of hydrog en-rich fluid and is therefore a
d ifferent pathophysiolog ic process and cannot be appropriately termed contraction alkalosis.
7
Antacod e abohc ao .aoosis Hypovolemia Hydrochloric acid Diuretic Gastric acid PH •omiting A .alosis Hyperaldosteronism Blood plasma Stomach Metabolism
8 Hyd ogen Hydronium Respiratory system
.9
A is not correct. 7% chose this .
• 10 Th is profile represents metabolic acidosis, which can be anion gap or non-anion gap. pH is low due to increased levels of H+ or other acid. Hco3· Is low
because It Is used to buffer excess H+. PC02 is low as a result of respiratory compensat ion for the increased levels of acid. causes of anion gap metabolic
• 11
acidosis can be recalled using the mnemonic MUDPILES (Methanol, u rem ia, Diabetic ketoacidosis, Pa raldehyde/phenformin, I ron/ isoniazid, Lactic
• 12 acidosis, Ethylene glycol, and Salicylat es), and causes of non -anion gap metabolic acidosis include diarrhea, glue sniffing, renal tubular acidosis, and
hyperchloremia .
• 13 Metabolic acidosis Anion gap Respiratory compensation Renal tubular acidosis Ethanol PH Diarrhea Acidosis Ketoacidosis Hyperchloremia Intoxicative inhalant
• 14 Anion Mnemonic Metabolism Kidney

• 15 B is not co rrect . 50fo chose this .

• 16 This profile represents respirat ory acidosis, which is commonly caused by hypoventilation (chronic obstructive pulmonary disease, paralysis of respiratory
muscles, opfolds, or airway obstruction ). The PC02 is high due to the decreased respiratory rate, which increases t he level of acid in the blood, causing a
• 17 low p H. The HC03- will increase t o com pensate for t he increa sed carbon dioxide/acid levels in the blood .
Respiratory acidosis Chronic obstructive pulmonary disease Hypoventilation Respiratory rate Acidosis Respiratory tract Opioid Airway obstruction Paralysis
. 18
Respiratory disease Pulmonology

C i s n ot correct. 120/o ch ose this.

This profile represents respiratory alkalosis, most commonly caused by hyperventilation (anxiety, acute pain, or alt it ude). The Pco 2 is low due to the
Increased respiratory rate, which decrea ses t he level of acid in the blood, causing a high pH. The Hco3· will decrease t o compensate for decreased carbon
rlinxirlP/ ilrirl IPVPI<; on thP hlnnrl.

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. . ..... .- ... - .
Respiratory acidosis Chronic obstructive pulmonary disease Hypoventilation Respiratory rate Acidosis Respiratory tract Opioid Airway obstruction Paralysis
2 Respiratory disease Pulmonology

3 C is n ot correct. 120/o ch ose this.

4 This profile represents respiratory alkalosis, most commonly caused by hyperventilation (anxiety, acute pain, or altitude). The Pco 2 is low due to the
Increased respiratory rate, which decreases the level of acid in the blood, causing a high pH. The Hco3 • will decrease t o compensate for decreased carbon
5 dioxide/ acid levels in the blood.
Respirato f a1 .alosis Hyperventilation Respiratory rate Alkalosis An ... oety
6
0 is not correct. 230/o chose this.
7
This profile represents mixed respiratory and metabolic alka losis in which the pH Is high due to decreased leve ls of C0 2 from increased respiratory rate as
8 well as Increased levels of HCo3 ·.
Metabolic a alosis PH Resporatory rate Alkalosis Metabolism
.9
• 10
• 11 Bottom Line:

• 12 Metabolic alkalosis, commonly due to excessive vomiting and hydrogen ion loss, is characterized by an increase in pH > 7.4 and elevated plasma
(HC03·]. In response to the increased pH, the respiratory system compensates by decreasing ventilation and increasing the Pco 2 .
• 13 Metabolic alkalosis Hydrogen ion PH Alkalosis Blood plasma Respiratory system Vomiting Ion Metabolism Hydrogen Ventilation (physiology)

• 14
• 15
• 16 laJ;fil;1i•J to r yea r: 20 17 ..
FIRST AIO FAC TS
• 17
. 18 FA17 p 561 .2

Acidosis and alkalosis

Check arterial pH

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Cal culat o r

1 •

2 FA17 p 561 .2

3 Acidosis and alkalosis

4
Check arterial pH
5
pH< 7.35 pH > 745
6
7 Acidemia Alkalemia
8
Pco2 < 36 mm Hg
.9
• 10
Respiratory Respiratory
• 11 Metabo~c acidosis Metabolic alkalosas
acidosis alkalosis
• 12
• 13 Hypovtntit.tion Check anion gap Hyptrvtntit.tion H• loss/HC0 1- excess
Airway obstruction
=Na' - {CI- +HCO; l
• 14 Hysteria loop diuretics
Acute lung disease Hypoxemia {eg, high altitude) Vomiting
• 15 Chronic lung disease Sallcylates {early) Antacid use
Opioids, sedatives Tumor Hyperaldosteronism
• 16
Weakening of respiratory Pulmonary embolism
• 17 muscles

. 18

> 12 m£q/L 8-12 m£q/l

I 45
40 Resporatory
I Anion gap Normal anion gap acadosls
~ 35

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 Lactic acidosis Resporatory
Ethylene glycol (.... oxalic acid} MetaboliC

-
alkaloSIS
2 Salicylates (late} acidosis

3 6.9 70 71 7.2 B 7.4 7.5 7.6 77 7.8 7.9

pH
4
5
6 FA17 p 561 .1
Acid-base physiology
7
pH Pco [HCO COMPENSATORY RESPONSE
8
•9 Metabolic acidosis l l l Hyperventilation (immediate)

• 10 Metabolic alkalosis t t t Hypovcntilation (immediate)

· 11 Respiratory acidosis l t t t renal [HC03-J reabsorption (delayed)
• 12 Respirato ry alkalosis t l l l renal [HC03-J reabsorption (delayed)
• 13 Key: t ~ = 1° disturbance; l t =compensatory response.
• 14

Henderson-Hasselbalch equation: pH = 6.1 +log 6~~~~~~

• 15
• 16
2
• 17 Pred icted respira tory compensation for a simple metabolic acidosis can be calculated using the
Winters formula. lf measured Pco2 >predicted Pco2 - concomitant respirato ry acidosis; if
• 18
measured Pco2 < pred icted Pco2 - concomitant respiratory alkalosis:
Pco2 = 1.5 IHC03-] + 8 + 2

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1
A 35-year-old man with decreased gastrointestinal motility is shown to have no slow waves on electric potential and force transducer recordings from
gastrointestinal muscles over a period of 60 seconds.
IA•A] •
2

3
Which of the following is the best description of slow waves in the gastrointestinal tract?
4
5 :
A. Contraction of skeletal muscle
6
B. Depolarization and repolarization of smooth muscle cells
7
8 c. Hyperpolarization of smooth muscle ce lls
.9
D. Increase in secretions of smooth muscle cells
• 10
E. Relaxation of smooth muscle cells
• 11

• 12
• 13
• 14
• 15
• 16
• 17
. 18

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1 Th e co rrect a nsw er i s B. 68% ch ose this. •

2 Slow waves are precisely timed, rhythmic depolariza tions and repolarlzatlons of the muscularis propria of the stomach and intestines, independent of the
presence or absence of stimulus. They move in an oral-to-anal direction. They occur in a frequency specific to each organ, with the stomach having the
3 lowest frequency (3 cycles per minute) and the duodenum of the small Intestine having the highest frequency ( 12 cycles per minute). They represent the
basal electric rhythm of gastric and intestinal motility. Hormones and neurotransmitters released near the gastrointestinal smooth muscle cells can
4 modulate the amplitude of the slow waves. Not all slow waves induce action potentials and stimulate smooth muscle contraction. Depending on the slow-
5 wave amplitude and smooth muscle excitability, an action potential can be Initiated if the hormones and neurotransmitters increase the slow-wave
depolarization enough to reach threshold. Only when contractile events occur at the peak of cell depolarization during a slow wave does coordinated
6 smooth muscle contraction occur in order to fadlitate movement through the digestive tract.
Action pote• t1a Duodenum Muscular layer Depolarization Small 'ntestine Ne otlansmitte• Muscle contraction Gastrointestinal tract Smooth muscle tiss<Je Moti .ty
7
Hormone Stomach Human gastrointestinal tract Gastrointestinal physiology Muscle Slow-wave potential
8
A i s not correct. 4 % chose this.
9 When slow waves are accompanied by action potentials, smooth muscle contract ion, not skeletal muscle contraction, occurs.
• 10 Skeletal muscle Muscle contraction Smooth muscle tissue Action potential Slow-wave potential Muscle

• 11 C i s n ot co rrect. 11 Ofo chose this •

Slow waves cause depolarization (the potential becomes more positive, moving toward threshold), not hyperpolarization (the potential becomes more
• 12 negative, moving further away from the threshold).
• 13 Hyperpolarization (biology) Depolarization Hyperpolarization (physics)

• 14 D is not co rrect. 40/o chose t his .

