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Review / Wrong Answers > 6/12 UWorld > Flashcards

6/12 UWorld Flashcards

1
Q

What are the cartilage, muscle, and nerve derivatives of the 1st branchial arch?

A
  • Cartilage:
    • Maxillary process, mandibular process, incus, malleus
  • Muscles:
    • Muscles of mastication, mylohyoid, tensor tympani, tensor veli palatine
  • Nerves:
    • CN V2 and V3
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2
Q

What are the cartilage, muscle, and nerve derivatives of the 2nd branchial arch?

A
  • Cartilage:
    • Stapes, styloid, stylohyoid
  • Muscles:
    • Muscles of facial expression
    • Stapedius, stylohyoid
  • Nerves:
    • CN VII
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3
Q

What are the cartilage, muscle, and nerve derivatives of the 3rd branchial arch?

A
  • Cartilage:
    • Greater horn of hyoid
  • Muscles:
    • Stylopharyngeus
  • Nerves:
    • CN IX
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4
Q

What are the cartilage, muscle, and nerve derivatives of the 4-6th branchial arch?

A
  • Cartilage
    • Arytenoids, cricoid, thyroid
  • Muscles:
    • 4th à Cricothyroid, most pharyngeal constrictors, levator veli palatini
    • 6th à All laryngeal muscles except cricothyroid
  • Nerves:
    • 4th à CN X superior laryngeal branch (swallowing)
    • 6th à CN X recurrent laryngeal branch (speaking)
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5
Q

Antibiotic associated with serotonin syndrome

A

Linezolid

MOA - inihibits 50S ribosomal subunit

Also has MAOI action

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6
Q

Differences between lesions in the right vs. left frontal lobe

A

Deficits in executive functioning, concentration, orientation, judgment, personality

Left sided lesions – associated with apathy and depression

Right sided lesions – associated with disinhibited behavior

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7
Q

What is HELLP syndrome

A
  • Stands for:
    • H = Hemolysis (anemia)
    • EL = Elevated Liver enzymes (RUQ pain, jaundice)
    • LP = Low Platelets (bruising bleeding)
  • Preeclampsia + thrombotic microangiopathy
    • Hemolysis = thrombi causing schistocytes
    • Liver enzymes = lack of RBCs leads to infarction of liver tissue
    • Platelets = all used up in thrombi
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8
Q

MOA of Eptifibatide

A
  • GP2b/3a antagonists
    • Monoclonal IgG antibody that binds GP2b/3a receptors, preventing platelet aggregation
  • Sketchy = Tied game
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9
Q

MOA of Ticagrelor

A
  • ADP receptor antagonist – Blocks platelet ADP surface receptors (P2-Y12 receptor blocker) - prevents expression of G2b/3a and thus prevents platelet aggregation
  • Sketchy: hot dog grill
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10
Q

MOA of Tirofiban

A

GP2b/3a antagonists

Monoclonal IgG antibody that binds GP2b/3a receptors, preventing platelet aggregation

Sketchy = Tied game

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11
Q

MOA of Abciximab

A

GP2b/3a antagonists

Monoclonal IgG antibody that binds GP2b/3a receptors, preventing platelet aggregation

Sketchy = Tied game

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12
Q

What is agranulocytosis

A

Usually refers to low neutrophils

Increased risk of infection

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13
Q

What are the names of the phosphodiesterase inhibitors involved in inhibiting platelet aggregation

MOA?

A
  • Phosphodiesterase inhibitors à “Don’t PHOSTER DISINTEREST in sports” sign
    • Cilostazol = lost the ball
    • Dipyridamole = two pyramids as top of tent
  • MOA:
    • Inhibition of phosphodiesterase leads to increases cAMP within the platelet which will activate protein kinase A, and impairing platelet function and aggregation
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14
Q

Lab findings (BT, PT, PTT) + treatment in von Willebrand disease

A
  • Genetic vWF deficiency
  • Findings:
    • Increased bleeding time – decreased platelet adhesion
    • Increased PTT – vWF normally stabilizes Factor VIII
    • Normal PT
  • Treatment
    • Desmopressin – increases vWF release from Weibel-Palade bodies of endothelial cells
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15
Q

Lab findings in DIC

A
  • Increased bleeding time – low platelets
  • Increased PT and PTT
  • Low fibrinogen – being used up
  • High D-dimer (fibrin split products)
  • Schistocytes
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16
Q

Describe the cause + treatment of immune thrombocytopenia

A
  • IgG autoantibodies to GP2b3a
  • Antibodies produced by plasma cells of spleen and antibody-bound platelets consumed by macrophages of spleen
  • Treatment = splenectomy
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17
Q

Describe the defect in Thrombotic thrombocytopenic purpura (TTP)

