GI physiology (digestion, absorption, motility)

GI physiology (digestion, absorption, motility) US Medical PG Question 1: A 25-year-old male presents to his primary care physician for fatigue, abdominal pain, diarrhea, and weight loss. He states that this issue has occurred throughout his life but seems to “flare up” on occasion. He states that his GI pain is relieved with defecation, and his stools are frequent, large, and particularly foul-smelling. The patient has a past medical history of an ACL tear, as well as a car accident that resulted in the patient needing a transfusion and epinephrine to treat transfusion anaphylaxis. His current medications include vitamin D and ibuprofen. He recently returned from a camping trip in the eastern United States. He states that on the trip they cooked packed meats over an open fire and obtained water from local streams. His temperature is 99.5°F (37.5°C), blood pressure is 120/77 mmHg, pulse is 70/min, respirations are 11/min, and oxygen saturation is 98% on room air. Physical exam reveals poor motor control and an ataxic gait on neurologic exam. Cardiac and pulmonary exams are within normal limits. Laboratory studies are ordered and return as below: Hemoglobin: 9.0 g/dL Hematocrit: 25% Haptoglobin: 12 mg/dL Leukocyte count: 7,500 cells/mm^3 with normal differential Platelet count: 255,000/mm^3 Serum: Na+: 140 mEq/L Cl-: 102 mEq/L K+: 5.0 mEq/L HCO3-: 24 mEq/L BUN: 24 mg/dL Glucose: 82 mg/dL Creatinine: 1.0 mg/dL Ca2+: 9.0 mg/dL LDH: 457 U/L AST: 11 U/L ALT: 11 U/L Radiography is ordered which reveals a stress fracture in the patient’s left tibia. Which of the following is the best confirmatory test for this patient’s condition?

• A. Stool ELISA
• B. Vitamin B12 and folate level
• C. Vitamin E level (Correct Answer)
• D. Bowel wall biopsy
• E. Iron studies

GI physiology (digestion, absorption, motility) Explanation: ***Vitamin E level*** - The patient's presentation suggests **celiac disease** causing **malabsorption** with secondary **vitamin E deficiency**, which is causing the specific complications seen here. - The **neurological findings** of **ataxic gait** and **poor motor control** combined with **hemolytic anemia** (low haptoglobin 12 mg/dL, elevated LDH 457 U/L, anemia) are **pathognomonic for vitamin E deficiency**. - Vitamin E deficiency causes **spinocerebellar degeneration**, **peripheral neuropathy**, and **hemolytic anemia** due to oxidative damage to RBC membranes and neuronal lipids. - The **stress fracture** suggests bone disease from calcium/vitamin D malabsorption, but the neuro-hematologic picture is most specific for vitamin E. - **Serum vitamin E level** is the **confirmatory test** for this specific deficiency syndrome causing the patient's neurological and hematological complications. - While the underlying condition is likely celiac disease, confirming vitamin E deficiency directly explains the constellation of findings and guides immediate treatment. *Bowel wall biopsy* - A **small intestine biopsy** would confirm the underlying diagnosis of **celiac disease** (villous atrophy, crypt hyperplasia) causing the malabsorption. - However, the question asks for confirmation of "this patient's condition" - referring to the specific syndrome presenting with the characteristic triad of **ataxia + hemolysis + malabsorption**. - This triad is pathognomonic for **vitamin E deficiency**, making direct measurement more confirmatory for the presenting complication than tissue diagnosis of the underlying cause. *Vitamin B12 and folate level* - **Vitamin B12 deficiency** can cause **subacute combined degeneration** with ataxia and neurological symptoms, but typically presents with **posterior column signs** (loss of proprioception, vibration) and **peripheral neuropathy**, not primarily cerebellar ataxia. - **Folate deficiency** causes **megaloblastic anemia** but does **not** cause neurological deficits or the hemolytic pattern seen here (low haptoglobin, elevated LDH with normal liver enzymes). - The **hemolytic anemia** is specific to vitamin E deficiency, not B12/folate deficiency. *Stool ELISA* - Could detect **Giardia lamblia** given the history of drinking stream water during camping, which can cause acute diarrhea and malabsorption. - However, this does not explain the **lifelong, recurring symptoms**, **neurological deficits**, **hemolytic anemia**, or **stress fracture**. - The chronic nature points to a primary malabsorption disorder, not acute infection. *Iron studies* - **Iron deficiency** commonly occurs with celiac disease due to duodenal malabsorption and could contribute to the **anemia**. - However, iron deficiency causes **microcytic anemia**, not hemolytic anemia, and does **not** explain the **low haptoglobin**, **elevated LDH**, **ataxic gait**, or **motor control issues**. - These findings are specific to vitamin E deficiency.

