Renal Flashcards

1
Q

Why is aspirin and acetominophen bad for the kidney?

A

1) Aspirin inhibits PGE2 leading to vasoconstriction of the afferent arteriole, which decreases blood flow to renal medulla 2) Acetominophen creates free radicals that damage renal tubules in the medulla.

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2
Q

How does multiple myeloma affect the kidney?

A

1) Bence Jones proteins produce tubular casts - the light chains are toxic to renal tubular epithelium. These casts also incite foreign body giant cell reaction involving tubules and interstitium leading to renal failure. 2) Nephrocalcinosis - hypercalcemia secondary to the lytic bone lesions produces metastatic calcification of the basement membrane of collecting tubules, 3) primary amyloidosis producing nephrotic syndrome.

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3
Q

What is can renal osteodystrophy cause?

A

1) Osteitis fibrosa cystica (Secondary to hypovitaminosis D –> increased PTH –> hyperparathyroidism which increases bone resorption in places like the jaw. 2) osteomalacia (decreased mineralization of the organic bone matrix (osteoid)), 3) osteoporosis (loss of osteoid and mineralized bone) due to chronic metabolic acidosis since bone is used to buffer H+.

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4
Q

What cells secrete renin?

A

The juxtaglomerular appartatus of the afferent arteriole.

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5
Q

What is the most common cause of death in SLE?

A

Diffuse proliferative glomerulonephritis. You will see “wire-looping” of capillaries on LM; subendothelial and sometimes intramembranous IgG-based ICs often with C3 deposition.

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6
Q

Why are patients hyperchloremic with non-anion gap metabolic acidosis?

A

There is an increase in chloride reabsorption to help replace the lost HCO3- in the metabolic acidosis. Diarrhea can cause a metabolic acidosis.

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7
Q

What is hepatorenal syndrome?

A

condition of intense renal vasoconstriction due to a loss of renal autoregulation occurring as a complication of severe, chronic liver disease (i.e., cirrhosis). It is characterized by splanchnic vasodilation and concomitant vasoconstriction in the renal vascular beds due to the activation of R-A-A-S. GFR is reduced, but kidney anatomy is normal. It leads to a pre-renal azotemia (trying to conserve volume for reabsorbing urea).

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8
Q

What is the best treatment for aspirin overdose?

A

Sodium bicarbonate to alkalinize the urine. Signs of an aspirin overdose are tinnitus, nausea, vomiting, and lethargy combined with fever and tachypnea.

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9
Q

In patients with renal disease, how do you adjust loading and maintenance doses?

A

Loading dose (= Cp x Vd / F) should remain the same because this only depends on volume of distribution, no excretion or metabolism. The maintenance dose (= Cp x CL x dose interval / F) should be lowered to due reduced excretion (reduced CL, or clearance).

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10
Q

Patients with Turner syndrome have increased likelihood of developing what renal disease?

A

Wilm’s tumor (nephroblastoma) - 25-30% of patients with Turner’s syndrome will develop horseshoe kidney, pelvic kidney, or duplicated collecting systems. Horseshoe kidney increases likely (4x) of developing Wilm’s tumor.

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11
Q

What microorganisms can lead to staghorn calculus?

A

Any urease-producing microorganisms - this includes Staphyloccus species, Ureaplasma, Proteus (most common), Klebsiella, and Pseudomonas. Staghorn calculus are made of ammonium magnesium phosphate, also known as struvite.

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12
Q

What is causes urine to dark color upon being oxidized?

A

Alkaptonuria, which a deficiency of homogentisic oxidase, an enzyme of tyrosine degradation pathway that converts homogentisic acid to maleylacetoacetic acid. Homogentisic acid when exposed turns a dark black.

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13
Q

Why do patients with alkaptonuria develop arthralgias?

A

Homogentisic acid is toxic to cartilage.

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14
Q

Why is a horseshoe or pelvic kidney lower down from its usual anatomic position?

A

The fused kidneys gets stuck on the inferior mesenteric artery.

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15
Q

What is the most common tumor type of the urinary tract system?

A

Transitional cell carcinoma. It presents with painless hematuria with no casts. Major risk factor is smoking in addition to aniline dyes, phenacetin, and cyclophosphamide.

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16
Q

What are lab values of patients on thiazide diuretics?

A

Hyperglycemia, metabolic alkalosis, low urinary calcium excretion. Inhibit the Na/Cl cotransporter. The drug attaches to the Cl− site and inhibits Na+ and Cl− reabsorption. This leaves the Na+ channel open for Ca2+ reabsorption. They also lead to hypokalemia becuase thiazide diuretics (most common cause): excessive exchange of Na+ for K+ in late distal and collecting tubules. H+ also secreted a lot from the intercalated disk cells.

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17
Q

What antibiotics are associated with nephrotoxicity?

