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RENAL > Concepts to review > Flashcards

Concepts to review Flashcards

1
Q

What is pulmunary-renal syndromes and what causes it (4)?

A

pulmonary-renal syndrome include Goodpasture syndrome, granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis, and systemic lupus erythematosus.

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2
Q

Hypersensitivity of GoodPaustures?

A

Type 2.

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3
Q

Glomerular subendothelial immune complex deposits are associated…..

A

Glomerular subendothelial immune complex deposits are associated with diffuse proliferative glomerulonephritis, seen in systemic lupus erythematosus.

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4
Q

Glomerular intramembranous immune complex deposits are associated

A

Glomerular intramembranous immune complex deposits are associated with diffuse proliferative glomerulonephritis, seen in membranoproliferative glomerulonephritis due to hepatitis C.

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5
Q

Creatinine
BUN
-mechanism of flow kidney

A

-Creatinine:secrted
-BUN:reabsp
-Ratios.

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6
Q

FSGN associated conditions and symptoms?

A

-Obesity, Sickle cell, Heroin use, IV drug use, HIV.
-Effacement EM (sub epitjeleal deposits)
-Effacement + Hilynosis (similar to RPGN).

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7
Q
A

-This patient, who has a history of intravenous drug use, presents with heavy proteinuria and dysmorphic RBCs on urine microscopy. The biopsy specimen indicates glomerular hypercellularity, increased mesangial matrix, and thickening and splitting of the peripheral capillary walls (double contour), which are classic signs of membranoproliferative glomerulonephritis (MPGN) type I. The most common cause of MPGN type I is hepatitis C infection, common in those with a history of intravenous drug use. Hepatitis B is a less common possibility. MPGN is classified as a nephritic syndrome but often presents with a nephrotic syndrome as well (>3.5 gm protein per 24 hr). Serum hypocomplementemia is common.

The other choices are incorrect:
Diabetic glomerulosclerosis is characterized by dramatic thickening of the capillary basement membrane without immune complexes.
Goodpasture syndrome presents with rapidly progressive glomerulonephritis and basement membrane thinning.
Membranous nephropathy is not associated with glomerular hypercellularity and mesangial proliferation.
Minimal change disease is associated with normal light microscopy findings, with podocyte effacement on electron microscopy.

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8
Q

History of Hepatitis C +arthralgia + Palbable Purpura + Fatigue/weakness

A

-MPG ass with Cryoglobunemia

-Precipitation of cryoglobulins in the vasculature may cause palpable purpura, skin necrosis, and peripheral neuropathy. Most but not all patients will also test positive for rheumatoid factor

-Other complications of mixed cryoglobulinemia may include liver disease, Raynaud phenomenon, and renal disease. Renal biopsy in patients with mixed cryoglobulinemia will show cryoglobulin deposition, which appears as subendothelial dense deposits on electron microscopy. Light microscopy of the glomeruli will show basement membrane thickening and mesangial proliferation.

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9
Q

TRAM-TRACK

A

-MPGN due to mesangial interposition but deposits is in Subendothelium.

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10
Q

What happens to phosphate in early stages of Renal/Kidney Faliure ?

A

-Remain normal due to FGF23–>promotes excretion through kidney.

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11
Q

What role does your RAAS system play in Chronic kidney injury?

A

-Leads to hyperfiltration –>Glomerulosclerosis(by TGF-Beta activation).
-prevented by ACHE inhb.

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12
Q

What do you except to decrease in excretion in renal faliure?

A

-Creatinine depends highly on filtration to be cleared from body–> if RPF is depleted you expect to incr creatinine in blood.
-H+ ion has other ways to exit.

-The most likely to decr. EXCRETION is creatinine.

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13
Q

Ipimumab used,A.E.

A

-RCC, acts on B7(APC) - CTLA4(T cells) inhibit intercation–>inactivates T cell interaction with Tumor cell.
-All -itis
-Patient fills weak after treatment (flu symptoms)

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14
Q

Diagnose of Renal Cancer.

-immature tubules with abortive glomerular formation.
-Groups and sheets of transitional epi. cells.
-Large cell with prominent eosinphilic cytoplasm containing numerous mit.
-Uniform cells with clear cytoplasm containing glycogen and lipid.-

A

-Wilson
-Urothelial Carcinoma
-Oncocytoma
-RCC

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15
Q
A

-Renal cell carcinoma usually occurs in the sixth decade ;combination of costovertebral pain, a palpable mass, and hematuria is the classic triad of symptoms. Histologically, renal cell carcinoma is predominantly of the clear cell type (clear cell carcinoma) with intracytoplasmic glycogen and lipid.