GI physiology (digestion, absorption, motility) US Medical PG Question 2: A 37-year-old man with Crohn disease is admitted to the hospital because of acute small bowel obstruction. Endoscopy shows a stricture in the terminal ileum. The ileum is surgically resected after endoscopic balloon dilatation fails to relieve the obstruction. Three years later, he returns for a follow-up examination. He takes no medications. This patient is most likely to have which of the following physical exam findings?

• A. Dry skin and keratomalacia
• B. Weakness and ataxia (Correct Answer)
• C. Hyperreflexia with tetany
• D. Gingival swelling and bleeding
• E. Pallor with koilonychia

GI physiology (digestion, absorption, motility) Explanation: ***Weakness and ataxia*** - This patient with a history of **Crohn disease** and significant **ileal resection** is at high risk for **vitamin B12 deficiency** due to the removal of the primary site of absorption in the terminal ileum. - **Vitamin B12 deficiency** can lead to subacute combined degeneration of the spinal cord, manifesting as **weakness**, **ataxia**, and **paresthesias**. *Dry skin and keratomalacia* - This presentation is indicative of **vitamin A deficiency**, which can occur in malabsorption but is less specific to ileal resection than B12 deficiency. - While fat-soluble vitamins (A, D, E, K) are absorbed in the small intestine, severe isolated vitamin A deficiency causing keratomalacia is not the most likely primary finding after ileal resection. *Hyperreflexia with tetany* - These symptoms typically suggest **hypocalcemia** or **hypomagnesemia**, often due to vitamin D deficiency or malabsorption of minerals. - Although possible with generalized malabsorption, it is not the most characteristic neurological complication following isolated ileal resection compared to vitamin B12 deficiency. *Gingival swelling and bleeding* - This is a hallmark of **scurvy**, caused by **vitamin C deficiency**, which is typically absorbed in the small intestine and does not correlate specifically with ileal resection. - This would be a less likely complication given the specific history compared to micronutrient deficiencies related to terminal ileum function. *Pallor with koilonychia* - **Pallor** and **koilonychia (spoon nails)** are characteristic signs of **iron deficiency anemia**. - While iron is absorbed in the duodenum and proximal jejunum, and anemia is common in Crohn disease, the specific neurological symptoms from B12 deficiency are generally more prominent after ileal resection.

GI physiology (digestion, absorption, motility) US Medical PG Question 3: A 21-year-old woman presents to the clinic complaining of fatigue for the past 2 weeks. She reports that it is difficult for her to do strenuous tasks such as lifting heavy boxes at the bar she works at. She denies any precipitating factors, weight changes, nail changes, dry skin, chest pain, abdominal pain, or urinary changes. She is currently trying out a vegetarian diet for weight loss and overall wellness. Besides heavier than usual periods, the patient is otherwise healthy with no significant medical history. A physical examination demonstrates conjunctival pallor. Where in the gastrointestinal system is the most likely mineral that is deficient in the patient absorbed?

• A. Large intestine
• B. Ileum
• C. Jejunum
• D. Stomach
• E. Duodenum (Correct Answer)

GI physiology (digestion, absorption, motility) Explanation: ***Duodenum*** - The patient's symptoms (fatigue, conjunctival pallor, heavy periods, vegetarian diet) are highly suggestive of **iron deficiency anemia**. The **duodenum** is the primary site for the absorption of dietary iron. - Iron absorption is tightly regulated here to maintain iron homeostasis, and conditions like a vegetarian diet can reduce bioavailable iron, leading to deficiency. *Large intestine* - The large intestine is primarily involved in **water and electrolyte absorption** and the formation of stool. - It does not play a significant role in the absorption of essential minerals like iron. *Ileum* - The ileum is the main site for the absorption of **bile salts** and **vitamin B12**. - While it absorbs some nutrients, it is not the primary site for iron absorption. *Jejunum* - The jejunum is the main site for the absorption of most **nutrients**, including carbohydrates, proteins, and fats. - While some iron absorption can occur here, the **duodenum** is the specialized and most significant site for this process. *Stomach* - The stomach's main roles include **digestion** of proteins and production of **intrinsic factor** for vitamin B12 absorption. - While **acidic pH** in the stomach aids in converting ferric iron (Fe3+) to ferrous iron (Fe2+), which is more readily absorbed, direct iron absorption in the stomach lining is minimal.

