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USMLE World Missed Questions > Renal > Flashcards

Flashcards in Renal Deck (84):
1

What is a renal angiomyolipoma?

A benign tumor composed of blood vessels, smooth muscle and fat.

2

What condition is associated with angiomyolipomas?

Tuberous sclerosis (especially when bilateral)

3

What is Tuberous Sclerosis and how does it present?

AD condition characterized by cortical tubers and subependymal hamartomas in the brain with seizures and mental retardation; cardiac rhabdomyomas, facial angiofibromas, and ash leaf patches may also occur.

4

What renal pathology is associated with von Hippel Lindau?

Bilateral renal cell carcinomas.

5

What is the effect of beta adrenergic action on renin?

NE binds to beta-1 receptors of JGA cells to stimulate renin release

6

What effect do beta blockers have on renin, angiotensin I and II and aldosterone?

Decreases all. They do not affect ACE activity.

7

Where is greater than 60% of water absorbed from regardless of hydration status?

Proximal tubules- it is reabsorbed iso-osmotically here

8

Where is the region of the highest osmolarity in the kidney?

Medullary interstitum

9

What action foes ADH have on urea?

It increases the number of passive urea transporters in the inner medullary collecting duct, allowing a substantial fraction of the highly concentrated urea to diffuse down its concentration gradient into the medullary interstitum. This contributes significantly to total osmolarity of the medulla which increases water-absorbing capacity of the nephron.

10

Why is RCC often golden yellow on macroscopic examination?

High lipid and glycogen content

11

From where do RCCs originate?

From the epithelium of the proximal renal tubules.

12

Name two risk factors associated with RCC.

Smoking and obesity (occurs typically in patients aged 60-70 yrs).

13

How is acute angle-closure glaucoma treated?

Acetazolamide (it inhibits carbonic anhydrase and bicarb which is present in aqueous humor)

14

What is the mechanism of action of acetazolamide?

Inhibits carbonic anhydrase which is found in high concentrations in the proximal tubule. By inhibiting carbonic anhydrase, acetazolamide blocks HCO3- reabsorption in the proximal tubules

15

What are the most common side effects associated with carbonic anhydrase inhibitors?

Somnolence, paresthesias, urine alkalinization

16

What is necessary in the workup of metabolic alkalosis?

Volume status and urine chloride

17

Name four common causes of metabolic alkalosis.

Vomiting, nasogastric suctioning, Thiazide/ Loop diuretics, mineralocorticoid excess state.

18

Which causes of metabolic alkalosis are saline responsive and which are not?

Saline responsive: vomiting, NG suctioning, thiazide/ loop diuretic use; unresponsive: mineralocorticoid excess

19

What is the most common cause of urinary tract obstruction in an elderly male?

BPH

20

Hos is poststerptococcol glomerulonephritis treated?

Loop diuretics and vasodilators to relieve edema and hypertension.

21

What is the most important prognostic factor in patients with post-streptococcal glomeurlonephritis?

Age. 95% of children recover completely, in adults only about 60% of cases resolve completely.

22

Describe the pathway of blood through the kidney.

Interlobar arteries --> arcuate arteries --> radial arteries --> afferent arterioles --> glomerular capillaries --> efferent arterioles --> peritubular capillaries --> interlobar veins.

23

What is the calculation for filtration fraction?

FF= GFR/RPF.

24

What happens to RPF due to severe efferent arteriolar constriction?

Substantially increased capillary oncotic pressure results in an overall decrease in GFR.

25

What is PAH?

An organic acid that is avidly filtered from the blood in the glomerulus and secreted by cells lining the proximal tubule of the nephron. It is used to measure renal plasma flow because it is both filtered and secreted by the glomerulus and renal tubules

26

What changes in secretion occur when blood concentration of PAH increases?

Secretion of PAH by proximal tubular epithelial cells increases only up to a maximum value (transport maximum of secretion enzymes)

27

What effect does primary hyperaldosteronism have on renin levels?

Decreases renin due to feedback inhibition

28

What causes secondary hyperaldosteronism?

Overproduction of aldosterone occurs secondary to increased renin synthesis

29

Name four causes of secondary hyperaldosteronism.

Renal artery stenosis, diuretic use, malignant hypertension, renin-secreting tumors.

30

What are reninomas?

Rare, small solitary benign juxtaglomerular cell neoplasms.

