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UWorld - Renal > Path / Pathophys > Flashcards

Path / Pathophys Flashcards

1
Q

A patient presents with hematuria and oliguria. Kidney biopsy with silver stain is shown below.

  1. What is the diagnosis?
  2. The abnormal deposition is made up of what?
A
  1. Rapidly Progressive Glomerulonephritis

(crescents in bowman space)

  1. Crescents are filled will fibrin and macrophages
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2
Q

A biopsy of a cancerous lung lesion is shown below.

Where did this cancer originate from and why?

A

The Kidneys (renal cell carcinoma)

Due to the empty/clear cytoplams

(clear cell renal carcinoma - most common type)

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3
Q

How and does Benign Prostatic Hyperplasia affect the ability to urinate? Why? Major complication?

A

It increases resistance to urine flow due to compressing the urethra (increasing the hydroostatic pressure required to overcome resistance to flow)

This results in incomplete emptying of the bladder.

(as bladder empties urinary pressure will soon fall below the bladders leaving a residual volume of urine)

Most common complication is UTI

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4
Q

In poststreptococcal glomerulonephritis (PSGN) what is the most important poor prognostic factor?

A

Increased Age

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5
Q

In a patient recovering from acute tubular necrosis, what is the major complication and why?

A

Major complication: Electrolyte Imbalances + Oliguria

(hypokalemia, hypocalcemia, hypophosphatemia)

This occurs due to GFR improving before tubular cell recovery

(tubular cells are stable cells and take some time to reenter cell cycle)

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6
Q

How would the following be altered in a hypovolemic patient in comparison to a regular person:

  1. RPF (renal plasma flow)
  2. GFR (glomerular filtration rate)
  3. FF (Filtration Fraction)
A

1. RPF is decreased

(RPF = amount of blood going to kidneys)

2. GFR is decreased

(GFR = amount of filtered blood in kidneys)

3. FF is increased

(FF = GFR/RPF)

(FF is increased during hypovlemia to try to maintain GFR)

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7
Q

Which toxic agents can result in Acute Tubular Necrosis?

A
  • Aminoglycosides (ex: gentamycin)
  • Heavy metals (ex: lead)
  • myoglobinuria (ex: from crush injury to muscle)
  • ethylene glycol/antifreeze
  • radiocontrast dye
  • urate (used for chemotherapy, prevented by also giving allopurinol)
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8
Q

How can Heart Failure affect the renal system?

A

Cardiorenal Syndrome

  1. HF results in decreased renal perfusion
  2. Activation of RAAS + ADH release + sympathetic stimulation
  3. Na and H2O reabsorption and systemic vasoconstriction
  4. Exacerbation of HF and further renal hypoperfusion
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9
Q

How would hypovolemia affect the following:

  1. Vasopressin
  2. Norepinephrine
  3. Angiotensin II
  4. Endothelin 1
A

All will be increased

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10
Q

In minimal change disease, what are the effects of albumin loss on:

  1. Plasma Oncotic Pressure
  2. Lipoprotein production
A
  1. decreased plasma oncotic pressure
  2. increased lipoprotein production –> hyperlipedemia

(stimulated by decreased oncotic pressure)

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11
Q

In acute tubular necrosis, which structures are most susceptible to ischemic damage?

A
  • medulla
  • proximal tubule
  • thick ascending limb
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12
Q

How would uterolithiasis (stone in ureter) present?

A

- hydronephrosis (swelling of kidney due to build up urine)

- Hematuria (RBCs with no RBC casts)

- Stone crystals

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13
Q

How/why does Osteodystrophy occur with chronic renal disease/failure?

A
  1. Impaired renal fcn –> hyperphosphatemia + hypocalcemia

2. Increased PTH (secondary hyperparathyroidism)

3. Increased osteoclast function

4. Osteodystrophy

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14
Q

What is the earliest sign of diabetic nephropathy?

A

Albuminuria

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15
Q

What are 2 general things that can decrease renal stone formation?

