Blood and Inflammation Drugs Flashcards
Heparin MOA
-binds Antithrombin III
-
Heparin-ATIII complex irreversibly inactivates thrombin and factor Xa
(“Trapped throm-beaver and foX”)
which lab value should be monitored when Heparin therapy is initiated ?
-aPTT - activated partial thromboplastin time
- measures the function of the intrinsic pathway of the coagulation cascade
(“Birdwatching father looking at Woodpecker inside tree trunk”)
what can Heparin be used for ?
- can be used for deep vein thrombosis prophylaxis
(“heppy hunter Hunting at the iliofemorial river”)
-heparin can be used for acute treatment of deep vein thrombosis
(“Beaver dam ion the iliofemoral river”)
-can be used for prophylaxis and acute treatment of pulmonary embolism (PE)
(“Birds nest on ischemic tree branch”)
- Continuous heparin drip can help reduce the development of the PE
-Heparin is used in the setting of an acute MI, heparin is used to prevent clot formation and extension
(“Broken heart strings”)
-IV heparin adminstration useful in the setting of acute DVT, PE, and MI
(“poison ivy on tree”)
Adverse effects of Heparin
- INCREASED RISK OF BLEEDING! - moniter aPTT !
- Heparin induced thrombocytopenia, - occurs when antibodies are made against heparin complex with platelet factor 4
(“Heppy hunter Shooting four clay plates” )
(“plates on the floor”)
- HIT results in paradoxical thrombosis in the setting of thrombocytopenia [HITT]
(“Throm-beaver dam around broken plates”)
-heparin can cause hyperaldosteronism even in low doses
(“depleted mineral mine” )
- leads to Hyperkalemia
(“Big K on depleted mine entrance”)
-heparin can cause osteoporosis
(“Porous termite damage”)
what can reverse the anticoagulant effect of Unfractioned Heparin?
Protamine Sulfate- positively charged peptide
(“positively charged protection fence stopping the heppy heparin hunter”)
**less effective for LMWH and fondaparinux**
LowMolecularWeightHeparin Properties
(“Heppy hunter’s daughter”)
_Enoxa /_parin
_Dalte /_parin
-LMWH-antithrombin complex inhibits factor Xa with less of an effect on thrombin
(“Heppy hunter’s daughter holding 1 FoX in small trap”)
-LMWH has a prolonged half-life
(“Long tapering flag”)
-Does not require aPTT monitoring
-LMWH is eliminated renally (Heparin in liver ) and can stay in the system if there is renal insufficiency
(“Decay flag breaking a kidney shaped rock”)
-heparin/LMWH is safe during pregnancy. “keep that baby heppy with heparin”
(“Heppy pregnant hunter momma”)
-less likely to induce HIT
(“intact pigeon clay plates”)
Fondaparinux properties
(“Fido the dog with a pair of FoXes”)
-binds antithrombin III with higher specificity that LMWH
(“Fido the dog holding 2 foX cages”)
-fondaparinux-antithrombin complex inhibits factor Xa with less of an effect on thrombin
(“fido the dog holding 2 foX cages with no beavers “)
-Lowest risk of HIT
(“no broken plates around Fido the dog”)
Name Direct Thrombin inhibitors
(“intruding gator lunching on that thrombeaver”)
“no intRUDIN - BIG GATOR“
- **BivaliRUDIN
- ar-GAT-Roban
- Dabi-GAT-Ran**
when should Direct Thrombin inhibitors be administered ?