31

How do ACE inhibitors cause nephrotoxicity and acute renal failure?

Block of angiotensin mediated efferent arteriole vasoconstriction. This leads to a reduced filtration fraction and can precipitate acute renal failure in patients dependent on efferent arteriole constriction to maintain renal perfusion.

32

During ascent of the kidney, a horseshoe kidney gets trapped behind what vessel?

IMA

33

Hypoaldosteronism may cause what renal pathology?

Type IV renal tubular acidosis.

34

What drugs are most commonly used as therapy for Conn's syndrome?

Aldosterone antagonists- spironolactone, eplerenone.

35

Name the side effects of loop diuretics- 3 common, 5 less common.

Common: hypokalemia, hypomagnesemia, hypocalcemia; less common: ototoxicity, hypotension, decreased GFR, hyponatremia, volume depletion.

36

Name four classes of drugs associated with ototoxicity.

Loop diuretics, aminoglycosides, salicylates, cisplatin.

37

What is an adverse effect and concern associated with initiation of ACE inhibitor use?

First dose hypotension- risk increases with hyponatremia, hypovolemia secondary to diuretics, low baseline blood pressure, high renin or aldosterone levels, renal impairment, heart failure.

38

What deposits are seen in the basement membranes of nephrons in patients with poststreptococcal glomerulonephritis?

Granular deposits of IgG, IgM, C3.

39

Which three type of urinary calculi are radiopaque and which type is radiolucent?

Opaque- calcium oxalate or calcium phosphate; struvite; cystine. Lucent- uric acid. Lucent stones can be visualized by abdominal US or CT.

40

What defines nephrotic syndrome?

Massive proteinuria (more than 3.5 g/day), hypoalbumemia, hyperlipidemia, lipiduria, generalized edema. NO RBC CASTS in urine with normal renal function.

41

What characterizes nephritic syndrome?

Hypertension, mild proteinuria (<1g per day), RBC casts or dysmorphic red cells in urine, azotemia.

42

What renal pathology is associated with goodpasture's syndrome?

Rapidly progressive glomerulonephritis (RPGN) which is characterized by cresent formation on light microscopic examination.

43

Renal vein thrombosis and thrombotic/ thromboembolic complications of nephrotic syndrome are associated with what underlying deficiency?

Loss of anticoagulant factors (esp. antithrombin III)

44

What is the pathophysiology associated with lithium induced diabetes insipidus?

Caused by lithium's antagonizing effect on the action of vasopressin on principle cells within the collecting duct system.

45

What is the main mechanism underlying renal stone formation?

Urine supersaturation; Risk of this can be decreased by increasing fluid intake.

46

What adverse effect may be caused by acyclovir if adequate hydration is not provided?

Crystalline nephropathy and renal tubular damage.

47

What is C-ANCA?

An autoanitbody directed against lysosomal enzymes of human neutrophils and monocytes. Found in Wegners (or granulomatosis with polyangiitis).

48

What renal disease is most commonly associated with Wegener's?

Rapidly progressive (cresenteric) glomerulonephritis (RPGN).

49

What is the mechanism of action of Foscarnet and what toxicities are associated with its use?

Pyrophosphate analog that can chelate calcium and promote nephrotoxic renal magnesium wasting- this can cause symptomatic hypocalcemia and hypomagnesemia.

50

What is the preferred method for diagnosis of incipient diabetic nephropathy?

Microalbuminuria detection

51

Homogeneous deposition of eosinophilic hyaline material in the intima and media of small arteries and arterioles characterizes what pathologies?

Hyaline arteriolosclerosis- this is produced by longstanding nonmalignant HTN and/or diabetes

52

What side effects may occur during the recovery phase of acute tubular necrosis?

Gradual increase in urine output causing high volume diuersis. Electrolyte abnormalities may include decreased concentrations of K, Mg, PO4, and Ca due to slowly recovering function. Dehydration may also occur with hypotonic urine.

53

What condition may underlie recurrent nephrolithiasis in a young patient?

Inborn error of metabolism- cystinuria

54

What is pathognomic on UA of cystinuria?

Hexagonal cystine crystals

55

What test determines the presence of urine cystine?

Sodium cyanide-nitroprusside test

56

Where does the highest osmolarity occur in the nephron in the setting of low ADH?

At the bottom of the loop of Henle.

57

What effect does aldosterone have on potassium and hydrogen ion secretion?

