Renal (Uworld)

Question 1

Renal vein thrombosis risk factors?

Answer 1

hypercoagulability: nephrotic syndrome,malignancy( particularly renal), oraql contra pills; volume depletion ( infants), trauma.

Question 2

Renal vein thrombosis clinical features?

Answer 2

hematuria, flank or abdominal pain, elevated LDH (lactate dehydrogenase) with or without acute kidney injury, enlarged kidney on imaging.

Question 3

Renal vein thrombosis diagnosis?

Answer 3

CT or MRI angiography, renal venography.

Question 4

Renal vein thrombosis treatment?

Answer 4

anticoagulation, thrombolysis/thrombectomy (if AKI is present).

Question 5

Renal vein thrombosis presents with?

Answer 5

hematuria, renovascular congestion (increased glomerular pressure), and flank pain (capsular stretch).

Question 6

Renal vein thrombosis causes?

Answer 6

nephrotic syndrome, malignancy, and trauma ( acquired hypercoagulability).

Question 7

Uretrolithiasis presentation?

Answer 7

acute flank pain and nausea.

Question 8

ureterolithiasis stones

Answer 8

if less or = 5 passes spontaneously, increased oral fluid intake to ensure adequate flow of dilute urine

Question 9

Alpha-blockers (ureterolithiasis)

Answer 9

facilitate passage of larger stones (6 - 10 mm)

Question 10

urologic consultation ?

Answer 10

if stone is 10 or more and for refractory pain, anuria, aki, and signs of urosepsis.

Question 11

nephrolithiasis presentation?

Answer 11

flank pain and hematuria also nausea and vomiting.

Question 12

hyperoxaluria

Answer 12

can be caused by crohn disease or any other small intestines disease that leads to fat malabsorption.

Question 13

Symptomatic hyperoxaluria

Answer 13

the result of increased oxalate absorption in the gut ( ca with fat instead of ca binding to oxalate) also decreased bile salts reabsorption in the small intestine damage the colonic mucosa and increase oxalate absorption.

Question 14

Diabetic nephropathy

Answer 14

the early stages of diabetic nephropathy are characterized by a period of glomerular hyperfiltration involving an increase in the fraction of plasma that is filtered by each glomerulus. this period may be clinically recognized by slightly reduced serum creatinine as well as the onset of moderately increased albuminuria ( 30 - 300 mg/g).

Question 15

Glomerular filtration in early DN?

Answer 15

primarily driven by an increase in hormonal mediators that favor afferent arteriole vasodilation ( natriuretic peptides, prostaglandins) and efferent arteriole vasoconstriction ( angiotensin 2) this causes an increase in glomerular hydrostatic pressure which increase the glomerular filtration rate, however, it also stimulates a sclerotic response in the glomerular capillaries and facilitates the gradual progression of DN.

Question 16

pharmacologic therapy

Answer 16

Ace inhibitors ( ex: lisinopril) or angiotensin 2 receptor blocker (ex: losartan) slows the progression of DN primarily by blocking angiotensin 2 mediated renal efferent arteriole vasoconstriction. this reduces glomerular hydrostatic pressure, decelerating the development of glomerular capillary sclerosis.

Question 17

history of diabetic nephropathy

Answer 17

hyperfiltration, incipient DN, overt Dn.

Question 18

Hyperfiltration

Answer 18

glomerular hypertrophy, increased GFR.

Question 19

Incipient DN

Answer 19

mesangial expansion, glomerular basement thickening, arteriolar hyalinosis. Moderately increased albuminuria. HTN.

Question 20

Overt DN

Answer 20

Mesangial nodules (kimmelstiel-wilson lesion), tubulointerstitial fibrosis. overt proteinuria. nephrotic syndrome, decreased GFR.

Question 21

acute gallstone pancreatitis led to hypovolemia

Answer 21

colicky abdominal pain after eating, severe epigastric pain, vomiting, elevated lipase.
pt develop hypovolemia due to vomiting, oral fluids intolerance, and third space extravasation.

Question 22

hypovolemia presentation?

Answer 22

dry mucous membranes, hemoconcentration, tachycardia, hypotension, and/or shock. the kidneys respond by releasing Renin from the juxtaglomerular cells.

Question 23

Renin angiotensin system

Answer 23

renin converts angiotensinogen to angiotensin 1 which then converted to angiotensin 2 by ACE.

Question 24

angiotensin 2 has the following systemic effects?

Answer 24

vasoconstriction : increases efferent and systemic arteriolar resistance, which improve the glomerular filtration rate and blood pressure.
sodium and water reabsorption: directly increases proximal tubule sodium reabsorption.
aldosterone secretion: increases sodium and water reabsorption in the distal tubule.