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Internal Medicine > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Define Acute Kidney Injury

A

A rapid decline in renal function with an increase in serum creatinine.

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2
Q

Define RIFLE

A
  • Risk
  • Injury
  • Failure
  • Loss
  • ESRD
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3
Q

Define RISK from RIFLE

A

A 1.5 fold increase in the serum creatinine or GFR decrease by 25% or urine output <0.5 mL/kg/hr for 6 hours.

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4
Q

Define INJURY from RIFLE

A

Twofold increase in serum creatinine of GFR decrease by 50% or urine output of <0.5 mL/kg/hr for 12 hours

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5
Q

Define FAILURE from RIFLE

A

Threefold increase in the serum creatinine or GFR decrease by 75% or urine output of <0.5 mL/kg/hr for 24 hours or anuria for 12 hours.

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6
Q

Define LOSS from RIFLE

A

complete loss of kidney function requiring dialysis for more than 4 weeks

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7
Q

Define ESRD from RIFLE

A

Complete loss of kidney function requiring dialysis for more than 3 months.

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8
Q

What are the 2 most common findings in someone with AKE?

A

Weight gain and edema. This is due to a positive water and sodium balance.

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9
Q

Define Azotemia

A

Elevated BUN an Cr

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10
Q

What are the 2 most common causes of death in AKI?

A

Infection and cardiorespiratory problems.

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11
Q

Define prerenal failure

A

Caused by a decrease in systemic arterial blood flow or renal perfusion. Most common cause of AKI and potentially reversible.

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12
Q

What are some causes of prerenal failure?

A
  • CHF
  • Hypovolemia
  • Hypotension
  • Renal arterial obstruction
  • Cirrhosis/Hepatorenal syndrome
  • NSAIDs, ACE-inhibitors, and cyclosporine
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13
Q

What are the things that you want to monitor in a patient with AKI?

A
  • Daily weights, intake and output
  • Hb and Hct for anemia
  • Signs of infection
  • Serum electrolytes
  • BP
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14
Q

Describe the pathophysiology of prerenal AKI

A

-Renal blood flow decrease enough to lower the GFR which leads to decreased clearance of metabolites (BUN, Cr, uremic toxins). However, since the renal parenchyma is undamaged, tubular function and concentrating ability remains intact. Therefore the kidney responds appropriately conserving as much sodium and water as possible.

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15
Q

What are the lab findings in prerenal AKI

A
  • Oliguria: to preserve volume
  • Increased BUN:Cr ration: >20:1
  • Increased urine osmolality: >500 mOsm/kg because the kidney is able to resorb water
  • Decreased urine Na+: <20 mEq/L with FeNA <1% because Na+ is avidly reabsorbed
  • Increased urine:plasma Cr ratio >40:1 because much of the filtrate is reabsorbed.
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16
Q

Define intrinsic renal failure

A

Kidney tissue is damaged such that the GFR and tubular function are significantly impaired. THe kidneys are unable to concentrate urine effectively.

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17
Q

What are some causes of intrinsic renal failure?

A
  • Tubular disease (ATN): can be caused by ischemia, nephrotoxins
  • Glomerular disease: (Acute glomerulonephritis) Goodpastures, Wegeners, Post-strep GN, lupus
  • Vascular disease: renal artery occlusion, HUS, TTP
  • Interstitial Disease: allergic interstitial nephritis
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18
Q

What lab abnormalities are seen in Rhabdo?

A

-hyperkalemia, hypocalcemia, hyperuricemia, elevated CPK

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19
Q

How do you treat rhabdo?

A

-IV fluids, mannitol, bicarb (which drives k+ back into cells)

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20
Q

What are the lab findings seen in intrinsic renal failure?

  • BUN:Cr
  • Urine Na+
  • FeNa
  • Urine Osmolality
  • urine:plasma cr ratio
A
  • Decreased BUN:Cr ratio (<20:1) in comparison with prerenal failure. Both BUN and Cr are still elevated but less urea is reabsorbed in comparison with prerenal.
  • Urine Na+ increased >40 mEq/L
  • FeNA >2-3% Because Na+ is poorly reabsorbed
  • Decreased urine osmolality <350 mOsm/kg because renal water absorption is impaired
  • Decreased urine:plasma Cr ratio <20:1 because filtrate cannot be reabsorbed
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21
Q

What are two causes of acute tubular necrosis?

A
  1. Ischemic AKI 2/2 to shock, hemorrhage, sepsis or DIC which leads to death of tubular cells.
  2. Nephrotoxic AKI which is injury 2/2 substances that directly injury renal parenchyma and result in cell death.
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22
Q

What are some agents that can cause nephrotoxic AKI?

