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Step 1 Smart Book > Renal > Flashcards

Renal Flashcards

1
Q

What are the most common causes of acute bacterial prostatitis? What is the MOST common the U.S.?

A

Same as UTI: E coli, Klebsiella, Proteus, Pseudomonas, Enterobacter, Serratia, Enterococcus, Staphylococcus

In the U.S. - E coli

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2
Q

What pathogenic attribute do uropathogenic strains of E coli share?

A

P-pili = pyelonephritis-associated pili (pilus adhesins)

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3
Q

What metabolic acid-base disturbance does acute renal failure lead to?

A

Metabolic acidosis (increased H+ and decreased HCO3- in the blood)

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4
Q

What are the three things recommended in a diet for renal failure patients?

A
  1. Low protein
  2. Restrict salt and fluid
  3. High carbohydrate - provides body with exogenous glucose so prevents gluconeogenesis which also prevents protein catabolism and nitrogen production
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5
Q

For the loop of Henle (medullary thin descending, medullary thick ascending, cortical thick ascending), which parts are permeable to water? List them in order of osmolality.

A

Thin descending is permeable to water while both the medullary and cortical thick ascending are impermeable to water

MOST hypoosmolalic: cortical thick ascending > medullary thick ascending > medullary thin descending (i.e. the tubular fluid gets more hypotonic as it travels through the loop)

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6
Q

How do you calculate changes in body osmolality due to urine loss?

A

(total body osmoles - urine osmoles) / (total body water - urine volume)

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7
Q

What are the presenting symptoms of ADPKD?

A
  1. HTN - from decreased renin
  2. renal failure (with elevated BUN and Cr)
  3. anemia - from decreased epo

Patients typically in their 40s

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8
Q

When is spironolactone contraindicated? How would you be able to tell this on EKG?

A

Spironolactone is potassium sparing so it is contraindicated in patients with hyperkalemia who are at increased risk of arrhythmia. Hyperkalemia on EKG shows absent P waves, tall peaked T waves.

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9
Q

What is a dangerous renal complication of aortic dissection and how does it present?

A

The dissection may run distally and occlude the renal arteries causing bilateral renal infarction. It presents with flank pain and hematuria.

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10
Q

What is the signature histologic finding in diabetic nephropathy?

A

Kimmelstiel-Wilson lesion - nodular (ovoid) PAS+ deposits of mesangial matrix and thickened basement membrane in the periphery of the glomerulus

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11
Q

What is the characteristic histologic feature of post-streptococcal glomerulonephritis?

A

Subepithelial electron dense humps

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12
Q

What is the characteristic histologic finding of Goodpasture syndrome?

A

Linear deposits of IgG (antibodies against the basement membrane)

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13
Q

How do you calculate the filtered load of a substance?

A

FL = GFR x plasma concentration

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14
Q

Bilateral renal agenesis is typically caused by a malformation of what?

A

ureteric buds

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15
Q

When is diffuse cortical necrosis typically seen?

A

DIC

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16
Q

What are the most common causes of papillary necrosis?

A

Diabetes, analgesic abuse, urinary tract obstruction, sickle cell disease

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17
Q

What is pseudomonas known to cause?

A

PSEUDO: pneumonia, sepsis, external otitis (swimmer’s ear), UTI, diabetic osteomyelitis

also: hot tub folliculitis

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18
Q

How might large kidney stones present?

A

Can be clinically silent for a while until the present with microhematuria and recurrent episodes of pyelonephritis

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19
Q

Describe the two mechanisms by which PAH reaches the tubular fluid and their regulatory mechanisms.

A
  1. Freely filtered - this is a constant fraction
  2. Secreted by the PCT cells - this is a carrier mediated process so it can be saturated with increasing blood concentration of PAH
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20
Q

What part of the nephron contains the most dilute tubular fluid? What is this value?

A

DCT - around 100 mOsm/L

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21
Q

What are the characteristic IF and LM findings in Goodpasture Syndrome?