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16
Q

Pee CHUNKS?? what kind bacteria is associated

A

-Urease+

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17
Q

Please SHiNE my SKiS??
-What organ is associated with there clearance?

A

Pseudomonas Aruginosa
Sterp peumoniea
Hemophilus Influenza tybe B
Nesseria meningitis
E.Coli
Strep Groub B
Klebsiella pneumoniea
Salmonella

-All encapsulated bacteria–>opzonized by spleen to remove them. People with ASPLENIA should get vaccinated against this organisms.

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18
Q

What can a sterile pyuria indicate? (2)

A

-Chlamydia + Nesseria UTI’s
-Interstitial Nephritis

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19
Q

Urianalyzes on indicate?
-RBC cast
-Myoglobin ATN

A

-Will tell you RBC present.
-Myoglobinuria will present with brown/reddish urine and NO RBC cells but Heme in urine. Also, complains of muscle aches, fatigue and weakness.

-Rhabdomyolysis occurs in hypo/hyper-kalemia as well.

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20
Q

Can Vancomycin cause Acute Tubular Necrosis?

A

-Yes, in the setting of prolonged use.

-Contrast dyes cause ATN within 24 hours of use, whereas aminoglycosides do so after 7 to 10 days of treatment and accumulation in the renal interstitium.

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21
Q

Main problem in ESRD

A

-Svere uremia (toxin)–>weakness,fatigue, pericarditis…
Reasson for dialysis.

22
Q

Most common cause of death in ESRD?

A

Patients with ESRD die most often of myocardial infarction (MI). The uremic environment accelerates atherosclerosis, making** MI** more likely. Other common causes of death in this population include increased infections and arrhythmias due to hyperkalemia and cardiac disease.

23
Q

-mannitol are unable to freely cross cell membranes and draw water out of the cells. When this occurs in the kidney, it leads to osmotic diuresis with polyuria. However, this patient has minimal renal function because of decreasing urine output due to postoperative sepsis. In this circumstance, the osmotically active mannitol stays in the circulation, causing a high serum osmolality rather than being filtered into the nephron, and it draws water out of the cells, leading to hyponatremia. Giving mannitol to patients with** poor renal function** may lead to volume overload and hyponatremia.

A
24
Q

What does High urine specific gravity tell us in regards to AKI?

A

-High urine gravity=concentrated urine–>you will see it in Pre-Renal AKI.

25
Q

Acute Drug Induced Interstitial Nephritis Hypersensitivity?

A

-Type 1 (Eosinphils present)

26
Q

What nephritic syndrome is mesangial proliferation associated with?

-Mesangial expansion is seen where?

A

-Type 1 Membranous proliferative Glomerulonephritis (interposition of mesangial cells)–>TRAM-TRACK appearance.

-**IgA Nephropathy and Diabetus Nephropathy. **

27
Q

Why RPGN has a rapid onset of nephritis and oliguria?

A

-Because it will destroy completly the glomeruli suddenly and rapidly.

28
Q

Membrabous nephropathy casues

A

-1:** unkown cause (phospholipase A2 receptors) (75% cases)**
-2: due to immune complex formation (SLE, drug reaction like Heroin), aslo solid tumors, MALARIA, HEPATITIS B and C

29
Q

Complication of M.M?

A

-Systemic amyloidosis (nephrotic syndrome).

30
Q

What nephrotic syndrome has SELECTIVE PROTENURIA?

A

Minimal change (only albumin passes, NOT Ig)

31
Q

What does long term Glucocorticoids cause and what will you give if patient has hypertension along side?

A

-Osteoporosis and you give ACHE inhb.

32
Q

How ACHE INHB are teratogenic in 3th trimester?

A

-Cause renal faliure by reducing GFR–>oligohydramnios.

33
Q

What are the complement disorders?
-Complement defic.
-Complement regulatot defic.

A
34
Q

Multiple kidney lesion look similar, how to differentiate between them?

A

-Nephrolitiasis: don’t have anemia nor incr ALK, but it will have flank pain and hematuria and maybe ass with elevated PTH–>elavated Ca++
-APKD: Bilateral cyst, No Hypercalcemia.
-Pyelonephritis: Feer,WBC cast, costovertebral angle tenderness
-RCC:elavated Ca++ and ALK, palbable mass and anemia.