A
  • Abx: aminoglycosides and Vanc
  • Radiocontrast agents
  • NSAIDs
  • Poisons
  • Myoglobinuria
  • Hemoglobinuria
  • Chemo: cisplatin
  • Kappa and gamma light chains (MM)
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23
Q

Define postrenal AKI

A

Obstruction of any segment of the urinary tract with an intact kidney can cause increased tubular pressure therefore urine cannot be excreted and this leads to a decreased GFR. Blood supply and renal parenchyma are intact. note that the kidneys must be obstructed for the creatinine to rise.

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24
Q

What are some causes of postrenal AKI?

A
  • BPH
  • obstruction of solitary kidey
  • Nephrolithiasis
  • Obstructing neoplasm
  • Retroperitoneal fibrosis
  • Ureteral obstruction-must be bilateral
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25
Q

What are the 3 phases of ATN?

A
  • Onset
    1. ) Oliguric phase
    2. ) Diuretic phase
    3. ) Recovery phase
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26
Q

What are hyaline casts associated with?

A

Prerenal failure

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27
Q

What are RBC casts associated with?

A

Glomerular disease

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28
Q

What are WBC casts associated with?

A

renal parenchymal inflammation

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29
Q

What are fatty casts associated with?

A

nephrotic syndrome

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30
Q

What are muddy brown casts assocaited with?

A

ATN

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31
Q

Lists the complications of AKI

A
  • Hyperkalemia
  • Metabolic acidosis: decreased H+ excretion
  • Hypocalcemia
  • +/- Hyponatremia
  • Hyperphosphatemia
  • Hyperuricemia
  • Uremia
  • Infection
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32
Q

What are the general treatments for AKI?

A
  • Avoid medications that decreased RBF or are nephrotoxic
  • Normalize the fluid imbalance
  • Adjust the medication doses for the level of renal function
  • Correct electrolyte disturbances
  • Optimize cardiac output
  • Dialysis if necessary
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33
Q

Treatment for prerenal AKI

A
  • Treat the underlying disorder
  • Give NS to maintain euvolemia and restore BP (unless they have edema or ascites)
  • Eliminate offending agent s
  • If unstable Swan-Ganz monitoring for accurate assessment of intravascular volume
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34
Q

Treatment for intrinsic AKI

A
  • Once ATN develops, therapy is supportive. Eliminate the cause/offending agent.
  • If oliguric, a trial of furosemide may help to increase urine flow and improve fluid balance.
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35
Q

Define Chronic Kidney Disease

A

Decreased kidney function (GFR <60) or kidney damage (functional or structural) for at least 3 months.

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36
Q

What are the most common causes of CKD?

A
  • Diabetes (#1)
  • HTN (#2)
  • Chronic GN
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37
Q

What is uremia?

A

-The clinical syndrome associated with the accumulation of nitrogenous wastes due to impaired renal function.

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38
Q

What are the cardiovascular manifestations of CKD?

A
  • CHF
  • HTN: decreased GFR stimulates RAAS which leads to increased BP
  • Pericarditis
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39
Q

What are the neurologic manifeststions of CKD

A

-Hypocalcemia

=Lethargy, somnolence, confusion, neuropathy, uremic symptoms

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40
Q

What are the hematologic manifestations of CKD?

A
  • Normocytic normochromic anemia

- Bleeding secondary to platelet dysfunction (uremia)

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41
Q

What are the calcium/phosphate disturbances that can occur with CKD?

A

-Hyperphosphatemia
-Hypocalcemia
–> both lead to increased PTH release (secondary hyperparathyroidism)
Secondary hyperparathyroidism can cause renal osteodystrophy which causes weakening of bones and possibly fractures.
-Vascular calcifications

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42
Q

What tests do you want to order to diagnose CKD?

A
  • UA
  • Cr and GFR
  • CBC (anemia, thrombocytopenia)
  • Serum electrolytes)
  • Renal ultrasound
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43
Q

Treatment for CKD

A
  • Low protein diet
  • Low salt diet
  • Restrit potassium phosphate, and magnesium intake
  • ACEi’s or ARBS
  • BP Control
  • Glycemic control
  • Smoking cessation
  • Correction of anemia and electrolyte abnormalities
  • -Dialysis or transplant if necessary
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44
Q

What are 3 life threatening complications that can occur with CKD?

A
  • Hyperkalemia: EKG!
  • Pulmonary edema: 2/2 to volume overload
  • Infection: pneumonia, UTI, sepsis
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45
Q

Absolute indications for Dialysis

A

A-acidosis
E-electrolytes: hyperkalemia (sever and persistent)
I-ingestion: methanol, ethylene glycol, lithium, aspirin
O-overload: not managed by other means
U-uremia: uremic pericarditis!

