Test type questions for 2.4 Flashcards
What automaticy differences at the SA node make it different than other cardiac tissue?
Which wave responds to atrial depolarization?
Which wave responds to atrial repolarization and ventricular depolarization?
No plateau phase(phase 1 and 2), influx of Ca other than Na.
P wave.
QRS complex.
Which wave responds to ventricular repolarization?
What are 4 differences between arteries and veins?
What are the EDRF’s and what predominates?
T wave.
Veins have valves, thinner elastic membrane, thinner smooth muscle layer, thick connective tissue layer.
Nitric Oxide(predominates, released in response to acetylcholine), prostacyclin(changed through cox2)
What are the EDCF’s and which one is strongest?
Beta stimulation causes what? Alpha stimulation causes what?
What is stroke volume? What is cardiac output?
Endothelin I(strongest), ACE, Thromboxane.
Beta causes vasodilation, Alpha causes vasoconstriction.
EDV-ESV. Stroke volume x Heart Rate.
What is an inotrope?
Is force of contraction influenced by intrinsic or extrinsic factors?
What is a chronotrope?
Something that affects the strength of muscle contraction. Dobutamine(positive), Metoprolol(negative)
Extrinisic.
Something that affects the rate at which the heart contracts. Dilitiazem(negative), epinephrine(positive).
What is a dromotrope?
What does the proximal tubule reabsorb(9 things)?
Where/how do cardiac anhydrase inhibitors work? What is one?
Something that effects AV node conduction. Atropine(positive), Digoxin(negative).
NaCl, H20, HCO3, glucose, amino acids, K, Ca, Mg, Urea.
Work in proximal tubule to block HCO3 reabsoprtion which helps treat alkaline states in the body. Acetazolamide.
What does the ascending loop reabsorb?
What does the descending loop reabsorb?
What does the distal convoluted tubule reabsorb? Is this the site of action for diuretics?
Highly solute permeable, where NaCl is pulled out, can also reabsorb Ca, Mg, NaCl.
Highly water permeable, where H2O is pulled out, can also reabsorb Ca, Mg, NaCl.
NaCl, Calcium. YES!
What is the site of action for amiloride and triamterene?
What are the functions of the collecting duct?
What are the 3 categories of prerenal AKI?
Collecting duct
Reabsorbs Na, secretion of potassium, Reabsorbs H2O, Acid base disorder last place to alter, regulates final composition of urine.
Volume depletion, Decreased effective circulating volume, Functional(medicines).
If you see WBC’s and RBC’s in the urine what does that normally tell you concerning AKI?
What is RISK criteria in RIFLE?
What is INJURY criteria in RIFLE?
You have AIN.
SCr up by 1.5 fold. Urine out put <0.5 mL/kg/hr for >6 hours.
SCr up by 2 fold. Urine output < 0.5 mL/kg/hr for >12 hours.
What is FAILURE criteria in RIFLE?
What is loss of kidney function and end stage renal disease?
Is AKIN staging the same as RIFLE?
SCr up by 3 fold. Anuria for >12 hours.
Complete loss of function for >4 weeks and renal replacement therapy for >3 months
Yes, except if you need ANY renal replacement therapy you are stage 3.
What is the FeNa equation?
What is the FeNa cutoff for prerenal?
When are loop diuretics appropriate for AKI?
(Una x Scr)/(Ucr x Sna) x 100
<1
If patients are volume overloaded and still producing urine, otherwise it can make it worse.
What is the pneumonic to look for when considering renal replacement therapy?
What happens with Digoxin in AKI? What is the symptoms(and hallmark one) of digoxin overdose?
What happens with phenytoin in AKI?
A(acidbase)E(electrolytes)I(intoxication)O(overload)U(uremia)
Stays in body longer, GI upset, blurred vision, Yellow halos is hallmark, weakness, dizziness, confusion.
Stays in body longer, nystagmus, ataxia, slurred speech, mental status changes.