A

Aminoglycosides (gentamicin, neomycin, streptomycin, tobramycin, amikacin)

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18
Q

What is the mechanism of action of cyclophosphamide?

A

It is an alkylating agent that cross-links DNA and prevents DNA synthesis and cell division.

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19
Q

What is tubulointerstitial nephritis (acute or chronic inflammation of tubules and interstitium) commonly cuased by?

A

Drug toxicity - Penicillin (particularly methicillin), rifampin, sulfonamides, NSAIDS, diuretics

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20
Q

How does tubulointerstitial nephritis present?

A

Pyuria (classically eosinophils) and azotemia, occurring after administration of drugs that act as haptens, including hypersensitivity.

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21
Q

What usually causes chronic pylonephritis?

A

Typically requires predisposition to infection such as vesicoureteral reflux or chronically obstructing kidney stones.

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22
Q

What causes the proteinuria associated with MCD?

A

Effacement of foot processes supporting the epithelial podocytes with weakening of slit-pore membranes. T-cell cytokine release attacks the BM and results in less charge barrier allowing negatively charged proteins like albumin to leak through into urine. Decreased albumin leads to less oncotic pressure in plasma so more fluid goes in interstitium leading to edema. Steroid treatment has a good response.

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23
Q

What is maple syrup urine disease?

A

Patients can’t degrade branched amino acids (I Love Vermont - isoleucine, Leucine, Valine) due to decreaed alpha-ketoacid dehydrogenase.

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24
Q

How long after a Group A beta-hemolytic strep infection does a person present with signs of PSGN?

A

About 1-3 weeks - RBCs will be seen in urinalysis.

25
Q

What is the mechanism of angiotensin II on efferent aterioles?

A

A II works by binding to angiotensin receptor type I, which is a seven-transmembrane domain receptor couples to Gq that activates phospholipase C. PLC cleave PIP2 to form IP3 and DAG. IP3 opens calcium channels which increase intracellular calcium and DAG activates protein kinase C.

26
Q

What is nephrogenic diabetes insipidus?

A

Kidneys do not respond to ADH, so urine osmolarity is decreased markedly and there is an increase in thirst along with increased urine output (polyuria, polydipsia). Administration of desmopressin/vassopressin and no response differentiates this from central DI, which would have a response (increase urine osmolarity).

27
Q

What are findings of tumor lysis syndrome?

A

Metabolic acidosis, hypocalcemia, and hyperphosphatemia. Rapidly dividing cancer cells die and dump their contents into the bloodstream, including large amounts of phosphate and purine derived from DNA. Purines are metabolized and secreted in the form of uric acid.

28
Q

How does allopurinol work?

A

It inhibits the enzyme xanthine oxidase, which subsequently reduces the conversion of xanthine to uric acid. It can beused in lymphoma and leukemia to prevent tumor lysis-associated urate nephropathy.

29
Q

Which loop diuretic is not sulfa derived?

A

Ethacrynic acid. Its side effects include ototoxicity, metabolic alkalosis, hypokalemia, hyperglycemia, and hyperuricemia.

30
Q

Why does hypokalemia lead to muscle weakness?

A

Less K+ outside cell, so more K+ flows out, making the membrane potential more negative and less excitable.

31
Q

What happens when the allantois fails to regress?

A

Urachal fistula which predisposes to UTIs; urine will be discharged through the umbilicus.

32
Q

Explain the evolution from yolk sac to urachus.

A

In the 3rd week the yolk sac forms the allantois, which extends into the urogenital sinus. Allantois becomes the urachus, a duct between fetal bladder and yolk sac. The urachus eventually regresses and becomes the median umbilical ligament.

33
Q

What do urachal remnants predispose a patient to?

A

Infection and adenocarcinoma.

34
Q

What are the remnants of the fetal umbilical arteries?

A

Medial umbilical ligaments.

35
Q

What are renal bruits a sign of?

A

Renal artery stenosis. This leads to decreased perfusion of the kidney. This results in a drop in intraglomerular pressure and GFR. ACE inhibitors are contraindicated because they prevent vasoconstrictive effect of AII on the efferent aterioles, which decreases RBF and increases GFR. ACEi would decrease GFR.

36
Q

What is an expected type of adjustment in blood pH that will occur after starting treatment with furosemide?

A

Natriuresis and diuresis occurs so volume falls and aldo secretion is increased. This causes sodium and water reabsorption in the principal cells of the collecting duct, while potassium is secreted. Sodium is taken up via the Na-H exchanger, which leads to a contraction alkalosis. Additionally, potassium and protons are exchanged in the intercalated cells - increase in sodium reabsorption results in K+ into the lumen, which then exhcnages for H+ so urine is more acidic.

37
Q

What is spironolactone?