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46
Q

Complications of hemodialysis

A
  • Hypotension
  • First use syndrome
  • Anticoagulation complications
  • Infection of the vascular access site
  • Amyloidosis of beta-2 microglobulin
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47
Q

Complications of peritoneal dialysis

A
  • Hyperglycemia
  • Hyperlipidemia
  • Abdominal/inguinal hernia 2/2 to increased intraabdominal pressure
  • Protein malnutrition
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48
Q

How does ADPKD present?

A
  • Abdominal pain
  • Hematuria
  • HTN
  • Flank mass
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49
Q

Complications of ADPKD

A
  • Intracerebral berry aneurysm
  • Infection of the renal cysts
  • Renal failure
  • Kidney stones
  • heart valve abnormalities (MV prolapse)
  • Cysts in liver, spleen, pancreas, bone
  • Diverticula
  • Hernias
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50
Q

How do you diagnose ADPKD

A

-U/S, CT or MRI

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51
Q

Treatment of ADPKD

A
  • Drain cysts
  • Transplant
  • Treat infection
  • Control HTN
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52
Q

What is the pathology of ARPKD?

A

It ic characterized by cysts predominantly in the renal collecting ducts as well as hepatic fibrosis.

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53
Q

Clinical picture of ARPKD

A
  • Hepatic involvement is always present
  • HTN
  • Enlarged kidneys
  • Pulmonary hypoplasia/insufficiency
  • Potters Syndrome
  • Oligohydramnios in mom
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54
Q

What is medullary sponge kidney

A
  • it is characterized by cystic dilation of the collecting ducts
  • Thought to be associated with hyperparathyroidism and parathyroid adenoma
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55
Q

What is the most common cause of secondary HTN?

A

-Renal artery stenosis

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56
Q

What are the two main causes of renal artery stenosis?

A
  • Fibromuscular dysplasia

- Atherosclerosis

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57
Q

Clinical features of renal artery stenosis

A
  • HTN: sudden onset in someone w/o fam hx, resistent to tx
  • Decreased renal function
  • abdominal bruit
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58
Q

How do you diagnose renal artery stenosis?

A
  • Renal arteriogram but be careful with contrast dyes!
  • MRA
  • Duplex doppler u/s
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59
Q

Treatment of renal artery stenosis?

A

-Revascularization with percutaneous transluminal renal angioplasty
-Surgery (bypass)
conservative medical therapy (ACE-is, CCBs)

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60
Q

In what situations might you see renal vein thrombosis?

A

-Nephrotic syndrome, invasion of the renal vein by RCC, trauma, pregnancy/OCPs, extrinsic compression by retroperitoneal fibrosis, aortic aneurysm, lymphadenopathy) or severe dehydration in infants.

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61
Q

Define hypertensive nephrosclerosis

A

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

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62
Q

Define benign nephrosclerosis

A

Thickening of the glomerular afferent arterioles develops in patients with long standing HTN

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63
Q

Define malignant nephrosclerosis

A

This can develop in a patient with long standing or benign HTN or in a previously undiagnosed person. It is characterized by a rapid decrease in renal function and accelerated HTN due to diffuse intrarenal vascular injury.

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64
Q

Symptoms of benign nephrosclerosis

A
  • Moderate increase in Cr levels
  • Microscopic hematuria
  • Mild proteinuria
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65
Q

Symptoms of malignant nephrosclerosis

A
  • Markedly elevated BP
  • Rapid increase in Cr, proteinuria, hematuria
  • RBC and WBC casts in urine, maybe nephrotic syndrome
  • MAHA may also be present
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66
Q

What are the 4 classifications of proteinuria?

A
  • Glomerular
  • Tubular
  • Overflow
  • Other
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67
Q

What is the pathogenesis of glomerular proteinuria?

A
  • It is due to increased glomerular permeability to proteins.
  • Can lead to nephrotic syndrome
  • May be seen in all types of glomerulonephritis
  • Protein loss tends to be more severe than in nonglomerular causes
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68
Q

What is the pathogenesis of tubular proteinuria?

A

Small proteins normally filtered at the glomerulus and then reabsorbed by the tubules appear in the urine because of abnormal tubules. This proteinuria is less severe than glomerular proteinuria.

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69
Q

What are some causes of tubular proteinuria?

A
  • Sickle cell disease
  • UTI
  • interstitial nephritis
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70
Q

Example of overflow proteinuria

A

-Bence Jones Proteinuria due to Multiple Myeloma

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71
Q

What are other causes of proteinuria?

A
  • UTI
  • Fever
  • Exertion/Stress
  • CHF
  • Pregnancy
  • Orthostatic proteinuria
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72
Q

What are the 3 key features of nephrotic syndrome?