What is treatment for Nephrolithiasis?
When is lithrotripsy preferred and CI’d?
What is the main difference of SCr from other kidney function markers?
Aggressive hydration(90% of stones pass without surgical intervention), restriction of dietary proteins and sodium, oral A1 adrenergic blockers, thiazide diuretics, allopurinol, alkalinizing agents(potassium and sodium citrate).
Preferred in large stones(>5mm), CI’d in uncontrolled hypertension, bleeding disorders, pregnancy, urinary tract anomalies or UTI.
Cheaper, Endogenous, lower accuracy.
What is the CockCroft-Gault equation?
Ideal body weight formula?
What BUN:SCr is suggestive of a prerenal cause?
Evaluates CrCl. ((140-age) x (IBW))/(72-SCr)) (times all by .85 if female). Normal range 75-115 mL.
Men: 50+ (2.3 x in over 5 ft). Female: 45.5 + (2.3 x in over 5 ft)
20:1 value.
What medications cause Prerenal injury?
What medications cause ATN?
What medications cause AIN?
ACEI’s/ARB’s,NSAIDS, Loop Diuretics, Cyclosporine, Tacrolimus, PTU, Allopurinol,Adalimumab, Bevacizumab, Methamphetamines, Warfarin.
Aminoglycosides, Contrast Dye, Cisplatin/Carboplatin, Amphotericin B, Cidofovir, Zalendronate.
All Beta lactams, PPI’s, Ciprofloxacin, NSAID’s/Cox-2 inhibitors, Loop Diuretics, Cyclosporine.
What medications cause glomerular disease?
What medications cause Postrenal disease?
How to treat NSAID and ACEI/ARB renal injury?
Gold, Pamidronate.
Acyclovir, Sulfonamides, Methotrexate, Triamterene.
Discontinue, Start low and go slow.
How to treat Calcineurine induced kidney injury?
How do aminoglycosides cause AKI? What is the most nephrotoxic aminoglycoside? Least? Treatment?
What drugs can you give to help AKI with contrast media?
CCB’s, Bridge to less toxic immunosuppresant.
Create and ROS which wreaks havoc. Amikacin, Neomycin. Renal Replacement therapy, reversible upon discontinuation.
Hydration, Sodium Bicarbonate, N-acetylcysteine(4 doses, 1 before and 3 after).
What is a hallmark finding of cisplatin AKI?
How can you prevent cisplatin AKI?
What formulation of Amphotericin B is most nephrotoxic?
Hypomagnesia
Amifostine pre treatment(chelates cisplatin) can treat with discontinuation and renal replacement therapy.
Conventional, use lipid version in high risk patients.
How long does it take for NSAIDS to produce an AIN reaction?
What is an AIN treatment?
How do you treat lithium AIN?
6 months, every other drug is around 2 weeks.
discontinue and note as a drug allergy,Corticosteroids.
Amiloride, renal replacements.
What are some hallmark signs of Acyclovir AKI and how do you treat it?
What is toxic Ca X Phos?
When do you start ESA’s?
Can have significant flank pain, crystal sediment in urine. Avoid rapid doses, avoid in renal dysfunction, hydration with high urine flow.
> 55 mg/ dL
dialysis: <10 hg, non dialysis: consider at <10 hg
Most common Side effect with ESA’s?
How much iron should you shoot for?
How much iron is in Ferrous Sulfate? Ferrous Fumarate? Ferrous gluconate?
Hypertension(should not be used with uncontrolled hypertension).
200 mg/day.
20%, 12%, 33%
Preferred vascular access port for hemodialysis?
How to manage hypotension in dialysis?
How to manage muscle cramps in dialysis?
AV fistula, disadvantage is requires 1-2 months to mature.
place in trendelenberg position, give midodorine, decrease filtration rate, Give bolus of IV fluids.
Vitamin E, IV fluids.
