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USMLE Pathoma > Block 2 Exam total prep (GI/Gallbladder/Male-repro/Pancreas) > Flashcards

Block 2 Exam total prep (GI/Gallbladder/Male-repro/Pancreas) Flashcards

1
Q

Describe the following for a Horseshoe kidney:

What is it?

A

The kidney gets caught on the IMA casing a conjoined kidney connected at the lower pole

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2
Q

conjoined kidney connected at the lower pole

A

Horseshoe kidney

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3
Q

Describe the following for a unilateral Renal agenesis:

What is it?

A

One kidney gets hypertrophied & hyperinflated to compensate for the other being atrophied/not formed this carries the risk of renal failure later on though

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4
Q

One kidney gets hypertrophied & hyperinflated to compensate for the other being atrophied/not formed this carries the risk of renal failure later on though

A

Unilateral renal agenesis

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5
Q

Describe the following for a bilateral Renal agenesis:

What is it?

A

Both kidneys are atrophied & don’t function causing potter sequence (oligohydramnios, lung hypoplasia, flat face/low set ears, & extremity defects)

This one is fatal :(

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6
Q

Both kidneys are atrophied & don’t function causing potter sequence (oligohydramnios, lung hypoplasia, flat face/low set ears, & extremity defects)

This one is fatal :(

A

Bilateral renal agenesis

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7
Q

What are the symptoms of Potter sequence & what congenital condition is it associated with?

A

oligohydramnios, lung hypoplasia, flat face/low set ears, & extremity defects

ass with bilateral renal agenesis

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8
Q

Describe the following for a Dysplastic kidney:

What is it?

A

a congenital defect causing abnormal kidney tissue & cysts it’s usually bilateral (but not always)

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9
Q

a congenital defect causing abnormal kidney tissue & cysts it’s usually bilateral (but not always)

A

Dysplastic kidney

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10
Q

Describe the following for a polycystic kidney disease:

What is it?

A

It causes enlarged kidneys with cysts in the renal cortex/medulla it can be autosomal dominant or recessive

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11
Q

What are the features of autosomal dominant polycystic kidney disease?

What is it?
- who/what

What causes it?

What conditions is it associated with?

A

Patho:
Usually in young adults it presents with HTN, hematuria, & worsening renal failure.

Causes:
It is caused by either an APKD1/2 mutation

Ass conditions:
It’s associated with Berry aneurysm, MVP, or hepatic cysts

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12
Q

Usually in young adults it presents with HTN, hematuria, & worsening renal failure. It is caused by either an APKD1/2 mutation and it’s associated with Berry aneurysm, MVP, or hepatic cysts

A

Autosomal dominant polycystic kidney disease

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13
Q

What are the features of autosomal recessive polycystic kidney disease?

What is it?
- who/what

A

Patho:
It typically affects infants & it presents as HTN, worsening renal failure, & eventually as potters (this one is fatal)

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14
Q

It typically affects infants & it presents as HTN, worsening renal failure, & eventually as potters (this one is fatal)

A

Autosomal recessive polycystic kidney disease

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15
Q

Describe the following for a Medullary cystic kidney disease:

What is it?

A

Aka the medullary sponge kidney.

It’s an autosomal dominant mutation that causes cysts in the medullary collecting ducts & fibrosis of the kidney. It makes the kidneys shrink & causes worsening renal failure

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16
Q

Cystic dilatation of the collecting ducts & fibrosis of the kidney parenchyma

A

Medullary cystic kidney disease

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17
Q

What is the most common cause of kidney failure in children & what organisms cause it?

A

Hemolytic uremic syndrome, which can be caused by E.coli, VTEC, or Shigella (i.e undercooked ground beef)

It forms platelet fibrin thrombi in the glomerular capillaries which cause thrombotic microangiopathy

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18
Q

The most common cause of renal failure in children, can be caused by E.coli, VTEC, or Shigella (i.e undercooked ground beef)

It forms platelet fibrin thrombi in the glomerular capillaries which cause thrombotic microangiopathy

A

Hemolytic uremic syndrome

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19
Q

Describe the following for prerenal azotemia:

What is it?

What are the lab findings?

A

Path:
Reduced blood flow to the kidneys (like from heart failure) cause worsening renal failure

Labs:
Azotemia (BUN:CR >15/20) Elevated
Oliguria (urine osmo >500)
Reduced GFR

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20
Q

It causes reduced blood flow to the kidneys (like from heart failure) cause worsening renal failure

Labs show the following:
Azotemia (BUN:CR >15/20) Elevated
Oliguria (urine osmo >500)
Reduced GFR

A

Prerenal Azotemia

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21
Q

Describe the following for postrenal azotemia:

What is it?

What are the lab findings?

A

Path:
Due to an obstruction downstream from the kidneys (i.e in the ureters) that reduces the glomerular filtration rate

Early stage only has azotemia, oliguria & reduced GFR but as it progresses to late stage the labs show this:

Reduced GFR

Azotemia (BUN:CR >15/20) Elevated

Inability to concentrate the urine (urine osmo >500)

Reduced Na resorption (FENa >2%)

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22
Q

Due to an obstruction downstream from the kidneys (i.e in the ureters) that reduces the glomerular filtration rate

Labs show:

Reduced GFR

Azotemia (BUN:CR >15/20) Elevated

Inability to concentrate the urine (urine osmo >500)

Reduced Na resorption (FENa >2%)

A

Post renal azotemia

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23
Q

Describe the following for acute tubular necrosis:

What is it? What are the symptoms?

A

Path:
Reduced blood flow to the kidneys tubules causes ischemia/necrosis it tends to happen after prerenal azotemia in the PCT & Medullary seg of the thick ascending LOH

Signs:
1) Renal failure
2) Brown granular casts in the urine

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24
Q

What are the lab findings in acute tubular sclerosis?

A

Labs:

decreased reabsorption of BUN (serum BUN:Cr ratio < 15), decreased reabsorption of sodium (FENa > 2%), and inability to concentrate urine (urine osm < 500 mOsm/kg).

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25
Q

What can cause acute tubular necrosis?

A

Causes:
1) Severe hypotension (hypovolemic, hemorrhage, severe dehydration), septic shock)

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26
Q

What are the two types of acute tubular necrosis?