A

-Edema
-Proteinuria
-Hyperlipidemia
-Hypoalbuminemia
Other: hypercoagulable state, increased incidence of infection

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73
Q

What is the underlying cause of nephrotic syndrome?

A

-Significant glomerular disease resulting in abnormal glomerular permeability

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74
Q

Treatment for asymptomatic proteinuria?

A

If it is transient, no further workup is necessary. If it is persistent, further testing is indicated. Start by checking BP and examining urine sediment. Treat the underlying disease and associated problems.

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75
Q

Treatment for symptomatic proteinuria?

A
  • Treat the underlying disease
  • ACE inhibitors (decrease albumin loss)
  • Diuretics
  • Limit dietary protein and sodium
  • Treat hypercholestolemia
  • Vaccinate against flu and pneumococcus
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76
Q

Definition of hematuria?

A

> 3 RBCs/HPF on UA

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77
Q

Microscopic hematuria is more associated with?

A

Glomerular origin

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78
Q

Gross hematuria is more associated with?

A

Nonglomerular or urologic in origin

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79
Q

What should you consider when you see gross painless hematuria?

A

Bladder or kidney cancer until proven otherwise

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80
Q

What are some causes of hematuria

A

-Bladder or Kidney Cancer
-Infection
-Kidney stones
-Glomerular disease
-Trauma
-Strenuous exercise
-Systemic disease
-SCD
-Bleeding disorder
-Meds
-Polycystic kidney disease, simple cysts
-BPH
Just to name a few

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81
Q

What are the 4 common sites of obstruction by stones?

A
  1. ) Uterovesicular junction
  2. ) Calyx of the kidney
  3. ) Uteropelvic junction
  4. ) Intersection of the ureter and the iliac vessels
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82
Q

Risk factors for nephrolithiasis

A
  1. ) Low fluid intake
  2. ) Family history
  3. ) Conditions that precipitate stone formation: gout, Crohn’s, RTA type 1, hyperparathyroidism
  4. ) Medications: loops, acetazolamide, antacids, chemo)
  5. ) Male gender
  6. ) UTIs
  7. ) Dietary factors: low calcium and oxalate
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83
Q

What is the most common type of kidney stone?

A

Calcium: either oxalate or phosphate

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84
Q

What do calcium stones look like?

A

bipyramidal or biconcave ovals

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85
Q

Are calcium stones visible on a KUB?

A

Yes, they are radiodense

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86
Q

What type of urine promotes uric acid stone formation?

A

Acidic <5.5

87
Q

What are uric acid stones associated with? (conditions?)

A
  • Gout

- Chemotherapy

88
Q

What do uric acid stones look like?

A

Flat squate planes

89
Q

Can uric acid stones be seen on a KUB?

A

No they are radiolucent. They require CT, U/S or IVP for detection

90
Q

Are struvite stones visible on a KUB?

A

Yes they are radiodense.

91
Q

What causes struvite stones?

A

Infection with urease producing organisms (proteus, klebsiella, serratia, enterobacter). These urea splitting bacteria convert urea to ammonia, thus producing alkaline urine. Alkaline urine promotes the formation of struvite stones.

92
Q

What causes cystine stones?

A

-Genetic predisposition, cystinuria

93
Q

What do cystine stones look like?

A

They are hexagon shaped crystals that are poorly visualized.

94
Q

What size are stones that pass spontaneously?

A

<0.5 cm

95
Q

Classic presentation of nephrolithiasis?

A
  • Colicky pain/flank pain that radiates to the groin
  • Hematuria
  • N/V may also be present
96
Q

How do you workup nephrolithiasis?

A
  • UA
  • Urine Cx if possible infection
  • Serum chemistry
  • 24 hour urine collection
  • KUB (CT w/o is gold standard), IVP or renal U/S) CT scan can pick up all stones, even radiolucent ones.
97
Q

What is the general treatment for all types of kidney stones.

A
  • Fluids/hydration
  • Analgesics
  • Antibiotics if UTI is present
98
Q

What are the indications for hospital admission w/ nephrolithiasis

A
  • Pain not controlled w/ oral meds
  • ANuria
  • Renal colic + UTI + fever
  • Large stones >1 cm that are unlikely to pass spontaneously.
99
Q

Extracorporeal shock wave lithotripsy is best for stones of what size?

A

> 5 mm <2 cm

100
Q

Percutaneous nephrolithotomy is best for stones of what size?

A

> 2 cm or if lithotripsy fails

101
Q

What pharmacologic measures can be taken to reduce the chance of future kidney stones

A
  • Thiazides: reduce urinary calcium, especially in pts w/ hypercalciuria
  • Allopurinol: esp for patients with high levels of uric acid
102
Q

Lower urinary tract obstruction occurs where and affects what?