A
  1. Increased fluid intake
  2. increased urinary citrate
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16
Q

A 65 yo patient comes in complaining of abdominal pain after eating who has a BP of 175/110.

CT scan of the abdomen reveals the following:

What condition is this patient most likely suffering from?

A

Renal artery stenosis

  • marked unilateral kidney atrophy
  • commonly occurs in elderly with other atherosclerotic diseases (in this case: mesenteric ischemia)
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17
Q

How can chronic kidney disease cause spasms?

A
  1. impaired kidney function results in hyperphosphatemia

2. Phosphate binds calcium

3. hypocalcemia

4. spasms

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18
Q

IgA Vasculitis / Henoch-Schonlein Purpura

  1. What is it?
  2. Who comonly gets it?
  3. How does it present?
A
  1. Small vessel vasculitis due to IgA immune complex deposition
  2. Most commonly occurs in children

3.

- palpable purpura on buttocks

- GI pain + bleeding

- joint pain

- Hematuria

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19
Q

Interstial Nephritis

  1. What is it?
  2. What can cause it?
  3. How does it present?
  4. What can it progess to?
A
  1. Drug-induced hypersensitivity that results in acute renal failure (intrarenal azotemia)
  2. P’s

Diuretics (Pee), NSAIDs (Pain-free), Penicillins, PPIs, RifamPin

  1. Oliguria, fever, rash (eosinophils may be present in urine)
  2. Renal Papillary necrosis
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20
Q

Renal Papillary Necrosis

  1. How does it present?
  2. What causes it?
A
  1. Flank pain and Hematuria
  2. “SAAD”

Sickle cell disease/trait

Acute Pyelonephritis (kidney infection)

Analgesic/NSAID abuse

Diabetes

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21
Q

How can BPH damage the kidney structure?

A
  1. BPH blocks prostatic urethra
  2. Hydronephrosis occurs
  3. Build-up of urine causes parenchymal pressure atrophy of kidney
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22
Q

IgA Nephropathy (Berger’s Disease)

  1. Clinical presentation?
  2. Microscopic Presentation?
A
  1. hematuria that occurs following a mucosal infection

2. IgA deposition in mesangium of glomeruli

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23
Q

Hemolytic Uremic Syndrome

  1. What is the classical ‘triad’ presentation?
  2. What causes the kidney effects?
A

1. Triad of:

  • Thrombocytopenia
  • Microangiopathic Hemolytic Anemia
  • Acute Kidney Injury
    2. Acute kidney injury occurs due to microthrombi in small blood vessels
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24
Q

How would the following values in a patient with long-standing Polycysitic Kidney Disease compare to a healthy individual:

  1. Phosphate
  2. PTH
  3. Calcitriol
A

Chronic Kidney Disease (in this case PKD) results in:

  1. Phosphate is increased (causes hypocalcemia)
  2. PTH is increased (to try and increase Ca levels
  3. Calcitriol is decreased

(even though it functions to increase Ca, it is inhibited by phosphate)

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25
Q

If a normal patient PTH and calcium are represented by “C” in the circle, what letter would represent a patient with chronic kidney disease?

A

A

chronic kidney disease results in:

  • hypocalcemia (due to hyperphosphatemia)
  • secondary hyperparathyroidism (to try and increase Ca)
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26
Q

Fibromuscular Dysplasia

  1. What is it?
  2. What does it commonly effect?
A
  1. Abnormal tissue growth within arterial walls resulting in:
    - fibromuscular webs –> arterial stenosis
    - aneurysms
    - loss of internal elastic lamina
  2. Brain –> stroke , Kidneys –> renal artery stenosis
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27
Q

Tumor Lysis Syndrome

  1. What is it? How does it happen?
  2. How can it be prevented?
  3. Where in the kidney would precipitation most commonly occur?
A
  1. It is a cause of acute kidney injury/failure that can occur after chemotherapy due to increased lysis of cells that release intracellular substances into the blood, namely uric acid
  2. Prevented with: hydration + allopurinol

3. Precipitation into a stone occurs in the distal tubules or collecting ducts due to their low pH

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28
Q

Autosomal Dominant Polycystic Kidney Disease

  1. How does it present?
  2. What is it associated with?
A

1.