A
  • Platelets used up in pathologic formation of microthrombi in small vessels
  • Due to decreased ADAMTS13, enzyme that normally cleaves vWF for degradation
    • No vWF degradation = abnormal platelet adhesion = microthrombi
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18
Q

Findings in TTP vs. HUS

A
  • TTP:
    • Findings (Pentad):
      • Thrombocytopenia = platelets being used up
      • Microangiopathic hemolytic anemia = RBCs sheared by microthrombi
      • Renal insufficiency (thrombi involve vessels of the kidney)
      • Neurological symptoms (confusion, HA, seizures, coma) – thrombi involve vessels of CNS
      • Fever
  • HUS:
    • Findings (triad):
      • Microangiopathic hemolytic anemia
      • Renal insufficiency (thrombi involve vessels of the kidney)
      • Thrombocytopenia
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19
Q

Compare the defect in Bernard-Soulier syndrome vs. Glanzmann thrombasthenia

A
  • Bernard-Soulier syndrome
    • Defect of glycoprotein 1b
    • Platelet can’t bind to vWF on collagen = defect of platelet plug formation
    • Platelet count is only slightly low – moderate thrombocytopenia
  • Glanzmann thrombasthenia
    • Genetic GP2b3a deficiency
    • Defect in platelet aggregation
    • Platelet count is normal (they aren’t being destroyed, just can’t aggregate)
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20
Q

Describe the basic difference between Hodgkin and Non-Hodgkin lymphoma

A

Hodgkin - Rare neoplastic cells (Reed-Sternberg cells) which secrete cytokine that draw in inflammatory cells, leading to a mass

Non-Hodgkin - Whole mass composed of malignant cells

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21
Q

What are the surface markers of Reed Sternberg cells

A
  • 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
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22
Q

Which lymphoma is more associated with B symptoms

A

Hodgkin - Due to cytokine released by RS cells

23
Q

Most common type of Hodgkin lymphoma

A

Nodular sclerosing type

24
Q

Hodgkin lymphoma with best prognosis

A

Lymphocyte-predominant

25
Q

Describe age distribution of Hodgkin vs. Non-hodgkin lymphoma

A
  • Hodgkin - bimodal distribution (peak at 20 and 65 y/o)
    • Think of 2 owl eyes as 2 humps
  • NHL - variable age range
26
Q

What is the translocation in follicular lymphoma

A
  • t(14;18) = heavy chain Ig (14) and BCL-2 (18)
    • Overexpression of BCL-2 = decreased apoptosis
      • Recall that BCL2 stabilizes mitochondrial membranes, preventing leakage of cytochrome C, and thus preventing apoptosis
      • Follicle is where B-cells are produced, so lack of apoptosis = malignant B-cell proliferation
    • THNK: 18 y/o is when you can buy a gun and start killing people (apoptosis)
      • Apoptosis occurs in the follicle
27
Q

What lymphoma presents with “starry sky” histology

A

Burkitt lymphoma

  • “Starry sky” appearance – sheet of lymphocytes with interspersed “tingible body” macrophages
  • THINK: Burkitt = Africa - sleeping under the stars
28
Q

What is small lymphocytic lymphoma

A

Lymphoma equivalent of CLL

SLL/CLL

29
Q

What diseases are associated with marginal zone lymphoma

A
  • Associated with chronic inflammatory states:
    • Sjogren syndrome
    • Hashimoto thyroiditis
    • H. pylori
  • Marginal zone = area surround the mantle zone
    • Marginal zone is present when the cells in germinal center are activated (i.e. inflammation), so it makes sense that this lymphoma occurs in chronic inflammatory states
30
Q

What is Sezary syndrome and what do Sezary cells look like?

A
  • If malignant T-cells of Mycosis fungoides leave the skin lesions and get into the blood it is called Sezary Syndrome
    • Sezary cells = lymphocytes with cerebriform nuclei on blood smear
31
Q

What serum markers indicate ALL

A
  • TdT (+) and PAS (+)
32
Q

Translocation and surface marker associated with B-ALL

A
  • CD10 (+)
  • t(12;21) = better prognosis
  • t(9;22) = poor prognosis
33
Q

Markers and histology associated with AML

A
  • MPO (+) and PAS (+)
  • Auer rods
    • Crystal aggregates of MPO
    • Especially seen in Acute promyelocytic leukemia, AML
34
Q

Common presentation of AML

A
  • DIC is a common presentation
    • Auer rods activate coagulation cascade
35
Q

Translocation of AML

A
  • t(15;17)
    • Translocation of retinoic acid receptor
    • Think:
      • Auer sounds like Fuer (Hitler) – Sound of music
      • I am 16 going on 17 (15;17)
      • Poke Hitler in the eye with a carrot – treat with retinoic acid
36
Q