A

1) Ischemic type: due to reduced to the tubules which is proceeded by prerenal azotemia in the PCT & Medullary thick ascending limb of the LOH

2) Nephrotic type: caused by toxic agents like heavy metals (lead), myoglobinuria (crushing injury), ethylene glycol (antifreeze) & radiocontrast (tumor lysis syndrome) cause necrosis in the PCT

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27
Q

1) Ischemic type: due to reduced to the tubules which is proceeded by prerenal azotemia in the PCT & Medullary thick ascending limb of the LOH

2) Nephrotic type: caused by toxic agents like heavy metals (lead), myoglobinuria (crushing injury), ethylene glycol (antifreeze) & radiocontrast (tumor lysis syndrome) cause necrosis in the PCT

Are features of which condition?

A

Acute Tubular necrosis

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28
Q

How does acute tubular necrosis (aka intrarenal azotemia) cause brown casts in the urine?

A

The ischemia/necrosis of the tubular epithelium causes necrotic plugs in the tubules which cause the renal dysfunction & brown/granular casts

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29
Q

What is acute interstitial nephritis?

A

Aka drug induced nephritis (a hypersensitivity reaction) it can cause renal papillary necrosis

Key signs include:
1. Oliguria
2. Fever/rash
3. Elevated eosinophils in the urine

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30
Q

Aka drug induced nephritis (a hypersensitivity reaction) it can cause renal papillary necrosis

Key signs include:
1. Oliguria
2. Fever/rash
3. Elevated eosinophils in the urine

Describes which condition?

A

Acute interstitial nephritis

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31
Q

What is renal papillary necrosis?

A

Necrosis of the renal papillae due to chronic conditions like analgesic abuse (phenacetin/aspirin), diabetes mellitus, sickle cell T/D, or severe acute pyelonephritis

Key signs:
1. Gross hematuria
2. Flank pain

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32
Q

What condition can lead to renal papillary necrosis as a complication?

A

Acute interstitial nephritis

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33
Q

What is Minimal change disease?

A

Aka Nil disease, its the most common cause of nephrotic syndrome in children. It’s the production of too many cytokines & it causes the effacement of podocytes resulting in selective albuminuria & lipid droplets in the urine.

Signs:
Pitting edema
Hyperlipidemia
Cholesterolemia

It has an excellent response to steroids & its associated with Hodgkin Lymphoma

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34
Q

Nephrotic vs Nephritic syndromes are related to what in the urine &

A

Nephrotic = protein in the urine
1. Minimal change disease
2. Focal segmental glomerulonephritis
3. Diabetic mellitus
4. systemic amyloidosis
5. Membranoproliferative glomerulonephritis
6. membranous nephropathy)

Nephrotic = Blood in the urine
1. Post Streptococcal Glomerulonephritis
2. IgA Nephropathy (Bergers)
3. Alport Syndrome
4. Rapidly progressive glomerulonephritis (Goodpasture’s, Wegner’s, Chrug-strauss, & micro polyangiitis)

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35
Q

Aka Nil disease, its the most common cause of nephrotic syndrome in children. It’s the production of too many cytokines & it causes the effacement of podocytes resulting in selective albuminuria & lipid droplets in the urine.

Signs:
Pitting edema
Hyperlipidemia
Cholesterolemia

It has an excellent response to steroids & its associated with Hodgkin Lymphoma

Describes which condition?

A

Minimal change disease

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36
Q

What are the lab findings seen in minimal change disease?

A
  1. Lipids in the PCT
  2. -ve immunofluorescence
  3. Hypoalbuminemia
  4. Effacement of foot processes
  5. Fatty casts in the urine
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37
Q
  1. Lipids in the PCT
  2. -ve immunofluorescence
  3. Hypoalbuminemia
  4. Effacement of foot processes
  5. Fatty casts in the urine

Are the lab findings of which condition?

A

Minimal change disease

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38
Q

What is focal segmental glomerulonephritis?

A

The most common cause of nephrotic syndrome in Hispanics & African Americans. It’s associated with HIV infection, Heroin use, & sickle cell disease which can progress to chronic renal failure. The lesions can be focal or segmental on H&E staining

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39
Q

The most common cause of nephrotic syndrome in Hispanics & African Americans. It’s associated with HIV infection, Heroin use, & sickle cell disease which can progress to chronic renal failure. The lesions can be focal or segmental on H&E staining

Which condition?

A

Focal segmental glomerulonephritis

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40
Q

Key words:

  1. Focal/segmental lesions
  2. Hispanic & African Americans
  3. Heroine, HIV, SLE, & Sickle cell association
  4. Subepithelial & spike/dome app
A

Membranous nephropathy

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41
Q

What is Diabetic Nephropathy?

A

Elevated serum glucose causes hyaline arteriosclerosis that causes non-enzymatic glycosylation of the blood vessel walls making them more permeable to protein (i.e the proteins leak through) resulting in more glomerular infiltration pressure & hyperinflation which can cause injury & nephrotic syndrome

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42
Q

Elevated serum glucose causes hyaline arteriosclerosis that causes non-enzymatic glycosylation of the blood vessel walls making them more permeable to protein (i.e the proteins leak through) resulting in more glomerular infiltration pressure & hyperinflation which can cause injury & nephrotic syndrome

Formation of Kimmestiel-wilson nodules

Describes which condition?

A

Diabetic nephropathy

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43
Q

What are the lab findings of diabetic nephropathy?

A
  1. Hypoalbuminemia (loss of albumin)
  2. Hyperglycemia
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44
Q

What is used to treat diabetic nephropathy?

A

ACE inhibitors

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45
Q

Hypoalbuminemia & formation of Kimmestiel-wilson nodules are indicative of which condition?

A

Diabetic nephropathy

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46
Q

What is systemic amyloidosis?

A

Amyloid deposits in the mesangium of the kidney that is associated with chromic inflammatory conditions

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47
Q

Amyloid deposits in the mesangium of the kidney that is associated with chromic inflammatory conditions

Describes which condition?

A

Systemic amyloidosis

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48
Q

Amyloidosis deposits are pink amorphous materials in the mesangium of the kidney that show apple-green birefringent under polarized light

A

Systemic amyloidosis

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49
Q

What is membranoproliferative glomerulonephritis?