GI physiology (digestion, absorption, motility) US Medical PG Question 4: An 82-year-old woman presents with 2 months of foul-smelling, greasy diarrhea. She says that she also has felt very tired recently and has had some associated bloating and flatus. She denies any recent abdominal pain, nausea, melena, hematochezia, or vomiting. She also denies any history of recent travel and states that her home has city water. Which of the following tests would be most appropriate to initially work up the most likely diagnosis in this patient?

• A. Fecal fat test (Correct Answer)
• B. Tissue transglutaminase antibody test
• C. Stool O&P
• D. Stool guaiac test
• E. CT of the abdomen with oral contrast

GI physiology (digestion, absorption, motility) Explanation: ***Fecal fat test*** - The patient's symptoms of **foul-smelling, greasy diarrhea**, along with **fatigue, bloating, and flatus**, strongly suggest **malabsorption**, specifically **steatorrhea** (excess fat in stool). - A **fecal fat test** (e.g., Sudan stain or 72-hour quantitative stool fat collection) directly assesses fat malabsorption and would be the most appropriate initial diagnostic test. *Tissue transglutaminase antibody test* - This test is used to screen for **celiac disease**, which can cause malabsorption symptoms. - While celiac disease is a possibility, a fecal fat test is a more general and appropriate initial step to confirm fat malabsorption before looking for specific causes. *Stool O&P* - Stands for **Stool Ova and Parasites**, used to detect parasitic infections like **Giardia** or **Cryptosporidium**, which can cause diarrhea. - However, the absence of recent travel, city water, and the prominent greasy nature of the stool make this less likely as the primary initial investigation compared to confirming malabsorption. *Stool guaiac test* - This test detects **occult blood in stool**. - The patient denies **melena or hematochezia**, and there are no signs pointing to gastrointestinal bleeding, making this test irrelevant for her presenting symptoms. *CT of the abdomen with oral contrast* - A CT scan with contrast might be used to investigate structural abnormalities or inflammation if other tests confirm malabsorption or point to a specific organ pathology (e.g., pancreatitis, Crohn's disease). - It's an imaging study and generally not the most appropriate *initial* test for evaluating the described symptoms of malabsorption.

GI physiology (digestion, absorption, motility) US Medical PG Question 5: A 31-year-old woman visits the clinic with chronic diarrhea on most days for the past four months. She also complains of lower abdominal discomfort and cramping, which is relieved by episodes of diarrhea. She denies any recent change in her weight. Bowel movements are preceded by a sensation of urgency, associated with mucus discharge, and followed by a feeling of incomplete evacuation. The patient went camping several months earlier, and another member of her camping party fell ill recently. Her temperature is 37° C (98.6° F), respiratory rate is 15/min, pulse is 67/min, and blood pressure is 122/98 mm Hg. Her physical examination is unremarkable. A routine stool examination is within normal limits and blood test results show: Hb% 13 gm/dL Total count (WBC): 11,000/mm3 Differential count: Neutrophils: 70% Lymphocytes: 25% Monocytes: 5% ESR: 10 mm/hr What is the most likely diagnosis?

• A. Giardiasis
• B. Ulcerative colitis
• C. Crohn’s disease
• D. Irritable bowel syndrome (Correct Answer)
• E. Laxative abuse

