Renal and Urinary Flashcards
(114 cards)
Laboratory Findings of [Post Strep GN] / [Post infectious GN] (4)
- INC ASO (Anti-Streptolysin)
- INC [Anti-DNase B]
- [DEC C3 and total compliment]
- Cryoglobulins
3 MAIN ways to avoiding [Catheter Associated UTI]
- REMOVE CATHETER AS SOON AS IT IS NOT INDICATED ANYMORE (DURATION IS THE GREATEST RISK)
- Avoid Unnecessary catheterization
- Use Sterile technique during insert
Most common cause of nephrOtic syndrome in Children and its Tx
A: Minimal Change Dz
B: REVERSIBLE with Corticosteroids
What is almost always associated for Acute Pyelonephritis? (2)
[VUR -Vesicoureteral Reflux] (Anatomical vs. Functional) and [WBC Cast]
Diabetic Autonomic Neuropathy
A: Clinical Presentation (2)
B: Dx method
C: What’s the earliest sign/detection method for Diabetic Nephropathy
D: Diabetic Nephropathy is the leading cause of _____
A: [Overflow incontinence 2° to inability to sense full bladder] and [incomplete emptying when voiding]
B: [PVR-PostVoid Residual] testing with US vs. Catheter to confirm [incomplete emptying when voiding]
C: [INC Albuminuria ( urine will be)]
D: [ESRD Chronic Kidney Dz]
Describe the Differential Dx for Metabolic ALKalosis
A: How does Multiple Sclerosis affect the Bladder?
B: Describe the 3 Different etiologies of Urinary Incontinence and their sx
A: [Loss of CNS inhibition on [Bladder Detrusor Contraction] allows bladder to always stay contracted –> Urge Incontinence–>eventually progresses [Bladder Atony and Dilation] –> Overflow Incontinence
A: Most common cause of [Nephrolithiasis/Kidney Stones]
B: Most common Risk Factor
C: Other Risk Factors (3)
D: Name 2 inhibitors of [Nephrolithiasis] (2)
A: Idiopathic Hypercalciuria = [Normocalcemia + Hypercalcuria]
B: Hypercalcuria
C:
- [Crohn Dz / Fat Malabsorption / Spinach]–> HyperOxaluria
- [Distal RTA Type 1] –> hypOcitraturia
- Gout –> Hyperuricosuria
D: Citrate vs. INC Water intake
Pts are Normocalcemic due to intact serum regulations by Vitamin D and PTH
ADPKD- Autosomal Dominant Polycystic Kidney Disease
A: Genetic MOD
B: Clinical MOD (2)
Benign Prostatic Hyperplasia
Clinical Manifestation (3)
- [Intermittent Bladder Outlet Obstruction]–>Urinary Retention –> Reflux Nephropathy
- Overflow Incontinence
- Later: Hydronephrosis–>[Renal Interstitial atrophy] –> Chronic Renal Failure
A: How do you Calculate Anion Gap
B: What is the normal Anion Gap
C: Name the Etiologies for [INC Anion Gap Acidosis] (9)
A: Never Carry Hotsauce: [Na+ - (Cl + HCO3)]
B: [10 - 12]
C: “The MUDPILES INC our Gap”
Methanol
Uremia
DKA (Tx= IV normal saline + Insulin)
Paraldehyde
[Isonizid vs. Iron]
Lactic Acid
Ethylene Glycol
Salicylates
DKA- Diabetic KetoAcidosis
A: Tx (2)
B: MOD (2 pathways)
C: What type of Anion Gap Acidosis does this cause
D: What’s the pH of the Urine during DKA? Why (2)?
A: [IV Normal Saline + Insulin]
B: image
C: [INC Anion Gap Acidosis] (MUDPILES)
D: Urine is ACIDIC (HCO3 is completely reAbsorbed in acidotic states by PCT & INC production of NH4 & H2PO4)
A: Which Renal Structure is subject to Injury from Pelvic Surgery and why?
B: Clinical manifestation (3)
A: Ureters can become unintentially ligated during [Pelvic surgery] –> Obstruction–> [Hydronephrosis w/Flank pain]
B:
- [Flank pain radiating to groin (from ureter and renal pelvis distension]
- [Ballotable Flank Mass developing within weeks of pelvic surgery]
- [Normal Urine output & Serum creatinine (contralateral kidney compensates)]
[Post Strep Glomerulonephritis / Post infectious GN]
A: Clinical Presentation (5)
B: What part of the Kidney is affectred
A: [Older Child/Young Adult] with [Edema / Hematuria (Cola Colored Urine) / ProteinUria] few weeks after [Impetigo vs. pharyngeal infection]
B: Affects BOTH Kidneys (enlarged and swollen)
[Pauci Immune ANCA-associated RPGN]
A: Histology (3)
B: Clinical Presentation (2)
Is a type 2 Hypersensitivity
A:
1) Absence of Ig and C3 deposit
2) Crescent formation
3) Focal Necrosis
B: [Renal Failure] + [Pulm (epistaxis vs. chronic sinusitis)
Acute Tubular Necrosis
A: Clinical Course (3 Phases)
B: Outcomes (2)
A:
- Initiation phase =36 hour period = slight DEC in urine output from ischemic/toxic injury
- Maintenance Phase= 1-2 week period= Tubular damage is established –> [Oliguria/Fluid overload/Electrolyte abnormalitities]
- Recovery Phase= [Tubular Re-epithelization] which clears cast –> Transient polyuria and [loss of electrolytes from still impaired tube reabsorption]
B: ([Tubular Re-epithelization] + [Renal Function imprvmnt]) vs. [Foci of interstitial scaring associated w/permanent renal impairment (rare)]
NephrOtic Syndrome
A: Classic Presentation (5)
B: COMMON Renal Complication from this. What are the sx (3)
A: CLag + [Proteinuria > 3.5 gm/day–>FOamy Urine] =
[INC Coagulability from loss of AT3]
[INC Lipidemia]
[DEC alubuminemia] –> Edema
[DEC gammaglobinemia]
B: Renal Vein Thrombosis –>
- Acute Flank Pain
- Hematuria
- [RIGHT Varicocele]
A: Describe Histology for Hyaline Arteriolosclerosis
B: Causes (2)
A: [Homogenous deposition of eosinophilic hyaline in intima and media of small vessels]
B:
1) Benign HTN
2) [Diabetic Autonomic NephrOpathy:–> will also have [Kimmelsteil Wilson Nodules from Mesangial Sclerosis]
Where in the Renal Tubule is PAH secreted into?
PCT (but also some PAH is freely filtered by Glomerulus)
so PAH concentration is lowest in Bowman’s Capsule
A: Which substances INCREASE along the PCT (5)
B: Which substances DEC along the PCT (3)
Describe Tubular Solute Concentrations for PAH along the renal tubule (PCT –> Loop–>DCT –> CD)
Describe Tubular Solute Concentrations for Creatinine along the renal tubule (PCT –> Loop–>DCT –> CD)
Basically the same path as [Innulin & Mannitol]
Describe Tubular Solute Concentrations for [Innulin & Mannitol] along the renal tubule (PCT –> Loop–>DCT –> CD)
Basically the same path as Creatinine
Describe Tubular Solute Concentrations for Urea along the renal tubule (PCT –> Loop–>DCT –> CD)