05 GI
Antiemetics
- Solitary track runner: the nucleus tractus solitarius (NTS, or vomiting center) located in the medulla, receives inputs from the GI tract, vestibular system, and area postrema
- Vomit on track: the NTS projects neurons to other medullary nuclei to coordinate the vomiting response
- Stomach hammer throw area: the GI tract communicates directly with the NTS (via CN X)
- Vegas sign at the stomach area: vagal afferents from the GI tract communicate with the NTS
- Smiley hammer at the stomach area: GI irritation (due to infection, chemotherapy, distention) causes mucosal serotonin release
- “1-2-3 Hammer Throw!”: serotonin activates 5HT-3 receptors on the vagal afferents
- Semicircular canal: the vestibular system communicates directly with the NTS (via CN VIII)
- Vests at the semicircular canal: the vestibulocochlear nerve (CN VIII) from the vestibular system communicates with the NTS
- Seasick at the canal: the vestibular system cis responsible for vertigo and motion sickness (vestibular nausea)
- Extreme postures next to the track: the area postrema (chemoreceptor trigger zone) is located adjacent to the NTS (outside the BBB in the 4th ventricle) and responds to emetogenic substances (e.g. chemotherapeutic agents)
- Ribbon dancer blocking the Hammer Throw: ondansetron antagonizes 5HT-3 receptor on vagal afferents in the GI tract (treats chemo-induced or post-op vomiting)
- Hammer tightening gut: ondansetron can cause constipation
- Hammer hitting head: ondansetron can cause headache and dizziness
- Twisted torsades streamer: ondansetron can prolong the QT interval and induce torsades
- Pile of smiley faces: ondansetron can cause serotonin syndrome (symptoms include rigidity, tremor, hyperthermia, confusion)
- Allergy inducing, Q shaped dandelions: the vestibular system contains H1 histamine receptors (coupled to Gq)
- Bee swatters: 1st generation H1 receptor blockers (e.g. diphenhydramine, meclizine) treat vestibular nausea (motion sickness)
- M1 motorcycle parking: the vestibular system contains M1 muscarinic receptors
- Telescope: scopolamine (muscarinic antagonist) treats vestibular nausea (motions sickness)
- Seasick sailor outfits: motion sickness (vestibular nausea) is treated with 1st generation H1 antagonists (e.g. diphenhydramine) and scopolamine (muscarinic antagonist)
- 2 D-ring ropes: the area postrema contains D2 receptors
- Tickler blocking the D-rings: metoclopramide antagonizes D2 receptors in the area postrema (treats chemotherapy induced vomiting)
- Contracted stomach: metoclopramide has upper GI prokinetic effects (useful for treatment of delayed gastric emptying due to post-surgical disorders and diabetic gastroparesis)
- “Do not obstruct”: metoclopramide (D2 antagonist) is contraindicated in small bowel obstruction
- Mud puddle: metoclopramide can cause diarrhea (prokinetic effect)
- Sleeping judge: metoclopramide can cause drowsiness (central D2 blockade)
- Crying coach: metoclopramide can cause depression (central D2 blockade)
- EXTRA pyramidal newspaper hat: metoclopramide can cause extrapyramidal effects due to central D2 blockade (e.g. dystonia, akathisia, parkinsonian features)
- Sticking out tongue: metoclopramide can cause tardive dyskinesia with chronic use (central D2 blockade)
- Now More Spicy chicken: metoclopramide (D2 antagonist) can cause neuroleptic malignant syndrome (symptoms include fever, rigidity, mental status changes, autonomic instability, rhabdomyolysis)
- Elevated milk release: metoclopramide can cause elevated prolactin levels (central D2 blockade)
- Twisted torsades streamer: metoclopramide can cause QT prolongation and induce
torsades
- PlaNK 1: the area postrema contains neurokinin 1 (NK1) receptors (activated by substance P)
- “Substance pee check”: substance P binds NK1 receptors in the area postrema
- “Participants”: aprepitant antagonizes the NK1 receptors in the area postrema (treats chemotherapy induced vomiting)
GERD
- “Pour-it-all” table: parietal cells in the gastric mucosa are responsible for acid secretion
- Battery powered puree pump: H+/K+ ATPase (proton pump) on the luminal membrane pumps H+ into the lumen
- Banana into the pump, lemons out: the H+/K+ ATPase exchanges one K+ for one H+ at the luminal membrane
- Three P batteries: ATPase
- Sidewalk: lumen of the stomach
Histamine
- “Enter CarefulLy”: enterochromaffin-like (ECL) cells
- Bees released from ECL tree: the ECL cell releases histamine (activates the parietal cells)
- Bees swarming honey pot: histamine (released by the ECL cell) activates H2 receptors on the parietal cell
- Honey pot with 2 “S” handles: H2 histamine receptors (coupled to Gs) on the basolateral membrane
- Honey pot kid knocking over acid pitcher: activation of H2 receptors upregulates the H+/K+ ATPase → increased acid secretion
Gastrin
- Gas truck releasing gas tanks: G-cells release gastrin (which stimulates ECL and parietal cells)
- Vegas sticker: vagal stimulation stimulates the G cell to release gastrin (via GRP)
- Gate release pull: gastrin releasing peptide (GRP) from the vagus nerve activates G cells
- Gas powered blower releasing bees from ECL tree: gastrin (released by G cells) stimulates the ECL cell to release histamine (CCK receptor)
- Gas powered acid pump: gastrin (released by G cells) stimulates the parietal cell to secrete H+ (minor effect)