How to manage thrombosis in dialysis?
Advantages of Hemodialysis?
Disadvantages of hemodialysis?
Saline flush, refer to vascular surgeon, possibly use t-PA
Takes place in HD center, easy to measure effectiveness, technique failure is low, high solute clearance
loss of patients independence, side effects listed and disequilibrium, vascular access causes thrombosis, decline in renal function is more rapid than with PD
Advantage of Peritoneal Dialysis?
What factors does warfarin inhibit?
What is the therapeutic INR for most conditions? What about for prosthetic mechanical heart valves?
Higher clearance of large solutes, better preservation of residual renal function, suitable for elderly and pediatric patients, patient independence.
2,7,9,10.
2-3. 2.5-3.5.
What does a higher INR mean? What does a lower INR mean?
What does protamine reverse?
How do we reverse warfarin?
Increased anticoagulation=bleeding. Decreased anticoagulation=clotting.
UFH, LMWH
Vitamin K.
What does Aminocaproic Acid reverse?
How do we reverse Dabigatran?
What are the 3 steps to HIT treatment? Should we ever infuse platelets?
Fibrinolytics
Idarucizumab
Discontinue Heparin–> Arbagtroban–> Overlap with Warfarin for at least 5 days. NO!!!
How often do we need to monitor warfarin?
What to do if there is an INR dose on warfarin that is out of range on a stable patient?
What to do if patient is on warfarin and has a significant bleed and any INR increase?
Daily upon initiation, then q2-3 days, then weekly until stable–> then monthly until 3 therapeutic INR’s are achieved and then every 12 weeks.
if 0.5 difference above or below continue current dose and then retest INR in 1-2 weeks.
Give PCC and then IV Vitamin K.
When should you give oral vitamin K with warfarin?
What are your major counseling points for warfarin?
What are some benefits of using UFH?
When patient has INR over 10 and no significant bleed.
Compliance, ask pharmacist before taking any new OTC medications, consistent Vitamin K intake, watch alcohol, watch for signs and symptoms of bleeding and clotting.
Cheap, Effective, Easily Reversible, Can be used in pregnancy and pediatrics.
What are some benefits of using LMWH?
What are the 3 LMWH?
What is the Enoxaparin dose for VTE prevention? How do you adjust this for a CrCl<30?
Long half life(also a negative), no monitoring, less incidence of major bleed, HIT, and osteoperosis vs UFH, increased subQ bioavailability, drug of choice in pregnancy
Enoxaparin, Dalteparin, Tinzaparin.
30 mg subQ every 12 hours or 40 subQ once daily. 30 mg subQ daily.
What is Heparin dose for VTE prevention?
What is heparin dose for VTE acute treatment? What aPTT do we aim for?
What is Enoxaparin dosing for VTE acute treatment? How do we adjust for CrCl<30?
5000 units subQ every 8-12 hours.
80 units/kg bolus followed by 18 units/kg/hr drip. 60-100 seconds.
1 mg/kg SubQ BID. 1mg/kg subQ once daily.
What is Fondaparinux dosing? Do we use when CrCl <30?
What are the LMWH’s MOA?
What is UFH’s MOA?
5-10 mg subq daily based on weight or just 2.5 mg daily, cut off zeros. NO.
Potentiates action of AT3, Inhibits factor Xa and 2a(thrombin).
Potentiates action of AT3, inactivates thrombin and factors 9,10,11,12, and plasmin
What is the only factor Xa inhibitor that has AT3 action?
What are the Factor Xa inhibitors?
Is fondaparinux 100% bioavailable subq?
Fondaparinux
Fondaparinux, Rivaroxaban, Apixaban, Edoxaban
YES
What renal cutoff is fondaparinux not used?
What renal cutoff is Edoxaban not used? Does it require bridging?
What renal cutoff is Rivaroxaban not used?
<30 CrCl.
If 10-15 it’s 30mg po daily. Yes, 5-10 days of bridging with parenteral anticoagulant.
