05 GI
Last updated
Last updated
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)
“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)
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)
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
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
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
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
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
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)
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)
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