A

Immune complex deposition in the glomerular basement membrane causing mesangial proliferation giving it a tram-track appearance

Type 1 sub endothelium & type 2 intramembranous both progress to chronic renal failure

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50
Q

Which conditions present with

1.Proteinuria (>3.5 g/day)

2.Hypoalbuminemia (pitting edema)

3.Hypercoagulability (reduced anti thrombin 3)

4.Hyperlipidemia/cholesterolemia (fatty casts in urine)

  1. Hypogammaglobulinemia (inflammation)
A

Nephrotic syndromes:

Minimal change disease

Diabetic nephropathy

Focal/Segmental glomerulonephritis

Systemic amyloidosis

Membranoproliferative glomerulonephritis

Membranous nephropathy

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51
Q

Nephrotic syndromes:

Minimal change disease

Diabetic nephropathy

Focal/Segmental glomerulonephritis

Systemic amyloidosis

Membranoproliferative glomerulonephritis

Membranous nephropathy

All present with which common lab findings?

A

1.Proteinuria (>3.5 g/day)

2.Hypoalbuminemia (pitting edema)

3.Hypercoagulability (reduced anti thrombin 3)

4.Hyperlipidemia/cholesterolemia (fatty casts in urine)

  1. Hypogammaglobulinemia (inflammation)
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52
Q

What is type 1 membranoproliferative glomerulonephritis

A

Type 1 is subendothelial & is associated with HBV & HCV infections

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53
Q

What is type 2 membranoproliferative glomerulonephritis

A

Intramembranous infiltration associated with IgG mediated C3 factor (chemotactic)

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54
Q

Key words:

  1. Affects children (nephropathy)
  2. Mesangial proliferation & tram track appearance
  3. Thickened & splitting basement membrane
  4. Immune complex deposition
A

Membranoproliferative glomerulonephritis

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55
Q

What is membranous nephropathy

A

The most common cause of nephrotic syndrome in white men that is associated by HBV/HCV, SLE, & Malignant cancers.

There is subepithelial immune complex deposition causing thickening glomerular basement membrane with an epi-membranous spike & done appearance

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56
Q

The most common cause of nephrotic syndrome in white men that is associated by HBV/HCV, SLE, & Malignant cancers.

There is subepithelial immune complex deposition causing thickening glomerular basement membrane with an epi-membranous spike & done appearance

A

membranous nephropathy

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57
Q

What is seen of immunofluorescence in membranous nephropathy

A

Granular fluorescence

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58
Q

What is a complication of membranous nephropathy

A

Chronic renal failure

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59
Q

Key words:

  1. Most common nephrotic syndrome in white men
  2. Subepithelial immune complex depositions
  3. Thickened GBM with epimembranous spikes & a dome appearance
  4. Associated with conditions like Hep B/C, SLE, & Malignant cancers
A

Membranous nephropathy

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60
Q

What is cystitis (UTI)? & What are the symptoms?

A

A bladder infection from E.coli (usually)

Signs:
1) Dysuria
2) Increased urinary frequency & urgency
3) Suprapubic pain

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61
Q

A bladder infection from E.coli (usually)

Signs:
1) Dysuria
2) Increased urinary frequency & urgency
3) Suprapubic pain

A

Cystitis

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62
Q

What lab work up would indicate cystitis?

A

1) Cloudy urine with elevated WBC (>10)

2) +ve leukocyte esterase
3) +ve nitrates

4) >100,000 CFU

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63
Q

1) Cloudy urine with elevated WBC (>10)

2) +ve leukocyte esterase
3) +ve nitrates

4) >100,000 CFU

These labs indicate which condition?

A

Cystitis

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64
Q

What are the organisms that can cause a cystitis infection?

A

Number one is E.coli

Others:
K. pneumoniae

Proteus microbilis (alkalinizes the urine to make it smell like pneumonia)

Enterococcus faecalis

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65
Q

What is urethritis & how does it differ from cystitis?

A

It has the same symptoms (dysuria, urine frequency/urgency, & suprapubic pain), but it is caused by C. trachomatis & N. gonorrhea

Labs:
Sterile pyuria (-ve bacterial cultures)

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66
Q

It has the same symptoms (dysuria, urine frequency/urgency, & suprapubic pain), but it is caused by C. trachomatis & N. gonorrhea

Labs:
Sterile pyuria (-ve bacterial cultures)

What type of UTI?

A

Urethritis

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67
Q

What is acute pyelonephritis? & what are the symptoms?

A

Infection of the kidney that ascends causing scarring of the upper/lower poles giving it a staghorn appearance. Acute pyelonephritis is a progression of ascending infections like cystitis caused by E. coli & proteus mirabilis

Signs:
1) Fever & chills
2) Flank pain
3) Costovertebral angle tenderness
4) Dysuria & hematuria

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68
Q

Infection of the kidney that ascends causing scarring of the upper/lower poles giving it a staghorn appearance. It’s a progression of ascending infections like cystitis caused by E. coli & proteus mirabilis

Signs:
1) Fever & chills
2) Flank pain
3) Costovertebral angle tenderness
4) Dysuria & hematuria

A

Acute pyelonephritis

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69
Q

What are the lab findings in acute pyelonephritis?

A

Elevated cysteine (in children)

WBC casts

Leukocytosis

Elevated CRP & ESR

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70
Q

What are risk factors associated with pyelonephritis?

A
  1. Being female (shorter UT)
  2. The vesicoureteral reflex (urine backflow usually in children)
  3. Obstruction (BPH or cervical cancer)
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71
Q
  1. Being female (shorter UT)
  2. The vesicoureteral reflex (urine backflow usually in children)
  3. Obstruction (BPH or cervical cancer)

Are all associated with an increased risk of developing which condition?

A

Pyelonephritis

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72
Q

What is chronic pyelonephritis? What condition is it associated with?

A

It is a complication of recurrent bouts of acute pyelonephritis which leads to interstitial fibrosis & atrophy of the renal tubules. It is associated with all the risk factors for acute pyelonephritis as well as multiple myeloma

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73
Q

It is a complication of recurrent bouts of acute pyelonephritis which leads to interstitial fibrosis, atrophy of the renal tubules, & thyroidization of the kidney. It is associated with all the risk factors for acute pyelonephritis as well as multiple myeloma

A

Chronic pyelonephritis

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74
Q

What are the lab findings in chronic pyelonephritis?

A

1) Blunted calyces/cortical scarring
2) Thyroidization of the kidney
3) Waxy & colloid casts in the urine

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75
Q

Key words:

1) Vesicoureteral reflux
2) Recurrent pyelonephritis
3) Blunted calyces
4) Thyroidization of kidney
5) Waxy & colloid casts

A

chronic pyelonephritis?

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76
Q

What is rapidly progressive glomerular nephritis & what conditions can lead to it?

A

An inflammatory disease of the kidney that rapidly destroys the renal glomeruli & leads to end-stage renal disease.