A

Occurs below the uterovesical junction and affects urination

103
Q

Upper urinary tract obstruction occurs where and affects what?

A

Occurs above the uterovesical junction and causes renal colic

104
Q

What are some causes of lower urinary tract obstruction?

A
  • BPH
  • Prostate cancer
  • Urethral stricture
  • Kidney stone
  • Neurogenic bladder (MS, DM)
  • Trauma (saddle or pelvic injury)
  • Bladder cancer
105
Q

What are some causes of upper urinary tract obstruction?

A 
Intrinsic causes: 
-Kidney stones 
-Blood clots 
-Sloughed papillae 
-Crystal deposition 
-Tumors 
-Strictures 
-Ureteropelvis or ureterovesical junction dysfunction 
Extrinsic causes: 
-Pregnancy 
-Tumors 
-AAA 
-Retroperitoneal fibrosis 
-Endometriosis 
-Prolapse 
-Hematomas 
-Crohn's Disease 
-Diverticulosis
106
Q

Clinical features of urinary tract obstruction

A
  • Renal colic and pain
  • Oliguria
  • Recurrent UTIs
  • Hematuria or Proteinuria
  • Renal failure
107
Q

Workup of urinary tract obstruction

A
  • Renal U/S is the best test. It will show urinary tract dilation
  • U/A, CBC, electrolytes, BUN/Cr )
  • KUB: to look for stones
  • IV urogram/IVP: gold standard of diagnosis for ureteral obstruction
  • Voiding cystourethrography
  • Cystoscopy
  • CT scan
108
Q

Risk factors for prostate cancer

A
  1. ) Age
  2. ) AA
  3. ) High fat diet
  4. ) + Fam Hx
  5. ) Exposure to herbicide and pesticides (industry, farming)
109
Q

How does prostate cancer grow?

A

It begins in the periphery and grows centrally, therefore obstructive symptoms occur late in the disease. By the time prostate cancer causes urinary obstruction, it often has mets to bone or LN

110
Q

Later symptoms of prostate cancer

A
  • Difficulty voiding
  • Dysuria
  • Increased urinary frequency
  • Bone pain from mets
  • Weight loss/cachexia
111
Q

How does carcinoma feel on DRE?

A

Hard, nodular and irregular

“like a knuckle”

112
Q

If DRE is abnormal, what is the next best step?

A

Transrectal ultrasound (regardless of the PSA level!)

113
Q

Besides prostate cancer, what else might cause elevated PSA?

A
  • Prostatitis
  • Prostatic massage
  • Needle biopsy
  • Cystoscopy
  • BPH
  • Advanced age
114
Q

What are indications for a transrectal ultrasound with biopsy?

A
  • PSA >10
  • PSA velocity of >0.75 / yr
  • Abnormal DRE
115
Q

Treatment of localized disease in prostate cancer?

A
  • Radical prostatectomy

- Watchful waiting if asymptomatic and natural life span is <10 years expected

116
Q

Complications of radical prostatectomy?

A
  • Erectile dysfunction

- Urinary incontinence

117
Q

Treatment of locally invasive disease in prostate cancer?

A

-Radiation therapy plus androgen deprivation therapy

118
Q

Treatment of metastatic prostate cancer?

A

Reduce amount of Testosterone with:

  • Orchiectomy
  • Antiandrogens
  • LH agonists (Leuprolide)
  • GnRH antagonist
119
Q

Stage A prostate cancer

A

Nonpalpable confined to the prostate

120
Q

Stage B prostate cancer

A

palpable nodule but confined to the prostate

121
Q

Stage C prostate cancer

A

extends beyond the capsule w/o metastasis

122
Q

Stage D prostate cancer

A

metastatic disease

123
Q

What syndrome is RCC associated with?

A

VHL (AD)

124
Q

Where is RCC likely to metastasize to?

A

lung, liver, brain, bone, but also don’t forget tumor thrombus into renal vein or IVC.

125
Q

Risk factors for RCC

A
  • Cigarette smoking
  • Pheacetin analgesics
  • ADPKD
  • Chronic dialysis
  • Exposure to heavy metals (mercury, cadmium
  • HTN
126
Q

Clinical features of RCC

A
  • Hematuria
  • Abdominal or flank pain
  • Abdominal or flank mass
  • Weight loss, fever
127
Q

What paraneoplastic syndromes are associated with RCC?

A
  • PTHrP secretion–> causing hypercalcemia
  • EPO secretion–> causing polycythemia
  • Renin–> causing HTN
  • Cortisol–> causing Cushings
  • Gonadotropin –> causing feminization or masculinization
128
Q

Diagnosis of RCC

A
  • Renal ultrasound

- Abdominal CT

129
Q

How does bladder cancer spread?