It increases ion secretion from principle and intercalated cells of the renal collecting tubules respectively; these ions are lost in tubular fluid when aldosterone levels are high.

58

What is cystinuria?

An inborn defect of the transporter of cystine, ornithine, arginine, and lysine. It is inherited autosomal recessive

59

How is acute pyelonephritis distinguished from a normal kidney on microscopic presentation?

Diffusely increased cellularity and WBC casts; tubular eptihelial disruption may be seen along with microabscesses in the interstitium.

60

What is the first line drug used to treat post-surgery urinary retention?

Muscarinic agonists- bethanechol; also a1 blockers can be used

61

What are severe complications associated with overaggressive treatment with osmotic diuretics?

Excessive volume depletion, hypernatremia. and pulmonary edema

62

What is myeloma kidney?

Excess excretion of free light chains causes cast nephropathy. Casts are eosinophilic.

63

What condition is associated with circulating IgG4 antibodies to the phospholipase A2 receptor?

Idiopathic membranous nephropathy.

64

What is the major renal pathophysiologic abnormality associated with prolonged NSAID use?

Chronic interstitial nephritis

65

What is seen on light microscopy of chronic interstitial nephritis?

Interstitial inflammation with subsequent fibrosis, necrosis and scarring of papillae, distortion of caliceal architecture, tubular atrophy.

66

What electrolyte and fluid abnormalities are associated with nephrotic syndrome?

Increased aldosterone synthesis, increased ADH release, sodium and water retention, hyperlipidemia, lipiduria.

67

What are the electron-dense deposits on the epithelial side of the glomerular basement membrane in patients with PSGN?

Immune complexes of IgG, IgM, and C3.

68

Which class of drugs reduces prostate gland size to improved bladder outlet obstruction?

5-alpha-reductase inhibitors (finasteride, dutasteride)

69

Which parts of the nephron are most susceptible to hypoxia?

Proximal tubules and the thick ascending limb of Henle's loop; these areas are in the outer medulla which has low blood supply.

70

What nephrotic syndrome is most common in patients with solid tumors (lung, colon, etc.)?

Membranous glomerulonephropathy.

71

What does electron microscopy of membranous glomerulonephropathy show?

Membrane thickening caused by irregular dense deposits between the membrane and epithelial cells- these protrusions resemble spikes/domes when stained with silver.

72

What is the difference in light microscopy between membranoproliferative glomerulonephritis and membranous glomerulonephritis?

Membranoproliferative is hypercellular; membranous is not.

73

What is the presentation of patients with pauci immune glomerulonephritis?

Renal failure, pulmonary sx (cough, hemoptysis, dyspnea), respiratory tract symptoms (epistaxis, mucosal ulceration, chronic sinusitis). Crescents on light microscopy.

74

From what type of cells does renal clear cell carcinoma arise?

Renal tubular cells.

75

Why do cells in renal clear cell carcinoma appear polygonal with abundant clear cytoplasm?

Because they are packed with glycogen and lipids

76

The abrupt onset of gross hematuria in a patient with family history of sickle cell disease suggests what pathology?

Renal papillary necrosis.

77

Name four conditions associated with renal papillary necrosis.

Sickle cell disease/trait, analgesic nephropathy, DM, acute pyelo/UTI

78

What are the classic symptoms of papillary necrosis?

Acute colicky flank pain, gross hematuria, passage of tissue fragments in urine.

79

What pathologic changes occur as a result of urinary retention due to BPH?

Increased urinary tract pressure, reflux nephropathy, hydronephrosis, renal interstitial atrophy and scarring.

80

What test must be used to see podocyte effacement in minimal change disease?

Electron microscopy.

81

What renal condition is characterized by fever, rash, and oliguria several weeks after use of b-lactam antibiotics, NSAIDS, sulfonamides, rifampin, or diuretics?

Drug induced acute interstitial nephritis.

82

What cellular changes are associated with acute interstitial nephritis?

Infiltration of mononuclear cells- lymphocytes/macrophages and plasma cells and eosinophil infiltraiton.

83

The presence of multiple calcium oxalate crystals in the renal tubules is indicative of toxic renal injury caused by what substance?

Ethylene glycol. Also present is anion gap metabolic acidosis and increased osmolar gap

84

Describe the appearance of tubular epithelial damage due to poisoning by ethylene glycol.

Ballooning and vacuolar degeneration, predominately of the proximal convoluted tubules.