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

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High Yield Sigs

Study Slideshow

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

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Explain how alterations in components of the filtration barrier would result in hematuria and proteinuria (and define proteinuria). (SIGS/LGS 6.8a)

Proteinuria (>300 (Slater)): podocyte damage-> impaired charge barrier-- NEPHROTIC; Hematuria: glomerular inflam-> GBM damage-> loss of RBC to urine-- NEPHRITIC

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Describe the anatomical and physiological features of the glomerulus. (SIGS6.8a)

afferent arteriole, efferent arteriole, mesangial cells & matrix, fenestrated endothelium, GBM, podocytes, Bowman's capsule; size & charge barriers

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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

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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)

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Explain why blood urea nitrogen and serum creatinine levels increase in a patient with AKI. (SIGS6.8b)

Norm: BUN/serum creatinine ratio 10:1; AKI: incr sodium reabsorb in PCT in hypovolemia-> parallel urea reabsorb-> decr. urea excretion& incr BUN/cr ratio >20:1

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Explain the effects of AKI on the electrolyte balance in serum and urine. (SIGS6.8b)

GFR, azotemia, uremia, oliguria, anuria, polyuria: measures of what is going on

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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

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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)

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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

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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

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Discuss the utility of routine cultures and interferon gamma release assay in the workup of pulmonary vasculitis. (Case 6.9a)

to rule in/out TB; interferon-y release assays rely on the fact that T lymphocytes will release IFN-y when exposed to specific antigens

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

See image

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Define respiratory acidosis and metabolic alkalosis. (SIGS 6.9b)

Resp. acid: lungs retain CO2 (hypoventilation);Met. Alk.: increase HCO3- (loss in acid) etiologies: vomiting&dehydration, incr. mineralocorticoid act., Cl- loss

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Describe the approach to interpreting an arterial blood gas and naming the disorder. (SIGS 6.9b)

Assess pH--> PaCO2 & HCO3 --> compensation of primary disorder (inconsistent PaCO2/HCO3 with pH)--> assess PaO2

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Define the CO2-bicarbonate buffering system. (Case 6.9b)

acid-base homeostatic mechanism to balance H2CO3, HCO-3, and CO2 to maintain pH in the blood, duodenum, and tissues to support metabolic function

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