in case of HIT
( Heparin Induced Thrombocytopenia)
name the Direct Factor Xa inhibitors
(“BANNED foXes”)
XABAN-suffix
- *Rivaro**/XABAN
- *api**/XABAN
Direct Factor Xa inhibitors properties
-factor Xa inhibitors bind directly to Xa
(“angry overall jeans gal directly grabbing foX”)
-are oral medications
(“blonde dude wearing overall jeans opens his mouth”)
-used for long term anticoagulation in atrial fibrillation
(“tv showing irregularly irregular signal”)
Warfarin MOA
-vitamin K is a cofactor for the enzymatic activation of clotting factors via gamma carboxylation at glutamic acid residue
(“Vitamin K medic stopping the bleeding”)
(“Vit K medic applies gamma shaped bandage”)
-Warfarin blocks vitamin K epoxide reductase, this is required for activation of Vitamin K thus preventing clotting factors 2,7,9,10, and protein C and S from being produced
(“Warhead destroying V-KOR supply ship from which the vit K medic is getting the gamma bandages”)
- Proteins C and S are anticoagulants
(“Corporal and sergeant hold their troops back”)
Warfarin Properties
-Onset of action is not immediate, not for acute thrombotic events
- onset of action is 8-12 hours, full clinical effect takes 3 days
(“Delayed warhead detonation”)
-factor VII (7) is the first clotting factor to be reduced when starting warfarin
(“soldier VII is wounded”)
-
oral administration
(“Soldier with open mouth leaning on warfarin bomb”)
-Long half life (6 hours)
(“Long tapering flag”)
which lab value should be monitored when Warfarin therapy is indicated ?
-PT time (Prothrombin time)
- a measure of the function of the extrinsic coagulation pathway - factor VII is the main component
(“Para trooping soldier VII landing extrinsically”)
-INR [international normalized ration] is also used to measure warfarin activity
- Goal INR 2-3 for prevention and treatment of thrombosis
(“INtercom Radio worn by paratrooper calibrated to 2-3”)
Warfarin is used to treat …
- long term anticoagulation in atrial fibrillation
- 3-6 months
-used as DVT prophylaxis
(“warship protecting the ileofemoral river”)
- acute treatment for DVT is IV Heparin because Warfarin has delayed onset
(“tv showing Irregularly irregular heart signal”)
Warfarin Side effects
- INCREASED RISK OF BLEEDING !
- may precipitate to intracerebral hemorrhage
-can cross the placental barrier and can cause a hemorrhagic disorder or prevent carboxylation reactions in bone.
(“Tarantula symbol on warfarin warhead”)
-vit K deficiency
-the anticoagulation protein C is reduced early in warfarin therapy, resulting in a hypercoagulable state initially
(“Soldiers charging past the injured corporal”)
- warfarin induced skin necrosis due to early hypercoagulable state (“Black soot on corporal”)
- coadministration of heparin when starting warfarin therapy prevents the early hypercoagulable state-heparin bridge
(“Heparin hunters patrolling the bridge”)
→ skin necrosis risk is increased with a hereditary protein C deficiency
- warfarin is a substrate of cytochrome P-450
(“CYP-450 chrome tank crushing warhead”)
-
increase P450→decrease effects
rifampin
phenobarbital
phenytoin -
decrease P450→ increase effects
antibiotics
antifungals
SSRI’s
how can warfarin antiacoagulation be reversed?
-delayed effect-warfarin anticoagulation can be reversed with vitamin K
(“distant Vit K medic reinforcements”)
-immediate reversal-fresh frozen plasma (FFP) provides coagulation factors for immediate warfarin anticoagulation reversal
(“FFP fighter pilot”)
Platelet Adhesion _A_ctivation Aggregation MOA
-tissue damage → collagen +VWf exposed →GPIb on platelet binds collagen +vwf→ activation → release of TXA2 ,ADP , serotonin
- ADP⇒ binds PLT receptor P2Y12 ⇒aggregation
- TXA2 ⇒aggregation and activation
- Serotonin ⇒aggregation and vasoconstriction
(“Peeling von Willie brand field”)
(“Holding 1b bat”)
(“Home plate”)
(“Aggregated players”)
(““ADP” aggregate Da players! Play youth ball 2-12y”)
(“Thrown happy face helmet”)
(“Batter’s box”)
Thromboxane Synthesis pathway
-Cyclooxygenase 1 (COX1) synthesizes prostaglandins (prostaglandins, TXA2) within platelets
(“Head coach cox”)
-COX-1 synthesizes TXA-2 from the precursor molecule arachidonic acid (AA)
(“AA minor league dugout”)
-TXA2 (synthesized by COX-1) causes vasoconstriction
(“Coach Cox twisting hat”)
-COX-2 expression is induced during inflammation, so he is inactive until some inflammatory event
(“Sleeping assistant coach”)
Aspirin MOA
-aspirin irreversibly acetylates COX-1 and COX2
-aspirin irreversible inhibits COX-1 and COX-2 reducing platelet activation and aggregation
(“ASA umpire ejecting the coaches”)
-aspirin inhibits COX 1 and 2 thus shifting AA pathway towards LOX enzyme causing “pseudo-allergy” due to excess leukotriene synthesis, seen in asthma or nasal polyposis pts.
