Also: EGF, kallikrein, R-proteins (haptocorrin for B12)
LO 4 — Satiety & Ghrelin
What is ghrelin, where is it produced, and what is its relationship to appetite?
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Answer
Ghrelin: peptide hormone from stomach fundus (X/A cells) Function: "hunger signal" — ↑appetite, triggers meal initiation Timing: peaks BEFORE meals (anticipatory)
Mnemonic: "Growing" = ghrelin stimulates growth of appetite
LO 4 — Leptin & Obesity
What is leptin, how does obesity affect leptin levels, and what is leptin resistance?
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Answer
Leptin: satiety hormone from adipocytes; long-term appetite suppression In obesity: leptin levels are HIGH (↑fat = ↑leptin) Leptin resistance: cells unresponsive to elevated leptin despite high serum levels
Test trap: Leptin is HIGH in obesity, not low
LO 4 — Post-Prandial Satiety Hormones
Name three hormones that signal satiety after a meal and their primary stimuli.
In diarrhea: loss of HCO₃− → non-gap metabolic acidosis; loss of K+ → hypokalemia
LO 14 — Secretory vs. Osmotic Diarrhea
Distinguish between secretory and osmotic diarrhea by stool electrolytes and mechanisms.
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Answer
Secretory: intestinal epithelium secretes Cl− (water follows); stool osmotic gap = normal; persists during fasting Osmotic: non-absorbable solute (lactose, MgSO4) draws water into lumen; stool osmotic gap >50; stops with fasting
Example secretory: cholera toxin (↑cAMP), heat-stable toxin (↑cGMP)
LO 11 — Acid-Suppressive Drugs
Compare H2 blockers vs. PPIs: mechanism, potency, and clinical use.
The ___________ glands produce serous saliva rich in α-amylase, while submandibular and sublingual glands produce ___________ secretion.
FIB 02 — LO 2
Salivary secretion is unique because ___________ and ___________ both stimulate it (unlike most organs where they are antagonistic).
Hint: Both SNS and PSNS → salivation (test trap!)
FIB 03 — LO 2
In low-flow saliva, ___________ and ___________ are reabsorbed by ductal cells, while ___________ and ___________ are secreted, resulting in ___________ saliva.
FIB 04 — LO 4
___________ is a hunger hormone from gastric fundus X/A cells that peaks ___________ meals, while ___________ is a satiety hormone from adipocytes that shows resistance in obesity.
FIB 05 — LO 5
Parietal cells secrete ___________ (via H⁺/K⁺ ATPase) and ___________ (required for B12 absorption in the ___________).
FIB 06 — LO 5
The rate-limiting step in parietal cell acid secretion is the ___________ ATPase, NOT carbonic anhydrase. This pump is the target of ___________ (irreversible inhibitor).
Hint: Test trap — rate-limiting is the ATPase!
FIB 07 — LO 6
The three phases of gastric acid secretion are: ___________ (30–40%, vagus), ___________ (50–60%, distension & gastrin), and ___________ (5–10%, mostly inhibitory).
Hint: Test trap — antral H. pylori causes DU, not gastric ulcer!
FIB 09 — LO 8
Pancreatic zymogens (trypsinogen, chymotrypsinogen, etc.) are activated in the duodenum by ___________, which converts ___________ to ___________ (the first active enzyme).
Hint: Trypsin then autocatalytically activates the rest.
FIB 10 — LO 9
___________ glands in the duodenum secrete HCO₃⁻-rich mucus to protect the epithelium from acidic chyme, while crypts of Lieberkühn secrete ___________ and ___________.
FIB 11 — LO 13
Loss of colonic HCO₃⁻ in diarrhea → ___________; loss of colonic K⁺ → ___________. Colonic mucus is secreted by ___________ cells.
FIB 12 — LO 14
___________ diarrhea persists during fasting and is caused by active epithelial secretion of Cl⁻, while ___________ diarrhea stops with fasting and is caused by non-absorbable solutes.
Instructions: Drag and drop the items into the correct order, then click "Check Order." Use "Show Answer" if you get stuck.
Drill 1 — Parietal Cell Acid Generation: Steps in Order
Arrange the biochemical steps of HCl production in parietal cells.