Slow waves do not play a role in secretions of smooth muscle cells .
• 15 Smooth muscle tissue Slow-wave potential Muscle
• 16 E i s not co rrect . 130/o ch ose this.
• 17 Relaxation of smooth muscle cells occurs after an action potential has been triggered to contract smooth muscles.
Action potential Smooth muscle tissue Muscle
. 18

Bottom Lin e:
Slow waves determine the frequency of contractions of the gastrointestinal tract. They are rhythmic depolarizations and repolarizations of the
muscularis orooria of the stomach and intestines and are indeoendent of stimulus.

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1 Relaxation of smooth muscle cells occurs after an action potential has been triggered to contract smooth muscles.
Action potential Smooth muscle tissue Muscle
2

3
Bottom Line:
4
Slow waves determine the frequency of contractions of the gastrointestinal tract. They are rhythmic depolarizations and repolarizations of the
5 muscularis propria of the stomach and intestines and are independent of stimulus.
Human gastrointestinal tract Gastrointestinal tract Muscular layer Slow -wave potential Depolarization
6
7

8
lijl;fiiJI•l toryear:[ 2017 • ]
9 FI RST AID FAC T S

0 10
o ll FA17p347.1

0
12 Digestive tract Laye rs of gut wall (inside to outside-MSJ\IS):
0
13
anatomy • M ucosa-epithelium, lamina propria, muscularis mucosa
• Submucosa- includes Submucosal nerve plexus (Meissner), Secretes fluid
0 14
• M uscularis externa- includes l\ lyenteric nerve plexus (Auerbach), l\lotility
15
0
Serosa (when intraperitoneal), adventitia (when retroperitoneal)
0
16 Ulcers can extend into subm ucosa, inner or outer muscular layer. Erosions are in the mucosa only.
0 17
Frequencies of basal electric rhythm (slow waves):
0
18 • Stomach-3 waves/min
• D uodcnum- 12 waves/min
Ileum- 8- 9 waves/min

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2
A 35-year-old woman with a history of rheumatoid arthritis is diagnosed with peptic ulcer disease. The doctor plans to prescribe her a medication that
Is known to be contraindicated in pregnancy. Before writing the prescription, he confirms that the patient is not pregnant and that she understands
lA• A] •
the risks were she to become pregnant while being treated .
3
4 What Is the mechanism of action of the drug the doctor most likely prescribed?
5
:
6 A. Acts as a H2-receptor agonist
7
B. Acts as a H2-receptor antagonist
8
c. Acts as a prostaglandin agonist
9
• 10 D. Acts as a prostaglandin antagonist

• 11 E. Acts as a proton pump inhibitor

• 12
• 13
• 14
• 15
• 16
• 17
. 18

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1
The co rrect a nswer is c. 55 % cho se this.
2
Misoprostol is the medication that was most likely prescribed. It is a prostaglandin E1 analog and acts as an agonist at the prostaglandin receptors on
3 pariet al cells. This, in turn, results in increa sed mucus production and decrea sed acid secretion . Misoprostol may be used in patients with gastric ulcers
induced by nonsteroidal anti-inflammatory ( NSAID) use (this patient was likely t aking chronic NSA!Ds, given her history of rheumatoid arthritis) when the
4 patient needs to continue NSAID use despite the gastrointestinal adverse effects. Another clinical use for misoprostol is in medically induced abortions,
where it is used in combination with mifepristone, a progesterone antagonist.
5
Mifepristone Nonsteroidal anti-inflammatory drug Misoprostol Rheumatoid arthritis Prostaglandin Progesterone Peptic ulcer Receptor antagonist Agonist Mucus
6 Anti-inflammatory Parietal cell Arthritis Pharmaceutical drug Structural analog Prostaglandin E Human gastrointestinal tract Gastrointestinal tract
7 Receptor (biochemistry) Equine gastric ulcer syndrome

8 A is no t co rrect. 3 % cho se this.

9 H2-receptor agonists would not help reflux but in fact would worsen the symptoms.
Gastroesophageal reflux disease Reflux Agonist
10
B is no t co rrect. 1 4 % cho se this.
· 11 H2-receptor antagonists such as ranitidine, cimetidine, and famotidine inhibit acid secretion at the histamine receptor. Some H2 blockers, such as
• 12 cimetidine, cross the placenta, but are not explicitly contraindicat ed in pregnancy because they have been frequently used in pregnant patients without
complications. However; ranitidine is preferred to cimetidine in pregnancy, as somes studies in animals and nonpregnant humans have raised concerns
• 13 about feminization of the fetus with cimetidine use .
Cimetidine Famotidine Ranitidine Histamine Placenta Histamine receptor Secretion Contraindication Fetus Pregnancy
• 14
D is no t co rrect. 1 7 % cho se this •
• 15
Misoprostol is a prostaglandin E1 analog and acts as an agonist at prostaglandin receptors on pariet al cells. It does not act as a prostaglandin antagonist .
• 16 Misoprostol Prostaglandin Agonist Parietal cell Receptor antagonist Structural analog Receptor (biochemistry) Prostaglandin E

• 17 E is no t co rrect. 11% cho se this.

• 18 Proton pump inhibitors ( PPis), such as omeprazole and lansoprazole, work to inhibit acid secretion . These drugs are a preferred trea tment for peptic ulcer
disea se and may even be used to trea t NSAID-induced ulcers. However; PP!s are not contraindicat ed in pregnancy.
Peptic ulcer Omeprazole lansoprazole Proton-pump inhibitor Proton pump Proton Contraindication Pregnancy Secretion Ulcer

Botto m Li ne:

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1 E is not correct. 11% chose this.

Proton pump inhibitors (PPis), such as omepra zole and lansoprazole, work to inhibit acid secretion. These drugs are a preferred treatment for peptic ulcer
2 disease and m ay even be used to treat NSAID-induced ulcers. However; PPis are not contraindicated in pregnancy.
Peptic ulcer Omeprazole lansoprazole Proton-pump inhibitor Proton pump Proton Contraindication Pregnancy Secretion Ulcer
3
4
5 Bottom Line:

6 In NSAID-induced peptic ulcer disease, misoprostol, a prostaglandin agonist, m ay be used. In these patients it inhibits acid secretion and protects the
mucosa. Misoprostol is contraindicated in pregnant patients.
7 Peptic ulcer Misoprostol Prostaglandin Agonist Mucous membrane Contraindication

8
9
10 I ill ;fi 1!1 I•J for year:[ 2017 ..
FI RST AI D FA CTS
· 11
• 12 FA17 p 382.3
• 13 Misoprostol
• 14 MECHANISM A PGE 1 analog. t production and secretion of gastric mucous barrier, ~ acid production .
• 15 CLINICAL USE Prevention of l SAID-induced peptic ulcers (i SA IDs block PGE 1 production). Also used off-label
• 16 for induction of labor (ripens cervix).
• 17 ADVERSEEFFECTS Diarrhea. Contraindicated in women of childbearing potential (abortifacient).
• 18