(“Swollen ASA umpire”)
- use Clopidogrel ( ADP inhibitor)
(“Acetyl-whistle)
ADP receptor inhibitors MOA
-Irreversibly Inhibit ADP surface receptor P2Y12 on platelets
(“ADP” aggregate Da players! Play youth ball 2-12y”)
what are Antiplatelet agents used for ?
- antiplatelet agents (aspirin, ADP receptor inhibitors) reduce cardiovascular events in patients with peripheral artery disease,
- they do not reduce the symptoms of peripheral artery disease such as atypical pain and claudication in the effected extremity
-antiplatelet agents (aspirin, ADP receptor inhibitors) reduce cardiovascular events in patients with coronary artery disease
(“Angina anvil grill”)
-use antiplatelet therapy (aspirin, ADP receptor inhibitors) in the setting of MI and other acute coronary syndromes, give as soon as possible to a patient with a STEMI
(“Broken heart strings”)
- give chewable aspirin tablets initially in an acute MI for immediate effect
(“ASA umpire chewing tablets”)
-dual antiplatelet therapy (aspirin and ADP receptor inhibitors) prevent coronary stent thrombosis
(“Corked bat”)
-antiplatelet therapy (aspirin and ADP receptor inhibitors) prevents ischemic stroke in patients with atherosclerosis and known cerebrovascular disease
(“Black paint stroke”)
(“Greasy grill pipe”)
Ticlopidine is an ADP P2Y12 receptor inhibitor that may cause …
(“Ty Cobb”)
-Neutropenia in 2% of patients
-can cause granulocytopenia, you must obtain white cell and rbc count when starting therapy
(“Falling granules in neutrophil shaped hour glass”)
names and MOA of GP IIb/IIIa receptor inhibitor
1) ABCiximab - irreversible
- abciximab is a monoclonal IgG antibody
(“Antibody shaped microphones”)
-abciximab inhibit platelet surface receptors GP IIb/IIIa from binding to fibrinogen to promote platelet aggregation
(“Crowd of spectators from seats 2b-3a jump on fries guys”)
- *2) Eptifibatide , Tirofiban -Reversible**
- must be given IV continuously
(“ABC sportscaster grabbing fries”)
GP IIb/III receptor inhibitors Side effects
-cause thrombocytopenia
(“Broken plates”)
which measurement will increase following an antiplatelet therapy ?
-antiplatelet therapy increases bleeding time- a measure of platelet function
(“Ketchup time”)
Names and MOA of Phosphodiesterase inhibitors
(“Don’t Phoster disinterest”)
Dipyridamole
(“two pyramids”)
Cilostazol
(“player that lost the ball”)
——————————————————————————–
-phosphodiesterase inhibitors increase cAMP impairing platelet function
(“SIGN UP FOR CAMP BOOTH”)
Cilostazol can be used to treat
-treats symptoms of claudication due to peripheral artery disease
(“dirt clods hitting leg”)
Cilostazol is a Phosphodiesterase inhibitor that causes
(“player that lost the ball”)
-causes arterial vasodilation
(“kid who lost the ball has dilated red sleeves”)
-causes coronary artery dilation
(“kid who lost the ball wearing dilated red crown”)
- can cause coronary steal, this will dilate all of the other coronary arteries preventing blood flow to the ischemic areas exacerbating ischemia
(“Stolen steal heart base”)
Name Surface ADP receptor P2Y12 receptor inhibitors
(THI-ENO-pyridines)
-GREL-suffix (“Hot dog grill”)
- ClopidoGREL
- PrasuGREL
- TicaGRELor
- Ticlopidine
Name Fibrinolytics
1) tissue plasminogen activator (tPA)
- Alt /eplase,
- Ret /eplase
-
Tenect /eplase
(“Toy Pl_A_yset”)
2) Streptokinase-synthesized by streptococci
(“Strepto-kinectors”)
(“Purple sphere chain”)
which lab values will be increased following a fibrinolytics therpay ?