VTE: CrCl<30. NVAF: CrCl<15
What renal cutoff is Apixaban not used?
What are the components of Virchow’s triad?
Who is at low risk for VTE and how do you treat?
Reduced dosing for >1.5 SCr. No data for CrCl.
Hypercoaguble state(malignancy, gene mutations(factor V leidin), hereditary dysfunction(Protein C&S), Pregnancy), Vascular injury(major orthopedic surgery, trauma, fracture, indwelling venous catheters), Venous stasis(illness, HF, paralysis, surgery, polycythemia vera, obesity, varicose veins).
Minor surgery, fully ambulatory. Ambulation +/- IPC.
Who is at moderate risk for VTE and how do you treat?
Who is at high risk for VTE and how do you treat?
Who is at very high risk for VTE and how do you treat?
most non surgical patients, medically ill with bedrest, major trauma. LMWH, Low dose UFH, Fondaparinux(medically ill only) OR IPC alone.
Surgical patients or medically ill with risk factors. Spinal cord injury patients. LMWH, Low does UFH AND IPC.
Ortho surgery. Any of the medicines really.
VTE prophylaxis rivaroxaban dose? VTE treatment dose?
VTE prophylaxis dabigatran dose?
VTE prophylaxis Apixaban dose? VTE treatment dose?
VTE treatment dose for Edoxaban?
10 mg PO daily. Avoid in renal impairment. 15 mg PO BID for 3 weeks then 20 mg daily.
110 mg PO for 1 dose then 220 mg PO daily.
2.5 mg PO BID. 10 mg PO BID for 7 days then 5 mg PO BID.
> 60 kg: 60 mg PO daily. <60: 30 mg PO daily
How long should treatment last for long term?
Slowest onset of ADP agonists? Which one do we need to stop a week in advance?
Which GP inhibitor causes the most thrombocytopenia? Which one is CI’d in dialysis and causes renal issues?
Provoked- 3 months. 1st or 2nd unprovoked 3 months then reevaluate.
Clopidogrel. Prasugrel.
Abciximab. Eptifitbatide.
What fibrinolytics causes antibody formation?
Preferred anticoagulation in pregnancy? What about Cancer patients?
What are the CYP2C9 inducers(decrease INR, decrease warfarin)?
What are the CYP2C9 inhibitors(increase INR, increase warfarin)?
Streptokinase
LMWH is preferred to UFH. LMWH is preferred to Warfarin.
Barbiturates, Carbamazepine, Phenytoin, Rifampin.
Amiodarone, Disulfiram, Fluconazole, Metronidazole, TMP/SMZ, Zafirlukast, Cranberry juice.
When does prevalence of PAD start to progress?
What is the most common site of claudication pain in PAD?
What is normal ABI? Mild to moderate? Severe?
Age 40.
Calf
0.91-1.3. 0.4-0.9. <0.4
What is first line therapy for PAD? What are the drugs we need to make sure we give them?
When is Cliostazol CI’d in PAD?
Is pentoxifylline recommended to be used according to chest guidelines?
Daily supervised exercise program. ASA, Statin, ACEI.
Heart Failure patients.
NO! but it is 2nd line therapy according to ACC/AHA.
What is low HDL in men? Women?
When are triglycerides considered high?
1st line therapy for acute angina relief?
<40, <50.
> 150 mg/dL.
Nitrates
What is third line treatment for angina prophylaxis? Do we need to have daily intervals without this?
What is our goal HR when giving beta blockers? Should we abruptly stop this?
What is the ONLY indicated Glycoprotein inhibitor indicated when planning a PCI? Does it prevent fibrinogen binding?
Long acting nitrates. YES.
50-60 BPM. NO.
Abciximab, yes.
What is the drug of choice for variant angina?
What are the side effects of non dihydropine CCB’s?
Which CAD treatment drug has no effect on BP or HR?