GI physiology (digestion, absorption, motility) Explanation: ***Irritable bowel syndrome (IBS)*** - The patient's symptoms of chronic diarrhea, abdominal discomfort relieved by defecation, urgency, and incomplete evacuation, without significant weight loss or alarming signs, are highly characteristic of **Irritable Bowel Syndrome** meeting **Rome IV criteria**. - The camping history suggests possible infectious gastroenteritis, but the **chronic duration (4 months)**, **normal stool examination**, and **absence of systemic illness** make infectious causes unlikely. - The mild WBC elevation and normal ESR are non-specific findings; IBS is a **functional disorder** without inflammatory markers. *Giardiasis* - While giardiasis can cause chronic diarrhea, it often presents with **malabsorption symptoms** such as fatty stools, weight loss, and nutrient deficiencies. - The routine stool examination being within normal limits makes giardiasis less likely, as **Giardia cysts or trophozoites** would typically be detected on microscopy. *Ulcerative colitis* - Ulcerative colitis is an **inflammatory bowel disease** typically characterized by bloody diarrhea, abdominal pain, and systemic symptoms like fever and weight loss. - The patient's symptoms include the absence of blood in stools and no weight loss, with **normal ESR**, which makes ulcerative colitis unlikely. *Crohn's disease* - Crohn's disease is another **inflammatory bowel disease** that can affect any part of the GI tract and presents with chronic diarrhea, abdominal pain, and often systemic symptoms like weight loss, fever, or perianal disease. - The lack of weight loss, systemic inflammation markers (normal ESR), and absence of blood or inflammatory markers in the stool make Crohn's disease less probable. *Laxative abuse* - Laxative abuse can cause chronic diarrhea, but it's typically associated with a history of **eating disorders** (anorexia nervosa, bulimia nervosa) or other psychological conditions, which are not mentioned in this case. - The patient's description of abdominal discomfort relieved by defecation, urgency, and incomplete evacuation is more consistent with **IBS** (a functional bowel disorder) rather than solely laxative-induced diarrhea.

GI physiology (digestion, absorption, motility) US Medical PG Question 6: A 54-year-old man presents to his primary care physician with a 2-month-history of diarrhea. He says that he feels the urge to defecate 3-4 times per day and that his stools have changed in character since the diarrhea began. Specifically, they now float, stick to the side of the toilet bowl, and smell extremely foul. His past medical history is significant for several episodes of acute pancreatitis secondary to excessive alcohol consumption. His symptoms are found to be due to a deficiency in an enzyme. Which of the following enzymes is most likely deficient in this patient?

• A. Enterokinase
• B. Amylase
• C. Colipase
• D. Lipase (Correct Answer)
• E. Chymotrypsin

GI physiology (digestion, absorption, motility) Explanation: ***Lipase*** - The patient's history of **recurrent pancreatitis** likely led to **exocrine pancreatic insufficiency**, reducing the production of digestive enzymes, particularly **lipase**. - **Steatorrhea** (foul-smelling, floating, sticky stools) is a classic symptom of **fat malabsorption**, which occurs due to insufficient lipase for triglyceride digestion. *Enterokinase* - **Enterokinase** is an enzyme produced in the **duodenum** that activates trypsinogen to trypsin, which then activates other pancreatic proteases. - A deficiency would primarily cause **protein malabsorption**, not the pronounced fat malabsorption (steatorrhea) seen in this patient. *Amylase* - **Amylase** is responsible for **carbohydrate digestion**. - While chronic pancreatitis can lead to amylase deficiency, the primary symptom of this patient's diarrhea, steatorrhea, points more directly to **fat malabsorption** rather than carbohydrate malabsorption. *Colipase* - **Colipase** is a co-enzyme that helps **lipase** bind to the fat-water interface to digest triglycerides. - While essential for fat digestion, lipase itself is the primary enzyme responsible, and a direct deficiency in colipase alone is less commonly implicated as the sole cause of severe steatorrhea than a general pancreatic enzyme insufficiency affecting lipase production. *Chymotrypsin* - **Chymotrypsin** is a **protease** primarily involved in **protein digestion**. - A deficiency would lead to **protein malabsorption**, which typically presents with symptoms like muscle wasting and edema, rather than the prominent steatorrhea described.

GI physiology (digestion, absorption, motility) US Medical PG Question 7: A 24-year-old man comes to the physician with a 2-day history of fever, crampy abdominal pain, and blood-tinged diarrhea. He recently returned from a trip to Mexico. His temperature is 38.2°C (100.8°F). Abdominal examination shows diffuse tenderness to palpation; bowel sounds are hyperactive. Stool cultures grow nonlactose fermenting, oxidase-negative, gram-negative rods that do not produce hydrogen sulfide on triple sugar iron agar. Which of the following processes is most likely involved in the pathogenesis of this patient's condition?