Vagal
- Motorcycle attached to stand in M3: M3 acetylcholine receptors are located on the parietal cell
- Vegas sticker: vagal stimulation stimulates the parietal cell to secrete acid (via M3 receptors)
- 2 bee swatters: H2 histamine receptor antagonists (e.g. ranitidine, cimetidine) inhibit acid secretion by parietal cells
- Tie-dye: “-tidine” suffix of the H2 receptor antagonists (e.g. ranitidine, cimetidine, famotidine, nizatidine))
- Gargling: H2 blockers (e.g. ranitidine, cimetidine) treat GERD (PPIs are first line)
- Ulcerated sidewalk: H2 blockers (e.g. ranitidine, cimetidine) treat gastric and duodenal ulcers (PPIs are first line)
- Tie-dye kid on the cement: cimetidine (H2 blocker with antiandrogenic side effects)
- Dented chrome bumper: cimetidine inhibits cytochrome P-450
- Pot lids on chest: cimetidine can cause gynecomastia
- Droopy honey wand: cimetidine can cause impotence
- Milk shooting from nose: cimetidine can cause elevated prolactin levels
- Girl scout blocking puree pump: proton pump inhibitors (PPIs) irreversibly inhibit the H+/K+ ATPase (the final common pathway for H+ secretion)
- PRIZE: “-prazole” suffix of PPIs (e.g. omeprazole, lansoprazole, rabeprazole)
- Jumbo gas tank: gastrinoma causing hypersecretion of gastric acid (Zollinger-Ellison syndrome - treat with PPIs)
- Helicopter hat: PPIs treat Helicobacter pylori infection
- Chocolate fondue fountain: PPIs increase the risk of Clostridium difficile infection (gastric acid important for bacteria proliferation)
- Dirty lung spots: PPIs increase the risk of respiratory infections (e.g. pneumonia)
- Medals bound to wagon: PPIs decrease the absorption of Ca2+, Mg2+, and Fe2+ (requires acidic environment)
- Fractured axel: PPIs may increase the risk of osteoporotic hip fractures (due to decreased Ca2+ absorption)
- Porous wood: PPIs may worsen osteoporosis (due to decreased Ca2+ absorption)
- Falling magnets: PPIs can cause hypomagnesemia
- Stop sign: somatostatin (SST) inhibits the release of histamine by ECL cells
- Stop sign: somatostatin (SST) inhibits the release of gastrin by G cells (and SST receptor positive gastrinomas)
- Octagon: octreotide (a long acting SST analog) inhibits ECL cells
- Octagon: octreotide (a long acting SST analog) inhibits G cells (useful in the treatment of gastrinoma/Zollinger-Ellison syndrome)
Laxatives
- not direct stimulation of GI motility (prokinetics, muscarinic agonists)
- changes consistency
- Spa water: osmotic laxatives (e.g. magnesium compounds, lactulose, polyethylene glycol) are nonabsorbable substances that draw water into the intestinal lumen → distention → peristalsis. Rapid action. Rapidly decompressing
- Magnets over water: magnesium compounds (e.g. magnesium hydroxide, magnesium citrate) are osmotic laxatives
- Peg drain cover: polyethylene glycol (PEG) is an osmotic laxative (nonabsorbable sugar), electrolyte balanced and used for preendoscopic prep
- Relaxulose: lactulose is an osmotic laxative (nonabsorbable sugar)
- Cirrhotic liver and brain coral: hepatic encephalopathy (a neurologic complication of cirrhosis due to the buildup of ammonia and other toxins)
- Relaxulose into the liver and brain coral tank: lactulose is useful in the treatment of hepatic encephalopathy
- Fish eating lactulose: intestinal bacteria metabolize lactulose into acidic metabolites
- Acidic pH meter: acidic metabolites decrease the pH of the intestinal lumen
- NH4+ release valve: ammonia (NH3) is trapped as ammonium (NH4+) in the acidic intestinal lumen and excreted
- Fisherman removing fish: rifaximin (a poorly absorbed antibiotic) eradicates ammonia producing intestinal bacteria (treats hepatic encephalopathy)
- Spilling mud bath: laxatives can cause diarrhea and dehydration
- Bulky seaweed: psyllium is a bulk-forming laxative (indigestible hydrophilic colloid → absorbs water → distention → peristalsis)
- Water penetrating canoe at the DOCK: docusate is a stool softener (surfactant agent that facilitates penetration of stool by water and lipids)
- Stimulating suntan lotion: senna is a stimulant laxative a.k.a cathartic (stimulation of enteric nervous system and colonic secretions)
- Brown gut: chronic use of senna causes melanosis coli (brown pigmentation of the colon)
- Muddy slippers left outside: antidiarrheal agents (featured in massage room)
- Utopia: opioid agonists (e.g. diphenoxylate, loperamide) treat diarrhea
- μssage: opioids treat diarrhea by activating μ-opioid receptors in the GI tract
- Lop-eared rabbit: loperamide treats diarrhea (μ-opioid agonist that does not cross the BBB → no analgesia or potential for addiction)
- Lop-eared rabbit hopping back and forth: opioid agonists (e.g. loperamide) increase colonic phasic segmenting activity → increased colonic transit time
- Dolphins: diphenoxylate treats diarrhea (μ-opioid agonist with some ability to cross the BBB → combined with atropine to prevent abuse)
- Red stool and inflammatory candles outside door: antidiarrheal agents are contraindicated in patients with bloody diarrhea or fever
- Clogged: opioids can cause constipation
- VIP CUSTOMERS only crab: VIPoma and carcinoid tumor cause secretory diarrhea
- Octagon stop sign: octreotide (a somatostatin "stop" analog) treats the symptoms of VIPoma and carcinoid syndrome (e.g. secretory diarrhea)