A

By local invasion

130
Q

Risk factors for bladder cell/transitional carcinoma?

A
  • Cigarette smoking
  • Industrial carcinogens (aniline dye, azo dyes)
  • Long term tx w/ cyclophosphamide
131
Q

Clinical features of bladder cancer

A
  • Hematuria (painless)

- Irritable bladder symptoms: dysuria, frequency

132
Q

How do you workup bladder cancer

A
  • UA and UCx
  • Urine cytology to detect malignant cells
  • IVP
  • Cystoscopy and biopsy
  • CXR and CT scan
133
Q

What is the most common type of testicular cancer in men 20-40 yo

A

Germ Cell Tumors

134
Q

Describe seminomas

A
  • Most Common Germ Cell tumor
  • Slow growth
  • Late invasion
  • Most radiosensitive
135
Q

Describe embryonal carcinoma

A
  • Non-seminomatous germ cell cancer
  • High malignant potential
  • Hemorrhage and necrosis are common
  • Mets to the abdominal lymphatics and lung occur early
136
Q

Describe choriocarcinomas

A
  • Non-seminomatous germ cell cancer
  • Most aggressive
  • Mets occur early by the time of diagnosis
  • Rare
137
Q

Describe yolk sac carcinoma

A
  • Non-seminomatous germ cell tumor

- Uncommon in adults, usually occur in young boys

138
Q

What are the two non-germ cell tumors? Are they scary?

A
  • Leydig Cell
  • Sertoli Cell
  • No they are usually benign
139
Q

Risk factors for testicular cancer

A
  • Cryptorchidism

- Klinefelter Syndrome

140
Q

Clinical features of testicular cancer

A
  • Painless mass/lump/firmness of the testicle

- Gynecomastia if hormone producing

141
Q

Workup of testicular mass

A
  • PE
  • Testicular ultrasound
  • Tumor markers
142
Q

What tumor is AFP associated with?

A

-Yolk sac embryonal tumor

143
Q

What tumor is beta-hCG associated with?

A

Choriocarcinoma

144
Q

What else is in the ddx for testicular caner?

A
  • Varicocele
  • Testicular torsion
  • Spermatocele
  • Hydrocele
  • Epidiymitis
  • Lymphoma
145
Q

What viruses is penile cancer associated with?

A
  • HPV 18

- Herpes simplex

146
Q

how does penile cancer present?

A

-As an exophytic mass on the penis

147
Q

Tx of penile cancer?

A

-local excision

148
Q

Tx of testicular cancer

A
  • Removal surgically (be careful w/ seeding)
  • CT scan of chest, abdomen and pelvis for staging
  • Perform beta-hCG and AFP measurements for comparison of pre-op values
  • Depends on the histology
149
Q

Clinical presentation of testicular torsion

A
  • Acute severe testicular pain
  • swollen and tender scrotum
  • elevated testicle
150
Q

Tx for testicular torsion

A

-Surgical fixation within 6 hours!

151
Q

What is epididymitis and what is the msot common organism in old men? what about young sexually active men?

A
  • Infection of the epidiymitis
  • Children and old men: E. Coli
  • Young sexually active men: Gonorrhea, Chlamydia
152
Q

Clinical presentation of epididymitis

A
  • Swollen tender testicle, dysuria, fever/chills, scrotal pain, scrotal mass
  • RULE OUT TESTICULAR TORSION and then give Abx
153
Q

Clinical features/pathogenesis of glomerular disease

A

Glomerular disorders are characterized by impairment in selective filtration of blood, resulting in excretion of larger substances such as plasma proteins and blood cells. As disease advances, GFR decreases proportionately, leading to renal failure and the possible need for dialysis and/or transplantation

154
Q

How do you diagnose glomerular disease?

A
  1. ) UA (proteinuria, hematuria, RBC casts)
  2. ) Blood test (renal function test)
  3. ) Needle biopsy of the kidney
155
Q

What are some possible clinical presentations of glomerular disease?

A
  • Isolated proteinuria
  • Isolated hematuria
  • Nephritic syndrome: HTN, hematuria, azotemia
  • Nephrotic syndrome: proteinuria, edema, hyperlipidemia, hypoalbuminemia
156
Q

Pathogenesis of Nephritic syndrome

A

-Inflammation of the glomeruli due to any of the causes of glomerulonephritis

157
Q

Pathogenesis of Nephrotic syndrome

A

-Abnormal glomerular permeability due to a number of conditions

158
Q

What is the most common cause of nephritic syndrome?

A

-Poststreptococcal glomerulonephritis

159
Q

What is the most common cause of nephrotic syndrome in adults?

A

-Membranous glomerulonephropathy

160
Q

Is minimal change disease nephritic or nephrotic?