• A. Dissemination via bloodstream
• B. Overactivation of adenylate cyclase
• C. Flagella-mediated gut colonization
• D. Invasion of colonic microfold cells
• E. Inhibition of host cytoskeleton organization (Correct Answer)

GI physiology (digestion, absorption, motility) Explanation: ***Inhibition of host cytoskeleton organization*** - The patient's symptoms (fever, crampy abdominal pain, blood-tinged diarrhea) and the microbiological findings (**nonlactose fermenting, oxidase-negative, gram-negative rods** that do not produce hydrogen sulfide) are characteristic of **Shigella infection**. - **Shigella** invades colonic epithelial cells and manipulates the host cell's **actin cytoskeleton** through effector proteins (IpaA, IpaB, IpaC) delivered via a **Type III secretion system**. - This cytoskeletal disruption enables **intracellular movement** via actin-based motility and **cell-to-cell spread**, allowing Shigella to evade immune defenses while causing characteristic inflammatory dysentery. *Dissemination via bloodstream* - While some bacterial infections cause bacteremia, **Shigella** infections are typically localized to the **gastrointestinal tract** and do not commonly disseminate systemically via the bloodstream. - **Bacteremia** due to *Shigella* is rare and usually occurs only in immunocompromised individuals or young children with severe disease. *Overactivation of adenylate cyclase* - **Overactivation of adenylate cyclase** producing **cyclic AMP** and leading to **secretory diarrhea** is characteristic of toxins like **cholera toxin** or **heat-labile enterotoxin of E. coli**. - **Shigella** primarily causes **inflammatory dysentery** through mucosal invasion and damage, not through this mechanism of fluid secretion. *Flagella-mediated gut colonization* - Many bacteria use **flagella** for motility and colonization, but **Shigella** species are notably **non-motile** and **lack flagella**. - Their pathogenesis relies on invasion and intracellular spread rather than flagella-driven colonization. *Invasion of colonic microfold cells* - While **Shigella does initially invade through M cells (microfold cells)** in the colonic epithelium to gain entry into the lamina propria, this is just the **initial entry step**, not the primary pathogenic mechanism that causes disease. - The key pathogenic process that leads to the characteristic symptoms is the **disruption of the host cytoskeleton** that enables intracellular replication and lateral spread through epithelial cells, causing the inflammatory dysentery seen in this patient.

GI physiology (digestion, absorption, motility) US Medical PG Question 8: Which neurotransmitter primarily mediates slow synaptic transmission in the enteric nervous system?

• A. Substance P
• B. Serotonin
• C. Acetylcholine
• D. Nitric oxide (Correct Answer)

GI physiology (digestion, absorption, motility) Explanation: **Nitric oxide** - **Nitric oxide (NO)** is a key **non-classical neurotransmitter** in the **enteric nervous system (ENS)**, mediating **slow synaptic transmission** due to its gaseous nature allowing for diffusion and longer-lasting effects. - It is involved in **smooth muscle relaxation**, **vasodilation**, and diverse gastrointestinal functions, including **peristalsis** and **sphincter relaxation**. *Substance P* - **Substance P** is a **neuropeptide** that acts as an **excitatory neurotransmitter** in the ENS, primarily mediating **fast synaptic transmission** and smooth muscle contraction. - It is involved in pain perception, inflammation, and is released by sensory neurons and some enteric neurons. *Serotonin* - **Serotonin (5-HT)** is a major neurotransmitter in the ENS, largely mediating **fast excitatory or inhibitory synaptic transmission** depending on the receptor subtype. - It plays a crucial role in regulating gut motility, secretion, and visceral sensation, and is involved in both rapid signaling and neuromodulation. *Acetylcholine* - **Acetylcholine (ACh)** is the primary **excitatory neurotransmitter** of the **parasympathetic nervous system** within the ENS, mediating **fast synaptic transmission** by binding to nicotinic and muscarinic receptors. - It is crucial for stimulating **smooth muscle contraction** (promoting peristalsis), increasing glandular secretions, and generally enhancing gut motility.