⠿CO₂ + H₂O → H₂CO₃ (via carbonic anhydrase)
⠿Cl⁻ enters canaliculus via apical Cl⁻ channel
⠿CO₂ enters parietal cell from blood
⠿H⁺/K⁺ ATPase pumps H⁺ into canaliculus (rate-limiting)
⠿H₂CO₃ → H⁺ + HCO₃⁻
⠿H⁺ + Cl⁻ → HCl in canaliculus lumen
CO₂ enters from blood
CO₂ + H₂O → H₂CO₃ via carbonic anhydrase
H₂CO₃ → H⁺ + HCO₃⁻
H⁺/K⁺ ATPase pumps H⁺ apically (RATE-LIMITING)
Cl⁻ enters via apical Cl⁻ channel
H⁺ + Cl⁻ → HCl in canaliculus
Drill 2 — Three Phases of Gastric Acid Secretion
Arrange the phases of gastric secretion in chronological order of a meal.
⠿Gastric phase: 50–60% of total HCl; triggered by gastric distension & gastrin
⠿Cephalic phase: 30–40% of total HCl; sight/smell/taste of food → vagus
⠿Intestinal phase: 5–10% of total HCl; MOSTLY INHIBITORY (secretin, PYY)
Cephalic phase — 30–40%; anticipatory, before food
⠿Acinar cells secrete isotonic NaCl + water + enzymes
⠿Result: HYPOTONIC saliva at low flow; approaches ISOTONIC at high flow
Acinar cells: isotonic NaCl + water
Ductal cells reabsorb Na⁺ & Cl⁻
Ductal cells secrete K⁺ & HCO₃⁻
Final result: hypotonic at low flow, isotonic at high flow
Instructions: Click an item on the left, then click its match on the right. Correct pairs turn green; wrong pairs flash red.
Set 1 — Gastric Cell Type → Secretory Product
Match each gastric cell type to its primary secretory product.
Cell Type
Parietal cell
Chief cell
G cell
D cell
Primary Product
Gastrin (↑HCl)
HCl + Intrinsic factor
Somatostatin (inhibits all)
Pepsinogen (→ pepsin)
Score: 0/4 correct
Set 2 — GI Hormone → Source Cell
Match each hormone to the cell type that secretes it.
Hormone
Gastrin
CCK
Secretin
Ghrelin
Source Cell
I cells (duodenum)
G cells (antrum)
S cells (duodenum)
X/A cells (gastric fundus)
Score: 0/4 correct
Set 3 — Acid-Suppressive Drug Class → Mechanism of Action
Match each drug class to how it suppresses gastric acid.
Drug Class
H2 blocker (cimetidine)
PPI (omeprazole)
Anticholinergic (atropine)
Sucralfate
Mechanism
Irreversibly inhibits H⁺/K⁺ ATPase (most potent)
Reversibly blocks H2 receptor
Blocks ACh (M3) stimulation of parietal cells
Forms protective barrier (does not block acid)
Score: 0/4 correct
Set 4 — Salivary Gland → Secretion Type & Key Component
Match each gland to the type of secretion and its key enzyme/function.
Gland
Parotid
Submandibular
Sublingual
Type & Component
Serous (α-amylase for starch digestion)
Mixed (mucous & serous)
Mixed (predominantly mucous)
Score: 0/3 correct
Test Trap Mode: Each statement is either TRUE or FALSE as written. Many are designed to catch common exam errors. Click T or F — then read the explanation carefully.
Trap 01 — LO 2
"Both sympathetic and parasympathetic nervous systems inhibit salivation (as in most organs)."
FALSE. Salivation is UNIQUE: BOTH SNS & PSNS STIMULATE it (not antagonistic as in other organs). PSNS dominant (M3 → watery, enzyme-rich); SNS brief (α1/β → thick, mucous). This is a classic test trap.
Trap 02 — LO 3
"Saliva is ISOTONIC at both low and high flow rates because acinar cells produce isotonic secretion."
FALSE. Saliva is HYPOTONIC at low flow (ductal cells have more time to reabsorb Na⁺/Cl⁻) and approaches ISOTONIC at high flow (less time for modification). The ducts are the key to understanding saliva osmolarity.
Trap 03 — LO 4
"Obese patients have HIGH ghrelin levels that drive their continued overeating."
FALSE. This is partially true for leptin resistance but NOT for ghrelin. In obesity: leptin is HIGH (but cells are unresponsive = resistance). Ghrelin is often NORMAL or even LOW. The trap is confusing leptin and ghrelin.
Trap 04 — LO 5
"Carbonic anhydrase is the rate-limiting step in parietal cell HCl production."
FALSE. The H⁺/K⁺ ATPase is the rate-limiting step, not carbonic anhydrase. PPIs target this pump. This is a high-yield trap on standardized exams.
Trap 05 — LO 6
"Antral H. pylori infection damages parietal cells, leading to DUODENALulcer."