-PT (prothrombin time , extrinsic)
(“kid holding para trooper”)
-aPTT (activated partial thromboplastin time, intrinsinc)
(“kid holding shooting trooper and making the sound PTTTT”)
Fibrinolytics treatment is used for …
-IV fibrinolytics may be used in the setting of ischemic stroke (“Black paint stroke”)
- Administer IV fibrinolytics within 3-4.5 hours of ischemic stroke symptoms
(“After school painting session 3:00-4:30”)
-IV fibrinolytics can be used for acute treatment of severe DVT and PE
(“Birds nest on ischemic branch”)
-fibronolytics may be used in the acute management of MI
(“Broken heart strings”)
-
percutaneous coronary intervention is the preferred reperfusion option in ACUTE STEMI
(“Corked Bat”)
when is Fibrinolytics therapy contraindicated ?
-perform PCI ideally within 2 hours of acute STEMI
(“far far player calling for two”)
-Recent head trauma is a contraindication for fibrinolytic therapy
(“Traumatic plasma beam”)
-recent intracranial surgery is a contraindication for fibrinolytic therapy
(“Red palette knife”)
-White area on CT indicates cerebral hemorrhage – a contraindication for fibrinolytic therapy
(“white area on brain ct”)
-severe hypertension is a contraindication for fibrinolytic therapy
(“High pressure paint tube”)
side effects of fibrinolytic therapy
-hemorrhagic stroke
(“Red pain stroke on painting”)
-Streptokinase only can cause allergic reaction and even anaphylaxis
(“strepto-kid choking on streptokinetctors”-choking hazard)
what can be used to reverse fibrinolysis?
Aminocaproic acid
- aminocaproic acid competitively inhibits plasminogen activation
(“Plasma general tucked under mom’s arm”)
Transexamic acid
(“mom holding Exams”)
- can be used to reverse tPA
(“Cap on paint tube”)
what can reverse coagulopathies?
FFP -Fresh Frozen Plasma
(“yellow kid holding FFP Pilot”)
Cryoprecipitate
(“Cryo ice pack”)
Statins MOA
(“steam punk pirate”)
HMG-CoA reductase inhibitors →reduce production of mevalonate from HMG-CoA → reduced levels of cholesterol in hepatocytes
(“steam punk pirate knocking over HMG crude ore reducer “)
-statins cause increased LDL receptor expression on hepatocytes, clearing LDL’s from circulation
(“Statin-punk threatening workers to pull in LDL ship”)
-statins are most effective drugs for lowering LDL’s (30-60%)
(“Sinking LDL ship”)
-statins can lower triglycerides (mild effect)
(“Statin-punk pirate kicking off trident passenger”)
-statins can increase HDL (mild effect)
(“Raised HDL submarine”)
Statins are effective because they …
1ST LINE AGENT FOR HYPERCHOLESTEROLEMIA
(“Gold bar plunder”)
-Statin therapy initiated in setting of MI and other acute coronary syndromes (ACS)
(“broken heart strings”)
-are the most effective lipid lowering medication for preventing future cardiovascular events
(“Guardian angel”)
-statins are the only lipid lowering drug consistently proven to reduce risk of atherosclerotic heart disease
(“Yellow filled coronary crown”)
-
reduce risk of cardiovascular events and mortality in high risk diabetics
(“Candy jar”)
