Unit 6b SIGs Cases 6.8a-6.10a | Baamboozle - Baamboozle

Explain how the fractional excretion of sodium can be used to differentiate the potential etiologies of AKI. (SIGS6.8b)

measures % filtered Na in urine; differentiates 2 common causes of AKI: transient decr. GFR/ poor renal perfusion vs. ATN; See image for values

Oops!

Check

Okay!

Check

Define pulmonary-renal syndrome and list possible etiologies. (Wild card- Sigs 6.9a)

renal failure w/ respritory failure; Etiologies: autoimmune-mediated RPGN & diffuse alveolar hemorrhage

Oops!

Check

Okay!

Check

Explain how IgG immune complex deposition alters glomerular structure. (SIGS6.10a)

IgG complex formation: cell walls antigen-> deposition-> inflammation-> WBC and complement-> injury-> opens glomerular filter-> hematuria

Oops!

Check

Okay!

Check

Explain the physiologic basis of protein handling in the kidney. (SIGS6.8a)

GFB-> fenestrated capillaries, BM (heparin sulfate; charge barrier)-> podocytes (nephrin; size & charge); destruction= proteinuria

Oops!

Check

Okay!

Check

Define the expected laboratory findings in ANCA-associated vasculitis. (SIGS6.9a)

leukocytosis+inflam marker(CRP), anemia, azotemia (prerenal), proteinuria, RBC cast, norm complement, decr PCO2, -anti-GBM & ANA, +p-ANCA (MPO), = cANCA (PR3)

Oops!

Check

Okay!

Check

Differentiate ischemic ATN from toxin-mediated ATN. (SIGS6.8b)

Ischemic: due to decreased/interrupted BF (ex: pre-renal azotemia); Toxin: direct toxic injury to tubules (ex: endogenous/exogenous agents)

Oops!

Check

Okay!

Check

trap

No points!

Oops!

shark

Other team loses 20 points!

Okay!

fairy

Take points!

banana

Go to last place!

Oops!

boom

Lose 50 points!

Oops!

seesaw

Swap points!

Okay!

gift

Win 5 points!

Okay!

baam

Lose 20 points!

Oops!

lifesaver

Give 25 points!

Oops!

gift

Win 15 points!

Okay!

fairy

Take points!

baam

Lose 25 points!

Oops!

Detail the mechanism of injury to the glomerulus in pauci-immune crescentic glomerulonephritis. (SIGS6.9a)

nephritic synd-> RPGN (AKA crescentic glom.nephr.-- crescents composed of fibrin & inflam cells *macrophages*)-> collect in Bowman's-> compress glomerular tuft

Oops!

Check

Okay!

Check

Discuss the role of immunosuppressive therapy in the treatment of lupus nephritis. (SIGS6.10a)

Goal: decrease inflam. and immun. activity--> decrease glomerular damage, decrease nephron loss

Oops!

Check

Okay!

Check

Describe how MPO-ANCA and PR3-ANCA lead to vasculitis. (Case 6.9a)

ANCA-mediated activation neutrophils-> ROS&lytic enzymes-> injury endothelial; stim. NETs-> damage endothel & glomeruli

Oops!

Check

Okay!

Check

Name the drug class to which canagliflozin belongs and explain why this drug is or is not a viable treatment option. (Wild card, LGS6.8.3 WFA6.8)

SGLT2 inhibitor; normally used in combo with metformin for diabetes (HbA1c>9.0), BUT not for pt. with eGFR less than 45 mL/min/1.73m2 (AE renal impairment)

Oops!

Check

Okay!

Check

Explain the pulmonary and renal mechanisms that compensate for alkalosis and acidosis. (SIGS 6.9b)

See image

Oops!

Check

Okay!

Check

seesaw

Swap points!

Oops!

seesaw

Swap points!

Okay!

fairy

Take points!

baam

Lose 10 points!

Oops!

Explain the pathophysiologic changes that occur in MCD and other etiologies of nephrotic syndrome. (SIGS6.8a)

MCD: LM: no changes; EM: effacement of podocyte foot processes; IF: negative; selective glomerular proteinuria; most common nephrotic syndrome in children

Oops!

Check

Okay!

Check