Diabetes
- Welcome INSIDE mat: insulin (the storage and anabolic hormone of the body)
- LangerHansel: islets of Langerhans in the pancreas (the site of beta cells that produce insulin)
- Beta-2 tuba: pancreatic beta cells produce insulin (stimulated by many factors including glucose and sympathetic activation of beta-2 receptors)
- LangerHansel’s candy: glucose - the most potent stimulant of insulin secretion
- Closed gate around banana candy flowers: glucose increases ATP levels in the beta cell → ATP dependent K+ channels CLOSE
- Gretel rushing in on calci-yum icecream flower: closing the ATP dependent K+ channels causes the beta cell to depolarize → voltage gated Ca2+ channels open → Ca2+ INFLUX → insulin secretion
- C wrapper: C-peptide (cleaved from proinsulin in the secretory granule) is released with endogenous secretion of insulin
- Tyrosine tire swing: the insulin receptor contains an intracellular tyrosine kinase domain
- 4 on open door: insulin inserts glucose transporter type 4 (GLUT4) into the membrane of peripheral tissues (primarily adipose and muscle)
- Full liver candy jar: insulin increases hepatic glycogen stores (increased glycogenensis, decreased glycogenolysis)
- Glycogen glazed ham: insulin increases glycogen storage and protein synthesis in muscle
- Full fatty donut jar: insulin increases triglyceride storage in adipocytes
- Eaten banana candy: insulin decreases serum K+ (increased Na+/K+ATPase in skeletal muscle drives K+ into the cells)
- Girls And Lads: insulin Glulisine, Aspart, Lispro (rapid acting, short duration)
- Tall immediate peak: insulin glulisine, aspart, and lispro have a rapid onset and short duration of action
- Birds nibbling the peak: insulin glulisine, aspart, and lispro control the postprandial glucose spike
- Rest Now: Regular insulin, NPH insulin (Neutral Protamine Hagedorn) (intermediate acting)
- Delayed peak: regular and NPH insulin have a delayed onset and intermediate duration of action (NPH is more delayed)
- Ivy under “R”: regular insulin can be administered IV
- Ivy next to eaten banana: IV regular insulin is useful in the management of hyperkalemia (administer with glucose!)
- Candy key: diabetic ketoacidosis (DKA - presents with vomiting, fatigue, polyuria)
- Ivy next to candy key: IV regular insulin is useful in the management of DKA (watch K+ levels!)
- Don’t Go: insulin Detemir, Glargine (long acting)
- Flat roof: insulin detemir and glargine have long durations of action and provide a steady background level of insulin (glargine has no peak)
- Falling candy: insulin therapy can cause hypoglycemia (presents with tachycardia, palpitations, sweating, nausea)
- Sulfa egg laying swan: sulfonylureas (e.g. glyburide, glipizide) are sulfa drugs
- Sulfa swan lake behind CLOSED banana gate: sulfonylureas bind the ATP-dependent K+ channels on beta cells → release of endogenous insulin
- Mother swan in a maid outfit: “-amide” suffix of 1st generation sulfonylureas (e.g. tolbutamide, chlorpropamide) (long duration of action, rarely used)
- Goslings riding on mother’s back: “-ride” suffix of 2nd generation sulfonylureas (e.g. glyburide, glimepiride (smaller dosing, long duration of action)
- Short zig-zagging gosling: glipizide (2nd generation sulfonylurea) has the shortest duration of action (less risk of hypoglycemia)
- Gliding: “-glinide” suffix of the meglitinides (e.g repaglinide, nateglinide)
- Gliding goose behind CLOSED banana gate: meglitinides (glinides) bind the ATP- dependent K+ channels on beta cells → release of endogenous insulin
- 2 fingers: sulfonylureas and meglitinides (glinides) are oral agents used in the treatment of TYPE 2 diabetes (require functional beta cells for endogenous insulin release)
- C wrapper: sulfonylureas and meglitinides (glinides) increase endogenous insulin release and C-peptide levels
- Father gliding goose can’t lay eggs: meglitinides (glinides) are NOT sulfa drugs (can be used in patients with an allergy to sulfonylureas)
- Falling candy: sulfonylureas and meglitinides (glinides) can cause hypoglycemia
- Fat old hag: sulfonylureas and meglitinides (glinides) can cause weight gain
- “Do not drink” next to mother sulfonylurea swan: some 1st generation sulfonylureas (e.g. chlorpropamide) cause a disulfiram-like reaction with ingestion of alcohol
- Chlorpropamide: SIADH
- 2 fingers: GLP-1 agonists and DPP-4 inhibitors are oral agents used in the treatment of TYPE 2 diabetes (require functional beta cells for endogenous insulin release)
- ExenaTIDE detergent: “-tide” suffix of GLP-1 agonists (e.g. exenatide, liraglutide)
- Gulp activated by hag: GLP-1 agonists (e.g. exenatide) activate the glucagon-like peptide-1 (GLP-1) receptor (increased insulin release and satiety, decreased glucagon release and gastric emptying)
- Gs protein AC
- 4 DRIPPING laundry items: dipeptidyl peptidase-4 (DPP-4) inhibitors (gliptins) prevent the breakdown of GLP-1
- Clipped in clothespins: “-gliptin” suffix of the DPP-4 inhibitors (e.g. sitagliptin, saxagliptin, linagliptin)
- Endogenous gulps: DPP-4 inhibitors (gliptins) increase levels of endogenously secreted GLP-1 (increased insulin release and satiety, decreased glucagon release and gastric emptying)
- Falling empty glucagon packets: GLP-1 agonists and DPP-4 inhibitors decrease glucagon secretion