-reduce risk of cardiovascular events and mortality in patients with peripheral artery disease
(“Clogged pipe”)
-reduce risk of future vascular events in patients with history of TIA or stroke
(“Black paint stroke”)
Statins side effects
(“steam punk pirate”)
-statins can cause myopathy weeks to months after starting therapy (proximal muscle weakness/soreness), difficulty raising arms above head
- can cause elevations in serum CK-myopathy
(“Crispy chicken bucket”)
-statins may be teratogenic
(“Tarantula on HDL submarine “)
-mild elevations in liver function tests (LFT’s) are
common -reversible with discontinuation of statin
(“Raised LFT flag”)
-all statins except pravastatin are metabolized by the cytochrome p450 (CYP-450) in the liver leading to an increased risk of developing myopathy
(“Chrome tank with CYP bumper”)
(“Bite out of crispy chicken”)
Name the Bile Acid Absorption Inhibitors
-Resins-
Cholestyramine (“Cho”lobetser”amine”)
Colestipol
Colesevelam
Resins MOA
-resins interrupt bile acid recycling and promote synthesis of new bile acids, depleting cholesterol stores
- causing HMG CoA reductase to synthesis more cholesterol
(“Activating HMG crude ore reducer”) - causing upregulation of LDL receptor and uptake of circulating LDL
(“Activating LoaD L receptor”)
(“Empty gold stores”)
Resins Side Effects
-bile acid resins (cholestyramine, colestipol, colesevelam) cause hypertryglycemia
(increased VLDL’s)
(“Cho”lobster”amine scaring airship away”)
- do not use this in hypocholesteremia with concomitant hypertriglycemia
-can cause cholesterol gall stones
(“Sea”gall” stones”)
-bile acid resins can cause constipation and bloating.
- do not use in pts with diverticulitis, or preexisting bowel disease
(“Cho”lobster”mine clamping pipe”)
- impair absorption of fat soluble vitamins A, D, E, K
(Cho”lobster”mine on DEcK-A”)
-bile acid resins decrease statin absorption-administer 4 hours apart
(“Cho”lobster”amin clashing with statin punk”)
Ezetimibe MOA
(“Z-shaped eel”)
-blocks intestinal absorption of cholesterol decreasing chylomicron carrier
(“Z shaped eel blocking gold delivery at intestinal airbase”)
-restricts liver’s access to exogenous cholesterol
(“Empty chest delivery”)
-causing HMG CoA reductase to synthesize more cholesterol
(“Activating HMG crude ore reducer”)
-causing upregulation of LDL receptors and uptake
of circulating LDL
(“Sunken LDL ship”)
Ezetimibe Side Effects
-may cause increased liver function tests (LFT’s)
(“Raised LFT flag”)
-may cause diarrhea / steatorrhea
(“Z shaped eel shitting oily water”)
Evolocumab MOA
(“Steam-ctopus man”)
-PCSK9 normally causes degradation of LDL receptors
(“Pesky “9” crabs inhibiting LoaD L receptor workers”)
-Evolocumab binds PCSK9 and prevents degradation of LDL receptors, increasing uptake of circulating LDL
(“Steam-octopus man removing pesky crabs”)
- Many PCSK9 inhibitors (evolcumab) are antibodies
(“Steam-ctopus man with antibody-shaped claws”)
Name Fibrates
Gemfibrozil
(“Gem-fibrozil jellyfish”)
Fenofibrate
Fibrates MOA
(“Gemfibrozil jellyfish”)
