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MS3 > Internal Med 9 > Flashcards

Internal Med 9 Flashcards

1
Q

What are the general principles of nephritic syndrome

A
  • Proteinuria < 3.5 g/day
  • Hematuria and RBC casts
  • Azotemia – increased serum BUN and Creatine
  • Hypertension – salt retention with periorbital edema
  • Oliguria
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2
Q

What are the different nephritic syndrome

A
  • PSGN
  • IgA nephropathy
  • Alport syndrome
  • Rapidly progressive (crescentic) glomerulonephritis
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3
Q

What will you see in biopsy in PSGN

A

♣ Hypercellular glomeruli
♣ Neutrophils
♣ EM: Immune deposits – subepithelial humps
♣ IF: “starry sky” granular appearance (“lumpy bumpy”)

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4
Q

What lab value might indicate PSGN

A

♣ Decreased C3 levels (complement is activated and used up)

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5
Q

Describe Henoch Schonlein purpura and what renal disease it is associated with

A

♣ Palpable purpura on butt and legs
♣ Arthralgias
♣ Abdominal pain
♣ Renal disease - IgA nephropathy

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6
Q

What will you see on biopsy in IgA nephropathy

A

♣ IgA immune complex deposited in mesangium

♣ Proliferation of mesangial cells

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7
Q

Describe Alport syndrome

A

o Due to defect in Type IV collagen (basement membrane)
- Leads to splitting of the basement membrane longitudinally

o Presents as isolated hematuria, sensory hearing loss, and ocular disturbances
♣ “Can’t see, can’t pee, can’t hear high C”

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8
Q

What are the 4 causes of rapidly progressive (crescentic) glomerulonephritis

A
  • Goodpastures
  • Granulomatosis with polyangiitis (Wegener’s)
  • Microscopic polyangiitis
  • Diffuse proliferative glomerulonephritis
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9
Q

Describe Goodpasture’s syndrome

A

• Type II HSR – antibodies against glomerular basement membrane
o Deposits comprised of IgG and C3
• Linear IF pattern
• Affects kidneys and the lungs (alveolar basement membrane)
• Presents as hematuria + hemoptysis

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10
Q

Describe Granulomatosis with polyangiitis

A

Wegener’s
• Affects kidney, lungs, and upper airway
• c-ANCA
• Negative IF

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11
Q

What is the most common kidney disease in lupus

A

Diffuse proliferative glomerulonephritis

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12
Q

Describe DPGN

A

• Anti-dsDNA seen subendothelially and within mesangium
• Granular IF
• Light microscopy – deposits make basement membrane look thick – “wire looping” of capillaries
o THINK: wire lupus
• Often presents as nephrotic + nephritic syndrome

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13
Q

Describe general principles of nephrotic syndrome

A
  • Proteinuria > 3.5 g/day
  • Hypoalbuminemia – protein lost in urine
  • Edema – decreased oncotic pressure due to hypoalbuminemia
  • Increased risk of infection – loss of immunoglobulin in urine
  • Increased risk of thrombosis – loss of antithrombin III
  • Hyperlipidemia – liver tries to make more lipoproteins in order to make up for decreased oncotic pressure
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14
Q

What are the subtypes of nephrotic syndrome

A

Foot process effacement

  • Minimal change disease
  • focal segmental glomerulosclerosis

Thickening of basement membrane:

  • membranous nephropathy
  • membranoproliferative glomerulonephritis

Other

  • Diabetic nephropathy
  • Amyloidosis
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15
Q

Describe minimal change disease

A

♣ H&E – normal
♣ EM – foot process effacement
♣ IF – negative

o Most common cause of nephrotic syndrome in children
o Triggered by infections or immunizations
o Treatment – steroids

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16
Q

Describe FSGS

A

♣ H&E – focal (affects some glomeruli), segmental (affects part of glomerulus)
♣ EM – foot process effacement
♣ IF – negative
o Poor response to steroids

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17
Q

Describe membranous nephropathy

A

o This is the nephrotic presentation of SLE
o Biopsy:
♣ H&E – thickening of basement membrane
♣ EM – “spike and dome” appearance with subepithelial deposits (IgG and C3)
♣ IF – granular

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18
Q

Describe membranoproliferative glomerulonephritis

A

• H&E – thick basement membrane with “tram track” appearance
o Due to mesangium proliferating between the basement membrane
o THINK: membranoproliferative = membrane proliferating = 2 membranes
• EM – subendothelial deposits
• IF – granular

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19
Q

Common causes of membranoproliferative glomerulonephritis

A

♣ Hepatitis B
♣ Hepatitis C
♣ Lupus
♣ Subacute bacterial endocarditis

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20
Q

Biopsy of diabetic nephropathy

A

o Non-enzymatic glycosylation of basement membrane

o Will show sclerosing of the mesangium with Kimmelstien-Wilson nodules (round acellular nodules)