A

It is a potassium-sparing diuretic often used in combination with thiazide diuretics to prevent hypokalemia. It is a weak androgen receptor antagonist, which leads to gynecomastia and decreased sex drive.

38
Q

How does spironolactone work?

A

It is a competitive aldosterone receptor antagonist.

39
Q

What is Conn’s syndrome?

A

It is primary hyperaldosteronism caused by a aldosterone-secreting adrenal adenoma. It results in hypertension, hypokalemia, metabolic alkalosis, and low plasma renin.

40
Q

What is acetazolamide’s mechanisms of action?

A

It is an inhibitor of carbonic anhydrase. Causes self-limited NaHCO3 diuresis and decreases total body HCO3- stores.

41
Q

Why are ACEi good to use in diabetics?

A

Since they dilate the efferent arterioles they help ease the effects of hyperfiltration, which leads to glomerular damage and renal failure. ACEi are protective against diabetic nephropathy.

42
Q

What does calcitonin do?

A

It tones down the bloodstream of calcium and puts it on bone.

43
Q

What is ADPKD?

A

It is autosomal dominant polycystic kidney disease that presents with innumerable cysts causing bilateral enlarged kidneys that ultimately destroy the kidney parenchyma. Mutation is in PKD1 or PKD2 gene. IT is associated with berry aneurysms, MVP, benign hepatic cysts, and hypertension (due to increased renin production).

44
Q

What is associated with crystal-induced nephropathy?

A

Protease inhibitors, like indinavir - drug precipitates in the urine and results in obstruction in urine flow.

45
Q

What diueretic is most beneficial for severe CHF and pulmonary edema?

A

A loop diuretic like furosemide

46
Q

A deficiency of 21-alpha-hydroxylase decreases the ability to make what?

A

Mineralcorticoids like aldosterone.

47
Q

What is a symptom associated with small cell lung cancer and what is a laboratory finding?

A

Paraneoplastic syndrome like SIADH, which leads to hyponatremia due to excessive water retention (and continued urinary Na+ excretion).

48
Q

In Goodpasture’s syndrome what is a PAS finding and what are the antibodies directed against?

A

Linear staining and autoantibodies against type IV collagen, a shared protein between alveolar and glomerular basement membranes. In kidneys, it causes rapidly progressive glomerulnephritis.

49
Q

Giving a child with a suspected viral illness will result in what condition?

A

Reye syndrome which is noted by fatty liver and cerebral edema.

50
Q

What is the effect of ATII on the PT for H+/HCO3- exchange?

A

It increases HCO3- reabsorption and has no change on H+ resorption. Hydrogen is pumped into tubule lumen where is combines with bicarbonate to yield water and carbon dioxide. CO2 diffuses back into PT cell where is it converted to bicarbonate and hydrogen via CA. Bicarbonate is pumped into the blood (increased resorption) and hydrogen is pumped back out into the lumen via the Na+/H+ exchanger where it undergoes another road of bicarbonate addition.

51
Q

What exposure can increase one’s risk of developing Goodpasture’s syndrome (RPGN and pulmonary hemorrhage)?

A

Exposure to hydrocarbon solvents such as those found in the dry-cleaning industry.

52
Q

Which antibodies normall provide the major defense for mucosal surfaces against bacterial colonization?

A

IgA - this is why Strep. pneumoniae is very virulent. It contains IgA protease which cleaves secretory IgA antibodies. N. meningitidis, N. gonorrhoeae, and H. influenzae also have IgA protease.

53
Q

Why can’t kids with chronic granulomatous disease fight off fungal and catalase-positive bacterial infections?

A

CGD is caused by a defective neutrophil phagocytosis due to a lack of NADPH oxidase activity. These individuals have negative nitroblue tetrazolium dye reduction tests.

54
Q

What is the function of leukotriene B4?

A

It is a neutrophil chemotactic agent.

55
Q

What is the function of LTC4, LTD4, and LTE4?

A

They cause bronchoconstriction, vasoconstriction, contraction of smooth muscle, and increased vascular permeability. 5-lipoxygenase converts arachodonic acid to 5-hydroxyperoxy-eicosatetraenoid acid, which produces leukotrienes.

56
Q

What does prostaglandin E2 doe to the lung?

A

It is a bronchodilator. Prostaglandins help keep things open (vasodilation, bronchodilation, smooth muscle relaxation, maintain a PDA).

57
Q

How does desquamative interstitial pneumonia (DIP) commonly present?

A

Gradual dyspnea in a middle-aged patient with a smoking history. It resembles IPF in its early stages (“honey-comb” lung).

58
Q

What is angioedema?

A

Rapid swelling of the dermis, subcutaneous tissue, mucosa, and submucosa tissues. It can be caused by ACE inhibitors. It is a Type I HSR.