The conditions that can cause it include good pastures, Microscopic polyangiitis, Churg Strauss syndrome, PSGN, Diffuse proliferative glomerulonephritis, or Wegner’s granulomatosis.

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77
Q

An inflammatory disease of the kidney that rapidly destroys the renal glomeruli & leads to end-stage renal disease.

The conditions that can cause it include good pastures, Microscopic polyangiitis, Churg Strauss syndrome, PSGN, Diffuse proliferative glomerulonephritis, or Wegner’s granulomatosis.

A

Rapidly progressive Glomerulonephritis

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78
Q

What are the symptoms & a key lab finding of glomerulonephritis?

A

Signs:
1) HTN
2) Oliguria
3) Hematuria + RBC casts
4) Edema
5) Azotemia (elevated BUN:CR serum)

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79
Q

Signs:
1) HTN
2) Oliguria
3) Hematuria + RBC casts
4) Edema
5) Azotemia (elevated BUN:CR serum)

A rapidly progressive renal condition

A

Rapidly progressive glomerulonephritis

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80
Q

If you see granular +ve immunofluorescence in rapidly progressive glomerulonephritis the causal condition is likely what?

A

PSGN or Diffuse proliferative glomerulonephritis

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81
Q

If you see linear +ve immunofluorescence in rapidly progressive glomerulonephritis the causal condition is likely what?

A

Good pastures

82
Q

If you see linear -ve immunofluorescence aka pauci glomerulonephritis in rapidly progressive glomerulonephritis the causal condition is likely what?

A

Wegner’s (C-ANCA +ve)

Microscopic polyangiitis (P-ANCA +ve)

Churg Strauss (P-ANCA +ve)

83
Q

What is good pastures?

What are the symptoms?

What is a complication of this condition?

A

It’s antibodies against type IV collagen (A3 chain) in the basement membranes of the glomeruli & alveoli

Signs:
1) Hematuria
2) Hemoptysis
3) +ve linear IF deposition

Complication is rapidly progressive glomerulonephritis

84
Q

It’s antibodies against type IV collagen (A3 chain) in the basement membranes of the glomeruli & alveoli

Signs:
1) Hematuria
2) Hemoptysis
3) +ve linear IF deposition
4) Bowmans space crescents

Complication is rapidly progressive glomerulonephritis

Describes which condition?

A

Good pastures

85
Q

What is Churg-Strauss?

What are the symptoms?

What are the key lab findings?

What is a major complication?

A

A P-ANCA +ve form of granulomatous inflammation divided into phases prodromal, eosinophilic, & vasculitic

Signs:
1) Prodromal (Asthma/allergic asthmatic reactions)

2) Eosinophilic (Pericarditis & Gi inv)

3) Vasculitic (Cutaneous lesions & palpable purpura)

Labs:
1) Bowmans space crescents
2) -ve IF deposition (Pauci GN)
3) Eosinophilia
4) Elevated IgEs

A complication is RPGN

86
Q

A P-ANCA +ve form of granulomatous inflammation divided into phases prodromal, eosinophilic, & vasculitic

Signs:
1) Prodromal (Asthma/allergic asthmatic reactions)

2) Eosinophilic (Pericarditis & Gi inv)

3) Vasculitic (Cutaneous lesions & palpable purpura)

Labs:
1) Bowmans space crescents
2) -ve IF deposition (Pauci GN)
3) Eosinophilia
4) Elevated IgEs

A complication is RPGN

A

Churg-Strauss syndrome

87
Q

What is Microscopic polyangiitis?

What are the symptoms?

What are the key lab findings?

What is a major complication?

A

P-ANCA +ve granulomatous inflammation affecting the lungs, kidneys, & skin

Signs:
1) Hemoptysis
2) Palpable purpura
3) HTN

Labs:
1. Bowman space crescents
2. -ve IF (Pauci’s GN)

A complication is RPGN

88
Q

P-ANCA +ve granulomatous inflammation affecting the lungs, kidneys, & skin

Signs:
1) Hemoptysis
2) Palpable purpura
3) HTN

Labs:
1. Bowman space crescents
2. -ve IF (Pauci’s GN)

A complication is RPGN

A

Microscopic polyangiitis

89
Q

What is Diffuse proliferative glomerulonephritis?

What are the key lab findings?

What is a major complication?

A

Diffuse antigen-antibody complex deposition in the subENDOthelial layers of tissues, that is very associated with SLE

Labs:
1. Bowman crescents
2. +ve granular deposition on IF

A complication is RPGN

90
Q

What is PSGN?

What are the symptoms?

What are the key lab findings?

What is a major complication?

A

Immune complex deposition in the glomerular basement membrane triggering complement activation & tissue damage after an infection with group A B-hemolytic strep (impetigo or strep throat)

Signs:
1. Hematuria
2. Azotemia (elevated BUN:CR)
3. HTN
4. Periorbital edema
5. Oliguria

Labs:
1) Bowman crescents (fibrin & macrophages)
2) Hypercellular & inflamed glomeruli
3) SubEPIthelial humps (a lumpy bumpy appearance)
4) +ve granular IF

Comp: RPGN

91
Q

Immune complex deposition in the glomerular basement membrane triggering complement activation & tissue damage after an infection with group A B-hemolytic strep (impetigo or strep throat)

Signs:
1. Hematuria
2. Azotemia (elevated BUN:CR)
3. HTN
4. Periorbital edema
5. Oliguria

Labs:
1) Bowman crescents (fibrin & macrophages)
2) Hypercellular & inflamed glomeruli
3) SubEPIthelial humps (a lumpy bumpy appearance)
4) +ve granular IF

Comp: RPGN

A

PSGN

92
Q

How does glomerular damage lead to edema & hyperlipidemia/cholesterolemia?

A

The edema comes from protein loss (i.e albumin & others) the hyperlipidemia/cholesterolemia comes from the liver making more lipoproteins to try to compensate for the proteins lost in the urine

93
Q

What is nephrolithiasis?

What are the symptoms?

What are the types of stones seen?

A

kidney stones that form when there is low urine volume output or high solute concentrations

Signs:
1) Colicky pain
2) Hematuria
3) Periumbilical & flank pain

Stone types:

Calcium oxalate or phosphate (most common)

Ammonium, magnesium, or phosphate (infection)

Cysteine (rare & in children)

94
Q

kidney stones that form when there is low urine volume output or high solute concentrations

Signs:
1) Colicky pain
2) Hematuria
3) Periumbilical & flank pain

Stone types:

Calcium oxalate or phosphate (most common)

Ammonium, magnesium, or phosphate (infection)

Cysteine (rare & in children)

A

Nephrolithiasis

95
Q

Nephrolithiasis:

What condition is associated with the formation of cysteine stones in children? How do you treat them?