FA17p381 .1

Acid suppression therapy

6
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1 gp ( )

3 FA17 p 381 .1

4 Acid suppression therapy

5
6 .4 GRP

7
$
Vagus n: : : _ _ . /
Gcells
8
9
~
10 Sornatostabn ProstaglandinS
• 11

• 12
• 13
Atropine --0--; t
• 14 M, receptor
• 15
• 16 G,
• 17
. 18
HcoJ--..,~;.;....­

·alkabne tide'- i blood pH -- -- --~

cAMP

after gastric ac1d secretion

leg. after meats. vomiting) H,CO. Gastric
a hydrase parietal
cell

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1 •
An overweight 37-year-old woman presents to her physician because of severe right upper quadrant abdominal pain. She has a low-grade fever.
2 Laboratory tests show a serum total bilirubin level of 0.8 mg/dl, a serum aspartate aminotransferase level of 18 U/l, a serum alanine
aminotransferase level of 20 U/l, and a leukocyte count of 15,000 cells/ Ill. Ultrasonography of the right upper quadrant is performed.
3
4 What Is the ultrasound image likely to show?
5
:
6 A. Adhesions along the hepat ic flexure of t he large colon
7
B. Engorgement of the splenic vessels
8
c. Mass at the head of the pancreas
9
10 D. Obstruction of the common bile duct by a gallstone

• 11 E. Papillary sloughing of the right kidney

• 12
F. Wall thickening and inflammation of the gallbladder
• 13
• 14
• 15
• 16
• 17
. 18

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1 •

3 The correct an swer i s F. 61% chose this.

This presentation is most consistent with acute cholecystitis, which usually presents In patients with the " 4
4
Fs": Fat, Female, Fertile, and Forty years old. These patients usually have severe and steady right upper
5 quadrant pain, low-grade fevers, leukocytosis, and slight elevations in transaminase levels. Elevations in
bilirubin and alkaline phosphatase concentrations are not common in uncomplicated cholecystitis since
6 biliary obstruction is limited to the gallbladder. The pain may radiate to the right upper shoulder or back.
Murphy sign IS conSidered present or positive if the patient has increased pain or suddenly halts inspiration
7 due to pain (inspiratory arrest). Acute chol ecystitis occurs when the cystic duct becomes acutely blocked by
8 a gallstone, lead1ng to irritation of the gallbladder mucosa and subsequent Inflammation. liver function
tests are usually normal but may occasionally be slightly elevated. Senstitlve findings include the presence
9 of cholelithasis and a positive Murphy sign as confirmed by ultrasound. As shown In the image, signs of
Inflammation such as gallbladder wall thickening (>3 mm) are important secondary findings that confirm
10 the diagnosis; the presence of gallstones supports the diagnosis, but is not diagnostic. Gallbladder wall
distension and pericholecystic fluid are not highlighted in the image, but are also significant.
11
It Is Important to remember that cholecystitis involves blockage of the cystic duct, whereas
• 12 choledocolithlasis is an obstruction of the common bile duct (and would manifest with much more elevated Image copyright © 2013 Cwik, eta/.
• 13 liver function tests [ LFTs]). Choledocolithiasis is especially dangerous because It often progresses to
ascending cholangitis, which is an infection of the biliary tract .
• 14
Gallstone Cholecystitis Bilirubin Cystic duct Leukocytosis Alkaline phosphatase Gallbladder Uver function tests Common bile duct Ascending cholangitis
• 15 Quadrant {abdomen) Murphy's sign Uver Medical ultrasound Ultrasound Inflammation Bile Bile duct Biliary tract Mucous membrane Infection Transaminase
• 16 A Is no t co rrect . soto ch ose this.
• 17 This would not be seen on ultrasound and does not correlate with the patient's clinical picture. Adhesions do not manifest with fever, hyperbilirubinemia,
or elevations In liver function tests .
. 18 Uver function tests Medical ultrasound Hyperbilirubinemia Ultrasound Uver Adhesion (medicine) Fever

B i s n o t correct. 2% ch ose this.

The spleen is located in the left upper quadrant of the abdomen, not the right, so it would not be seen on the ultrasound of this patient's right upper
quadrant.
Spleen Medical ultrasound Quadrant (abdomen) Ultrasound Abdomen

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I I I I I p p I I
' yp I I
1
or elevations in liver function t ests.
2 liver function tests Medical ultrasound Hyperbilirubinemia Ultrasound liver Adhesion (medicine) Fever

3 B is no t co rrect. 2% cho se this.

The spleen is locat ed in the left upper quadrant of the abdomen, not the right, so it would not be seen on the ultra sound of this patient's right upper
4
quadrant.
5 Spleen Medical ultrasound Quadrant (abdomen) Ultrasound Abdomen

6 c is no t co rrect. 3 % cho se this.

Although a mass at the hea d of the pancrea s could be seen on right upper quadrant ultra sound, it does not fit the clinical picture of this patient, because
7
an obstructive pancrea tic hea d mass is more likely to result in painless j aundice. This patient has severe right upper quadra nt pain more suggestive of
8 gallbladder -relat ed disea se.
Jaundice Medical ultrasound Pancreas Quadrant (abdomen) Ultrasound Head of pancreas
9
D is no t co rrect. 27% cho se this.
10
Obstruction of the common bile duct by a gallstone is indicative of choledocolithiasis. If the common bile duct were to be obstructed, as in
11 choledocolithiasis, one would see much higher serum bilirubin, aspartat e aminotransferase (AST), and alanine aminotransferase (ALT) as bile flows out of
both the liver and gallbladder would be obstructed. Acute cholecystitis is a more likely diagnosis, in which the cystic duct is blocked, lea ding to
• 12 inflammation and wall thickening in the gallbladder and only very mild eleva tions in liver function t ests ( LFTs), as is the case in this patient.
Gallstone Cholecystitis Bilirubin Cystic duct Alanine transaminase Aspartate transaminase Common bile duct Gallbladder liver function tests Bile duct Bile liver
• 13
Blood plasma Inflammation Alanine Aspartic acid
• 14
E is no t co rrect. 2% cho se this •
• 15
Although the kidneys can be visualized with ultrasound, papillary sloughing would not be picked up by this imaging modality. Furthermore, this does not
• 16 match the patient's clinical picture .
Ultrasound Medical ultrasound
• 17

• 18
Botto m Li ne:
In a patient with the " 4 Fs" who presents with acute right upper quadrant pain in the abdomen and mildly eleva t ed or normal LFTs, the most likely
diagnosis is acute cholecystitis due to obstruction of the biliary duct system at the level of the cystic duct.
Bile duct Cholecystitis Cystic duct Quadrant (abdomen) liver function tests Abdomen Bile

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1 Spleen Medical ultrasound Quadrant (abdomen) Ultrasound Abdomen

2 c is no t co rrect. 3% cho se this.