- Sealed gastric container: GLP-1 agonists and DPP-4 inhibitors decrease gastric emptying
- Clothespin clipping nose: DPP-4 inhibitors (gliptins) can increase the risk of nasopharyngitis and upper respiratory tract infections
- Squeezing pancreas sponge: GLP-1 agonists (e.g. exenatide) can cause pancreatitis
- Candies NOT falling: GLP-1 agonists and DPP-4 inhibitors do NOT cause hypoglycemia
- C wrapper: GLP-1 agonists and DPP-4 inhibitors increase endogenous insulin release and C-peptide levels
Diabetes 2
- 2nd grade: these agents are used in the treatment of TYPE 2 diabetes (require functional beta cells for endogenous insulin release)
- Metaphor: metformin (a biguanide) is the first line oral agent for the management of type 2 diabetes
- Bitten mitochondrial candy: metformin inhibits mitochondrial enzyme glycerophosphate dehydrogenase (mGDP)
- AMPKandy: metformin activates the enzyme AMP-activated protein kinase (AMPK) → decreased gluconeogenesis, increased insulin sensitivity
- Stopping candy release from liver bag: metformin modulates enzyme function to decrease hepatic gluconeogenesis
- INSIDE open candy box: metformin increases insulin sensitivity
- Spilled sour milk: metformin can cause lactic acidosis
- Cracked kidney tray: renal insufficiency increases the risk of metformin induced lactic acidosis. Excreted by kidney
- Nauseated: metformin can cause GI side effects (e.g. anorexia, nausea, vomiting, diarrhea)
- Skinny kid: metformin can cause modest weight reduction
- Glitter: “-glitazone” suffix of the thiazolidinediones (glitazones- e.g. rosiglitazone, pioglitazone)
- PPARy in circle: thiazolidinediones (glitazones) are ligands of peroxisome proliferator- activated receptor gamma (PPAR-γ) (an intranuclear receptor that regulates gene transcription)
- Turtle neck: PPAR-γ upregulates adiponectin (increased insulin sensitivity and fatty acid oxidation). Adiponectin low in diabetes pts
- Elevated fatty donut jar: thiazolidinediones (glitazones) increase the differentiation and number of adipocytes
- Eating fatty donut: thiazolidinediones (glitazones) increase triglyceride storage and fatty acid oxidation → decreased serum triglycerides
- 4 on open door: thiazolidinediones (glitazones) upregulate GLUT4 in peripheral tissues (increased glucose uptake)
- INSIDE open candy box: thiazolidinediones (glitazones) increase insulin sensitivity
- Fat belly: thiazolidinediones (glitazones) can cause weight gain
- Baggy pants: thiazolidinediones (glitazones) can cause fluid retention and peripheral edema in renal tubules
- Crushed failing heart balloon: thiazolidinedione (glitazones) induced fluid retention can exacerbate heart failure
- Fractured chair leg: thiazolidinediones (glitazones) can increase the risk of atypical extremity fractures in women (due to decreased bone mineral density)
- Amy and Lynn: amylin (islet amyloid polypeptide) analogues (e.g. pramlintide) (decreased glucagon, gastric emptying, and appetite)
- Falling candy: amylin analogues (e.g. pramlintide) can cause hypoglycemia
- Closed gastric water cooler: amylin analogues (e.g. pramlintide) decrease gastric emptying
- Falling empty glucagon packets: amylin analogues (e.g. pramlintide) decrease glucagon secretion
- 1 and 2: amylin analogues (e.g. pramlintide) can be useful in the management of type 1 and type 2 diabetes
- Eaten cupcake: amylin analogues (e.g. pramlintide) can be used to control the postprandial glucose spike
- Nauseated: pramlintide can cause GI side effects (e.g. nausea, vomiting, anorexia)
- A-Carb wigglers: acarbose and miglitol (alpha-glucosidase inhibitors)
- “Monosaccharide free”: inhibition of alpha-glucosidase enzymes decreases the conversion of disaccharides into absorbable monosaccharides
- Brush border flags: alpha-glucosidase inhibitors decrease the activity of disaccharidases on the intestinal brush border
- Delayed bag opening: alpha-glucosidase inhibitors delay carbohydrate absorption
- Eaten cupcake: alpha-glucosidase inhibitors (e.g. acarbose, miglitol) can be used to control the postprandial glucose spike
- Leaky bathroom puddle: alpha-glucosidase inhibitors can cause GI side effects (e.g. diarrhea, flatulence, abdominal pain) due to fermentation of the undigested carbohydrates by gut bacteria
- Flossing: “-flozin” suffix of the SGLT2 inhibitors (e.g. canagliflozin, dapagliflozin)
- Salty Glucose Co.: sodium-glucose cotransporter 2 (SGLT2) reabsorbs glucose in the proximal tubule (inhibition leads to urinary glucose loss)
- Pro Cart Track: proximal convoluted tubule of the nephron (site of action of SGLT2 inhibitors)
- Bladder cup: SGLT2 inhibitors (e.g. canagliflozin, dapagliflozin can increase the risk of UTI (due to increased urine glucose concentration)
- Snow hitting crotch: SGLT2 inhibitors (e.g. canagliflozin, dapagliflozin) can increase the risk of vaginal candidiasis
- Canada: Candida albicans
- Fainting: SGLT2 inhibitors (e.g. canagliflozin, dapagliflozin) can cause hypotension (due to osmotic diuresis)
- Cracked kidney tray: SGLT2 inhibitors are contraindicated in renal insufficiency
Thyroid
PTU
- Evil follicu-LAIR: thyroid follicular cell (site of iodine uptake and thyroid hormone production)
- Salty sodium peanuts entering lair: sodium enters thyroid follicular cell through the sodium-iodide symporter