A

Cysteine stones are associated with cystinuria a genetic tubule defect with impaired cysteine resorption & the tendency to form staghorn in the kidney

Rx: Hydration & alkalinize the urine

96
Q

Nephrolithiasis:

Which conditions are associated with the formation of uric acid stones? What is the treatment?

A

Conditions like Gout or hyperuricemia (i.e leukemia or myeloproliferative disease) tend to form uric kidney stones

They can be treated with hydration & by alkalinizing the urine

97
Q

Nephrolithiasis:

Which conditions are associated with the formation of calcium oxalate or phosphate stones? What is the treatment?

A

The formation is either idiopathic or from states of hypercalcemia/hypercalciuria.

It could be associated with Crohn’s or indicate acute tubular necrosis syndrome or consumption of ethylene glycol

Treat them by giving a ca2+ sparring diuretic like hydrochlorothiazide

98
Q

Nephrolithiasis:

Which conditions are associated with the formation of ammonium, magnesium, & phosphate stones? What is the treatment?

A

They’re usually due to infections with urease +ve organisms (inflammation) via klebsiella or proteus vulgaris because they tend to alkalinize the urine causing staghorn calculi that are a niche for UTIs

99
Q

What is chronic renal failure & what conditions can lead to it?

What are the symptoms?

What are the lab findings?

What does it predispose to?

A

Long-standing pressure on the kidney from conditions like diabetes, HTN, & glomerular disease cause them be become shrunken (atrophy) & cystic

Signs:
1) Encephalopathy (waste in the blood)
2) HTN
3) Anemia (low EPO)
4) Edema (protein loss)
5) Osteodystrophy
6) Secondary hyperparathyroidism + osteoporosis
7) Asterixis
8) Platelet dysfunction

Labs:
Uremia (high nitrates)
Azotemia (high BUN:CR)
Metabolic acidosis
Hypercalcemia/phosphatemia/kalemia

High risk of progressing to Renal cell carcinoma!!

100
Q

What complication does chronic renal failure often lead to ?

A

Renal cell carcinoma

101
Q

Long-standing pressure on the kidney from conditions like diabetes, HTN, & glomerular disease cause them be become shrunken (atrophy) & cystic

Signs:
1) Encephalopathy (waste in the blood)
2) HTN
3) Anemia (low EPO)
4) Edema (protein loss)
5) Osteodystrophy
6) Secondary hyperparathyroidism + osteoporosis
7) Asterixis
8) Platelet dysfunction

Labs:
Uremia (high nitrates)
Azotemia (high BUN:CR)
Metabolic acidosis
Hypercalcemia/phosphatemia/kalemia

High risk of progressing to Renal cell carcinoma!!

A

Chronic renal failure

102
Q

Signs:
1) Encephalopathy (waste in the blood)
2) HTN
3) Anemia (low EPO)
4) Edema (protein loss)
5) Osteodystrophy
6) Secondary hyperparathyroidism + osteoporosis
7) Asterixis
8) Platelet dysfunction

Labs:
Uremia (high nitrates)
Azotemia (high BUN:CR)
Metabolic acidosis
Hypercalcemia/phosphatemia/kalemia

All indicate which condition?

A

Chronic renal failure

103
Q

What is a angiomyolipoma?

A

A benign hamartoma (made up of blood vessels, smooth muscle, & fat) that is very common in tuberous sclerosis

104
Q

What is hereditary renal cell carcinoma, papillary type?

A

A MET oncogene mutation that results in altered papillae tissue & psammoma bodies

105
Q

What is renal cell carcinoma?
- What are its subtypes?

What are the symptoms?

A

A malignant epithelial tumor of the tubules caused by genetic defects in tumor suppressor genes (VHL), growth (IGF-1) & transcription (HIF) factors. It can be either sporadic or hereditary.

1) Sporadic type is more common in older men (~60yrs) who smoke, it’s a single tumor in the upper pole of the kidney
- Clear cell
- Papillary
- Chromophobe

2) Hereditary type is more common in young adults & is associated with genetic conditions

Signs:
1) Triad (Hematuria, Palpable mass, & flank pain (never at the same time))
2) Fever
3) Weigt loss
4) Left varicocele (rare)
5) Large yellowish mass

106
Q

A malignant epithelial tumor of the tubules caused by genetic defects in tumor suppressor genes (VHL), growth (IGF-1) & transcription (HIF) factors. It can be either sporadic or hereditary.

1) Sporadic type is more common in older men (~60yrs) who smoke, it’s a single tumor in the upper pole of the kidney
- Clear cell
- Papillary
- Chromophobe

2) Hereditary type is more common in young adults & is associated with genetic conditions

Signs:
1) Triad (Hematuria, Palpable mass, & flank pain (never at the same time))
2) Fever
3) Weigt loss
4) Left varicocele (rare)
5) Large yellowish mass

A

Renal cell carcinoma

107
Q

What is the sporadic type renal cell carcinoma?

A

1) Sporadic type is more common in older men (~60yrs) who smoke, it’s a single tumor in the upper pole of the kidney

108
Q

common in older men (~60yrs) who smoke, it’s a single tumor in the upper pole of the kidney

A

Sporadic type RCC

109
Q

What is the sporadic clear cell type RCC

A

clear cell type is associated with a VHL mutation or pseudohypoxia that affects the PCT it has a higher risk of hemangioblastomas in the cerebellum or further RCC

110
Q

What is the sporadic papillary type RCC?

A

Papillary type is associated with MET oncogene mutations casing the formation of psammomas bodies in the renal papillae.

111
Q

What is the sporadic chromophobe type RCC?

A

Chromophobe RCC causes pale eosinophils in cells lining the DCT it is associated with mitochondrial mutations & TP53 mutations

112
Q

What is a Wilms tumor?

What are some conditions that can lead to it?

What are it’s symptoms?