Although a mass at the hea d of the pancrea s could be seen on right upper quadrant ultrasound, it does not fit the clinical picture of this patient, because
3 an obstructive pancrea tic hea d mass is more likely to result in painless j aundice. This patient has severe right upper quadra nt pain more suggestive of
4 gallbladder -relat ed disea se.
Jaundice Medical ultrasound Pancreas Quadrant (abdomen) Ultrasound Head of pancreas
5
D is no t co rrect. 2 7 % cho se this.
6 Obstruction of the common bile duct by a gallstone is indicative of choledocolithiasis. If the common bile duct were to be obstructed, as in
7 choledocolithiasis, one would see much higher serum bilirubin, aspartat e aminotransferase (AST), and alanine aminotransferase (ALT) as bile flows out of
both the liver and gallbladder would be obstructed. Acute cholecystitis is a more likely diagnosis, in which the cystic duct is blocked, lea ding to
8 inflammation and wall thickening in the gallbladder and only very mild eleva tions in liver function t ests ( LFTs), as is the case in this patient.
Gallstone Cholecystitis Bilirubin Cystic duct Alanine transaminase Aspartate transaminase Common bile duct Gallbladder liver function tests Bile duct Bile liver
9
Blood plasma Inflammation Alanine Aspartic acid
10
E is no t co rrect. 2 % cho se this.
11 Although the kidneys can be visualized with ultrasound, papillary sloughing would not be picked up by this imaging modality. Furthermore, this does not
• 12 match the patient's clinical picture .
Ultrasound Medical ultrasound
• 13
• 14
Bo tto m Line:
• 15
In a patient with the " 4 Fs" who presents with acute right upper quadrant pain in the abdomen and mildly eleva t ed or normal LFTs, the most likely
• 16 diagnosis is acute cholecystitis due to obstruction of the biliary duct system at the level of the cystic duct.
Bile duct Cholecystitis Cystic duct Quadrant (abdomen) liver function tests Abdomen Bile
• 17

• 18

lijj ;fi IJ l•l f o r year:l 2 0 1 7 ..

FI RST AID FAC T S

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2
As a student, you are working in a laboratory over the summer that focuses on the biochemistry of the gastrointestinal (GI) tract . Your mentor wants
to study the neural signaling processes and second-messenger pathways Involved In the secretions of digestive enzymes by the salivary glands In
lA• A] •
response to food. In preparation, you review your first-year biochemistry notes on the role of digestive enzymes in the tract . You visualize a scenario
3 where you consume a meal of mashed potatoes and you reflect on how the body would function in breaking down this meal for its nutrient value.
4
5 Which of the following is involved in the initial digestion of this macronutrfent?

6 :
A. a-Amylase
7
8 B. Bile salts

9 c. Enterokinase
10
o. Gastric acid
11
E. Pepsin
• 12
• 13
• 14
• 15
• 16
• 17
. 18

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2 The co rrect a nswer is A. 9 1% cho se this.

3 a-Amylase (ptyalin) is the first enzyme involved in starch digestion, the dominant macronutrient of potatoes. This substance typically is secret ed by the
pancrea s and the salivary glands.
4 Nutrient Enzyme Ptyalin Pancreas Digestion Starch Salivary gland
5 B is no t co rrect. 1 Ofo cho se this.
6 The liver produces bile salts, which the gallbladder stores and secret es. Bile salts are not involved in starch digestion but are critical for the digestion of
fatty foods because they help emulsify lipids.
7 Gallbladder Bile acid Bile liver Starch lipid Emulsion Digestion Salt (chemistry)

8 c is no t co rrect. 2 % cho se this.

9 The duodenum produces enterokinase, which converts trypsinogen, a pancrea tic proenzyme, into its activa t ed for trypsin . Trypsin is then able to digest
proteins by clea ving peptide chains. Neither enterokinase nor trypsin is involved in starch digestion.
10 Zymogen Trypsinogen Duodenum Enteropeptidase Trypsin Digestion Peptide Starch
11 D is no t co rrect. 3 % cho se this.
12 Pariet al cells of the stomach secret e gastric acid and intrinsic factor; this decrea ses stomach pH and helps with vitamin B12 binding, respectively. The
stomach mostly aids in the digestion of proteins. It is not involved in starch digestion .
• 13 Intrinsic factor Gastric acid Vitamin B12 PH B vitamins Parietal cell Digestion Starch Vitamin Protein Stomach
• 14
E is no t co rrect. 3 % cho se this.
• 15 Chief cells of the stomach secret e pepsin, which aids in the digestion of protein, not starch . Potatoes are a starch-hea vy food .
Pepsin Protein Chief cell Gastric chief cell Starch Parathyroid chief cell Digestion Stomach
• 16
• 17

• 18 Botto m Li ne:
Salivary glands secret e a-amylase (ptya lin), which begins starch digestion.
Ptyalin Salivary gland Digestion Starch

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1
Bottom Line:
2
Salivary glands secrete a-amylase (ptya lin), which begins starch digestion.
3 Ptyalin Salivary gland Digestion Starch

4
5
6 I ill ;fi 1!1 I•J for year:[ 2017 ..
FIRST AID FAC T S
7

8 FA17 p 358.1
9
Pancreatic secretions Isotonic Auicl; low flow --. high Cl-, high flow --. high HC0 3-.
10
ENZYME ROLE NOTES
11
a -amylase Starch digestion Secreted in active form
12
Lipases Fat digestion
• 13
Proteases Protein digestion Includes trypsin, chymotrypsin, elastase,
• 14
carboxypeptidases
• 15
Secreted as proenzymes also known as
• 16 zymogens
• 17 Trypsinogen Converted to active enzyme trypsin Converted to trypsin by enterokinase/
• 18 _. activation of other proenzymes and cleaving enteropeptidase, ;1 brush-border enzyme on
of additional trypsinogen molecules into active duodenal and jejunal mucosa
trypsi n (positive feedback loop)

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1 •
A 43-year-old overweight woman presents to her doctor's office because of right upper quadrant abdominal pain. She has experienced similar
2 episodes of this type of pain in the past and admits that it is worse after meals.

3
Increased secretion of which of the following is responsible for this patient's postprandia l pain?
4
5 :
A. Cholecystokmin
6
B. Gastrin
7
8 c. Pepsin

9
D. Somatostatin
10
E. Vasoactive intest inal peptide
11

12
• 13
• 14
• 15
• 16
• 17
. 18

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1 The co rrect a nswer is A. 71% cho se this.

2 This is a classic presentation of cholelithiasis, or gallstones. Patients with cholelithiasis experience pain after meals as a result of the duodenal relea se of
cholecystokinin (CCK ), which causes the gallbladder to contract while the stone obstructs the cystic duct. CCK is stimulat ed by fatty acids and amino acids.
3 Gallstone Cholecystokinin Cystic duct Gallbladder Duodenum Fatty acid Amino acid

4 B is no t co rrect. 19 % cho se this.

5 Ga strin is relea sed by the G cells of the stomach in response to proteins or peptides in the stomach . Ga strin lea ds to increa sed secretion of gastric acid
and low pH inhibits its secretion, lea ding to a negative feedback loop. However; in Zollinger -EIIison Syndrome (ZES), which is caused by a gastrin-
6 secreting tumor in the pancrea s, there is excessive gastric acid secretion in the stomach; these patients generally present with more severe symptoms
such as pain in the esophagus, stea torrhea, wheezing or hemat emesis. Ga strin does not have an effect on gallbladder contraction .
7 Hematemesis Gastrin Steatorrhea Esophagus Gallbladder Gastric acid Pancreas PH G cell Peptide Neoplasm Negative feedback Protein Secretion Stomach
8 c is no t co rrect. 5 % cho se this.
9 Pepsin is a digestive protea se relea sed by chief cells in the stomach . Its precursor; pepsinogen, autoclea ves in the acidic environment of the stomach . It is
relea sed under the influence gastrin and the influence of the vagus nerve. It does not cause gallbladder contraction .
10 Pepsin Gastrin Pepsinogen Vagus nerve Gallbladder Gastric chief cell Protease Chief cell Parathyroid chief cell Stomach
11 D is no t co rrect. 3 % cho se this.
12 Somatostatin is relea sed by the D cells of the duodenum, pyloric antrum, and pancrea tic islets. It reduces smooth muscle contractions and inhibits the
relea se of both insulin and glucagon from the pancrea s. It does not cause gallbladder contraction .
13 Pyloric antrum Somatostatin Glucagon Duodenum Gallbladder Pancreas Pancreatic islets Delta cell Insulin Smooth muscle tissue Antrum Pylorus Muscle
• 14
E is no t co rrect. 2 % cho se this.
• 15 Vasoactive intestinal peptide induces smooth muscle relaxation in the lower esophageal sphincter; stomach, gallbladder and stimulat es secretion of wat er
into pancrea tic juice and bile. It also inhibits gastric acid secretion and absorption from the intestinal lumen. It causes relaxation rather than contraction
• 16 of the gallbladder.
• 17 Pancreatic juice Vasoactive intestinal peptide lower esophageal sphincter Gallbladder Gastric acid lumen (anatomy) Gastrointestinal tract Bile
Smooth muscle tissue Human gastrointestinal tract Peptide Cardia Sphincter Muscle Secretion Stomach
• 18

Botto m Li ne:
Patients with gallstones experience pain after meals as a result of the duodenal relea se of cholecystokinin, which causes the gallbladder to contract
while the stone obstructs the cystic duct.

