Renal Flashcards
What kind of bone is affected, and what bone lesions are seen in the following diseases: Primary Hyperparathyroidism Low Vitamin D/Rickets/Osteomalacia Osteopetrosis Osteoporosis
Primary Hyperparathyroidism–> Cortical thinning/ subperiosteal erosions.
Low Vitamin D/Rickets/Osteomalacia–>Osteoid matrix accumulation around trabeculae is seen.Histologically, there is excessive unmineralized osteoid with widened osteoid seams
Osteoporosis—>Trabecular thinning with fewer interconnections is characteristic of postmenopausal osteoporosis.
Osteopetrosis–>Osteopetrosis (“marble bone disease”) is characterized by persistence of the primary spongiosa in the medullary cavity with no mature trabeculae. Woven bone seen.
Ultrasound reveals dilated calyces with overlying cortical atrophy bilaterally, mostly in the upper and lower poles. What is the most likely cause of this patient’s condition?
Renal scarring indicate recurrent pyelonephritis. And that occurs in vesicoureteral reflux.
Multicystic dysplastic kidneys–> cause shrunken kidneys so you confused cortical atrophy with this. But be careful.
(Posterior urethral valves, APKD, hydronephrosis–> all cause enlarged kidneys)
AIN will show what on urineanalysis?
Aiiiiin—> WBC CASTS
Cast ho gayayy, aayiiiin
What kind of urinary incontinence is seen in diabetic autonomic neuropathy?
Overflow incontinence is due to impaired detrusor contractility (eg, diabetic autonomic neuropathy)
Urinary incontinence story?
Stress–> For stress imagine urethra ka masla aur leakage of urine while intraabdominal pressure is increased.
(Urethral hypermobilization, urethral sphincter deficiency)
Urge incontinence–>Sudden, overwhelming urge to urinate.
Detruser HYPUR-activity.
Overflow incontinuous–> urinary dribbling. Occurs when there’s IMPAIRED DETRUSOR CONTRACTILITY ( diabetic autonomic neuropathy) or Bladder Outlet obstruction (tumour, BPH)
What is seen microscopically in Renal papillary necrosis?
Gray-white or yellow necrosis of the distal two-thirds of the renal pyramids is seen macroscopically and corresponds microscopically to coagulation necrosis with preserved tubule outlines; cortical surface scars can develop subsequently as inflammatory foci are replaced by fibrous depressions.
Renal Tubular acidosis story:
ABO:
Type 1 (DTA)--> α-intercalated H+ nahyin secrete ker rahay, iss waja sey Bicarb saara urine mein jaa raha hai. This is the only acidosis, jiss mein urine's PH is towards alkaline/more/greater than 5.5. Clinical association is INCREASED urine stone formation.
Type 2 (PTA, increased risk of hypophosphatemic rickets in fanconi syndrome, acetozolamide use)—> Bicarbonate reabsorb nahyin ho raha, tou abb blood kam bicarb bhaij raha hai kidney ko–> urine mein bicarb kam hoga, aur urine acidic hoga.
Type 4 (Hyperkalemic)—> Only acidosis jiss mein HYPERKALEMIA hoga (baaqi dono mein hypo hota hai)–> O is for HYPO-ALDOSTERONISM–> Decreased NH4 secretion. Occurs in K-sparing diuretics.
Aldosterone causes Hypokalemic Metabolic Alkalosis, and HTN–> State your story for this:
3 conditions where we see: HTN and Metabolic Alkalosis:
1–>Sirf Aldo increased hai, Rennin is decreased–> Aldosterone secreting tumour, B/L adrenal hyperplasia.
2—> Aldo aur Rennin dono INCREASED hein (Iss mein Renin pehlay increase hota hai, aur Rennin aagay Aldo ko bhee increase kerta hai)—> SECONDARY HYPERALDOSTERONISM–> Renal Artery stenosis, Malignanat HTN, Reninoma/JG cell tumour/ Renin-secreting tumour, Diuretic use, edema seen in cirrhosis, heart failure.
3—> Renin aur Aldo dono decreased hein per phir bhee HTN and Hypokalemia hai? HOW—> CAH, deoxycorticosterone producing tumour, Cushing, Exogenous Mineralocorticoids.
We don’t see edema in Primary hyperaldo, but we see it in conditions of SECONDARY hyperaldosteronism–> edema caused by CHF, cirrhosis.
Why?
Primary aldosteronism causes INCREASED sodium reabsorption—> But serum Na ko normal rakhnay kay liyay, there’s increased INTRAVASCULAR VOLUME.
When intravascular volume is raised it causes PRESSURE NATURESIS–> Hence, no edema!
Barter, Gittelman and Liddle’s syndrome, same?
Batter Syndrome–> Bart is a TALL guy, who runs in loops in his aldos sneakers. (Defect is TAL, characteristics of this condition are simillar to when the person is taking loop diuretics, Aldosterone and Rennin is increased. Causes metabolic alkalosis just like loop.
Gittelman–> Gentleman feels bad about not being in the mag this year because of his thighs, but gets up to go running in his aldo sneakers.
(Defect of NaCl in DCT, similar to when the person is on thiazide diuretics, HYPOMAGNESEMIA (sets it apart from other RTA)
Liddle’s syndrome–> Little boy is being adamant, but he doesn’t have aldo sneakers and can’t run because so little! Adamant–> Autosommal dominant (Only RTD which is Autosommal Dominant, all others are AR)
(Liddle’s and SAME both–> LOW RENNIN AND ALDO–> both being low is diagnostic for these RTA. )
Note: Low Aldo and Rennin is seen in Liddle, SAME, and SIADH–> 579 FA