-fibrates activate PPAR-alpha to upregulate LPL
-increase hydrolysis of VLDL and chylomicron triglycerides via LPL fibrates decrease serum triglycerides
(“Trident passengers escape airship”)
-fibrates stimulate LPL and reduce hepatic VLDL secretion decrease serum VLDL 35-50%
(“Gem-Fibozil jellyfish takes down airship”)
-decrease serum LDL (mild effect) by reducing VLDL
(“Gem-fibrozil jellyfish sinks ship”)
-fibrates increase serum HDL (mild effect) by activation of apolipoproteins A1 and A2 that will create nascent HDL’s
(“Elevates High density submarine”)
(“Lighthouse keeper lighting newsPPAR signal”)
Fibrates Adverse effects
-fibrates can cause cholesterol gall stones
(“Sea”gall” stones”)
-Fibrates combines with statins increases risk of myopathy
(“Elevated statin-punk eating crispy chicken”)
Niacin (vitamin B3) MOA
(“Loch Niacin monster”)
-MOST EFFECTIVE drug for increasing serum HDL (~30%)
(“Elevate High Density submarine”)
-niacin decreases serum triglyceride (reduces hepatic VLDL secretion)
(“Trident passengers escape airship”)
-Niacin decreases serum VLDL
(reduces hepatic secretion)
(“Loch Niacin monster takes down airship”)
-Niacin decreases serum LDL (mild effect) by lowering VLDL
(“Loch Niacin monster sinks ship”)
Niacin Adverse Effect
(“loch niacin monster”)
-can cause cutaneous flushing and warmth → prostaglandins (cause flushing) is a mediator of vasodilation and inflammation
(“Red fiery furnace”)
(“Pro slugger bat”)
-
NSAIDs (including aspirin) can be used to prevent flushing from niacin
(“Fire extinguisher”)
-niacin can cause hyperglycemia
(“Elevated candy”)
-niacin can cause hyperuricemia (can precipitate gout)
(“Yellow knitting needles”)
-can cause elevated liver function tests (LFT’s) leading to severe hepatotoxicity, requires monitoring
(“Raised LFT Flag”)
what is the benefit of including fish in your diet?
-fish oils are high in omega 3 fatty acids and can lower serum triglycerides
(by decreasing VLDL and apoB production)
(“Omega fish leaking oil”)
(“Sunken tridents”)
Names of NSAIDS
**Aspirin
Diclofenac , ketorolac**
(blue fan holding sign “ go BLAC sox”)
Indomethacin
(green fan holding sign “ don’t mess with indigo sox”)
Meloxicam , Piroxicam
(big screen in stadium streaming from “SOX CAM”)
Naproxen
(big screen in stadium saying :” apPROXimately 110 mph”)
what is the COX (1,2) Pathway ? what are the effects of the resultant products ?
COX 1
cell membrane →(PLA2)→AA→(COX1)→
-
TXA2 ⇒ platelet activation , vasconstriction
(batter’s box says “ SOX A2”) -
Prostaglandins
⇒ gastric cytoprotective
(proslugger protects catcher with GI pads)
⇒dilate afferent arteriole
COX 2 FOUND IN ENDOTHEL , ACTIVE DURING INFLAMMATION
cell membrane →(PLA2)→AA→(COX2)→
-
Prostacyclin (PGI2)
⇒ vasodilation
⇒inhibition of platelet aggregation - Prostaglandins-inflammation
⇒increase vascular permeability
⇒increase pain sensitivity
⇒induce fever
⇒dilate afferent arteriole
——————————————————————————–
Both COX 1 +2 synthesize prostaglandins that can dilate the afferent arteriole
what is the difference between COX 1 and COX 2?