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1
Smooth muscle tissue Human gastrointestinal tract Peptide Cardia Sphincter Muscle Secretion Stomach
2

3
Bottom Line:
4
Patients with gallstones experience pain after m ea ls as a result of the duodenal release of cholecystokinin, which causes the gallbladder to contract
5 while the stone obstructs the cystic duct.
Cholecystokinin Cystic duct Gallbladder Duodenum Gallstone
6
7

8
lijl;fiiJI•l toryear:[2017 • ]
9 FI RST AID FAC T S

10
FA17 p356.1
11
Gastrointestinal regulatory substances
12
REGULATORYSUBSTANCE SOURCE ACTION REGULATION NOTES
13
Gastrin G cells (antrum t gastric H+ secretion t by stomach t by chronic PPl use.
• 14
of stomach, t growth of gastric mucosa distention/ t in chronic atrophic gastritis
• 15 duodenum) t gastric motility alkalinization, (cg, H pylori).
• 16 amino acids, t t in Zollinger-Eilison
peptides, vagal syndrome (gastrinoma).
• 17
stimulation via
• 18 gastrin-releasing
peptide (GRP)
~ by pH< 1.5
Somatostatin D cells ~ gastric acid and t by acid Jn h ibits secretion of various
I . ... • 1 • .. I 1 I
•

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1
Ghrelin Stomach t appetite t in fasting stale t in Prader-Willi syndrome.
2
l b)' food l after gastric bypass surgery.
3
4
FA17 p 379.1
5
6
Gallstones t cholesterol and/or bilirubin, l bile salts, and Risk factors (.f f 's):
(cholelithiasis) gallbladder stasis all cause stones. l. Female
7
2 types of stones: 2. Fat
8
C holesterol stones (radiolucent with 10- 20% 3. Fertile (pregnant}
9 opaque due to calcification!>)- SO% of stones. 4. Fort~
10 Associated with obesitv,•
Crohn disease, Diagnose with ultrasound : . Treat" ith electi' e
11 ad,·anced age, estrogen therapy, multip:~rity, cholecystectomy if symptomatic.
rapid weight loss, 1 alive American origin. Can cause fistula between gallbladder and
12 2
Pigment stones · (black = radiopaque, Ca + C l tract - air in biliary tree (pneumobilia)
13
bilirubinate, hemolysis; brown = radiolucent, - passage of gallstones into intestinal tract
• 14 infection). Associated with C rohn disease, - obstruction of ileocecal V<llve (gallstone
• 15 chronic hemol)'sis, alcoholic cirrhosis, ileus).
• 16 advanced age, biliar)' infections, total
parenteral nutrition (TP ).
• 17
lost common compl ication is cholcc)'stitis;
. 18
can also cause acute pancreatitis, ascending
cholangitis.
RELATED PATHOLOGIES CHARACTERISTICS
Biliar v colic Associated with nausea/vomitin2 and dull RUO oain. 1 eurohormonal activation Ce2. bv CCK aft er
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3 FA17 p 353.1

4 Biliary structures Gallstones (filling defects in gallbladder and cystic duct, red arrows in fJ) that reach the con Auence
5 of the common bile and pancreal ic duels al I he ampulla of Vater can block both the common bile
and pancreatic ducts (double duel sign), causing both cholangitis and pancreatitis, respecti,·ely.
6
Tumors that arise in head of pancreas (usuall} ductal adenocarcinoma) can cause obstruction of
7 common bile duel .... enlarged g<1llbladder "ilh painless jaundice (Cour\'oisier sign).
8
9 Cystic duct - - - - - -
Liver
10
Gallbladder -........
11
- Common hepatic duct
12
13
• 14
• 15 Accessory - - - -
pancreatic duct
• 16 "'--Pancreas
• 17 Sphincter of Odd1 __/~ _,

. 18 Ampulla of Vater/ /
Main pancreatic duct /
Duodenum

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1 •
A variety of enzymes from the pancreas and small intestine are important to digestion and must undergo activation to become functional in the
2 duodenum.

3
The loss of which enzyme would be most detrimental to the activation of other enzymes important for the digestive process?
4
5 :
A. Amylase
6
B. Chymotrypsinogen
7
8 c. Enteroki nase

9
o. Lipase
10
E. Pepsi n
11

12
13
• 14
• 15
• 16
• 17
. 18

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1 The co rrect answer is c. 5 3 % chose this .

2 Loss of enterokinase would prove to be most detrimental. Enterokinase is embedded in the intestinal mucosa and is responsible for activa ting trypsinogen
into trypsin . The active trypsin then activat es the rest of the pancrea tic enzymes. Although enterokinase is not a pancrea tic enzyme itself, it is most
3 important for subsequent activation of enzymes from the pancrea tic exocrine organ.
Trypsinogen Trypsin Enzyme Enteropeptidase Pancreas Exocrine gland Intestinal mucosa Digestive enzyme Mucous membrane
4
A is not co rrect. 4 % chose this .
5
The loss of amylase from the pancrea s would not be too detrimental, especially because it is also made in the salivary glands.
6 Amylase Pancreas Salivary gland

7 B is not co rrect. 2 7 % chose this .

8 Chymotrypsinogen can be activat ed to chymotrypsin by trypsin . However; this process depends on the activation of trypsinogen to trypsin by enterokinase
in the first place, so it is not as crucial to the entire process.
9 Chymotrypsinogen Trypsinogen Chymotrypsin Trypsin Enteropeptidase

10 D is not co rrect. 4 % chose this .

11 lipase does not help activat e other enzymes. Deficiency in lipase may cause diarrhea, but would not be as detrimental as the total loss of enterokinase.
Enteropeptidase lipase Diarrhea Enzyme
12
E is not co rrect. 1 2 % chose this .
13 Although the digestion of proteins is indeed important, without enterokinase they would not even have a chance to be activa t ed. Pepsin does not play a
14 role in the activation of the other pancrea tic enzymes.
Pepsin Enteropeptidase Digestion Digestive enzyme Enzyme Protein
• 15
• 16
Botto m Line:
• 17
Enterokinase activat es trypsinogen into trypsin, which in turn activa t es the pancrea tic enzymes.
• 18 Trypsinogen Trypsin Enteropeptidase Digestive enzyme Enzyme

·-~~t~~~~f~)~~ fo r year:l 2 0 1 7 " J

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1
Bottom Line:
2
Enterokinase activates trypsinogen into trypsin, which in turn activa t es the pancreatic enzymes.
3 Trypsinogen Trypsin Enteropeptidase Digestive enzyme Enzyme

4
5
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7

8 FA17 p 358.1
9
Pancreatic secretions Isotonic Auicl; low Aow ... high CJ-, high Aow ... high I-IC03-.
10
ENZYME ROLE NOTES
11
a -amylase Starch digestion Secreted in active form
12
Lipases Fat digestion
13
Proteases Protein digestion Includes trypsin, chymotrypsin, elastase,
14
carboxypeptidases
• 15
Secreted as proenzymes also known as
• 16 zymogens
• 17 Trypsinogen Converted to active enzyme trypsin Converted to trypsin by enterokinase/
• 18 ... activation of other proenzymes and cleaving enteropeptidase, ;1 brush-border enzyme on
of additional trypsinogen molecules into active duodenal and jejunal mucosa
trypsi n (positive feedback loop)