  • bilateral enlarged kidneys with cysts in renal cortex + medulla
  • Hematuria and hypertension
    2. Berry aneurysm, hepatic cysts, mitral valve prolapse

“Cysts in kideys, brain, liver and heart”

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29
Q

A patient presents with hematuria and hypertension, CT scan of the abdomen is shown below, what is the diagnosis?

A

AD Polycystic Kidney Disease

  • enlarged kidneys with cysts
  • hepatic cysts
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30
Q

What would be the most likely diagnosis of a patient with signs and symptoms of SLE (lupus) and:

  1. Nephrotic Syndrome
  2. Nephritic Syndrome
A
  1. Membranous Glomerulonephritis
  2. Diffuse Proliferative Glomerulonephritis
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31
Q

Urothelial (Transitional Cell) Carcinoma

  1. What areas does it affect?
  2. Major risk factor?
A
  1. Urothelial lining of bladder, ureters, urethra and renal pelvis

2. Smoking (the major risk factor)

Occupational exposure to rubber, plastics and dyes

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32
Q

Postreptococcal Glomerulonephritis

  1. How does it present on histology?
  2. How are the following lab values affected:
    a. Total complement levels
    b. Levels of C3
    c. Levels of C4
A
  1. Enlarged hypercellular glomeruli

2.

a. Decreased total complement
b. decreased C3
c. normal C4

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33
Q

Minimal Change Disease

  1. What causes the effacement of foot proceses?
  2. What causes the selective loss of albumin?
A
  1. overproduction of glomerular permeabilty factor that damages podocytes
  2. Loss of anions / negative charge
34
Q

Which nephropathy is associated with IgG4 antibodies to the phospholipase A2 receptor?

A

Membranous Nephropathy

35
Q

Goodpasture Syndrome

  1. How does it present?
  2. What is it caused by?
A

1.

  • hemoptysis
  • hematuria (due to rapidly progressive glomerulonephritis)
    2. Antibody againt type 4 collagen in glomerular and alveolar basement membranes
36
Q

Is it normal for there to be microscopic or gross hematuria in a patient with BPH? Why?

A

Yes, BPH can result in the formation of new friable/easily torn blood vessels that can cause hematuria

37
Q

Why are the cells in clear cell renal carcinoma clear?

A

Due to their origination from the proximal tubule, they have a high glycogen and lipid content that dissolves during slide/tissue preperation

38
Q

What are the major risk factors for Uric Acid Stones? (3)

A

1. Increased Uric Acid Secretion

(gout, myeloproliferative disorders)

2. Increased Urine concentration

(hot, arid climates + dehydration)

  1. Low Urine pH –> favors insoluble uric acid

(chronic diarrhea due to loss of bicarbonate)

39
Q

Why do some patients with Multiple Sclerosis develop urinary frequency and incontinence?

A

Due to bladder hypertonia

(due to an upper motor neuron lesion)

40
Q

In what nepthropathy would you be most likely to see serum antineutrophil cytoplasmic antibodies (ANCA)?

A

Pauci- Immune (negative IF) Rapidly Progressive Glomerulonephritis (vasculitides):

  • Wegener (c-ANCA)
  • Microscopic Polyangitis (p-ANCA)
  • Churg-Strauss (p-ANCA)
41
Q

Calcium Kindey Stones

  1. Serum levels of calcium
  2. Urine levels of calcium
A
  1. Normocalcemia
  2. Hypercalciuria

NOTE: Calcium stones are most commonly caused by idiopathic hypercalciuria

42
Q

A patient comes in with left flank pain, hematuria and recurrent UTIs. CT of scan of the abdomen is shown below:

  1. What is the diagnosis?
  2. What causes this?
  3. What is the urine pH most likely to be?
A
  1. Ammonium Magnesium Phosphate (AMP / Struvite) Stone
  2. Urease producing organisms (Klebsiella, Proteus)

3. Urinary pH > 8, due to hydrolysis of urea forming ammonia which alkalinizes the urine

43
Q

What is most significant risk factor for UTI’s due to catheterization?