A

A malignant tumor of the kidney made from blastema (immature mesenchyme) & Primitive glomeruli/tubular stroma. It’s usually seen in children under 5yrs old and is associated with the following condition:

  1. WAGR
  2. Denys-Drash
  3. Beckwith-Wiedemann

Signs:
1) A large unilateral flank mass
2) Hematuria
3) HTN (high renin)

113
Q

A malignant tumor of the kidney made from blastema (immature mesenchyme) & Primitive glomeruli/tubular stroma. It’s usually seen in children under 5yrs old and is associated with the following condition:

  1. WAGR
  2. Denys-Drash
  3. Beckwith-Wiedemann

Signs:
1) A large unilateral flank mass
2) Hematuria
3) HTN (high renin)

A

Wilms tumor

114
Q

What is WAGR syndrome & what is a potential complication?

A

Due to a deleted WT1 gene (11p13)

Wilms tumor
Aniridia
Genitourinary abnormalities
Retardation (motor/mental)

Risk of metastasizing to the lungs

115
Q

What is Denys-Drash syndrome?

A

A mutated WT1 gene:

Male pseudo hermaphroditism

Progressive glomeruli disease (diffuse mesangial sclerosis)

Wilms tumor

116
Q

What is Beckwith-Weidmann syndrome?

A

Mutated WT2 clusters on (11p15.5) causing dysfunctional IGF1 (growth factor):

Organomegaly/macroglossia
Muscular hemihypertrophy
Neonatal hypoglycemia
Wilms tumor

“WOMMaN”

117
Q

What is an oncocytoma?

A

A benign tumor with increased levels of mitochondria & mahogany brown central hyaline scarring on microscopy

118
Q

What is transitional cell carcinoma?

A

Aka urothelial cell carcinoma, a malignant cancer of the lining of the bladder, renal pelvis, & urethra. Usually appearing in older adults as either flat (high grade malignancy) or papillary (low grade malignancy). These tumors are multifocal and tend to reoccur (field defect)

119
Q

Aka urothelial cell carcinoma, a malignant cancer of the lining of the bladder, renal pelvis, & urethra. Usually appearing in older adults as either flat (high grade malignancy) or papillary (low grade malignancy). These tumors are multifocal and tend to reoccur (field defect)

A

Transitional cell carcinoma

120
Q

What is a flat transitional/urothelial cell cancer?

A

A high-grade malignant cancer that invades surrounding tissue right away because of its early P53 mutations

121
Q

A high-grade malignant cancer that invades surrounding tissue right away because of its early P53 mutations (usually affects the bladder, renal pelvis, or urethra)

A

flat transitional/urothelial cell cancer

122
Q

What is a papillary transitional/urothelial cell cancer?

A

Low-grade malignancy that needs to progress to high-grade before invading any other tissues.

123
Q

Low-grade malignancy that needs to progress to high-grade before invading any other tissues. (usually affects the bladder, renal pelvis, or urethra)

A

papillary transitional/urothelial cell cancer?

124
Q

What is the sign of transitional cell carcinoma of the bladder (aka bladder cancer)?

What part of the bladder is likely affected?

What is the number one risk factor?

A

Painless hematuria

Lateral wall near the trigone

Smoking

125
Q

Naphythylamine exposure, Azodyes, long term cyclophosphamide or phenacetine use are all associated with which type of cancer?

A

Transitional cell caner of the bladder/renal pelvis, or urethra

126
Q

What is squamous cell cancer of the lower urinary tract?

What causes?

A

Malignant proliferation aka squamous metaplasia of the bladder, renal pelvis or urethra due to consistent stress/trauma

Causes:
1. Chronic cystitis (seen in older women)
2. Schistosomiasis (Egyptian men)
3. Long-term nephrolithiasis

127
Q

Malignant proliferation aka squamous metaplasia of the bladder, renal pelvis or urethra due to consistent stress/trauma

Causes:
1. Chronic cystitis (seen in older women)
2. Schistosomiasis (Egyptian men)
3. Long-term nephrolithiasis

A

Squamous cell carcinoma of the lower urinary tract

128
Q

What is adenocarcinoma of the lower urinary tract?

What causes it?

A

It is malignant proliferation of the glands involving the bladder. It can arise from

1) urachal remnants as a cyst like tumor in the dome of the bladder

or

2) From cystitis granularize or exstrophy of the bladder (when the anterior wall of the bladder fail to form)

129
Q

It is malignant proliferation of the glands involving the bladder. It can arise from

1) urachal remnants as a cyst like tumor in the dome of the bladder

or

2) From cystitis granularize or exstrophy of the bladder (when the anterior wall of the bladder fail to form)

A

Adenocarcinoma of the bladder

130
Q

What is squamous cell carcinoma of the penis?
- What are it’s precursors?

What are the major risk factors of this condition?

A

Malignant proliferation from in situ precursor lesions such as Bowen disease, Erythroplakia of Queyrat, & Bowenoid papulosis

Risk factors:
#1 HPV infection
Uncircumcision (site for inflammation)

131
Q

Malignant proliferation from in situ precursor lesions such as Bowen disease, Erythroplakia of Queyrat, & Bowenoid papulosis

Risk factors:
#1 HPV infection
Uncircumcision (site for inflammation)

A

squamous cell carcinoma of the penis

132
Q

How is Bowen disease a precursor for penile squamous cell carcinoma?

A

carcinoma of the shaft & scrotum presenting as leukoplakia

133
Q

How is Erythroplakia of Queyrat a precursor for penile squamous cell carcinoma?

A

(in situ carcinoma on the glans that presents as erythroplakia)

134
Q

How is Bowenoid papulosis a precursor for penile squamous cell carcinoma?

A

(an in situ carcinoma that presents as multiple reddish papules, seen in younger patients (40yrs) that don’t usually progress to invasive carcinoma)

135
Q

What is condyloma Acuminatum?

A

A benign watery growth on the genital skin from an HPV 6/11 infection. It’s characterized by Koilocytic change

136
Q

A benign watery growth on the genital skin from an HPV 6/11 infection. It’s characterized by Koilocytic change

A

condyloma Acuminatum?

137
Q

What is a lymphogranuloma venereum?

What causes it?

What are its complications?

A

Necrotizing granulomatous inflammation of the inguinal lymphatics & LN that heals over with fibrosis. It’s caused by C. Trachomatis (L1-3)

Complications include:
Rectal Strictures

138
Q

Necrotizing granulomatous inflammation of the inguinal lymphatics & LN that heals over with fibrosis. It’s caused by C. Trachomatis (L1-3)

Complications include:
Rectal Strictures

A
139
Q

What are hypospadias?

A

A congenital opening on the underside of the urethra because the urothelial folds failed to close

140
Q

What are epispadias?