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1
A 65-year-old woman presents to her doctor because of weakness, light-headedness, peripheral neuropathy, a recent 4.5-kg ( 10-lb) weight loss, and
diarrhea. She has a past medical history of hypothyroidism. A complete blood cell count is significant for a hemoglobin level of 7.5 g/dl, a hematocrit
IA•A] •
2
level of 28%, and a mean corpuscular volume of 115 fl (normal: 80-100 fL).
3
4 This patient Is most likely deficient in a substance produced by which of the following types of cells?
5
:
6 A. Chief cell
7
B. G cell
8
c. I cell
9
10 o. Mucous cell

11 E. Parietal cell
12
13
14
0 15
0
16
0
17
0
18

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1
The co rrect a nswer is E. 8 0 % cho se this.
2
The vignette describes symptoms of anemia with some gastrointestinal effects, which should make one suspicious of pernicious anemia. Anemia is
3 confirmed by the low hematocrit and hemoglobin levels, and the elevat ed mean corpuscular volume indicat es that this is a macrocytic anemia. A common
cause of macrocytic anemia is vitamin B12 and/or folat e deficiency. This patient is also experiencing neurologic symptoms, and while both vitamin B12 and
4 folat e deficiencies cause macrocytic anemia, only vitamin B12 deficiency causes neurologic deficits. One cause of vitamin B12 deficiency is pernicious
anemia. Pernicious anemia is more common in the elderly, those of northern European descent, and African-Americans. It is an autoimmune condition
5
that can cause decrea sed production of intrinsic factor (which is required for vitamin B12 absorption) or reduced function of ileal IF-B12 receptors.
6 Pernicious anemia is common in patients with other autoimmune conditions such as Hashimoto's thyroiditis and vitiligo. Intrinsic factor is produced in
pariet al cells of the stomach . This condition is trea t ed with regular intramuscular injections of cobalamin (vitamin B12 ) .
7 Pernicious anemia Vitiligo Hashimoto' s thyroiditis Macrocytic anemia Mean corpuscular volume Hematocrit Hemoglobin Intrinsic factor Folic acid Folate deficiency

8 Vitamin B12 Anemia Cobalamin B vitamins Parietal cell Autoimmunity Autoimmune disease Ileum Gastrointestinal tract Vitamin Stomach Intramuscular injection

Macrocytosis Human gastrointestinal tract

9
10 A is no t co rrect. 7% cho se this.
Chief cells of the stomach typically secret e pepsinogens. In the setting of low gastric pH, pepsinogen is converted to pepsin, which clea ves peptide bonds
11 and aids in protein digestion.
Pepsin Pepsinogen PH Chief cell Protein Peptide Gastric chief cell Parathyroid chief cell Digestion Proteolysis Stomach
12
13 B is no t co rrect. 4 % cho se this.
G cells locat ed in the stomach typically secret e gastrin, which serves to increa se gastric acid secretion, growth of gastric mucosa, and gastric motility.
14 Gastrin Gastric acid G cell Gastric mucosa Mucous membrane Motility Stomach

15 c is no t co rrect. 6 % cho se this.

• 16 I cells are locat ed in the duodenum and j ejunum. These cells relea se cholecystokinin, an enzyme that causes increa sed pancrea tic secretion, increa sed
gall bladder contraction, and decrea sed gastric emptying .
• 17
Jejunum Cholecystokinin Duodenum Enzyme Gallbladder Urinary bladder Stomach
• 18
D is no t co rrect. 3 % cho se this.
Mucous cells locat ed in the stomach typically secret e mucus to lubricat e the stomach and bicarbonat e to protect the surface from the acidic environment.
Mucus Bicarbonate Acid Stomach

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1 Jejunum Cholecystokinin Duodenum Enzyme Gallbladder Urinary bladder Stomach

2 D is not correct. 3% chose this.

Mucous cells locat ed in the stomach typically secret e mucus to lubricat e the stomach and bicarbonat e to protect the surface from the acidic environment.
3
Mucus Bicarbonate Acid Stomach
4
5
Bottom Line:
6
Pernicious anemia is an autoimmune condition that can cause decrea sed production of intrinsic factor by pariet al cells in the stomach . Because intrinsic
7 factor is required for the absorption of vitamin B12 , it can cause a macrocytic anemia.
Pernicious anemia Macrocytic anemia Intrinsic factor Vitamin 812 B vitamins Parietal cell Autoimmunity Macrocytosis Anemia Autoimmune disease Vitamin
8
9
10
I ill ;fi 1!1 I•J for year:[ 2017 ..
11 FI RST AI D FA CTS

12
FA17 p 398.1
13
Macrocytic (MCV > 100 fl) anemia
14
DESCRIPTION FINDINGS
15
Megaloblastic anemia Impaired Dl A synthesis .... maturation of RBC macrocytosis, hypersegmented
• 16
nucleus of precursor cells in bone marrow neutrophils a,
glossitis.
• 17 delayed relative to maturation of cytoplasm .
• 18

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1 •
thumbs) in up to 50% of cases.
2
3 FA17 p 357.1
4 Gastrointestinal secretory products
PRODUCT SOURCE ACTION REGULATION NOTES
5
6
Intrinsic factor Parietal cel ls Vitamin B1rbinding Autoimmune destruction
(stomach) protein (required for B12 of parietal cells .... chronic
7
uptake in terminal ileum) gastritis and pern icious
8 anemia.
9
Gastric acid Parietal cells l stomach pH t by histamine,
10 (stomach) ACh, gastrin
11 l by somatostatin,
12 GIP,
prostaglandin,
13
secretin
14
Pepsin Chief cells Protein digestion t by vagal Pepsinogen (inactive) is
15
(stomach) stimulation, converted to pepsin (active) in
• 16 the presence of H+.
local acid
• 17
Bicarbonate Mucosal cells eutralizes acid t by pancreatic Trapped in mucus that covers
• 18 (stomach, and bilia ry the gastric epithelium .
duodenum, secretion with
sal ivary glands, secretin
pancreas) and
l"trnnno .. rrl "ln,-1" •

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1 •
A 53-year-old patient presents to the clinic because of lethargy, malaise, and peripheral edema . His pulse is 96/min. Although his abdomen Is
2 distended, the remainder of his body habitus appears cachectic. His chart reveals that he was recently involved in several motor vehicle collisions.
Laboratory studies show:
3
wac count: 12,000/mm•
4 Hemoglobin: 11 g/ dL
5 Hematocrit: 35%
Aspartate aminotransferase: 120 U/ L
6 Alanine aminotransferase: so U/ L
Alka line phosphatase: 80 U/ L
7
8
What Is the major physiolog ic mechanism for this patient's edema?
9
:
10 A. Constriction of arterioles
11
B. Decreased production of serum proteins
12
13
c. Increased permeability of capillaries

14 D. Increased permeability of glomeruli

15 E. Lymphatic blockage
• 16
• 17
. 18

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2
The co rrect a nswer is B. 70% cho se this.
3 The patient has a presentation that is consistent with alcoholic hepatitis. This is evidenced by a ratio of aspartat e aminotransferase to alanine
4 aminotransferase (AST:ALT ratio) > 1.5 and a normal alkaline phosphat ase level (elevation would be more suggestive of biliary obstruction). He also
shows classic signs of met abolic encephalopathy, ascites, and edema. The mild anemia is the result of the suppressive effects of alcohol on the bone
5 marrow . The major mechanism contributing to edema in this disea se is the decrea sed production of serum proteins (eg, albumin) by the damaged liver.
Therefore, the plasma oncotic pressure is decrea sed, allowing fluid to flow out of the capillaries.
6 Alcoholic hepatitis Aspartate transaminase Oncotic pressure Ascites Alanine transaminase Alkaline phosphatase Human serum albumin Edema Albumin Anemia
7 Blood plasma liver Hepatitis Capillary Alkalinity Bone marrow Alanine Aspartic acid Encephalopathy Alcoholism Serum (blood) Bile Alcohol Protein Metabolism

8 Transaminase Bone

9 A is no t co rrect. 5 % cho se this.

Arteriolar constriction would lea d to decrea sed hydrostatic pressure in the capillaries downstream, resulting in decrea sed filtration of fluid into the
10 interstitium . The constriction of venules, however; would be more likely to increa se capillary hydrostatic pressure.
11 Hydrostatic pressure Capillary Arteriole Interstitial fluid Venule Starling equation Filtration Hydrostatics

12 c is no t co rrect. 14 % cho se this.