- Iodide vial smuggled in with salty peanuts: the sodium-iodide symporter concentrates iodide in the follicular cell
- Follicu-LAIR truck lumen: thyroid follicle lumen (site of iodide storage as thyroglobulin)
- TransPOrter: thyroid peroxidase (TPO - enzyme involved in iodide oxidation and organification)
- Rusty oxidized transport truck: TPO oxidizes iodide into iodine
- “Thyro-global” truck: thyroglobulin (tyrosine rich protein precursor to thyroid hormones located in the follicular lumen)
- Organic foods transporter truck: TPO facilitates iodine organification (iodination of tyrosine residues on thyroglobulin)
- Coupled tyres of transport truck: TPO facilitates coupling of iodinated tyrosine residues
- Time bomb prep table in the follicu-LAIR: thyroid hormones (T4 and T3) are cleaved from thyroglobulin in the follicular cell (T4 in greater quantities)
- T4 time bomb: tetraiodothyronine (thyroxine, T4)
- T3 time bomb: triiodothyronine (T3) is the more potent form of thyroid hormone
- T4 detonator in the periphery: 5’ deiodinase in the peripheral tissues converts T4 to T3
- Sensitive to catfish: thyroid hormone increases the sensitivity of peripheral tissues to catecholamines (increased number of beta-adrenergic receptors)
- Anxious henchman with big bowtie: hyperthyroidism is associated with hypermetabolic and hyperadrenergic symptoms (e.g. tachycardia, palpitations, insomnia, anxiety, tremor, heat intolerance, weight loss)
- Bulging infrared goggles: Grave’s ophthalmopathy (increased volume of retroorbital connective tissue, due to cellular proliferation, inflammation, and the accumulation of glycosaminoglycans) → exophthalmos
- Radioactive vial: hyperthyroidism due to Graves' disease can be treated with ablating doses of radioactive iodine (131-I)
- Bulging radioactive goggles: radioactive iodine treatment can exacerbate Grave’s ophthalmopathy
- “PTU!” agent firing at the transporter: propylthiouracil (PTU - a thionamide) treats hyperthyroidism by inhibiting TPO
- Evil math equations striking transporter: methimazole (thionamide) treats hyperthyroidism by inhibiting TPO
- “PTU!” agent firing at the bomb trigger: PTU treats hyperthyroidism by inhibiting 5’ deiodinase → decreased conversion of T4 into T3
- Silenced bugle gun pointed at catfish tank: beta blockers treat the hyperadrenergic symptoms of hyperthyroidism
- Silenced bugle gun pointed at trigger: beta blockers treat hyperthyroidism by inhibiting 5’ deiodinase → decreased conversion of T4 into T3
- Moon face death coaster blocking trigger: glucocorticoids treats hyperthyroidism by inhibiting 5’ deiodinase → decreased conversion of T4 into T3
- Moon face death coaster hitting goggles: glucocorticoids treat Grave’s ophthalmopathy
- Thwarted Dr. Storm: treat thyroid storm by 1) blocking sympathetic effects (beta blockers); 2) blocking thyroid hormone synthesis (PTU); and blocking conversion of T3 to T4 (beta blockers, PTU, glucocorticoids)
- Undone bowtie: radioactive iodine treatment can cause hypothyroidism
- Anxious radioactive henchman: radioactive iodine treatment can exacerbate HYPERthyroidism
- Broken liver beaker: PTU can cause severe hepatotoxicity
- Chemical spots: PTU can cause a maculopapular rash
- Self destruct sand timer: PTU and methimazole can cause agranulocytosis. Risk of infection
- Plastic chew bones: PTU and methimazole can cause aplastic anemia
- Guard wolf: PTU and methimazole can cause drug induced lupus
- Inflamed leash: PTU can cause ANCA-associated vasculitis
- Tarantula: methimazole is a first trimester teratogen
- Fat, cold, fatigued mixologist: hypothyroidism is associated with dry brittle hair, lethargy, fatigue, weakness, decreased BMR, cold intolerance, and myxedema
- Mixing cold drinks: untreated hypothyroidism can lead to myxedema coma (progressive weakness, stupor, hypothermia, hypoventilation, hypoglycemia, hyponatremia, death)
- Synthetic T4 time bombs: levothyroxine (synthetic T4) treats hypothyroidism
- Anxious agent taking cover: levothyroxine therapy can cause HYPERthyroidism
- Obstructive box of anions: anions such as perchlorate, pertechnetate, and thiocyanate competitively inhibit the sodium-iodide transporter (treat accidental radioactive iodine exposure). Decreased reduction of iodide uptake
Bisphosphonate
- Osteo-builders: osteoblasts
- Destructive class: osteoclasts
- DONATE: “-dronate” suffix of bisphosphonates (e.g alendronate, pamidronate, zoledronate), the first line treatment for osteoporosis
- Two P coins: bisphosphonates have a chemical structure similar to pyrophosphate
- Large T-rex appetite: bisphosphonates attach to hydroxyapatite in bone
- Classmate stuck in donation box: osteoclasts bind to the bisphosphonate, inhibiting their adherence to the bony surface
- Class waiting to enter: osteoclast precursors
- Preventing class from entering: bisphosphonates decrease the development and recruitment of osteoclast precursors
- Classmate’s popping balloon: bisphosphonates induce osteoclast apoptosis
- Elevated calci-yum icecream: bisphosphonates are useful in the acute treatment of hypercalcemia
- Massive calcified rock with metastatic crab fossils: hypercalcemia of malignancy is a common cause of severe hypercalcemia requiring acute treatment (with bisphosphonates and calcitonin)