GI physiology (digestion, absorption, motility) US Medical PG Question 9: A 54-year-old man comes to the physician because of diarrhea that has become progressively worse over the past 4 months. He currently has 4–6 episodes of foul-smelling stools per day. Over the past 3 months, he has had fatigue and a 5-kg (11-lb) weight loss. He returned from Bangladesh 6 months ago after a year-long business assignment. He has osteoarthritis and hypertension. Current medications include amlodipine and naproxen. He appears pale and malnourished. His temperature is 37.3°C (99.1°F), pulse is 76/min, and blood pressure is 140/86 mm Hg. Examination shows pale conjunctivae and dry mucous membranes. Angular stomatitis and glossitis are present. The abdomen is distended but soft and nontender. Rectal examination shows no abnormalities. Laboratory studies show: Hemoglobin 8.9 g/dL Leukocyte count 4100/mm3 Platelet count 160,000/mm3 Mean corpuscular volume 110 μm3 Serum Na+ 133 mEq/L Cl- 98 mEq/l K+ 3.3 mEq/L Creatinine 1.1 mg/dL IgA 250 mg/dL Anti-tissue transglutaminase, IgA negative Stool culture and studies for ova and parasites are negative. Test of the stool for occult blood is negative. Fecal fat content is 22 g/day (N < 7). Fecal lactoferrin is negative and elastase is within normal limits. Which of the following is the most appropriate next step in diagnosis?

• A. CT scan of the abdomen
• B. IgG against deamidated gliadin peptide
• C. Schilling test
• D. Enteroscopy
• E. PAS-stained biopsy of small bowel (Correct Answer)

GI physiology (digestion, absorption, motility) Explanation: ***PAS-stained biopsy of small bowel*** - The patient's history of travel to Bangladesh, chronic diarrhea, malabsorption (weight loss, fatigue, elevated fecal fat, macrocytic anemia), and negative celiac serology (anti-tissue transglutaminase IgA) are highly suggestive of **Whipple's disease**. - **Periodic Acid-Schiff (PAS) staining** of a small bowel biopsy is the gold standard for diagnosing Whipple's disease, revealing **PAS-positive macrophages** containing *Tropheryma whipplei*. *CT scan of the abdomen* - While a CT scan can identify structural abnormalities or masses, it is not the most direct diagnostic test for **malabsorptive conditions** like Whipple's disease. - It would likely show non-specific findings such as **bowel wall thickening** or **lymphadenopathy**, but not the definitive histological changes. *IgG against deamidated gliadin peptide* - This test is used to diagnose **celiac disease**, but the patient's IgA anti-tissue transglutaminase was already negative, and this IgG test is typically performed when IgA deficiency is suspected or in young children. - Given the strong suspicion of an infectious etiology due to travel history and systemic symptoms, focusing solely on celiac serology is less appropriate as the first next step. *Schilling test* - The Schilling test is an **obsolete test** that was historically used to assess **vitamin B12 absorption** and differentiate causes of B12 deficiency (pernicious anemia, bacterial overgrowth, or pancreatic insufficiency). - This test is **no longer performed in clinical practice** due to unavailability of radioactive B12; modern evaluation uses serum B12, methylmalonic acid, and homocysteine levels. - While the patient has macrocytic anemia, the test would not directly address the underlying cause of fat malabsorption and systemic symptoms present. *Enteroscopy* - Enteroscopy allows for visualization and biopsy of the small bowel beyond the reach of a standard upper endoscopy. - While useful for obtaining biopsies, simply performing an enteroscopy without knowing what to look for or what specific stain to request (referring to PAS) on the biopsy would be less targeted than ordering a **PAS-stained biopsy** specifically.

GI physiology (digestion, absorption, motility) US Medical PG Question 10: A 30-year-old woman was found lying down and unresponsive by her parents 2 hours ago. She has no significant medical history. Two years ago, the woman discovered that her husband of 8 years was having an extramarital affair; this revelation subsequently resulted in a drawn-out divorce. After the separation, she moved back in with her parents, who note that she stays in her room, sleeps a lot, and rarely eats. A physical exam shows obtundation. Her temperature is 37.1ºC (98.7ºF), pulse is 110/min, respirations are 24/min, and blood pressure is 126/78 mm Hg. The patient’s admission labs are as follows: TSH 3.2 µU/mL Morning cortisol 8 µg/dL Prolactin 15 ng/mL FSH 7 mIU/mL LH 6 mIU/mL Glucose 22 mg/dL C-peptide not detected Beta-hydroxybutyrate ≤ 2.7 mmol/L Which of the following is most true of the cell type that is likely involved in the production of the molecule causing this patient’s symptoms?