A

Goodpasture is a type I RPGN.
IF - linear deposits of IgG and C3 along the basement membrane
LM - glomerular crescent formation

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22
Q

What induces the development of the metanephros which will go on to form the definitive kidney?

A

Ureteric buds

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23
Q

What are the common causes of drug-induced interstitial nephritis?

A

NSAIDs (ibuprofen and indomethacin), beta lactam antibiotics, sulfonamides, diuretics, phenytoin, cimetidine, methyldopa

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24
Q

What is the only diuretic that acts solely upstream of the macula densa?

A

Acetazolamide (which acts on PCT) because thiazides and loops both act on transporters that are also located in the DCT thus interfering with the macula densa’s sensing of NaCl delivery

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25
Q

How does the clearance of creatinine differ from that of inulin?

A

Inulin is not filtered or reabsorbed. Creatinine is slightly secreted in the PCT - after that it is like inulin

26
Q

How does autonomic regulation affect renin release?

A

Sympathetic activation through renal nerves stimulates renin secretion

27
Q

What is the typical clinical presentation of IgA nephropathy?

A

Hematuria within a few days of viral infection (typically upper respiratory infection but can also be enterovirus)

28
Q

How does angiotensin II affect afferent/efferent arterioles?

A

Preferential constriction of the efferent arteriole - increasing GFR

29
Q

What are the most common causes of acute renal failure?

A

Prerenal azotemia due to renal hypoperfusion - can occur in one of three ways

  1. Change in vascular resistance (secondary to sepsis, anaphylaxis, anesthesia, ACE inhibitors)
  2. Decrease in intravascular volume
  3. Decreased cardiac output
30
Q

What are the two preferred pharmacologic treatments for urinary incontinence?

A

Antimuscarinic agents - oxybutynin and tolterodine

31
Q

What other drug is contraindicated when taking fluoroquinolones?

A

Antacids - reduce the bioavailability

32
Q

When a staghorn renal calculi is observed, what should you suspect?

A

Infection with a urease producing bug (e.g. proteus) - urease raises pH by splitting urea and forming ammonia which produces magnesium ammonia phosphate (struvite) which can precipitate as a stone

33
Q

What is the major nitrogen containing end product of protein catabolism?

A

Urea

34
Q

What neurovascular complication are ADPKD patients at risk for and why?

A

Subarachnoid hemorrhage from rupture of a berry aneurysm

35
Q

How can diabetes interfere with the action of ADH?

A

Hyperglycemia can prevent the reabsorption of glucose in the PCT which also leads to decreased reabsorption of water and sodium –> increased delivery of water and solutes overwhelms the loop of Henle –> reduces ability to maintain medullary osmolar gradient –> inhibits ADH’s ability to help concentrate urine since all it does is place water channels in the collecting duct

starts to look like nephrogenic diabetes insipidus

36
Q

How is hyperacute transplant rejection mediated?

A

Preformed recipient antibodies attack the transplanted organ (type II hypersensitivity)

37
Q

What is the classic clinical presentation of multiple myeloma?

A

Easy fatigability, back pain, constipation, and azotemia in an elderly patient

On kidney biopsy, look for large eosinophilic casts with Bence Jones proteins

38
Q

Which part of the nephron is impermeable to water?

A

Thick and thin ascending limbs of the loop of Henle

39
Q

What condition are bilateral renal angiomyolipomas associated with? What else is associated with this condition?

A

Tuberous sclerosis

Mnemonic HAMARTOMAS: hamartomas (in the brain), ash-leaf skin patches, mental retardation, angiomyolipoma (of the kidney), rhabdomyoma, tuberous sclerosis, autosomal dOminant, mitral regurgitation, angiofibroma (of the face), seizures and shagreen patches

40
Q

Describe how WBC casts in the urine tell you that the kidneys have been infected.

A

WBC casts form when leukocytes are compressed in the renal tubules so they imply that an infection involves the kidneys

41
Q

At what glucose level do you begin to see glucosuria?

A

180 - 200 mg/dL

42
Q

How can indomethacin lead to acute renal failure?