COX 1 - is constitutively expressed
COX 2 - expression is induced by inflammation
NSAIDs MOA
Reversible inhibition of COX 1,2
(“anti inflammatory fire extinguisher aiming towards head coach and assistant coach “)
Diclofenac
Ketorolac
(“BLAC sox”)
Indomethacin
(“INDIGO Sox “)
Piroxicam
Meloxicam
(“Sox Cam”)
Naproxen
(“approximately 110 mph”)
Irreversible inhibition of COX 1,2
Aspirin (“ASA umpire”)
- acetylates COX-1 and COX-2 resulting in irreversible inhibition
Reversible COX 2 inhibitor
Celecoxib
(“Celebrating catcher in the dugout drenching the assistant coach”)
Non-Anti Inflammatory COX2 Inhibitor
Acetaminophen
(“Icy-medicine spray on assistant coach”)
NSAIDs Side Effects
inhibition of COX-1
-can cause gastric inflammation, erosions, and ulceration
(“Burned hole in the gastrointestinal pads”)
-inhibition of COX-1 by NSAID’s can cause GI bleeding
(“Ketchup on the gastrointestinal pads”)
-inhibition of COX-1 by NSAIDs can prolong bleeding time
(“Ketchup on clock”)
——————————————————————————–
NSAIDs in General
-can increase blood pressure due to COX inhibition in the kidney, decreasing sodium excretion
(“Bursting from high pressure”)
-can cause acute interstitial nephritis
(“Baseball-filled kidney shaped containers”)
-NSAID’s cause afferent arteriole vasoconstriction, decreasing GFR ACE inhibitors will effect GFR greatly when used with NSAIDS due to the great decrease of GFR
(“Contracted proximal end of fire extinguisher hose”)
-cause renal papillary necrosis (sloughing of renal papillae)
(“Sloughing of cleat spikes”)
-NSAIDs can increase serum lithium concentrations
(“Elevated “lift-ium” balloons”)
-NSAIDs (indomethacin generally) can cause aplastic anemia
(“Plastic bone-shaped balloon”)
-NSAIDs will cause Impaired renin secretion leading to hyporaldosteronism (decreased mineralcorticoids) that will lead to hyperkalemia, type IV RTA
(“player number 4 falling into the depleted “mineral mine”, entrance of the mine has a “big K”)
Risk managment
-minimize NSAID use in patients of risk for acute kidney injury, because it can exacerbate renal insufficiency, same with MI, or any other issue that may decrease renal perfusion
(“Fire extinguisher behind cracked kidney-shaped glass”)
-avoid NSAIDs in 3rd trimester due to risk of premature closure of ductus arteriosus (highest risk with indomethacin and ibuprofen)
(“Exiting pregnant lady with 3 on her shirt “)
in which cases is Aspirin therapy useful?
- useful in Kawasaki’s disease (the most common vasculitis in children) manifests as fever, conjunctivitis, erythema of lips and oral mucosa, rash, and cervical lymphadenopathy
(“Child on Kawasaki’s ATV”)
Aspirin Side Effects
-aspirin use in children can lead to development of Reye’s syndrome
(“kid next to ATV wearing shirt with rays pattern”)
-Reye’s syndrome occurs when a child is given aspirin in the setting of a viral illness. Consists of rapidly progressive encephalopathy with hepatic dysfunction after apparent recovery of a viral illness
(“Cerebral baseball cap , Fat liver spot on cow”)
(“Tissue box”)
———————————————————————————aspirin toxicity can cause an anion gap metabolic acidosis
(“play sitting on Mudpile”)
-aspirin causes respiratory alkalosis priorto metabolic acidosis
(“ player sitting on mudpile blowing “OH-“”)
-aspirin can cause tinnitus
(“Tin Cans on ground”)
what can be used to control aspirin in the setting of acute toxicity ?
-activated charcoal , can be used to absorb aspirin in setting of acute toxicity
(“Charcoal lines on fan’s face”)
-alkalinization of the serum and urine with a basic solution (sodium bicarb) increases the renal excretion of aspirin
(“Base loaded hose sprinkles on ASA umpire”)
Celecoxib Properties
-celecoxib is a sulfa drug
(“Rotten sulfa eggs”)
-has reduced ulcer and bleeding risk by avoiding COX-1 inhibition
(“Clean gastrointestinal pads”)
-celecoxib may increase the risk of ischemic cardiovascular disease, avoid in acute MI and stable angina
(“spilled Thrombus ice cubes”)
Acetaminophen Properties
- NOT anti- inflammatory
- acting as an antipyretic and analgesic used for mild to -moderate pain, osteoarthritis and some Rheumatoid arthritis
-acetaminophen causes hepatotoxicity.