• A. Located in the periphery of islets of Langerhans and produce glucagon
• B. Located in the center of islets of Langerhans and produce insulin (Correct Answer)
• C. Located in the adrenal medulla and produce epinephrine
• D. Located in the anterior pituitary and produce growth hormone
• E. Located in zona fasciculata of the adrenal cortex and produce cortisol

GI physiology (digestion, absorption, motility) Explanation: ***Located in the center of islets of Langerhans and produce insulin*** - This patient presents with **severe hypoglycemia** (glucose 22 mg/dL), **undetectable C-peptide**, and **inappropriately low beta-hydroxybutyrate** (≤ 2.7 mmol/L). The clinical context (depression, isolation) combined with undetectable C-peptide strongly suggests **exogenous insulin administration** (factitious hypoglycemia or suicide attempt). - The molecule **causing this patient's symptoms** is **insulin**, which drives glucose into cells and suppresses counterregulatory mechanisms, resulting in profound hypoglycemia and neuroglycopenic symptoms (obtundation). - **Beta cells** located in the **center of the islets of Langerhans** are the cell type that normally produces insulin. Even though this patient's hypoglycemia is caused by exogenous insulin (not endogenous production, as evidenced by undetectable C-peptide), the question asks about the cell type involved in producing the causative molecule - which is insulin, produced by pancreatic beta cells. - The key distinction: C-peptide is co-secreted with endogenous insulin, so its absence confirms an exogenous source, but insulin itself (whether endogenous or exogenous) is still the molecule causing the pathophysiology. *Located in the adrenal medulla and produce epinephrine* - **Chromaffin cells** in the adrenal medulla produce **epinephrine**, a key counterregulatory hormone that responds to hypoglycemia by promoting glycogenolysis and gluconeogenesis to raise blood glucose. - While epinephrine is involved in the physiologic response to this patient's condition, it is not the molecule **causing** the hypoglycemia - it's attempting to correct it. *Located in the anterior pituitary and produce growth hormone* - The anterior pituitary produces **growth hormone (GH)**, which has anti-insulin effects and promotes gluconeogenesis. - Like epinephrine, GH is a counterregulatory hormone that opposes hypoglycemia rather than causing it. *Located in zona fasciculata of the adrenal cortex and produce cortisol* - The **zona fasciculata** produces **cortisol**, a glucocorticoid that raises blood glucose through gluconeogenesis. - The patient's morning cortisol of 8 µg/dL is within normal range. Cortisol is another counterregulatory hormone, not the cause of hypoglycemia. *Located in the periphery of islets of Langerhans and produce glucagon* - **Alpha cells** at the periphery of islets produce **glucagon**, which opposes insulin action by promoting glycogenolysis and gluconeogenesis. - In exogenous insulin overdose, excess insulin suppresses glucagon secretion and overwhelms counterregulatory mechanisms, but glucagon itself is not causing the hypoglycemia.

GI physiology (digestion, absorption, motility) Flashcard 1 of 10

Question: Intestinal peristalsis occurs in response to binding of _____ to intrinsic primary afferent neurons (IPANs)

Answer: 5-HT (serotonin)

GI physiology (digestion, absorption, motility) Flashcard 2 of 10

Question: Vasoactive intestinal polypeptide (VIP) is secreted from _____ neurons in the gallbladder, small intestine, and sphincters

Answer: parasympathetic

GI physiology (digestion, absorption, motility) Flashcard 3 of 10

Question: Mucosal defenses include normal _____, which provides nutrients and picks up leaked acids

Answer: blood supply

GI physiology (digestion, absorption, motility) Flashcard 4 of 10

Question: Secondary lactase deficiency occurs due to loss of the intestinal _____

Answer: brush border

GI physiology (digestion, absorption, motility) Flashcard 5 of 10

Question: Mucus is secreted into the GI tract via _____ cells in the stomach, duodenum, salivary glands, and pancreas

Answer: mucous

GI physiology (digestion, absorption, motility) Flashcard 6 of 10

Question: _____ contractions serve to mix intestinal contents; "back-and-forth movement"

Answer: Segmentation

GI physiology (digestion, absorption, motility) Flashcard 7 of 10

Question: satiety

Answer: ventromedial area of the hypothalamus

GI physiology (digestion, absorption, motility) Flashcard 8 of 10

Question: What is the function of the area postrema?

Answer: emetic center of brain

GI physiology (digestion, absorption, motility) Flashcard 9 of 10

Question: Give two cell types rich in rough endoplasmic reticulum (RER).

Answer: intestinal goblet cells, plasma cells

GI physiology (digestion, absorption, motility) Flashcard 10 of 10

Question: Is the plasma membrane symmetric or asymmetric?

Answer: asymmetric interior vs exterior asymmetric regionally on same side