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Step Up to Medicine > Renal > Flashcards

Renal Flashcards

1
Q

In ADPCKD, what causes progressive renal failure in patients? (2)

A

Patients get progressive renal failure from recurrent episodes of pyelonephritis and nephrolithiasis.

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2
Q

What % of patients with ADPCKD develop ESRD and what happens to the remaining %?

A

50% of patients develop ESRD by their late 50s and 60s. The others have a normal lifespan.

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3
Q

What five things does ADPCKD present with?

A
  1. Flank pain
  2. Hematuria
  3. Infection
  4. Kidney Stones
  5. HTN
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4
Q

What is one neurovascular complication of ADPCKD?

A

Intracerebral berry aneurysms (most do not rupture).

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5
Q

What confirms a diagnosis of ADPCKD?

A

Ultrasound

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6
Q

How does one treat ADPCKD

A

No curative therapy is available. Drain cysts if they are symptomatic, treat hypertension and infections

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7
Q

What two pathological process categorize ARPCKD?

A
  1. Hepatic fiborsis

2. Cysts in renal collecting ducts

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8
Q

What are some hepatic complications of ARPCKD? (2)

A

Portal HTN and cholangitis

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9
Q

What is the primary cause of morbidity and mortality in the neonatal period for patients with ARPCKD?

A

Pulmonary insufficiency from pulmonary hypoplasia

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10
Q

Besides pulmonary insufficiency and liver diseases what is one major symptom of ARPCKD?

A

Hypertension

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11
Q

What is seen in pregnant women with a baby with ARPCKD?

A

Oligohydramnios (decreased amniotic fluid)

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12
Q

How is ARPCKD treated?

A

Manage respiratory issues in newborns, and treat ESRD with renal replacement therapy

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13
Q

What is the underlying pathological cause of medullary sponge kidney?

A

Cystic dilation of the collecting ducts

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14
Q

What types of diseases are associated with medullary sponge kidney?

A

Hyperparathyroidsm and parathyroid adenoma

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15
Q

What are some symptoms of medullary sponge kidney?

A

Hematuria, UTI, kidney stones

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16
Q

Simple renal cysts increase with ______

A

Age

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17
Q

What is the treatment for simple renal cysts

A

Most are discovered incidentally and are usually asymptomatic. No treatment is necessary in most cases

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18
Q

What are three broad categories of injuries that can lead to acute kidney injuries?

A

Pre-renal, intra-renal, post-renal

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19
Q

What are 4 broad causes of pre-renal acute kidney injury?

A
  1. Pump problems (affect heart) = MI, CHF
  2. Leaky pipes (affect blood vessels) = nephrosis (nephrotic syndrome), gastrosis (GI loss of proteins), cirrhosis (loss of proteins), or malnutrition
  3. Hole in pipe = diarrhea, dehydration, diuresis, hemorrhage
  4. Clog = fibromuscular dysplasia in young women or atherosclerosis buildup in older person which leads to renal artery stenosis
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20
Q

What are three broad causes of intrarenal acute kidney injuries?

A
  1. Things that affect the glomerulus (glomerulonephritis)
  2. Things that affect the tubules (acute tubular necrosis)
  3. Things that affect the nephron’s interstitum (acute interstitial nephritis)
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21
Q

What are three broad causes of post-renal acute kidney injury?

A
  1. Affects ureter = cancer or stones
  2. Affects bladder = cancer, stones or neurogenic bladder
  3. Affects uretera = cancer, stones, BPH, or kinked foley
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22
Q

What kind of casts are seen in glomerulonephritis?

A

RBC casts

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23
Q

What kind of casts are seen in acute tubular necrosis?

A

Brown muddy casts

24
Q

What is seen in acute intersitital nephritis? (4)

A

inflammatory cells, WBCs, eosinophils, WBC casts

25
Q

What are two broad causes of acute interstitial nephritis?

A
  1. Infection (seen in pyelonephritis = WBC Casts)

2. Toxic agents

26
Q

What antibiotics are associated with acute interstitial nephritis? (3)

A
  1. TMP-SMX
  2. Penicillins
  3. Cephalosporins
27
Q

What are two broad categories of causes for acute tubular necrosis?

A
  1. Toxins (IV contrast or myoglobin)

2. Prolonged prerenal ischemia

28
Q

What are the three stages of acute tubular necrosis?

A
  1. increased Creatinine
  2. Oliguric phase
  3. Polyuric phase
29
Q

What are the acute indications for dialysis? (AEIOU)

A 
Acidosis
Electrolytes (K+/Ca2+)
Intoxication
Overload
Uremia
30
Q

What is the definition of acute kidney injury (give specific measurements for absolute and relative values)

A

A rapid decline in renal function with an increase in serum creatinine (relative increase in 50% or an absolute increase of 0.5 to 1.0 mg/dl)

31
Q

Define acute renal failure

A

Early stage of acute kidney injury where creatinine is normal (because it hasn’t had a chance to accumulate in the body) and GFR is declining fast

32
Q

What occurs to BUN and Creatinine in Acute kidney injuries?

A

Increased BUN and Creatinine

33
Q

What can causes elevated creatinine levels in serum?

