9 ⼀RENAL/UROLOGY/ID II Flashcards
(344 cards)
239
What is Conn’s syndrome?
________________
dx?
Primary Hyperaldosteronism
2/2 excessive adrenal gland secretion ➜ polyuria and polydipsia
________________
[Plasma aldosterone : Plasma Renin ACTIVITY] > 30
What type of acid base disturbance does TB cause? Why?
TB is a common cause of Addison’s primary adrenal insufficiency which –> ⬇︎Aldosterone –> Normal Anion Gap Metabolic Acidosis

How is Allopurinol used to prevent kidney damage during CA tx?
Allopurinol prevents [tumor lysis-associated urate crystal nephropathy] in pts receiving tx for lymphoma/leukemia
Which drugs cause renal tubular obstruction and ➜ [Crystalline nephropathy Acute Tubular Necrosis]? - 5.0
“crystal MAPES obstruct kidneys!”
- MTX
- Acyclovir IV
- Protease inhibitors
- Ethylene glycol
- Sulfonamides
Uremia constitutes a BUN of ⬜
Name the classic s/s (3)
> 50
_________________
LAC
Lethargy | Anorexia with vomiting | Confusion
Why are DM pts who take SGLT2 inhibitors at ⇪ risk for DKA?
because [SGLT2 inhibitors] prevent Glucose reabsorption ➜ easier/faster for [fasting, exercise, abrupt insulin ∆] to activate ketogenesis = ketogenesis may occur in setting of [euglycemic DKA < 250 BG]
(normally: DKA is observed
Hemodialysis via tunneled catheter is a/w high rates of catheter-related bloodstream infxn
Typical management for catheter-related bloodstream infxn involves leaving tunneled Catheter in place and what else? (2)
_________________
When is immediate removal of [infected tunneled Catheter] indicated ? (5)
{Vancomycin + [cefepime|gentamicin]} ➜ [once afebrile, change catheter over guidewire]
_________________
Severe Sepsis | HDUS | pus at site | sx > 72h after abx | metastatic infxn
Demeclocycline MOA
blunts Collecting Duct resposne to ADH during SIADH ➜ water excretion
preferred over lithium which is similar
How do you determine if renal artery stenosis is the underlying cause of HTN in Kidney transplant patients?
_________________
explain
Give [ACEk2 inhibitor]. If Creatinine INC ➜ Renal Artery stenosis was the cause of HTN
_________________
(2/2 improper surgical anastomosis), renal artery stenosis (BL or solitary uL) causes DEC GFR and when [ACEk2 inhibitor] is given ➜ even lower DEC GFR. This very low GFR activates the renin-angiotensin-aldosterone system ➜ INC [Angiotensin 1 and 2] HAVDEN ➜ ultimately resistant hypertension, flash pulm edema
How do you workup hypOnatremia?
Patients with Chronic Kidney Disease develop ⬜ anemia that is treated with ⬜
Prior to giving this treatment, why must iron be assessed first?
normocytic; Erythropoietin
_________________
[EPO ➜ vigorous hematopoiesis ➜ rapid depletion of iron stores ➜ IDAfn]
so MD must ensure iron stores are sufficienct prior to giving EPO
Erythrocytosis in patients with hematuria and smoking hx should always make you think of (and rule out) ⬜
RCC (HAWF) = GET CT abd!
_________________
RCC ➜ Erythropoietin secretion ➜ Erythrocytosis
HAWF= Hematuria/Abd mass/Wt loss/Flank Pain
⬜ is the most common cause of nephrOtic syndrome in kids and presents with ⬜
_________________
Tx?
Minimal change disease; [CLag]
_________________
CTS
_________________
[CLag = ⇪ Coagulation/Lipidemia /⬇︎albumin/gammaglobulin]
rapid remission with CTS but has HIGH relapse rate = frequent UA

Both AiN and Pyelonephritis involve intrusion of the tubulointerstitium. What’s the major difference?
[AiN = mononuclear cell]
vs
[Pyelonephritis = neutroPhil]
[AiN] MOD
[RiPAN –mo–> FAPES]
hypersensitivity to [RiPAN antigen] ➜ moNONUCLEAR CELLS infiltrating tubulointerstitium➜ FAPES
_________________
RiPAN = Rheum/iNfection/PPI/Abx/NSAIDs
FAPES = FEVER / AKI intrarenal / [Pyuria +/- WBC cast] / [Eosinophilia (blood +/- urine)] / Skin rash]

[AiN] sx (5)
FAPES = FEVER / AKI intrarenal / [Pyuria_sterile+/- WBC cast] / [Eosinophilia (in blood +/- urine)] / [Skin rash]
_________________
[RiPAN –mo–> FAPES]
RiPAN = Rheum/iNfection/PPI/Abx/NSAIDs
ATN MOD
[⬇︎renal perfusion] ➜ [Acute Tubular Necrosis of tubular epithelium] ➜ sloughing of necrotic medullary cells ➜ [mBGC and/or rTEC/C]
w
[💢flank]+/- hematuria (more common in GN)
💢= pain
🔎mBGC = muddy Brown Granular cast
🔎rTEC/C = renal Tubular Epithelial Cell/cast
clinical presentation of [radioContrast associated AKI]
24-48h after contrast ➜ = [contrast induced nephropathy] = nonoliguric intrarenal AKI⼀ATN⼀mBGC
🔎mBGC = muddy Brown Granular Cast
How do you determine cause of an AKI? -4
PHEOCHromocytoma
clinical features (6)
PHEOCHromocytoma
Palpitations
HA
Episodic SWEATING
Orthostatic hypOtension
([Catecholamine & Metanephrine 24h urine] or [free plasma metanephrine] = dx)
HTNrefractory
a patient with positive labs for PHEOCHromocytoma has negative imaging results
What’s the next diagnostic used?
_________________
When can surgical removal occur?
[MIBG scan]
_________________
Adrenalectomy only after [10 day preOp BP control with αB➜ (+ BB)]
_________________
MIBG = MetaIodoBenzylGuanidine (resembles NorEpi ➜ will be taken up by rogue adrenergic tissue = locates tumors not seen by imaging) // [αB = α R Blocker]
PHEOCHromocytoma patients undergoing adrenalectomy may experience hypOtension and HYPERtension intraoperatively
How is [PHEOCHromocytoma-related_hypOtension] treated?
_________________
[PHEOCHromocytoma-related_HTN] treated?
PHhypOtension ➜ [NS IV bolus]
_________________
PHHYPERtension ➜ give [phentolamineα1🟥 IV bolus]
_________________
Dopamine/Dobutamine can’t be used in PHEOCHromocytoma hypOtension 2/2 chronic α R Blockade
clinical features of BrIAn (3)
_________________
Berger IgA nephropathy
- [URI ➜ Recurrent GROSS hematuriia]
- [NORMAL COMPLEMENT (PSGN-PiG = low complement)]
- [POOR PROGNOSIS if Cr ⇪ / BP ⇪ / persistent prOteinuria]*
_________________
*BP>140/90 / [pp> 1 gm per day]
Why is rapidly worsening kidney function (⬇︎GFR or ⇪[urine albumin/Cr ratio]) highly concerning for Diabetic Kidney Disease?
Diabetic Kidney Disease is a SLOW PROGRESSIVE KIDNEY DETERIORATION.
Rapid Deterioration suggest ANOTHER ETX➜ WARRANTS RENAL BIOPSY




































































