A

A congenital opening on the upper side of the urethra because the genital tubercles were positioned abnormally during development it’s associated with bladder exstrophy

141
Q

A congenital opening on the upper side of the urethra because the genital tubercles were positioned abnormally during development it’s associated with bladder exstrophy

A

epispadias

142
Q

A congenital opening on the underside of the urethra because the urothelial folds failed to close

A

hypospadias

143
Q

What is a seminoma?

A

A germ cell tumor that is typically malignant but has a very good prognosis as it is radiosensitive & slow to metastasize

Labs will show
A painless testicular lump with large cells with clear cytoplasm without hemorrhage or necrosis

144
Q

A germ cell tumor that is typically malignant but has a very good prognosis as it is radiosensitive & slow to metastasize

Labs will show
A painless testicular lump with large cells with clear cytoplasm without hemorrhage or necrosis

A

seminoma

145
Q

What is a teratoma?

A

A tumor that is usually benign except in men, its made of mature fetal tissue that’s derived from 2-3 embryonic layers giving it things like teeth, hair, & skin

Labs:
Elevated AFP & B-hcG

Non-seminoma germ cell tumor

146
Q

List the non-seminoma Germ cell tumors?

A
147
Q

A tumor that is usually benign except in men, its made of mature fetal tissue that’s derived from 2-3 embryonic layers giving it things like teeth, hair, & skin

Labs:
Elevated AFP & B-hcG

Non-seminoma germ cell tumor

A

Teratoma

148
Q

What is an embryological carcinoma?

A

An aggressively malignant tumor with early hematogenous spread. It’s made of primitive glandular cells & forms a hemorrhagic mass with necrosis.

Labs:
Elevated AFP & B-hcG

Non-seminoma germ cell tumor

149
Q

An aggressively malignant tumor with early hematogenous spread. It’s made of primitive glandular cells & forms a hemorrhagic mass with necrosis.

Labs:
Elevated AFP & B-hcG

Non-seminoma germ cell tumor

A

embryological carcinoma

150
Q

What is a yolk sac tumor?

A

A malignant tumor more common in children it looks like a yolk-sac & has Schiller-Duval bodies (look like glomeruli)

Labs: Elevated AFP

151
Q

A malignant tumor more common in children it looks like a yolk-sac & has Schiller-Duval bodies (look like glomeruli)

Labs: Elevated AFP

A

yolk sac tumor

152
Q

What is a choriocarcinoma (testes)?

A

The most aggressive & malignant tumor it’s made up of syncytiotrophoblastic & cytotrophoblast multinucleated giant cells (placenta-like tissues) that spreads early through the blood

Labs: Elevated B-hcG

Complications can be hyperthyroidism & gynecomastia

153
Q

The most aggressive & malignant tumor it’s made up of syncytiotrophoblastic & cytotrophoblast multinucleated giant cells (placenta-like tissues) that spreads early through the blood

Labs: Elevated B-hcG

Complications can be hyperthyroidism & gynecomastia

A

choriocarcinoma

154
Q

What are two main risk factors for developing germ cell tumors?

A

Cryptorchidism & Klinefelter syndrome

155
Q

What is a mixed germ cell tumor?

A

A mix of seminoma & non seminoma that is always treated as a non-seminoma a. It is a mass with hemorrhage, and necrosis

156
Q

A mix of seminoma & non seminoma that is always treated as a non-seminoma a. It is a mass with hemorrhage, and necrosis

A

mixed germ cell tumor

157
Q

What is a Leydig cell tumor?

A

A Rare tumor that comes from leydig cells causing more production of testosterone. They usually develop after 4yrs old & are very rarely malignant

Labs:
They are golden brown in color with Reinke crystals on histology

158
Q

A Rare tumor that comes from leydig cells causing more production of testosterone. They usually develop after 4yrs old & are very rarely malignant

Labs:
They are golden brown in color with Reinke crystals on histology

A

Leydig cell tumor

159
Q

What is a Sertoli cell tumor?

A

a rare tumor made of Sertoli cells
that makes more estrogen and lead to gynecomastia in affected men

160
Q

a rare tumor made of Sertoli cells
that makes more estrogen and lead to gynecomastia in affected men

A

Sertoli tumor

161
Q

What is a lymphoma?

A

A very common testicular tumor in men over 60yrs. It tends to be bilateral & is made of diffuse B cells

162
Q

Where do testicular tumors spread to ?

A

Testicular tumors drain into the para-aortic (lumbar Ln) first then the mediastinal & supraclavicular LN)

163
Q

What is cryptorchidism?

What are the potential complications?

A

When the testes fail to descend into the scrotum (either resolves on its own or needs an orchidectomy)

Complications include:
Testicular atrophy & infertility
Higher risk of seminomas

164
Q

When the testes fail to descend into the scrotum (either resolves on its own or needs an orchidectomy)

Complications include:
Testicular atrophy & infertility
Higher risk of seminomas

A

Cryptorchidism

165
Q

What is orchitis?

A

Inflammation of the testicles usually caused by infection from C. trachomatis & N. gonorrhea (in young adults) & E.coli & pseudomonas (In older adults)

166
Q

What are the two other ways someone can experience orchitis not due to infection?

A

MUMPS virus (teens) & Autoimmune orchitis (granulomas of the seminiferous tubules)

167
Q

Inflammation of the testicles usually caused by infection from C. trachomatis & N. gonorrhea (in young adults) & E.coli & pseudomonas (In older adults)

A

Orchitis

168
Q

What is varicocele?

What condition is it associated with?

What are the signs?

A

Dilation of the spermatic veins giving it a bag of worm’s appearance due to reduced drainage

Associated with left sided renal cell carcinoma & infertility.

Signs:
1) Scrotal swelling
2) Bag of worm’s appearance

169
Q

Why does a varicocele appear on the left side?

A

Because the right testicle drains into the IMA whereas the left drains into the left renal vein where the RCC can spread to

170
Q

Dilation of the spermatic veins giving it a bag of worms appearance due to reduced drainage

Associated with left sided renal cell carcinoma & infertility

Signs:
1) Scrotal swelling
2) Bag of worms appearance

A

Varicocele

171
Q

What is testicular torsion?

What are the causes?

What are the symptoms?

A

Usually in adolescents it’s twisting of the spermatocord that causes vein obstruction causing congestion & hemorrhagic infarction.

Causes:
Congenital failure of the testes to attach to the processes vaginalis

Signs:
1) Sudden testicular pain
2) Absent cremasteric reflex
3) Negative Prehn sign

172
Q

Usually in adolescents it’s twisting of the spermatocord that causes vein obstruction causing congestion & hemorrhagic infarction.

