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STEP > High Yield Facts > Flashcards

High Yield Facts Flashcards

1
Q

What cells produce surfactant

A

Type 2 pneumocytes

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2
Q

How does pulmonary HTN present on cardiac exam

A

Loud P2. LUSB

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3
Q

What kind of emphysema is seen in smokers?

A

Centriacinar which effects upper lobes

“Smoke rises”

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4
Q

What cell reacts to silica in silicosis?

A

Macrophages
Leads to inflammation followed by fibroblasts and collagen deposition
High prevalence of TB and bronchogenic carcinoma

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5
Q

Immune response involved in sarcoidosis

A

Accumulation of TH1 CD4+ helper T cells

Also involves IL2 (stimulates TH1 proliferation) and IFN gamma (macrophage activation)

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6
Q

Classic sarcoidosis findings

A 
Hilar lymphadenopathy on CXR
Cough + SOB
African American female
Often asymptomatic
May have high ACE levels and hypercalcemia
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7
Q

Electrolyte disturbance in sarcoidosis

A

Hypercalcemia

Elevated 1 alpha hydroxylase activity in alveolar macrophages leads to increased active vitamin D

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8
Q

what cells are involved in regeneration of the lung following lobar pneumonia?

A

Type 2 pneumocytes

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9
Q

pneumonia + hyponatremia

A

most likely legionella

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10
Q

immune response in TB

A

Cell mediated –> TH1

CD4 T cell activation, INF gamma release–> macrophage activation and cytotoxic C cells

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11
Q

Primary TB findings on CXR

A

Hilar lymphadenopathy (like sarcoidosis)

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12
Q

Ghon complex

A

Seen in primary TB

Ghon foci + lymph nodes –> subpleural granuloma seen in mid to lower lung. Called a ranke complex once calcified

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13
Q

CXR in secondary TB

A

Cavitation in upper lobes

due to caseous and liquefactive necrosis

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14
Q

Delayed separation of the umbilical cord

A

LAD1 (leukocyte adhesion deficiency type 1)

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15
Q

First step of hemostasis and mediators involved

A

transient vasoconstriction of the vessel mediated by reflex neural stimulation and endothelin release

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16
Q

Where does von willebrand factor come from

A

Weibel-Palade bodies of endothelial cells

Alpha granules of platelets

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17
Q

Tromboxane A2 is a synthesized by what?

A

Platelet cyclooxygenase

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18
Q

Cause of TTP

A

Acquired autoantibody against ADAMTS13 - enzyme responible for vWF multimer degradation. results in impaired platelet adhession–>microthrombi

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19
Q

Major cause of HUS

A

E coli O157:H7

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20
Q

What happens to PT/PTT in HUS and TTP?

A

NORMAL -coagulation cascade not effected

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21
Q

Effect of Aspirin on cyclooxygenase

A

irreversibly inactivates it

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22
Q

How to distinguish Hemophilia A and coagulation factor inhibitor

A

Mixing study - patient plasma + normal donor plasma
Hemophilia A - PTT will correct
Inhibitor: PTT will remain elevated

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23
Q

Most common inherited coagulation disorder

A

Von willebrand Disease

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24
Q

Von willebrand disease test

A

Abnormal ristocetin test - induces platelet aggregation by causing vWF to bind platelet GPIb. Lack of vWF = no agglutination

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25
Q

Von willebrand treatment and mechanism

A

desmopression (ADH analog): increases vWF release from weibel-Palade bodies in endothelial cells

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26
Q

Coagulation factors requiring vitamin K

A

2, 7, 9, 10

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27
Q

rattlesnake bite

A

venom activates coagulation cascade –> DIC

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28
Q

Best screening test for DIC

A

D-dimer
product of lysing fibrin crosslinks (real final step after clotting -cause healing). DIC = massive amounts of microthrombi so you have increased fibrinolysis and thus increased D-dimer

29
Q

How do you differentiate disorders of fibrinolysis from DIC?

A

DIC will have elevated D-dimer and low platelets

DoF: d-dimer normal because cleaving serum fibrinogen rather than fibrin in clots. also normal platelet count

30
Q

Effective of elevated homocysteine and how it occurs

A

Vit B12 deficiency - cant take methyl from THF and transfer it onto homocysteine, which normally results in cystathionine. Thus homocysteine accumulates
High levels damages endothelium and leads to thrombosis
Genetic cause: Cystathionine beta synthase deficiency

31
Q

Major drug to be concerned about giving in protein C and S deficiency

A

Warfarin Skin necrosis risk is increased
Warfarin blocks vit K effects
Protein C and S are effected first followed by 2, 7, 9, 10
Since already deficient in C and S, drops to severely low levels if given warfarin so very low ratio compared to other factors. thrombosis ensues
run heparin at same time when initially given

32
Q

What makes amniotic fluid thrombotic?

A

LOADED with tissue thromboplastin

33
Q

Treatment for neutropenic patients receiving chemo?

A

GM-CSF or G-CSF - boosts granulocyte production

34
Q

Most sensitive cell to radiation?

A

Lymphocytes

35
Q

Describe “Left Shift” seen in leukocytosis

A

release of pools of neutrophils including immature neutrophils (left shift) from bone marrow. Immature forms lack the Fc receptors (CD16). important because Fc allows interaction with Ig

SO: DECREASED CD16

36
Q

mechanism of Eosinophilia in hodgkins lymphoma

A

increased IL5

37
Q

Basophilia is associated with what disease?