Common surface markers + histology of CLL

A
  • 95% have B-cell markers (rather than T-cell) à CD20+ and CD5+
  • Characteristic smudge cells
    • THINK: CLL = Crushed Little Lymphocytes = smudge cells
37
Q

What is the Richter transformation

A
  • Progression of CLL to aggressive lymphoma, usually diffuse large B-cell lymphoma
38
Q

Complications of CLL

A

Recall that CLL involves mostly B-cells

  • Hypogammaglobulinemia
    • Neoplastic B-cells don’t make Ig
  • May cause autoimmune hemolytic anemia (both warm of cold cell agglutinins)
    • If neoplastic B-cells do make Ig, it will be defective and can attack the body
  • Richter transformation
    • Progression to aggressive lymphoma, usually diffuse large B-cell lymphoma
39
Q

What are the myeloproliferative disorders

A

Aka chronic leukemias of myeloid cells:

  • Chronic myeloid leukemia (CML)
  • Polycythemia vera
  • Essential thrombocythemia
  • Myelofibrosis
40
Q

Compare progression of CLL to progression of CML

A

CLL may progress to diffuse B-cell lymphoma (Richter transformation)

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

41
Q

Treatment of CML

A
  • Responds to Imatinib (bcr-able tyrosine kinase inhibitor)
42
Q

Mutation and presentation of polycythemia vera

A
  • JAK2 kinase mutation
  • Increased red cell mass, without elevated EPO
  • Presentation:
    • Plethora (flushed face)
    • Blurred vision and HA (due to hyperviscosity)
    • Thrombosis (e.g Budd Chiari)
    • Itching after bathing
    • Erythromelalgia (severe, burning pain and red-blue coloration in the extremities)
43
Q

Mutation and presentation of essential thrombacythemia

A
  • JAK2 kinase mutation
  • Presentation:
    • Increased bleeding – dysfunctional platelets
    • Thrombosis – too many platelets
44
Q

What disorder presents with a “dry tap” on bone marrow aspiration

A

Myelofibrosis

Hairy cell leukemia (subtype of CLL that causes marrow fibrosis)

45
Q

Mutation in myelofibrosis

A

JAK2 kinase

All myeloproliferative disorders (polycythemia vera, essential thrombocythemia, myelofibrosis) except for CML have JAK2 kinase mutation

46
Q

Describe the problem in myelodysplastic syndrome

A
  • Defect in cell maturation of all non-lymphoid lineages
    • Stem-cell disorder and dysplasia involving ineffective hematopoiesis
    • Cause by de novo mutations or environmental exposures
47
Q

Histology of myelodysplastic syndrome

A
  • Pseudo-Pelger-Huet anomaly
    • Neutrophils with bilobed nuclei, connected by a thin strand
    • Typically seen after chemotherapy
48
Q

What disorders present with lytic bone lesions?

A

Multiple myeloma

Langerhans cell histiocytosis

Adult T-cell lymphoma

49
Q

Describe multiple myeloma and its classic presentation

A
  • Malignant proliferation of monoclonal plasma cell within the marrow
    • Recall: Plasma cells = mature B-cells that produce immunoglobulin
  • Presentation:
    • Anemia – plasma cells packed in bone marrow inhibit production of other cells
      • Rouleaux formation of RBC
    • Renal insufficiency – excessive antibodies plug up kidney and form casts
    • Lytic bone lesions - plasma cells activate RANK
      • Back pain – plasma cells stimulate osteoclasts
      • Hypercalcemia – plasma cells stimulate osteoclasts
    • M spike
    • Increased risk of infection (monoclonal antibodies lack antigenic diversity)
50
Q

Findings in Waldenstrom macroglobulinemia

A
  • B-cell lymphoma with monoclonal IgM production
  • Findings:
    • M spike due to increased IgM
    • Hyperviscosity:
      • Blurred vision
      • Raynoud phenomenon
    • Amyloidosis
  • No lytic bone lesions (vs. multiple myeloma)
51
Q

Describe predominant antibodies produced in multiple myeloma vs. Waldenstrom macroglobulinemia

A

Multiple myeloma = IgG and IgA

Waldenstrom macroglobulinemia = IgM (thing MACRO = IgM)

52
Q

Describe presentation of 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
53
Q

Presentation of Langerhans cell histiocytosis

A
  • Neoplastic proliferation of specialized dendritic cells (especially in skin)
  • Birbeck (“tennis racket”) granules seen on EM
  • S-100 (+) and CD1a (+)
  • Presentation:
    • In children
    • Lytic bone lesions
    • Skin rash
    • Recurrent otitis media
54
Q

What is the effect of the t(9;22) translocation seen in CML

A

BCR-ABL

Constitutively active tyrosine kinase)

Review / Wrong Answers (140 decks)

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