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.