CCB.
Bradycardia, hypotension, heart block, constipation(verapamil), worsening HF
Ranolazine.
Which heart attack has a higher mortality rate at 30 days?
What is the 1st cardiac marker detected?
What is Ivabradene common adverse effect?
STEMI, NSTEMI is 6 months.
Myoglobin.
Phosphenes.
When should you NOT give fibrinolytics to Heart attack patients?
What are some disorders that mimic MI?
What shows ischemia on a EKG?
When they are NSTEMI or after 30 minutes
Aortic dissection, Pericardiditis, Pleuritic chest pain, Pulmonary Embolism, Pneumothorax, Pneumonia, GERD, PUD, Esophageal spasm, anxity and panic attacks.
Flattening and then inversion T wave
What does ST Elevation mean on an EKG?
What does ST depression mean on an EKG?
What does a Q wave show on an EKG?
STEMI
NSTEMI
Necrosis.
What is the preferred cardiac marker? Why?
How long is troponin in the body?
Door to balloon time for STEMI?
Troponin, highly sensitive and specific and is only in cardiac muscle.
5-10 days.
90 minutes.
What is MONA therapy?
Does aspirin reduce mortality rate? When is it CI’d?
Does nitroglycerin and morphine reduce mortality rate?
Morphine, Oxygen, Nitroglycerin, Aspirin.
YES. Active GI bleed and Allergy
NO
What is heparin dosing for MI? What do we want to keep aPTT at?
Enoxaparin dosing for NSTEMI?
Enoxaparin STEMi dosing?
60 units/kg bolus then 12 units/kg/h after. 50-70.
1mg/kg subq every 12 hours, except in CrCl <30 than it’s q24 hours.
<75 years old 30mg IV bolus then 1 mg/kg q 12. >75 no bolus and .75mg/kg q 12.
Clopodigrel loading dose for MI?
Prasugrel loading dose for MI?
Which ADP receptor antagonists have the quickest onset?
300-600 mg then 75 mg daily
60 mg then 10 mg daily.
Prasugrel, Ticagrelor
How do you transition cangrelor to an oral agent?
Do CCB’s have mortality benefit in an MI? Should we start beta blocker in stead?
Fibrinolytic CI’s?
ticagrelor 180 mg, prasugrel 60 mg, clopodigrel 600 mg.
NO. YES.
ANY H/O stroke, suspected aortic dissection, aneursym, severe uncontrolled hypertension, recent surgery or head trauma in last 12 weeks,H/O CV accident in last 2 years,bleeding, pregnancy, active PUD, prolonged CPR.
If you have HIT and need to go to cath lab what do you use? STEMi drug regimen overall for PCI?
What is conservative/medical management for NSTEMI?
What is 0-2 TIMI score?
Bivalrudin. Aspirin, ADP receptor antagonist, GPI + UFH or Bivalrudin, Beta blocker.
Aspirin, ADP receptor antagonist, Antithrombin agent
Low, medical management.
What is 3-4 TIMI score?
What is 5-7 TIMI score?
What is early invasive medicine for NSTEMI?
Intermediate, early invasive management
High, immediate revascularization management.
Aspirin, P2Y12 inhibitor, Antithrombin agent, and consider GPI
What are medications to reduce mortality upon MI discharge(SCAAB)?
How long should you be on your P2Y12 inhibitor after MI?
When do we need to minimize calcium binders in hyperphosphatemia?
Statin, Clopidogrel(or other P2Y12 inhibitor), Aspirin, ACEI, Beta blocker.
12 months.
> 10.2
What Iron product requires a test dose?
What is your target Hb in ESA’s? Big side effect if too high?
Obesity dosing for LMWH in VTE treatment? Prophylaxis?
Iron dextran, also BBW for anaphylaxis
10-11 g/dL. STROKE.
1mg/kg BID. 0.5mg/kg once daily or 60 mg once daily