A

Nephrotic syndrome

161
Q

Who has MCD and what else is it associated with?

A

-Most common in children, associated with Hodgkin disease and non-hodgkin lymphoma.

162
Q

What is seen on EM in MCD?

A

-Fusion of the foot processes

163
Q

Treatment of MCD?

A

-corticosteroids for 4-8 weeks; excellent prognosis

164
Q

What is the theory for the pathogenesis of MCD?

A

Possible T-cell dysfunction

165
Q

Is FSGS nephritic or nephrotic?

A

Nephrotic

166
Q

Describe the prognosis of FSGS

A

Fair to poor. Generally resistant to steroid therapy. Patients develop renal insufficiency within 5-10 years of diagnosis. The course ifs progressive.

167
Q

Treatment of FSGS (understand that it’s complicated and controversial)

A

Combo of cytotoxic agents, steroids, and immunosuppressive agents

168
Q

Is membranous glomerulonephritis nephritis or nephrotic?

A

Nephrotic.

169
Q

What happens to the glomerular capillary walls in membranous glomerulonephritis?

A

The glomerular capillary walls become thickened

170
Q

What is membranous glomerulonephritis associated with? Both primary and secondary disease?

A

Primary: idiopathic
Secondary:
-Infection–> Hep C, Hep V, syphilis, malaria
-Drugs–> Gold, captopril, penicillamine
-Neoplasms
-Lupus

171
Q

What is the most common cause of glomerular hematuria?

A

-IgA Nephropathy

172
Q

How does IgA Nephropathy present?

A

-Gross hematuria after an upper respiratory infection

173
Q

What is seen on EM in IgA Nephropathy?

A

IgA and C3 deposition

174
Q

What is Hereditary Nephritis?

A
  • Aka Alport syndrome

- X-linked or Autosomal Dominant with variable penetrance

175
Q

What are the clinical features of Alport Syndrome?

A
  • Hematuria
  • Pyuria
  • Proteinuria
  • High frequency hearing loss w/o deafness
  • Progressive renal failure
176
Q

What is membranoproliferative glomerulonephritis associated with?

A
  • Hep C
  • Hep B
  • Syphilis
  • Lupus
  • Cryoglobulinemia
177
Q

How long after infection w/ strep does GN develop?

A

10-14 days

178
Q

What kind of strep infections can lead to post-strep GN?

A

-URI or skin (impetigo)

179
Q

What are the clinical features and important lab values in post-strep GN?

A
  • hematuria
  • Edema
  • HTN
  • low complement levels
  • Proteinuria
  • Elevated antistreptolysin O
180
Q

What is Goodpasture’s Syndrome?

A

Triad of:

  1. ) Proliferative glomerulonephritis (usually crescentic)
  2. ) Pulmonary hemorrhage
  3. ) IgG antiglomerular basement membrane antibody
181
Q

What is the clinical presentation of Goodpastures Disease

A
  • Rapidly progressive renal failure
  • Hemoptysis
  • Cough
  • Dyspnea
  • Lung disease precedes kidney disease by days to weeks
182
Q

What is seen on IF in Goodpastures disease?

A

linear IF pattern

183
Q

how do you treat Goodpastures?

A

-Treat with plasmapharesis to remove circulating anti-IgG antibodies. Cyclophosphamide and steroids can decrease the formation of new antibodies.

184
Q

What is the pathology of AIN?

A

It is inflammation involving the interstitium which is the tissue that surrounds the glomeruli and tubules.

185
Q

What should you inquire about with suspected AIN?

A
  • recent infection
  • new medication
  • rash, fever, aches/pains
  • Signs and symptoms of AKI
186
Q

What are 4 causes of AIN?

A
  1. ) Acute allergic reaction to medication (MOST COMMON CAUSE)
  2. ) Infection (esp. in children)
  3. ) Collagen vascular diseases (sarcoidosis)
  4. ) Autoimmune diseases (SLE, Sjogrens)
187
Q

What are the 3 classic findings associated with AIN?

A
  • Rash
  • Fever
  • EOSINOPHILIA
188
Q

What is seen on a UA that is diagnostic of AIN?

A

Eosinophils in the urine, given the proper history and findings.
Mild proteinuria or microscopic hematuria may also be present.

189
Q

What is the only way to definitively distinguish between AIN and ATN?

A

Renal biopsy

190
Q

What is chronic interstitial nephritis?

A

-It has a more indolent course and is associated with tubulointerstitial fibrosis and atrophy

191
Q

Treatment of AIN

A
  • Remove the offending agent

- Tx the underlying disease or infection if present

192
Q

What is renal papillary necrosis associated with?