(“Liver spot on goat”)
- toxic levels of acetaminophen deplete glutathione in the liver since glutathione will inactivate the toxic metabolite NAPQI
(“Goat scared by the icy medicine”)
what is the Antidote for Acetaminophen toxicity
N-acetylcysteine restores hepatic glutathione stores to treat acetaminophen hepatoxicity
(“Goat attracted to N-Flower seeds
-activated charcoal can be used to absorb acetaminophen in setting of acute toxicity
(“Charcoal lines on the fan above acetaminophen spray”)
Acute Managment of Gout/Pseudogout
Acute gout, will commonly manifest in the 1st metatarsal
——————————————————————————–
-NSAID s - 1st line treatment in acute gout
(indomethacin)
(Fire extinguisher”
-Glucocorticoids (prednisone) treat acute gout
(“Moon Face”)
-Colchicine treats acute gout
(“Choir sing”)
Cholchicine Properties
(“Choir Sing”)
-taken orally 12-24 hours
- colchicine binds intracellular tubulin preventing
polymerization of microtubules
(“Binding palm fronds”)
-colchicine disrupts the cytoskeleton of neutrophils thereby inhibiting neutrophil migration, phagocytosis, and degranulation
(“First responders blocked by choir”)
-can cause diarrhea
(“Muddy floor”)
what is the difference between Gout and Pseudogout (CPPD) ?
Gout
- Uric acid crystals
(“Knitting needles”) - Needle shaped
- (-) Birefringent
Pseudogout (“they should not lie”)
- Calcium pyrophosphate
- Rhomboid shaped
(“Blue rhomboid incense holder”) - (+) Birefringent
Chronic Managment of Gout
Allopurinol
(“Pure nun”)
Febuxostat
Probenacid
(“Probation officer Cid”)
Pegloticase
(“Just in case” plegoticase”)
Allopurinol MOA
(“Pure Nun”)
-inhibits xanthine oxidase
(“Nun grabbing XO notes”)
Allopurinol can be useful when …
- prevent uric acid deposition in setting of tumor lysis syndrome
- uric acid crystals can form in tumor lysis syndrome after starting cytotoxic chemotherapy
(“Shattered cancer crab glass”)
* most common with treatment of lymphoma and acute lymphoblastic leukemia
(“White T Cell crusaders”)
- Lesch-Nyhan syndrome -associated with hyperuricemia is managed with allopurinol.
- Will see picking of the skin or biting of the lips in a child where uric acid is causing pain
(“Needle in flesh and biting of finger of kid by stained glass window”)
(“Nun sweeping crystals from broken cancer vitrage”)
Allopurinol Side effects
-Allopurinol inhibits breakdown of purine analogs
- 6 mercaptopurine and azathioprine, thus increasing risk of toxicity and may cause a mild rash
(“Concentrated purine beads on nuns”)
-can cause Stevens-Johnsons syndrome
(“Sloughed off red mask”)
-can cause drug reaction with eosinophilia and systemic symptoms (DRESS syndrome)
(“Eosinophilic Dress”)
Probenacid MOA
(“Probation officer cid”)
-decreases renal tubular reabsorption of uric acid
(“Preventing punk from grabbing yarn”)
Probenacid Side Effect
(“probation officer cid”)
-may increase the risk of forming renal stones due to increased uric acid excretion.
(“Accumulating yarn and needles”)
-probenecid can inhibit the excretion of many drugs
(“probation officer cid holding back guy with “Drugs” tattoo”)
- prevents excretion of penicillin
(“probation officer Cid’s purple pencil”)
-probenecid is a sulfa drug
(“Rotten sulfas eggs”)
THE ASPIRIN PARADOX IN GOUT DISEASE
-aspirin at low doses inhibits uric acid excretion
-at high doses can prevent tubular reabsorption of uric acid
(“Little ASA umpire yarn”)
(“ASA umpire preventing son from grabbing yarn”)
Pegloticase MOA
(holy water “jusT InCASE”)
-pegloticase converts uric acid into water soluble allantoin
(“Holy water just in case!”)
-pegloticase is administered IV
(“poison ivy next holy water stand”)
Pegloticase Side Effects
(holy water “jus_T I_nCASE”)
-can cause hemolysis in G6PD deficiency (bite cells)
(“Watermelon with bite”)
-pegloticase can cause anaphylaxis
(“Choking Kid”)