Capillary permeability is usually caused by inflammation, and this may lea d to edema. However; there is minimal inflammation in the peripheral
13 vasculature in this case, as evidenced by the WBC count .
14 Vascular permeability Edema Capillary Inflammation Circulatory system Semipermeable membrane

15 D is no t co rrect. 4 % cho se this.

The permeability of renal glomeruli is increa sed in disea ses such as nephrotic syndrome, lea ding to the protein loss in the blood and a subsequent
16 decrea se in oncotic pressure. However; the kidneys are not the source of the problem in this case.
• 17 Nephrotic syndrome Glomerulus (kidney) Oncotic pressure Glomerulus Protein Semipermeable membrane Kidney

• 18 E is no t co rrect. 7% cho se this •

Lymphatic obstruction can cause edema, but it is not the underlying problem in this case.
Edema lymphatic system lymph lymphangiectasia

Rntt-n rn 1 i n .ca.•

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1
E is not correct. 7% chose this.
2
Lymphatic obstruction can cause edema, but it is not the underlying problem in this case.
3 Edema lymphatic system lymph lymphangiectasia

4
5 Bottom Line:
6 A decrease in oncotic pressure (as in liver failure or nephrotic syndrome), an increase in hydrostatic pressure (as in congestive heart failure), or a
lymphatic obstruction can lea d to edema. When eva luating a patient with edema, approach the patient in a systematic fashion to avoid missing the
7
underlying problem.
8 Nephrotic syndrome Oncotic pressure Heart failure Congestive heart failure Edema Hydrostatic pressure liver liver failure lymphangiectasia lymphatic system
lymph
9
10
11
I ill ;fi 1!1 I•J for year:[ 2017 ..
FI RST AID FA CTS
12
13
FA11p287.1
14
15
Capillary fluid Starling forces determine Auid movement through capillary membranes:
exchange • Pc =capillary pressure-pushes fluid out of capillary
16
Interstitial fluid • P; = interstitial Auid pressure- pushes Auid into capillary
• 17
• 7tc =plasma colloid osmotic (oncotic) pressure-pulls Auid into capillary
• 18 1t; = interstitial fluid colloid osmotic pressure- pulls fluid out of capillary
J,. = net fluid flow = Kr [(Pc - P;) - c;(nc -n;)]
Kr =capillary permeability to Auid
Capillary c; = reflection coefficient (measure of capillary permeabi lity to protein)
F.Cl t>m~-PW'PSS AniCI nntAmv intn in tt>rstitinm rnmmnn lv r~nst>Cl lw·

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1 •
t capillary permeability (t Kr; eg, toxins, infections, burns)
2 • t interstitial fluid colloid osmotic pressure (t n;; eg, lymphatic blockage)
3
4
FA17 p 374.1
5 Alcoholic liver disease
6 Hepatic steatosis lacrovesicular fall y change rJ that ma) be
7 re,·ersible with alcohol cessation.
8 Alcoholic hepatitis Requires sustained, long-term consumption. ~ l ake a
to.\ ST with alcohol:
9 Swollen and necrotic hepatoc}1es with AS'l > ALT (ratio usually> 2:1).
10 neutrophilic infiltration. lallory bodies
(intracytoplasmic eosinophilic inclusions of
11
damaged keratin filaments).
12
Alcoholic cirrhosis Final and usm11ly irreversible form.
13
Regenerative nodules surrounded b} fibrous
14 bands in response to chronic liver injury
15 - portal hypertension and end-stage liver
16 disease. Sclerosis around central ''cin (a rrows
in ~) may be seen in early disease .
• 17
. 18

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1 •
A 15-year-old boy presents to his pediatrician complaining that the right side of face and neck are swollen, just behind the angle of the jaw. Upon
2 further questioning he also says he has produced more saliva lately than usual.

3
Compared with normal saliva, which of the following would be lower in concentration in this patient's saliva?
4
5 :
A. Amylase
6
B. Bicarbonate
7
8 c. Chloride

9
D. Potassium
10
E. Sodium
11

12
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• 17
. 18

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Item: 17 of 18 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
QIO: 3 0 26 ..L ar Prev ious Next Lab~lues Notes Calculat o r

1 Th e co rrect a nswer i s D. 3 4 0/o chose this. •

2 This vignette describes a boy with parotitis, which is classically caused by mumps {Typical presentation
shown In the Image. The incidence of this infection has decreased significantly since the advent of the MMR
3 vaccine In 1967), but has a large range of causes, including autoimmune, bacterial, and idiopathic sources.
In general, saliva secreted from duct acini starts out isotonic to plasma. As saliva travels, the excretory
4 ducts and the Intercalated ducts reabsorb Na+ and Cl- and secrete K+ and HCo 3-. At higher rates of flow,
5 such as can be seen in the setting of parotitis, there is less time that saliva Is In contact with the ductal
epithelium, and less reabsorption of Na+ and Cl- and less secretion of K+. As a result, salivary K+
6 concentration decreases as flow rate increases. However, bicarbonate secretion Is increased independently
by the action of secretagogues. In add ition, at lower sa livary flows, sa liva In the mouth tends to be
7 hypotonic and sli ghtly acidic compared w ith plasma. At higher flows, sa liva Is nearl y ISOtonic to plasma and
becomes more basic.
8
Parotitis Mumps Blood plasma Epithelium Autoimmune disease vaccine MMR vaccine El<CI etion Idiopathy Saliva
9 Bicarbonate Infection Acinus Autoimmunity Tonicity

10 Image courtesy of CDC/Barbar Rice

11
A is not co rrect. 2 00/o chose this.
12
The concentration of amylase generally increases with the salivary flow rate.
13 Amylase

14 8 is not co rrect . 1 80/o chose this.

15 Bicarbonate {HCo 3 -) increases the pH and buffer capacity of saliva, especially during stimulation, in which secretagogues promote HCo 3 - secretion. The
HCo 3 - concentration generally increases with sa liva ry flow, resulting In a higher p H.
16 PH Bicarbonate Saliva Buffer solution

17 C is no t co rrect. 160/o ch ose this.

. 18 At higher rates of flow, there is less time that saliva is in contact with the ductal epithelium, which normally reabsorbs sodium chloride . Salivary chloride
concentration increases as salivary flow rate increases.
Sodium chloride Sodium Epithelium Saliva

E is n o t correct. 120/o ch ose this.

At higher rates of flow, there is less time that saliva is in contact with the ductal epithelium, which normally reabsorbs sodium chloride. Salivary sodium
rnnrPntr~t l nn inrn::a::.c;pc;. ~c;. c;Aii~rv flnw r;:::r;tp inrrp;:::r;~c:;:

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Item: 17 of 18 ~. I • M k <:] t> al ~· ~
QIO: 3026 .l. ar Previous Next lab 'Vfl1 ues Notes Calculator

1 c is not correct. 16% chose this.

At higher rates of flow, there is less time that saliva is in contact with the ductal epithelium, which normally reabsorbs sodium chloride . Salivary chloride
2 concentration increases as salivary flow rate increases.
Sodium chloride Sodium Epithelium Saliva
3
4 E is not correct. 12% chose this.
At higher rates of flow, there is less time that saliva is in contact with the ductal epithelium, which normally reabsorbs sodium chloride . Salivary sodium
5 concentration increases as salivary flow rate increases.
Sodium chloride Sodium Epithelium Saliva
6
7

8 Bottom Line:

9 Saliva is isotonic at high flow rates and hypotonic at low flow rates as the ductal epithelium has more time to modify the secretion by reabsorbing
sodium and chloride and secreting potassium. Bicarbonate secretion increases with salivary flow.
10 Saliva Tonicity Bicarbonate Sodium Epithelium Potassium Isotonicity Hypotonia Secretion

11

12
13 I ill ;fi 1!1 I•J for year:[ 2017 ..
FI RST AI D FA CTS
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15 FA11 p 166.3
16 Mumps virus A para myxovirus that causes mumps, Mumps makes your parotid glands and testes as
17 uncommon due to effectiveness of MMR big as POM-Poms.
• 18 vaecme.
Symptoms: Parotitis r.i], O rchitis (inAammation
of testes), aseptic M eningitis, and Pancreatitis.
Can cause steri lity (especially after puberty).