A
  • Analgesic nephropathy
  • UTI
  • Diabetic nephropathy
  • Sickle cell nephropathy
  • Urinary tract obstruction
  • chronci alcoholism
  • Renal transplant rejection
193
Q

How do you diagnose renal papillary necrosis?

A

-Excretory urogram and note changes in the papillae or medulla

194
Q

What is one complication of renal papillary necrosis?

A

Sloughed papillae can cause ureteral obstruction.

195
Q

What is analgesic nephropathy?

A

It is a form of toxic injury to the kidney due to excessive use of over the counter analgesics. It can manifest as interstitial nephritis or renal papillary necrosis. It may lead to acute or chronic renal failure.

196
Q

What metabolic abnormality is seen in RTAs?

A
  • Non-anion gap hyperchloremic metabolic acidosis.

- Glomerular function is normal.

197
Q

What is the problem in type I RTA?

A

A defect in the ability to secrete H+ at the distal tubule. Therefore new bicarb cannot be generated. This inability to acidify the urine leads to a metabolic acidosis.

198
Q

How low does the urine pH normally get? what about in Type I RTA?

A

As low as 4.7, but in Type I RTA it can’t get below 6!

199
Q

What electrolyte abnormalities does RTA type I lead to?

A

Type I RTA leads to increased excretion of ions (sodium calcium, potassium, sulfate, and phosphate) This results in:

  • Decrease in ECF
  • Hypokalemia
  • Renal stones/nephrocalcinosis due to increased calcium and phosphate excretion into alkaline urine.
  • Rickets/osteomalacia in children
200
Q

What is the primary symptom of Type I RTA?

A

-Kidney Stones!

201
Q

What are some causes of type I RTA?

A
  • Congenital
  • Multiple myeloma
  • Nephrocalcinosis
  • Nephrotoxicity (amphotericin B toxicity)
  • Autoimmune diseases (Lupus, Sjogrens)
  • Medullary sponge kidney
  • Analgesic nephropathy
202
Q

Treatment of type I RTA?

A
  • Correct the acidosis with sodium bicarb. This can also help prevent the formation of kidney stones.
  • Administer phosphate salts: helps with the excretion of titratable acids.
203
Q

What is the problem in Type II RTA?

A

The defect is an inability to resorb HCO3- at the proximal tubule, resulting in an increased excretion of bicarbonate in the urine and a metabolic acidosis. The patient also loses K+ and Na+ in the urine.

204
Q

What are some causes of Type 2 RTA?

A
  • Fanconi syndrome
  • Cystinosis
  • Wilsons Disease
  • Lead toxicity
  • Multiple myeloma: excretion of monoclonal light chains is a common feature so multiple myeloma should always be ruled out in a patient with proximal RTA
  • Nephrotic syndrome
  • Amyloidosis
205
Q

Do nephrolithiasis and nephrocalcinosis occur in Type 2 RTA?

A

NO!!!!

206
Q

Treatment of Type 2 RTA?

A
  • Treat the underlying cause
  • Do not give bicarb to correct the acidosis because it will be excreted in the urine
  • Sodium restriction increases sodium reabsorption and thus bicarb reabsorption in the proximal tubule.
207
Q

What is Type 4 RTA?

A

Hypoaldosteronism or renal resistance to aldosterone. It is characterized by decreased Na+ absorption and decreased H+/K+ secretion in the distal tubule

208
Q

What makes type 4 RTA different from type 1 and 2 RTA?

A
  • It causes hyperkalemia, not hypokalemia like type 1 and 2 do.
  • It causes acidic urine
209
Q

What is Hartnup syndrome?

A

-AR disease with defective amino acid transporter causing decreased intestinal and renal reabsorption of neutral amino acids such as tryptophan, causing nicotinamide deficiency

210
Q

Clinical features of Hartnup syndrome?

A

-Pellagra: dermatitis, dementia, diarrhea, ataxia, psych disturbances

211
Q

Tx of Hartnup Syndrome?

A

Give them nicotinamide if they are symptomatic

212
Q

What is Fanconi Syndrome?

A

An inherited or acquired proximal tubule dysfunction that leads to defective transport of the following: glucose, amino acids, sodium, potassium, phosphate, uric acid, and bicarb.

213
Q

How do you treat Fanconi Syndrome?

A

-Phosphate, potassium, alkali and salt supplementation and adequate hydration

214
Q

What is seen in Fanconi Syndrome?

A
  • Glucosuria
  • Phosphaturia (leads to rickets/impaired growth in kids/osteomalacia/osteoporosis and pathologic fractures in adults
  • Proteinuria
  • Polyuria
  • Dehydration
  • Type 2 RTA
  • Hypercalciuria
  • Hypokalemia

Internal Medicine (6 decks)

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