Causes:
Congenital failure of the testes to attach to the processes vaginalis

Signs:
1) Sudden testicular pain
2) Absent cremasteric reflex

A

Testicular torsion

173
Q

What is a hydrocele?

A

Fluid that collects in the tunica vaginalis, scrotal swelling that can be transilluminated

Caused by incomplete closure of the processus vaginalis

(causes a connection between the peritoneal cavity & the tunica vaginalis or blocked LN drainage in adults)

174
Q

Fluid that collects in the tunica vaginalis

Caused by incomplete closure of the processus vaginalis (causes a connection between the peritoneal cavity & the tunica vaginalis or blocked LN drainage in adults)

A

Hydrocele

175
Q

What is acute prostatitis?

A

Acute inflammation from a bacterial infection like E.coli & pseudomonas (older) & c.trachomatis & N. gonorrhea (younger)

Signs:
1) Dysuria
2) Fever & chills
3) Tender & boggy testes prostate on DRE

Labs:
WBC in prostatic secretions with +ve bacterial culture

176
Q

Acute inflammation from a bacterial infection like E.coli & pseudomonas (older) & c.trachomatis & N. gonorrhea (younger)

Signs:
1) Dysuria
2) Fever & chills
3) Tender & boggy testes prostate on DRE

Labs:
WBC in prostatic secretions with +ve bacterial culture

A

Acute prostatitis

177
Q

What is chronic prostatitis?

A

Chronic inflammation that’s not from infection

Signs:
1) Dysuria
2) Pelvic & lower back pain

Labs:
WBCs in the prostatic secretions with -ve bacterial cultures

178
Q

Chronic inflammation that’s not from infection

Signs:
1) Dysuria
2) Pelvic & lower back pain

Labs:
WBCs in the prostatic secretions with -ve bacterial cultures

A

Chronic prostatitis

179
Q

What is BPH?

What are the causes?

What are the symptoms?

A

Hyperplasia of the stroma & glands in the periurethral zone

causes:
1. old age
2. Increase in DHT (via 5 alpha reductase to increase the conversion of dihydrotestosterone in the stromal cells which act on androgen receptors causing hyperplasia)

Signs:
1) Difficulty starting/stopping a urine stream
2) Urine retention
3) Dribbling urine

180
Q

Hyperplasia of the stroma & glands in the periurethral zone

causes:
1. old age
2. Increase in DHT (via 5 alpha reductase to increase the conversion of dihydrotestosterone in the stromal cells which act on androgen receptors causing hyperplasia)

Signs:
1) Difficulty starting/stopping a urine stream
2) Urine retention
3) Dribbling urine

A

BPH

181
Q

What are the complications of BPH?

A

Risk on infection
Hydronephrosis
Bladder diverticula

182
Q

Risk on infection
Hydronephrosis
Bladder diverticula

Are complication of which condition?

A

BPH

183
Q

What are the lab findings of BPH?

A

Microscopic hematuria
Slightly elevated PSA (<10ng/day)

184
Q

Microscopic hematuria
Slightly elevated PSA (<10ng/day)
& difficulty starting/stopping urine

Is indicative of which condition?

A

BPH

185
Q

How would you treat BPH?

A

Alpha 1 antagonist (terazosin)
Selective alpa1 antagonist (tamsulosin)
5 alpha reductase inhibitors

186
Q

What is prostate adenocarcinoma?

A

Malignant proliferation of the prostate that arises in the peripheral & posterior region of the prostate

Labs:
PSA >10
Reduced free PSA
Palpation on DRE

Biopsy shows small invasive glands with prominent nucleoli

187
Q

Increased age (50+yrs), race (Afro Americans>white>Asians)
High saturated fat diet are all risk factors for which condition?

A

Prostate adenocarcinoma

188
Q

Malignant proliferation of the prostate that arises in the peripheral & posterior region of the prostate

Labs:
PSA >10
Reduced free PSA
Palpation on DRE

Biopsy shows small invasive glands with prominent nucleoli

A

Prostate adenocarcinoma

189
Q

What are the complications of prostatic carcinoma?

A

Osteoblastic metastases to the lower spine
(Lower back pain)
High serum alkaline phosphatase
High PSA & PAP

190
Q

Osteoblastic metastases to the lower spine
(Lower back pain)
High serum alkaline phosphatase
High PSA & PAP

Are all complications of which condition?

A

Prostatic adenocarcinoma

191
Q

What is acute pancreatitis?

A

Inflammation & hemorrhaging of pancreas due to autodigestion from prematurely activated enzyme trypsin which activates other pancreatic enzymes caused by alcohol & gallstones

Signs:
1) Grey turners (ecchymosis flank)
2) Cullen sign (ecchymosis umbilicus)
3) epigastric pain radiating to the back

192
Q

Inflammation & hemorrhaging of pancreas due to autodigestion from prematurely activated enzyme trypsin which activates other pancreatic enzymes caused by alcohol & gallstones

Signs:
1) Grey turners (ecchymosis flank)
2) Cullen sign (ecchymosis umbilicus)
3) epigastric pain radiating to the back

A

Acute pancreatitis

193
Q

What is MEN1?

A

Pituitary tumor
Parathyroid tumor
Pancreatic tumor

194
Q

Pituitary tumor
Parathyroid tumor
Pancreatic tumor

Describes which condition?

A

MEN1

195
Q

What is the MEN2 Type A tumor?

A

Due to RET oncogene mutations causing:

Parathyroid tumor
Pheochromocytoma
Medullary thyroid carcinoma

196
Q

Due to RET oncogene mutations causing:

Parathyroid tumor
Pheochromocytoma
Medullary thyroid carcinoma

A

MEN2 A

197
Q

What is the MEN2 Type B?

A

Mucosal neuromas
Pheochromocytomas
Medullary thyroid carcinoma
Marfan habitus

198
Q

Mucosal neuromas
Pheochromocytomas
Medullary thyroid carcinoma
Marfan habitus

A

MEN2B

199
Q

What is a glucagonoma?

What are the signs?

How do you treat it?

A

An aloha cell tumor that causes anemia, diabetes with mild hyperglycemia, & necrolytic migratory erythema

Treat it with octreotide

200
Q

An aloha cell tumor that causes anemia, diabetes with mild hyperglycemia, & necrolytic migratory erythema

Treat it with octreotide

A

Glucagonoma tumor

USMLE Pathoma (20 decks)

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