- Disorganized bone display: bisphosphonates and calcitonin are useful in the management of Paget disease (uncontrolled osteoclast resorption with secondary disorganized bone formation)
- Corroded neck: bisphosphonates can cause upper GI side effects (e.g. acid reflux, esophagitis, esophageal ulcers)
- Crumbling jaw bone: bisphosphonates can cause osteonecrosis of the jaw (rare)
- Falling calci-yum icecream: bisphosphonates can cause hypocalcemia
- Female symbol: estrogen therapy can treat and prevent postmenopausal osteoporosis (not recommended due to increased risk of breast cancer and other side effects)
- Female guarding class entrance: estrogen inhibits differentiation of osteoclast precursors
- Relax: raloxifene (a selective estrogen receptor modulator - SERM) is useful in the treatment and prevention of postmenopausal osteoporosis
- Relaxing the waiting classmates: raloxifene has estrogen agonist activity in bone (inhibits osteoclast differentiation) and estrogen antagonist activity in breast and uterus (reduced risk of breast cancer)
- PthD: parathyroid hormone (PTH)
- Convincing osteo-builder to give crank-drill: PTH stimulates osteoblasts to express RANKL
- Crank-drill: receptor activator of nuclear factor kappaB ligand (RANKL)
- Active classmate with crank-drill: RANKL binds to RANK on the osteoclast, increasing its activity
- Dino suit man grabbing crank-drill: denosumab (monoclonal antibody against RANKL) is useful in the treatment of osteoporosis
- Antibody spikes: denosumab is a monoclonal antibody
- Curator toning it down: calcitonin (“tones down calcium”) has some utility in the treatment of osteoporosis
- Curator grabbing classmate: calcitonin directly inhibits osteoclasts → decreased bone resorption
- Calci-yum ice cream pouring down flank: calcitonin promotes Ca2+ excretion by the kidney
- Falling calci-yum icecream: calcitonin can cause hypocalcemia
PTH
- Osteo-builders: osteoblasts (activated by teriparatide and vitamin D → increase bone mineral density)
- Destructive classmates: osteoclasts (indirectly activated by teriparatide and vitamin D → increase bone resorption/turnover)
- Released calcified bones: osteoclasts release calcium from bone
- Released P fossil: osteoclasts release phosphate from bone
- PthD paleontologist: parathyroid hormone (PTH)
- PthD lab: parathyroid gland
- Calcified bone receiving: calcium-sensing receptor on the parathyroid gland (senses increased serum calcium)
- PthD stuck behind bones: high serum calcium levels inhibit PTH production and secretion
- PthD convincing osteo-builder to give up crank-drill: PTH stimulates osteoblasts to release receptor activator of nuclear factor kappa-B ligand (RANKL) → activates osteoclasts
- Classmate receiving crank-drill: RANKL binds to RANK on the osteoclast surface → increased differentiation and activity → increased bone resorption
- PthD teaching osteo-builders: PTH stimulates maturation of osteoblasts → increased bone formation (net effect of PTH)
- PthD gathering bones and dropping P fossils: PTH increases calcium resorption by the kidney (and increases phosphate excretion)
- 1-head added to Calci-TRON: 1-alpha-hydroxylase in the kidney converts 25-hydroxyvitamin D into 1,25-dihydroxyvitamin D
- PthD adding final piece to Calci-TRON: PTH increases activity of 1-alpha-hydroxylase in the kidney → increased production of 1,25-dihydroxyvitamin D (calcitriol)
- PthD teaching assistant (TA): teriparatide (recombinant PTH)
- TA teaching osteo-builders: intermittent doses of teriparatide stimulates maturation of osteoblasts → increased bone formation. No osteoclast activity
- Fresh piece of calcified chalk: teriparatide can be used to treat osteoporosis (increase bone density)
- TA gathering bones and dropping P fossils: teriparatide increases calcium resorption by the kidney (and increases phosphate excretion)
- TA adding final piece to Calci-TRON: teriparatide increases activity of 1-alpha-hydroxylase in the kidney → increased production of 1,25-dihydroxyvitamin D (calcitriol)
- Solar D3 battery: vitamin D3 (cholecalciferol) is obtained via dairy products or UVB radiation in sunlight
- Earth-friendly D2 battery: vitamin D2 (ergocalciferol) is obtained via plants
- Robot body added to D battery in liver-barrow: 25-hydroxylase in the liver converts vitamin D to 25-hydroxyvitamin D
- Calci-TRON gathering bones and fossils from dump site: calcitriol stimulates reabsorption of calcium AND phosphate by the kidney
- Calci-TRON gathering bones and fossils from GI truck: calcitriol stimulates intestinal absorption of calcium AND phosphate
- Calci-TRONl delivering crank-drills: calcitriol stimulates osteoblasts to release RANKL → activates osteoclasts
- Calci-TRON collapsing PthD lab: calcitriol inhibits PTH production by the parathyroid gland
- Calci-TRON teaching osteo-builders: calcitriol stimulates maturation of osteoblasts → increased bone formation
- Fresh piece of calcified chalk: calcitriol can be used to treat osteoporosis (increase bone density)
- Calci-TRON stabilizing rickety tower: vitamin D (e.g. calcitriol) can be used to treat osteoporosis (increase bone density)
- Calci-TRON stabilizing broken kidney: calcitriol can be useful in chronic kidney disease (prevent hypocalcemia)
- Scaly knee and elbow pads: topical vitamin D can be used to treat psoriasis
- Calci-TRON saving falling calcified bones: calcitriol is useful in the long term management of hypocalcemia (e.g. hypothyroidism)