FALSE (partially). Antral H. pylori damages D CELLS (not parietal) → ↓somatostatin → ↑gastrin → ↑↑↑ HCl from parietal cells → DUODENAL ulcer. Corpus infection damages parietal cells → GASTRIC ulcer. Antral infection counterintuitively causes duodenal ulcers.
Trap 06 — LO 8
"Trypsin activates trypsinogen in the duodenum, starting the zymogen activation cascade."
FALSE.Enterokinase (brush border) activates trypsinogen → trypsin (first step). Trypsin then autocatalytically activates the other zymogens. Backwards activation is a classic trap.
Trap 07 — LO 9
"At high gastric pH (e.g., during PPI use), pepsinogen is maximally activated."
FALSE. Pepsinogen requires ACIDIC pH <3.5 to be converted to pepsin. High pH (from PPIs) → pepsinogen remains INACTIVE. Over-suppression of acid can impair protein digestion.
Trap 08 — LO 10
"Cystic fibrosis presents with thick pancreatic secretions because the pancreatic acinar cells produce abnormally viscous enzymes."
FALSE. Enzymes are normal; the problem is with DUCTAL CFTR (cystic fibrosis transmembrane regulator). CFTR defect → ↓HCO₃⁻ secretion → thick, acidic secretions (not enough water & alkali to dilute) → duct obstruction → autodigestion → steatorrhea.
Trap 09 — LO 13
"Loss of K⁺ in diarrhea is primarily due to decreased K⁺ intake."
FALSE. Hypokalemia in diarrhea is due to LOSS of K⁺ in stool (colonic epithelial cells secrete K⁺ via aldosterone-driven channels), not decreased intake. The colon normally reabsorbs K⁺; in diarrhea, transit is too rapid.
Trap 10 — LO 14
"Osmotic diarrhea persists even when the patient fasts overnight."
FALSE. Osmotic diarrhea STOPS with fasting because the osmotically active solute is no longer entering the gut. Secretory diarrhea PERSISTS despite fasting (active epithelial Cl⁻ secretion continues). This is the key clinical distinction.
Salivary Glands & Secretion
Gland
% of Total
Secretion Type
Key Component
Flow Rate Effect
Parotid
25%
Serous
α-amylase (starch → maltose)
Serous predominates at high flow
Submandibular
70%
Mixed
α-amylase + mucins
Mixed at all flow rates
Sublingual
5%
Mixed (mucous-dominant)
Mucins (lubrication)
Mucous predominates at low flow
Saliva (overall)
~1.5 L/day
Isotonic → hypotonic (low flow)
EGF, R-proteins (haptocorrin), IgA, lysozyme
Hypotonic at low (reabsorption), isotonic at high
Gastric Cell Types & Products
Cell Type
Location
Primary Product
Stimulated By
Clinical Significance
Parietal
Fundus/body
HCl (H⁺/K⁺ ATPase) + Intrinsic factor
ACh (M3), Histamine (H2), Gastrin (CCK-B)
Target of H2 blockers & PPIs; IF loss → B12 deficiency
Chief
Fundus/body
Pepsinogen (→ pepsin at pH <3.5)
ACh, gastrin (indirectly)
Inactive at high pH; requires acid activation
G cell
Antrum + duodenum
Gastrin → ↑HCl + motility
Protein/amino acids, gastric distension
Zollinger-Ellison = gastrinoma → severe ulcers
D cell
Antrum + duodenum
Somatostatin (inhibits ALL)
Acid (pH <3.5)
Antral D cell loss (H. pylori) → duodenal ulcer
ECL cell
Fundus glands
Histamine → H2 receptors on parietal cells
Gastrin (G17 main form)
PPI use → hyperplasia (benign if no MEN1)
Mucous cell
Gastric pits
Alkaline mucus + HCO₃⁻ (protective barrier)
Constant; ↑ by vagal stimulation
Lost in atrophic gastritis; NSAID ulcers penetrate this barrier
Three Phases of Gastric Secretion
Phase
Timing
% of Total HCl
Stimulus
Mechanism
Duration
Cephalic
Before food arrives
30–40%
Sight, smell, taste, thought of food
Vagus nerve (CN X) → ACh → parietal cells
~1 hour
Gastric
After food enters stomach
50–60%
Gastric distension + amino acids/peptides
Mechano- & chemoreceptors → gastrin release from G cells
~3–4 hours
Intestinal
As chyme enters duodenum
5–10%
Acid chyme + nutrients
Mostly INHIBITORY (secretin, PYY, GLP-1 suppress further gastrin & acid)