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Item: 18 of 18 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
QIO: 3925 ..L ar Pre v ious Next Lab~lues Notes Calcula t o r

1 •
A 22-year-old woman presents with dyspnea upon exertion, weakness, and fatigue . On physical examination, she has hair loss, spoon-shaped
2 fingernails, and pale mucous membranes. She has a history of heavy menstrual bleeding. Lab results revea l :

3 RBC count: 2 million/mm 3

Mean corpuscular volume: 65 fl (normal : 80- 100 fl)
4 Mean corpuscular hemoglobin: 24.0 pg (normal : 25.4-34.6 pg)
Ferritin: 6 ng/ml (normal: 12-150 ng/ml )
5 Red cell distribution width: 17o/o (norm al: 11.5- 14.5%).
6
7
Malabsorption In what part of the gastrointestinal tract will produce the type of anemia described in the stem?
8
:
9 A . Duodenum
10
B. Gastric fundus
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c. Ileum
12
13 o. Jejunum

14 E. Sigmoid colon
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. 18

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Item: 18 of 18 ~. I • M k <:] t> al ~· ~
QIO: 3925 .l. ar Previous Next lab 'Vfl1 ues Notes Calculator

1 The correct answer is A. 60% chose this.

2 One of the causes of microcytic anemia is iron deficiency. Iron is absorbed in the
duodenum via two independent mechanisms. Heme-associat ed iron is t aken up by a
De;,~~;ncy Chronic Dis~as.e
0•11

3 minor "'" m inor

heme transporter in the luminal plasma membrane of the duodenal epithelial cell. Anemia
Free ferric iron ions ( Fe 3 +) are converted to ferrous iron ions ( Fe 2 +) by a
~
~ or NO<mal ~ ~
4
cytochrome B enzyme on the luminal plasma membrane of the duodenal epithelial Normal lormal lormal
cell. Ferrous iron ions are t aken up by the divalent met al transporter channel, also in ~Fe ~O<mal lormal
5 IO<mal ronnar
the luminal plasma membrane. Within the cell, iron is transferred to mucosal ferritin r or l(l(rll81 IO<mal rormar
6 and then shuttled to transferrin in the plasma. Although some iron absorption may J\onnaJ Normal ~ormal .Hbl\2
occur in the upper j ejunum, most of it occurs in the duodenum. Thus, a deficiency in
7 duodenal absorption will cause iron deficiency, which is the most common cause of
8 microcytic anemia. Iron deficiency may lea d to decrea sed mean corpuscular hemoglobin (MCH ), which is the average amount of hemoglobin per red blood
cell in a blood sample. Other common lab findings in iron deficiency anemia are an increa sed red cell distribution and low ferritin . See the t able for further
9 information on differentiating types of anemia.
Red blood cell Microcytic anemia Jejunum Ferritin Duodenum Iron-deficiency anemia Heme Transferrin Hemoglobin Enzyme Epithelium Anemia Iron
10
Iron deficiency Blood plasma Cell membrane lumen (anatomy) Ferric Biological membrane Mean corpuscular hemoglobin Divalent Blood cell Iron{II) oxide
11
Cytochrome Ferrous
12
B is not correct. 5 % chose this.
13 The gastric fundus contains pariet al cells that secret e intrinsic factor; which is important in the absorption of vitamin B 12 · No major nutrient absorption
occurs in the gastric fundus. However; a deficiency in intrinsic factor will lea d to malabsorption of vitamin B12 in the t erminal ileum, which may lea d to
14 megaloblastic anemia from vitamin B 12 deficiency.
15 Megaloblastic anemia Ileum Intrinsic factor Vitamin B12 Anemia Malabsorption B vitamins Parietal cell Gastric fundus Nutrient Vitamin Fundus (stomach)

16 c is not correct. 17% chose this.

The ileum is the major site of absorption of vitamin B 12 , the fat -soluble vitamins (A, D, E, and K), fatty acids, and carbohydrat es. Vitamin B 12 deficiency
17 causes megaloblastic, not microcytic, anemia.
18 Ileum Anemia B vitamins Vitamin B12 Carbohydrate Fatty acid Vitamin Microcytic anemia lipophilicity

D is not correct. 16% chose this.

The j ejunum is a major site of folat e absorption. Decrea sed folat e levels is another cause of megaloblastic anemia, in addition to vitamin B12 deficiency.
To differentiat e between folat e and vitamin B12 deficiency, methylmalonic acid levels can be drawn, which will be eleva t ed in vitamin B12 deficiency but
normal in folat e deficiency.

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Item: 18 of 18 ~. I • M k <:] t> al ~· ~
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1 causes megaloblastic, not microcytic, anemia.

Ileum Anemia 8 vitamins Vitamin 812 Carbohydrate Fatty acid Vitamin Microcytic anemia lipophilicity
2
D is no t co rrect. 16% cho se this.
3
The j ejunum is a major site of folate absorption . Decreased folate levels is another cause of megaloblastic anemia, in addition to vitamin 8 12 deficiency.
4 To differentiate between folate and vitamin 8 12 deficiency, methylmalonic acid levels can be drawn, which will be elevated in vitamin 8 12 deficiency but
normal in folate deficiency.
5 Megaloblastic anemia Jejunum Methylmalonic acid Folic acid Folate deficiency Vitamin 812 Anemia 8 vitamins Vitamin
6 E is no t co rrect. 2 % cho se this.
7 The sigmoid colon is a site of water absorption . Malabsorption in the sigmoid colon will not affect R8C production.
Sigmoid colon Malabsorption Colon (anatomy)
8
9
10 Botto m Li ne:
Iron and calcium are predominately absorbed in the duodenum, and malabsorption in this segment of the gastrointestinal tract can lead to microcytic
11
anemia.
12 Microcytic anemia Duodenum Anemia Malabsorption Human gastrointestinal tract Gastrointestinal tract Calcium Iron

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15 I iii I;fi 1!1 I•J f o r yea r :l 2017 ..
FI RST AI D FA CTS

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17 FA17 p 396.2

18 Microcytic (MCV < 80 fl), hypochromic anemia

Iron deficiency ! iron clue to chronic bleed ing (eg, GI loss, menorrhagia), malnutrition, absorption disorders, GI
surgery (eg, gastrectomy), or t demand (eg, pregnancy) - l fina l step in heme synthesis.
Labs: l iron, t TIBC, l ferritin, t free erythrocyte protoporphyrin. Microcytosis and
h\lnf'\,..hrl\l"'r1'3C:i'l fr-P.n l ro:~ l n-:~l l "r\ n
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FA17 p 358.3
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Vitamin/mineral absorption
8
Iron Absorbed as Fc1+ in duodenum. Iron f ist, Bro
9
Folate Absorbed in small bowel. Clinically reb·ant in patients with small bowel
10
disease or after resection.
11 812 Absorbed in terminal ileum along with bile
salts, requires intrinsic factor.
12
13
FA17 p 358.5
14
15
Bile Composed of bile salts (bile acids conjugated lo glycine or taurine, making them water soluble),
phospholipids, cholesterol, bilirubin, we~ le r, and ions. Cholesterol 7o.-hydroxylase catalyzes
16
rate-limiting step of bile acid synt·hcsis.
17 Functions:
18 Digestion and absorption of lipids and fat-soluble vitamins
Cholesterol excretion (body's Io means of eliminating cholesterol)
Antimicrobial activity (via membrane disruption)

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