A

Duration of catheterization

(i.e. the best way to prevent a UTI is to remove the catheter whenever is it not needed)

44
Q

What type of kidney stone is pictured below:

A

Calcium Stone

‘envelope shaped’

45
Q

What type of kidney stone is pictured below:

A

AMP Stone

‘coffin-lid shaped’

46
Q

What type of kidney stone is pictured below:

A

Uric acid Stone

‘rhomboid shaped’

47
Q

What type of kidney stone is pictured below:

A

Cystine Stone

‘hexagonal shaped’

48
Q

Acute tubular necrosis with vacuolar degeneration and ballooning of the proximal convoluted tubule is most likely due to what?

A

Ethylene Glycol (Antifreeze) ingestion

49
Q

In most cases patients recover from acute tubular necrosis.

In this recovery phase, what would be seen on kidney biopsy?

A

Tubular re-epithelialization

50
Q

Renal Infarction

  1. How does kidney appear on gross pathology?
  2. How is it most commonly caused?
A
  1. Sharply demarcated, yellow-white, wedge shaped areas with hyperemia

2.

Cardioembolic Disease (usually due to Atrial Fribrillaiton)

51
Q

Where does renal cell carcinoma most commonly originate from?

A

Epithelial cells of proximal renal tubules

52
Q

What area of the kidney to ACE inhibitors affect?

A

Efferent Arteriole Dilation

(due to reduced AT II)

53
Q

In patient with renal artery stenosis, which cell type is most likely to undergo hyperplasia and why?

A

Modified smooth muscle (Juxtaglomerular) cells of the afferent arteriole

Due to decreases perfusion thet will secrete renin and activate the RAAS

54
Q

Which nephropathy is IgG4 antibodies to the phospholipase A2 receptor recetor associated with?

A

Membranous Nephropathy

55
Q

A 2 year old presents with failure to thrive, polyuria, glucosuria and normal serum glucose.

  1. Whats the main issue?
  2. Diagnosis?
A

1.

Defect in proximal tubule reabsorption

2.

Fanconi Syndrome

(Glucose, bicarbonate, calcium, phosphate, amino acids are lost. They also often present with rickets)

56
Q

What can occur following acute tubular necrosis? Why?

(during the recovery phase)

A

Ployuria and Electrolyte Wasting

(Decreased K, Ca, Mg, P)

This occurs since GFR improves before tubular function is restored

57
Q

A patient presents with hematuria following an upper respiratory infection.

  1. If serum complement is normal whats the diagnosis?
  2. If serum complement is low whats the diagnosis?
A
  1. IgA Nephropathy

(normal serum complement)

  1. Poststrep Glomerulonephritis

(low serum complement)

58
Q

Which organisms can cause a struvite/AMP stone?

A

Proteus and Klebsiella

59
Q

How to NSAIDs affect the kidney? (2)

A
  1. They could cause Acute Interstitial Nephritis

(Nephrotic syndorme with rash, fever, eosinophils in urine)

  1. They inhibit prostaglandin production which is needed to dilate the afferent arteriole and maintain GFR when a patient is volume depleted which can then lead to prerenal azotemia
60
Q

How does Poststreptococal Glomerulonephiritis appear on:

  1. Electron Microscopy
  2. Immunofluorecense
A
  1. Subepithelial humps
  2. Granular staining
61
Q
  1. What is the most common type of nephrotic syndrome in children?
  2. What is the most common type of nephritic syndrome in children?
A

Minimal Change Disease

Poststrep. Glomerulonephritis

62
Q

What lab changes would be seen in a patient with PSGN?

A

Elevated ASO

Decreased C3 (normal C4)

63
Q

Why do patients with multiple sclerosis have increased urinary frequency and urinary incontinence?

A

Spastic Bladder

64
Q

What is the most common type of renal cell carcinoma?

In what part of kidney does it originate?