A

CML

38
Q

What normally causes lymphocytic leukocytosis, and what is the exception to the rule

A

Viral infections - T lymphocytes undergo hyperplasia in response to virally infected cells
Bordetella pertussis infection is the exception - bacteria produces a lymphocytosis promoting factor whcih blocks circulating lymphocytes from leaving the blood to enter the lymph node

39
Q

what region of lymph nodes and spleen is affect in infectious mononucleosis

A

Nodes:Paracortex because this is where the T cells are. IM causes T cell hyperplasia (because viral infection - CD8 response)
Spleen: PALS hyperplasia in white pulp–>splenomegaly
EBV and CMV cause IM

40
Q

Classic presentation of Infectious mononucleosis but negative monospot test suggests what?

A

EBV is not the cause. Likely CMV

41
Q

Major complication of infectious mononucleosis to worry about?

A

splenic rupture. patients are advised to avoid contact sports for the next year to prevent this

42
Q

Leukemia and down syndrome

A

ALL seen after the age of 5

Acute megakaryobkastic leukemia seen after age of 5

43
Q

Acute promyelocytic leukemia genetic cause and mechanism

A

t(15;17) - RAR (retinoic acid receptor) mutation prevents promyelocyte (blast) maturation
also risk for DIC because of tons of auer rods

44
Q

APL treatment

A

ATRA - all trans retinoic acid - vit A derivative that binds altered receptor and causes blasts to mature

45
Q

Acute monocytic leukemia key presentation

A

infiltrate the gums

46
Q

Cause of splenomegaly in Hairy cell leukemia

A

RED PULP accumulates hairy cells (normally would expect it to be white pulp

47
Q

Hairy cell leukemia treatment

A

2-CDA (cladribine). ADA inhibitro so adenosine accumulates to toxic levels in neoplastic B cells

48
Q

Common cause of Adult T T cell Leukemia/Lymphoma - ATLL

A

HTLV-1 - seen in Japn and carribean

49
Q

Classic presentation of Adult T T cell Leukemia/Lymphoma (ATLL)

A

lytic bone lesions and hypercalcemia and RASH

Rash points you toward ATLL and away from multiple myeloma (which also presents with lytic bone lesions and hypercalcemia)

50
Q

Where is iron absorbed

A

Duodenum

51
Q

Why does gastrectomy cause Iron deficiency?

A

Less acid. Means iron cant stay in Fe2+ form as easily and changes to Fe3+. this isnt as readily absorbed

52
Q

How does iron deficency anemia initially appear on blood smear

A

As a normocytic anemia. Bone marrow notices less iron is available to make heme. So just makes less RBCs in roder to keep popping out normal cells. As things progress is when you end up with microcytic anemia.

53
Q

Explain FEP test and Iron deficiency anemia

A

Free erythrocyte protoporphyrin will be high
Good test for this type of anemia because Iron + protophorohyrin is what makes heme. Since decreased iron for binding, more protoporphyrin is floating free

Also elevated in ACD - anemia of chronic disease

54
Q

Plummer-Vinson Syndrome

A

iron deficiency anemia with esophageal web. Presents with anemia, dysphagia (web catches food), and beefy red tongue

55
Q

Where is iron located in sideroblastic anemia?

A

Trapped in the mitochondria - due to lack of protoporphyrin but iron keeps getting transferred in despite having nothing to combine with

56
Q

Most common cause of congenital sideroblastic anemia?

A

ALAS defect

57
Q

Most common acquired causes of sideroblastic anemia?

A

Alcoholism - mitochondrial poison
Lead poisoning - inhibits ALAD and ferrochelatase
B6 deficiency - required ALAS cofactor - may be seen as side effect of isoniazid

58
Q

What mechanism underlies beta thalassemias?

A

Gene mutations (point mutations in promoter or splice sites). Alpha thalassemias are DELETIONS

59
Q

Characteristic appearance of xray (skull) in B thalassemia?

A

Crew cut appearance from erythroid hyperplasia (hematopoeisis expands to site where it normally isnt

60
Q

Where is dietary folate absorbed

A

Jejunum

61
Q

Hemosiderinuria in Intravascular hemolysis mechanism

A

Start with hemoglobinuria during hemolysis. Hgb taken up by renal tubular cells and broken down into Fe, which accumulates as hemosiderin. eventually sloughs off and leaves in urine. This happens a few days after hemolysis

62
Q

Classic infant presentation in sickle cell disease

A

African American
6 months old
Dactylitis (swollen hands and feet due to vaso-occlusive infarcts in bones)

63
Q

Major complication of concern in sickle cell trait

A

generally asymptomatic because <50% sickle cell do NOT sickle
Exception: renal medulla. Extreme hypoxia and hypertonicity in medulla causes sickling–> microinfarctions –> Microhemturia –> decrased ability to concentrate urine

64
Q

Cause of paroxysmal nocturnal hemoglobinuria (PNH)

A

ACQUIRED defect in myeloid stem cells resulting in absent GPI (glycophosphatidylinositol). DAF and MIRL cant be expressed on RBC membranes and thus are susceptible to complement

65
Q

Cancer concern for aptietns with paroxysmal nocturnal hemoglobinuria (PNH)

A

Progression to AML (10% of patients will get AML)

Why? this condition is due to a mutation in myeloid stem cells, not hard to get another mutation

66
Q

What are causes of IgM mediated intravascular hemolysis

A

Infectious Mononucleosis

Mycoplasma pneumoniae

67
Q

Mutation in polycythemia vera and classic unique symtpom

A

JAK2 kinase

Itching after bathing due to mast cell histamine release

68
Q

Cause of ectopic EPO production

A

renal cell carcinoma

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