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

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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

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

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

Discuss the role of renal biopsy in the evaluation and management of glomerulonephritis. (SIGS6.10a)

establish specific etiology; Lupus Nephritis: definitive classification & progression (lesions, focal v. diffuse, activity-inflamm., chronicity index-scarring)

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

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

See image

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

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

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

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

How do thiazide diuretics cause hypokalemia and metabolic alkalosis and what is an alternative diuretic to manage hypertension? (Wild card- LGS6.9.1 WFA 6.9

block Na/Cl transporter lum DCT-> prevent Na reabsorb in DCT-> excess Na to coll duct-> incr urinary secretion K+ &H+ incr bicarb blood-> hypokalemia & met alk

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

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)

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

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

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

Explain the major renal physiologic mechanism of antidiuretic hormone (ADH) in water balance. (Wild card-LGS 6.9.1)

ADH-> antidiuresis (incr H2O reabsorb-> decr. urine form); binds V2 recp. principal cells in coll. ducts-> activate adenylate cyclase-> incr cAMP-> aquaporin 2

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

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

Describe the characteristic histopathologic and immunofluorescent features that differentiate the glomerulonephritides. (SIGS6.10a)

See image

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)

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)

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

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