A

Clear-Cell Carcinoma

Originates in the proximal renal tubule

65
Q

In a patient with kidney stones, what is most likely to been on urinalysis? (2)

A
  1. RBCs (hematuria)
  2. Crystals consistent with the type of stone
66
Q

What should be given to a patient with nephrogenic diabetes insipidus?

A

Thiazide diuretics + water replacement

(even though this makes them pee more it allows for better water retention overall)

67
Q

What is the first sign of diabetic nephropathy?

A

increased albumin in urine

68
Q

In a hypovolemic patient how would the kidney alter its absorption of the following:

  1. Sodium
  2. Chloride
  3. Water
  4. Urea
  5. Potassium
A
  1. Increased sodium absorption
  2. Increased chloride absorption
  3. Increased water absorption
  4. Increased urea absorption
  5. Decreased potassium absorption
69
Q

Which letter best represents a patient with chronic kidney disease? Why?

A

“A”

  • CKD results in hyperphosphatemia which binds serum Ca
  • CKD results in decreased levels of active vitamin D so theres less Ca absorption and Ca release from bone

These result in increase PTH release

70
Q

What part of the kidney to ACE-Inhibitors effect?

How does this effect GFR?

A

They dilate the efferent arteriole

This decreases GFR

71
Q

How does severe vomitting effect the following:

  1. Sodium
  2. Potassium
  3. Chloride
  4. Bicarbonate
A
  1. decreased sodium
  2. decreased potassium
  3. decreased chloride
  4. increased bicarbonate

Severe vomitting results in a hypokalemic, hypochloremic metabolic alkalosis

72
Q

How do ACE-Inhibitors effect the GFR?

A

They lower GFR by preventing constriction of efferent arterioles

73
Q

What are the 3 Thiazide diuretics?

Why can they cause muscle pain?

A

1. Hydrochlorothiazide

2. Chlorthalidone

3. Metolazone

Muscle pains due to hypokalemia

74
Q

Patiromer

  1. What is it used for?
  2. How does it work?
A
  1. Used to treat hyperkalemia
  2. Exchanges a calcium for a potassium
75
Q

Sevelamer

  1. What is it used for?
  2. How does it work?
A
  1. Treats hyperphosphatemia

2.

Binds intestinal phospate to reduce its absorption

76
Q

Patients with CKD often develop normocytic anemia due to EPO deficiency so they are given EPO.

What is the major risk of taking EPO for a prolonged amount of time?

A

Thromboembolism & Hypertension

77
Q

How would ACE-Inhibitors effect the following levels:

  1. Renin
  2. AT I
  3. AT II
  4. Aldosterone
  5. Bradykinin
A
  1. Increased renin
  2. Increased AT I

3. Decreased AT II

4. Decreased Aldosterone

  1. Increased Bradykinin
78
Q

How would a Vasopressin-V2-Antagonist (Vaptan) affect the following:

  1. Urine Output
  2. Serum Osmolality
  3. Urinary Sodium excretion
  4. Urinary Potasisum Excretion
A
  1. Increased urine output
  2. Increased serum osmolality

3. No change in sodium excretion

4. No change in potassium excretion

79
Q

What is first-line therapy for rapid-relief of symptoms in patients with HF?

A

Loop diuretics

80
Q

How would a Beta-Blocker affect the following:

  1. Renin
  2. AT I
  3. AT II
  4. Aldosterone
A

Beta-blockers inhibit renin release so they will all be decreased

81
Q

How would Furosemide affect the following

  1. Serum Bicarbonate
  2. Serum Chloride
  3. Urine Sodium
  4. Urine Potassium
A
  1. Increased serum bicarb (can cause contraction alkalosis)
  2. Decreased serum Cl (due to inhibition of Na/K,2Cl)
  3. Increased urine Sodium (since not being reabsorbed)
  4. Increased urine Potassium (since not being reabsorbed)

Furosemide causes decreased absorption of Na, K, Cl

(inhibits Na/K/2Cl transporter)

UWorld - Renal (2 decks)

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