35
Q

What does a NORMAL Hba1c tell you in regards to renal pathology?

A

-Is NOT diabetus Nephropaty.

-If elevated patients may have recurrent infections.

36
Q

What stage does shrunken kidneys represent?

A

-Usually End stage renal disease.

37
Q

What molecule is rels. in MI in the kidney mediating the renal ischemia due to endothelial damage (caused by ischemia)?

A

-Endothelin.

The most common cause of acute tubular necrosis is
ischemic injury. The hypotension that develops **after myocardial infarction **causes decreased renal blood flow, with
intrarenal vasoconstriction. Sublethal endothelial injury from
reduced renal blood flow leads to the increased release of the
vasoconstrictor endothelin **and diminished amounts of the vasodilators nitric oxide and prostaglandin. The ischemic form
of acute tubular injury is often accompanied by rupture of
the basement membrane (tubulorrhexis). An initiating phase
that lasts approximately 1 day is followed by a maintenance
phase during which progressive oliguria and increasing blood
urea nitrogen levels occur, with salt and water overload.
This is followed by a recovery phase, during which there is a
steady increase in urinary output and hypokalemia. Eventually, tubular function is restored. Treatment of this acute renal
failure results in recovery of nearly all patients.

38
Q

Papillary necrosis ass (2)

A

-Diabetus–> recurrent pyelonephritis
-Analgesics(damages interstitium)
-Sickle cell dis or trait.

39
Q

Diagnosis

Coarse and irregular
scarring resulting from ascending infection, blunting and deformity of calyces, and asymmetric involvement of the kidneys. The loss of tubules from scarring gives rise to reduced
renal concentrating ability; the patient had polyuria with a
low specific gravity of the urine. Urinary tract obstruction
favors recurrent urinary tract infection (UTI). Vesicoureteral
reflux propels infected urine from the urinary bladder to the
ureters and renal pelvis and predisposes to infection; it can
be unilateral.

A

-Chronic Pyelonephritis–>most common ass (obstruction reflux).

40
Q

-With respect to imaging of pregnancy patients with symptoms, unenhanced MR of the abdomen and pelvis is typically the most helpful evaluation of this patient’s symptoms, since this involves neither ionizing radiation or contrast injection. Contrast material is avoided because of potential teratogenic effects (for gadolinium based contrast used for MR studies)

CT scans, Enhanced MRI of the abdomen and pelvis as well as nuclear medicine renal scintigraphy (done with Tc-99m-DTPA) are typically avoided because of concerns regarding exposure to ionizing radiation, and contrast material is avoided because of concerns regarding adverse effects on fetal thyroid function (for iodinated contrast used for CT studies) and potential teratogenic effects

A
41
Q

A 37-year-old immigrant from Africa presenting with dysuria, hematuria, dyspareunia with CBC showing eosinophilia, urine analysis revealing 10–19 RBCs /hpf, colposcopy showing sandy patches on cervix and urine direct wet mount showing large egg with tapering anterior end and posterior end showing rudimentary spine, is suggestive of chronic infection by a trematode Schistosoma haematobium. The adult form of this parasite usually colonizes in venous plexus of bladder and causes dysuria and hematuria. It migrates to cervix causing sandy patches appearance which is seen on colposcopy. Transmission of this infection occurs due to contact with contaminated water. Infective form is cercaria, definitive host is man while intermediate host is snail.

A
42
Q

Ca++-Stones present with what in urine?

A

-Hypercalciuria.

43
Q

MEY gene mutation ass with what cancer?

A

-RCC Papillary type

44
Q

In UTI’s what’s the commonest empirical treatment that we use?

A

-SMX-TMP.

45
Q

3 causes of Euvolemic Hyponatremia?

A

-CKD, Thiazide and SIADH
-Na++ loss, Normal volume.

46
Q

medullary kidney dis.

A

-may present with NO cyst and normal renal ultrasound, inherited aut dominant,
-Presentation with gout.

47
Q

Where is dop. produced?

A

-Hypothalamus

48
Q

What value do you look at in Pituitary Somatotropes tumors ?

A

-IGF-1
-GH is pulsatile–>not viable.

49
Q

Can patients with Acromegaly present with diabetic neuropathy ?
-What test fails in this patients?

A

-Yes–>GH has Dibetogenic effects.
-Glucose supressor test. N decr when adm glucose.

50
Q

Can pituitary adenomas that are NOT H. secreting cause Hypopituitarism?

A

-Yes,compression effect

RENAL (17 decks)

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