- Falling PthD: hypocalcemia is commonly caused by hypoparathyroidism (decreased production of calcitriol by the kidney)
- Undone bowtie on PthD: thyroid surgery can cause hypoparathyroidism and hypocalcemia
- Shaking structure: hypocalcemia can cause seizure
- Tense fist: hypocalcemia can cause paresthesias, muscle cramps, trismus, and tetany
- Raised calci-yum ice cream: teriparatide and vitamin D therapy can cause hypercalcemia
- Calculator at the calcified bone receptor: cinacalcet (a calcimimetic) activates the calcium sensing receptor on the parathyroid gland → decreased production of PTH
- Calculating pile of calcified bones: cinacalcet is useful in the treatment of hypercalcemia due to hyperparathyroidism
- Shoveling fossils in the GI truck: sevelamer (a phosphate binding polymer) decreases absorption of phosphate in the GI tract
- Shoveling pile of fossils: sevelamer is useful in the treatment of hyperphosphatemia due to chronic kidney disease
Glucocorticoids
- Stone: “-sone” suffix of glucocorticoids (e.g. dexamethasone, fludrocortisone, prednisone)
- Adrenal cap: cortisol (an endogenous glucocorticoid) is released from the adrenal cortex
- Moon face: glucocorticoids
- Moon scepter in outer circle: the glucocorticoid receptor is located in the cytoplasm
- Activated scepter in inner circle: the activated glucocorticoid receptor enters the nucleus and regulates gene transcription
- Inhibited cataPuLt A2: glucocorticoids inhibit phospholipase A2 (PLA2 - the first step in the arachidonic acid inflammatory pathway)
- AA frame of catapult A2: glucocorticoids prevent production of arachidonic acid (AA) by inhibiting PLA2
- Inhibited pro-slugger bat: glucocorticoids prevent production of inflammatory prostaglandins by COX
- Inhibited lacrosse stick: glucocorticoids prevent production of inflammatory leukotrienes by LOX
- Inhibited N-Flame Krossbow: glucocorticoids inhibit NF-KB (transcription factor for pro-inflammatory cytokines, e.g. IL-2, TNF-alpha)
- Inhibited T-kight and antibody archer: glucocorticoids prevent activation of T-cells and B-cells (by inhibiting production of proinflammatory cytokines)
- Blocked adhesion of first responders: glucocorticoids prevent production of neutrophil adhesion molecules → demargination and decreased migration
- Crowded first responders: demargination of neutrophils causes neutrophilia
- Falling T-knight, helper T-squire, and antibody archer: glucocorticoids reduce T-cell and B-cell counts
- Helper T-squire lowest: glucocorticoids are most effective at reducing helper T-cell counts
- Falling eo-slingshot: glucocorticoids reduce peripheral eosinophil counts
- Eclipsed inflammatory sun: glucocorticoids are useful for treating inflammatory disorders (e.g. gout, rheumatoid arthritis, asthma, IBD)
- Cracked antibodies: glucocorticoids are useful for immunosuppressive therapy (e.g. transplant rejection prevention, treatment of autoimmune disorders)
- Locked welcome inside mat: glucocorticoids cause insulin resistance
- Liver bag producing candy: glucocorticoids stimulate gluconeogenesis
- Sugar-filled liver jar: glucocorticoids increase hepatic glycogen storage
- Cracked moon: adrenal insufficiency (can be due to Addison’s disease - primary adrenal insufficiency)
- Fainted druid: acute adrenal insufficiency can manifest as circulatory shock and death
- Falling candy: acute adrenal insufficiency can manifest as hypoglycemia
- Exogenous moon face: exogenous glucocorticoids treat/prevent acute adrenal insufficiency
- Shriveled adrenal hat: chronic exogenous glucocorticoid use causes adrenal cortical atrophy (secondary adrenal insufficiency)
- Falling meat: glucocorticoids promote proteolysis
- Falling fatty donut jar: glucocorticoids promote lipolysis
- Cushion: Cushing’s syndrome (due to chronic glucocorticoid use - fat redistribution, muscle weakness, skin thinning, osteoporosis, immunosuppression)
- Moon face: moon facies (due to fat deposition)
- Fat belly: fat redistribution → central adiposity
- Thin arms: myopathy, muscle wasting, proximal weakness
- Thin striped fabric: glucocorticoids inhibit fibroblast proliferation → skin thinning, striae, impaired wound healing
- Fractured osteoporotic altar: glucocorticoids decrease bone mass → osteoporosis, fractures
- Cracked head: glucocorticoid induced psychosis (hypomania, confusion, hallucinations)
- Banana peel: glucocorticoids can cause hypoglycemia (due to mineralocorticoid effects)
- Cane: glucocorticoids can cause immuno-suppression
- Pulmonary cacti: glucocorticoids can cause reactivation of latent infections (e.g. TB)
Hypothalamic
ADH
- Collecting duct (CD) - the site of action of antidiuretic hormone (ADH, vasopressin)
- Hydrating waterboy: antidiuretic hormone (ADH, vasopressin)
- Posterior water jug: ADH is released from the posterior pituitary
- V1 hole on the Q shaped green: ADH activates V1 receptors coupled to Gq (activates PLC → IP3 + DAG → increased intracellular Ca2+)
- Constricted golfclub: ADH activation of V1 on vascular smooth muscle causes vasoconstriction and increased BP
- V2 hole on the S shaped green: ADH activates V2 receptors coupled to Gs (activates adenylyl cyclase → increased cAMP)