A

Indomethacin is an NSAID which decreases the synthesis of prostaglandins. PGE2 is an important vasodilator that preferentially acts on the afferent arteriole (increases GFR). Inhibiting PGE2 can lead to decreased renal perfusion leading to ischemia.

43
Q

What is thought to mediate the underlying process in minimal change disease?

A

Altered cell-mediated immunologic response with abnormal secretion of lymphokines by T cells –> reduce the production of anions in GBM –> increasing glomerular permeability to albumin as well as podocyte effacement

44
Q

Which renal structure is most likely to be damaged in a sickle cell crisis?

A

Vasa recta

45
Q

Given constant filtration and maximal secretion, what happens to clearance of a substance as plasma concentration increases?

A

Decreases because clearance = urinary excretion/plasma clearance and urinary excretion in this case will basically max out as plasma clearance keeps increasing

46
Q

What is tolterodine?

A

Competitive muscarinic receptor antagonist used to treat urinary incontinence, urinary urgency, and urinary frequency

Blocks parasympathetic hyperactivity in patients with a neurogenic bladder

47
Q

What does inhibiting carbonic anhydrase do (e.g. with acetazolamide)?

A

Decreases H+ secretion which also decreases NH4 excretion (NH4+ substitutes with H+ in the Na/H exchanger)

48
Q

What are the common causes of drug-induced interstitial nephritis?

A

NSAIDs (ibuprofen and indomethacin), beta lactam antibiotics, sulfonamides, diuretics, phenytoin, cimetidine, methyldopa

49
Q

What kind of drug is indomethacin?

A

NSAID

50
Q

Why do NSAIDs exacerbate renal failure?

A

Decrease prostaglandin production which results in decreased blood flow to the kidneys

51
Q

How does hyperglycemia (e.g. like in diabetics) cause resistance to ADH?

A

Hyperglycemia can prevent proximal tubule reabsorption of glucose –> increased delivery of fluid and electrolytes to the loop of Henle –> reduces loop’s ability to maintain medullary gradient –> gradient is required for ADH action in the collecting duct

52
Q

What organisms can cause UTI with positive leukoesterase test and NEGATIVE nitrite test?

A

Enterococcus faecalis or staphylococcus saprophyticus

Enterobacter sp, Klebsiella, E. coli, Proteus are all nitrite POSITIVE

53
Q

Describe how an ACE inhibitor affects sodium and potassium handling by the kidney.

A

Decrease in sodium reabsorption and decrease in potassium excretion because ACE inhibitor blocks formation of angiotensin II (leading to decreased levels of aldosterone)

54
Q

How do we use fractional sodium excretion to differentiate between prerenal vs. intrarenal azotemia?

A

Prerenal - 2%

55
Q

When a staghorn renal calculi is observed, what should you suspect?

A

Infection with a urease producing bug (e.g. proteus) - urease raises pH by splitting urea and forming ammonia which produces magnesium ammonia phosphate (struvite) which can precipitate as a stone

56
Q

Which renal structures tend to be damaged in a sickle cell crisis?

A

Vasa recta of the renal medulla

57
Q

What is a dangerous renal complication of aortic dissection and how does it present?

A

The dissection may run distally and occlude the renal arteries causing bilateral renal infarction. It presents with flank pain and hematuria.

58
Q

How does autonomic regulation affect renin release?

A

Sympathetic activation through renal nerves stimulates renin secretion

59
Q

How do you calculate filtration fraction if you are given renal blood flow instead of renal plasma flow?

A

FF = GFR / (1 - Hct)(Renal Blood Flow)

Because RPF = (1 - Hct)(RBF)

60
Q

What do you see on electron microscopy for post-streptococcal glomerulonephritis?

A

Subepithelial humps

61
Q

Where does clear cell renal carcinoma originate from?

A

Epithelium of PCT

62
Q

Presentation: Adult patient with anorexia, hematuria, abdominal discomfort and liver cysts

Diagnosis?

A

ADPKD

Step 1 Smart Book (13 decks)

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