A

Muscle breakdown and acute kidney injury

34
Q

What can causes elevated BUN levels? (4)

A

Gi/soft tissue bleeding, acute kidney injury, increased protein intake and catabolic drugs (steroids)

35
Q

In patients with prerenal acute kidney injury what medications are potentially dangerous (2 and describe mechanism of action)

A
  1. NSAIDs (constrict afferent arterioles)

2. ACE Inhibitors (dilate efferent arterioles)

36
Q

What is seen on urinanalysis on pre-renal acute kidney injury (BUN/CR ratio, FENa, Urine Osmolality, and Urine Sodium) and why (explain these lab findings)

A
  1. BUN/CR > 20:1
  2. FENa < 1%
  3. Urine Osmolality > 500 mOsm
  4. Urine Sodium < 20

During prerenal acute kidney injury, renal blood flow decreases, however the renal parenchyma is undamaged, and tubular function (concentrating ability) is preserved. Therefore, the kidney responds appropriately conserving as much sodium and water as possible.

The kidney has an increased BUN/CR ratio because the kidney is able to reabsorb urea

It has an increased urine osmolality because the kidney is reabsorbing water.

It has decreased urine sodium and a decreased FeNa because the kidney is reabsorbing any sodium

37
Q

What is one symptom ALWAYS found in prerenal acute kidney injury?

A

Oliguria

38
Q

What kind of casts are seen in prerenal acute kidney injury?

A

Hylaline casts (bland urine sediment)

39
Q

What is the most common cause of secondary HTN and describe the basic pathological steps?

A

Renal artery stenosis causes a decrease in blood flow to the JGA, as a result RAAS becomes activated, leading to HTN

40
Q

What are two general causes of renal artery stenosis and what patient populations do they affect?

A
  1. Atherosclerosis - affects elderly men

2. Fibromuscular dysplasia - seen in young females

41
Q

What are two common clinical features (1 is vital sign and the other is physical symptom) seen in patients with renal artery stenosis?

A
  1. HTN - Look for a sudden onset of hypertension in a patient without a family history. The hypertension may be severe (malignant) and refractory to medical therapy.
  2. Abdominal bruit is present in 50-80% of patients, and is more commonly seen in patients with fibromuscular dysplasia that causes renal artery stenosis
42
Q

What is the gold standard for diagnosing renal artery stenosis? What should you be worried about using this gold standard? Great secondary choice in patients with renal failure?

A

Renal arteriogram is the gold standard, however, contrast dye can be nephrotoxic so do not use it in patients with renal failure. Magnetic renal arteriogram has a high sensitivity and specificity and is not nephrotoxic

43
Q

How is renal artery stenosis treated? (3)

A
  1. Revascularization with percutaneous transluminal renal angioplasty (PRTA) is the initial treatment in most patients, it has a higher success rate in fibromuscular dysplasia than the arterosclerotic type.
  2. Surgery if PRTA is not successful (bypass)
  3. Medical management with ACE inhibitors and calcium channel blockers may be tried
44
Q

How is renal vein thrombosis treated?

A

Anticoagulation to prevent pulmonary embolism

45
Q

What are some causes of renal vein thrombosis?

A

Pregnancy/oral contraceptives, invasion of renal vein by renal cell carcinoma, nephrotic syndrome

46
Q

What is atheroembolic disease of the renal arteries?

A

Showers of cholesterol crystals that dislodge from plaques in large arteries and embolize to the renal vasculature

47
Q

Define hypertensive nephroscolerosis?

A

Systemic Hypertension increases capillary hydrostatic pressure in the glomeruli leading to benign or malignant sclerosis

48
Q

What is the difference between benign nephrosclerosis and malignant nephrosclerosis?

A

In benign nephrosclerosis, thickening of the glomerular afferent arterioles develops in patients with long-standing HTN. It results in mild to moderate increase in creatinine levels, microscopic hematuria, and mild proteinuria.

Malignant nephrosclerosis, can develop in a patient with long-standing benign HTN or in a previously undiagnosed patient. It is characterized by a rapid decrease in renal function and accelerated hypertension due to diffuse intrarenal vascular injury. Clinical Manifestations include: rapid increase in CR, proteinuria, and rapid increase in BP.

49
Q

What is the treatment for benign and malignant hypertensive nephrosclerosis?

A

Controlling the blood pressure

50
Q

Define sickle cell nephropathy? What part of the kidney does it affect? What % progress to ESRD? How is it managed?

A

Sickling of RBC in the microvasculature which leads to infarction. Affects renal papilla. 5% go to ESRD. Managed using ACE Inhibitors

51
Q

What causes testicular torsion?

A

Twisting of the spermatic cord leading to arterial occlusion and venous outflow obstruction, ischemia can lead to testicular infarction

52
Q

What are 3 clinical signs indicating testicular torsion? (3)

A
  1. Acute severe testicular pain
  2. Swollen and tender scrotum
  3. Elevated testicle
53
Q

How is testicular torsion treated and what is the critical time value?

A

Surgery is treatment, if delayed longer than 6 hours, infarction may occur

54
Q

What is epididymitis?

A

Infection of the epididymis

55
Q

What is the most common cause of epididymitis?

A

E coli

56
Q

What are the clinical signs of epididymitis?

A

Swollen tender testicle, dysuria, fever, chills, scrotal pain and scrotal mass

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