- Green on basolateral side and translocation of pure water: ADH activation of V2 on the basolateral membrane of the CD causes translocation of aquaporin 2 to the apical membrane and reabsorption of free water
- Endothelial tile: extrarenal V2 receptors are located on the vascular endothelium
- von Wille brand pool table: ADH activation of V2 on vascular endothelium causes release of von Willebrand factor (vWF)
- 8-ball: ADH activation of V2 on vascular endothelium causes release of factor VIII
- Insipidus fountain: polyuria diabetes insipidus (DI)
- Dehydrating kidney sand trap: nephrogenic DI
- Ignoring water boy: nephrogenic DI occurs when the nephron does not respond appropriately to ADH
- Lift-ium balloons: lithium can cause drug-induced nephrogenic DI
- Chloro-thighs: thiazide diuretics treat nephrogenic DI
- Almond cart: amiloride (a K+ sparing diuretic) treats nephrogenic DI
- Falling lift-ium balloon man: amiloride treats lithium induced DI (blocks Li+ entry into collecting duct cells → increased Li+ clearance)
- Fire extinguisher: NSAIDs (e.g. indomethacin) treat nephrogenic diabetes insipidus
- Dehydrating brain sand trap: central DI
- Absent waterboys: central DI occurs when the pituitary does not release adequate amounts of ADH
- Waterboy entering exogenously: exogenous administration of ADH treats central DI
- Desert-mobile: Desmopressin acetate (DDAVP - a long acting synthetic analog of ADH) treats central DI
- V-2 engine: DDAVP has high specificity for the V2 receptor
- Scratched von Wille brand felt: DDAVP treats von Willebrand deficiency (releases vWF from vascular endothelium)
- Bruised with mucosal bleeding: von Willebrand disease (vWD - deficient vWF) can be associated with increased bruisability and mucosal bleeding (dental procedures, menstrual period)
- Missing 8-ball in “A” frame: DDAVP treats hemophilia A (releases factor VIII from vascular endothelium)
- Bleeding knee joint: hemophilia A (X-linked deficiency of factor VIII) can be associated with hemarthrosis and prolonged bleeding after minor procedures
- Wet mattress: DDAVP treats night enuresis (decreased urine production)
- Falling salty peanut shells: DDAVP can cause hyponatremia)
- Bulging venous golf clubs: ADH is useful in the management of esophageal variceal bleeding (constricts mesenteric arterioles → reduced portal pressure)
- Brain shaped water hazard: syndrome of inappropriate ADH (SIADH)
- Over-hydrating waterboy: SIADH is caused by the overproduction of ADH
- Vaporizer: “-vaptan” suffix of V2 ADH receptor antagonists (e.g. conivaptan, tolvaptan) used to treat SIADH
- Wet pants: vaptans promote free water excretion (correcting hyponatremia)
- Elevated peanuts hitting head: vaptans may cause hypernatremia or central pontine myelinolysis (osmotic demyelination syndrome - due to overly rapid correction of Na+)
- Bicycle: demeclocycline treats SIADH (vaptans are first line)
GH
- Magic growing beans: growth hormone (GH, somatotropin)
- Front of pituitary sack: GH is secreted from the anterior pituitary
- Big "welcome INSIDE" mat: octreotide treats insulinoma
- Sprouting from liver rock: GH stimulates the liver to produce IGF-1
- Tire swing: the GH receptor is associated with JAK tyrosine kinase. JAK STAT
- Striated muscle leaf: GH has anabolic effects in muscle
- Falling fatty donut jar: GH has catabolic effects in adipose tissue
- Growing “welcome INSIDE” mat: insulin-like growth factor 1 (IGF-1) (mediates the growth promoting effects of GH)
- Tall growing vine: IGF-1 is responsible for long bone growth (pubertal growth spurt)
- Short kid: GH therapy is useful in GH deficiency and idiopathic short stature (controversial)
- Turning “X” girl: GH therapy is useful for increasing growth in Turner syndrome (XO)
- Fadre Willi: GH therapy is useful for increasing growth in Prader Willi syndrome (growth failure, obesity, carbohydrate intolerance). Missing piece of chromosome donated by father
- Sermon: mecasermin (recombinant IGF-1) treats growth failure due to severe IGF-1 deficiency
- Falling candy: mecasermin (recombinant IGF-1) can cause hypoglycemia
- Giant: GH secreting pituitary adenoma causes acromegaly (in adults) or gigantism (in children)
- Octagon stop sign: octreotide (somatostatin analog) treats acromegaly and gigantism (inhibit secretion of GH)
- VIP only: octreotide treats VIPoma (neuroendocrine tumor secreting vasoactive intestinal peptide)
- Customers only: octreotide treats carcinoid tumor (ileal tumor with hepatic mets secreting serotonin)
- Giant glucagon packet: octreotide treats glucagonoma
- Giant gas tank: octreotide treats gastrinoma (Zollinger-Ellison syndrome)
- Exposed variceal pipes: octreotide can control bleeding of esophageal varices (decreased portal blood flow and variceal pressure)
- Nauseated: octreotide can cause GI side effects (e.g. nausea , vomiting, abdominal pain)
- Yellow stool: octreotide can cause steatorrhea (decreased pancreatic secretions and gallbladder contractility)
- Burglar with broomstick: cabergoline and bromocriptine (D2 receptor agonist) treat acromegaly (inhibit secretion of GH from pituitary). Also treats hyperprolactinemia
- Double rope ladder: D2 dopamine receptor (activated by cabergoline and bromocriptine)
- ANTS on the tire swing: pegvisomant (a GH receptor antagonist) treats acromegaly. Receptor activation not GH secretion
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