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21
Q

Describe kidney biopsy of amyloidosis

A

o Deposits within the mesangium

o Characterized by apple-green birefringence on Congo red staining

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22
Q

What chromosome is involved in CML

A

o t(9;22) – Philedalphia chromosome
♣ THINK: Carry Mai, Lord, because she is able
• Mai’s birthday is 9/22
• BCR-ABL (because she is able)

23
Q

What will you see in platelets and RBCs in acute leukemia

A

o Often associated with pancytopenia

♣ Blasts “crowd out” normal hematopoiesis

24
Q

Presentation of acute leukemias

A
  • Anemia = low RBC
  • Infection/fever = no good WBC
  • Bleeding = low platelets
25
Q

How do you officially diagnose leukemias

A

Bone marrow biopsy

26
Q

Describe characteristics of AML

A

When you think AML, think “All my life” = musicals
o Sound of music = Auer sounds like Fuer (Hitler) – for auer rods
o I am 16 going on 17 (15;17)
o Poke Hitler in the eye with a carrot – treat with retinoic acid

27
Q

Risk factors associated with AML

A

o Chemotherapy, radiation, myelodysplastic syndrome, Down syndrome

28
Q

What positive marker will you see in ALL

A

TdT+

29
Q

What positive marker will you see in AML

A

MPO+

30
Q

What leukemia occurs mostly in kids

A

ALL

31
Q

Tx of ALL

A

Chemo with prophylaxis of CNS

32
Q

Tx of CML

A

Responds to Imatinib (bcr-able tyrosine kinase inhibitor)

33
Q

Which leukemia do you have to worry about progression

A

CML may progress to AML (80%) or ALL (20%)

34
Q

Tx of CLL

A 
o	Young = stem cell transplant
o	Old (>65) and symptomatic = chemo
o	Old (>65) and asymptomatic = nothing
35
Q

Next step in management of non-tender lymphadenopathy

A
  • This most likely means cancer! Either lymphoma or met
  • Inflammatory lymph node would be usually be painful

So you you do an excisional biopsy!!

Do not choose FNA

36
Q

What will you see on biopsy of Hodgkin lymphoma

A

Reed-Sternberg cells
♣ Large cells with multiple/bi-lobed nuclei with clearing around the nuclei (“owl-eye”)
♣ RS cells are CD15+ and CD30+
• THINK: 2 owl eyes x 15 = 30

37
Q

Which lymphoma has a better prognosis?

A

Hodgkin

38
Q

Which lymphoma presents with B-symptoms

A

Hodgkin

39
Q

What is a unique signature feature of Hodgkin lymphoma

A

Alcohol lymph nodes - lymph nodes become painful when pt drinks alcohol

40
Q

Burkitt lymphoma is a subtype of what?

A

Non-Hodgkin

41
Q

What chromosomes are involved in Burkitt

A 
o	t(8;14)  c-myc (8) and heavy chain Ig (14)
♣	THINK: “B” in Burkitt = 8 and “tt” = 14
42
Q

What are the ears in chemo man

A

C = Cisplatin and Carboplatin = ototoxicity

43
Q

What is the heart in chemo man

A

D = doxorubicin = cardiotoxicity

44
Q

What are the lungs in chemo man

A

B = bleomycin = pulmonary fibrosis

45
Q

What are the limbs in chemo man

A

V = Vincristine = peripheral neuropathy

46
Q

What is the bladder in chemo man

A

C = Cyclophosphamide = hemorrhagic cystitis

47
Q

What are the bones in chemo man

A 
M = methotrexate
5 = 5-FU
6 = 6-MP

All cause myelosuppression

48
Q

What is multiple myeloma

A

♣ Malignant proliferation of monoclonal plasma cell within the marrow
• Recall: Plasma cells = mature B-cells that produce immunoglobulin

49
Q

Describe clinical presentation of multiple myeloma

A 
•	THINK: CRAB
o	C = hyperCalcemia
o	R = renal failure
o	A = anemia
o	B = bone pain
  • Anemia – plasma cells packed in bone marrow inhibit production of other cells
  • Renal insufficiency – excessive antibodies plug up kidney and form casts
  • Back pain – plasma cells stimulate osteoclasts
  • Hypercalcemia – plasma cells stimulate osteoclasts
50
Q

Tx of multiple myeloma

A
  • <70 y/o with donor = stem cell transplant

* >70 or without donor = chemo

51
Q

What is monoclonal gammopathy of undetermined significance (MGUS)

A

♣ Monocloncal proliferation of plasma cells
♣ Production of monoclonal immunoglobulins = M spike
♣ No symptoms
♣ 1-2% progress to multiple myeloma

52
Q

Describe cause of Waldenstrom macroglobulinemia

A

♣ B-cell lymphoma with monoclonal IgM production

• THINK: ‘W’ upside down is ‘M’

53
Q

Describe presentation of Waldenstrom

A 
•	M spike due to increased IgM
•	Hyperviscosity:
o	Blurred vision
o	Raynoud phenomenon
•	Amyloidosis 
♣	No lytic bone lesions (vs. multiple myeloma)

MS3 (88 decks)

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