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hematology Flashcards

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USMLE® Step 1 flashcards
1
Q

different degenrative diseases of back explain

RADUCLOPathy,spondyloarthopathy, spinal metastasis

A

Relieved with rest
• Cervical and lumbosacral
Radiculopathy
• Radiates to leg, positive straight leg raise
test Spinal stenosis
• Pain with standing, relieved with flexion
Spondyloarthropathy
• Relieved with exercise Spinal mets
• Constant pain, worse at night, no
response to position change Osteomyelitis
• Focal tenderness, fever, night sweats
Bone mets PB/KTL
• Prostate, Breast, Kidney, Thyroid, Lung

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2
Q

explain pathogeneisis of HEmochromatosis

A

HFE protein normally interacts with
transferrin recognizing Fe uptake from GI
tract > mutation leads to falsely low
detection of Fe > no hepcidin production >
increased DMT1

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3
Q

how to ifferentiate between hemophilia and antiphospholipid antibody syndrome

A

use mixing study

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4
Q

how to differentiate between pilocytic astrocytoma, and medulloblastoma

A 
Pilocytic astrocytomas are the
most common brain tumors in
children. They frequently arise in
the cerebellum and can be
differentiated from
medulloblastomas by the presence
of both cystic and solid
components on imaging.
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5
Q

histopath of brain tumora

A 
Medulloblastoma
• 2nd MC (MC malignant)
• MC in vermis
• Small blue cells with drop mets
Ependymomas
• Perivascular rosettes
• Usually in ventricle causing
hydrocephalus
Adults GBM
• Pseudopalisading
Oligodendroglioma
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6
Q

why vitk supplemetation necessary in newborn

A 
Newborns who don't receive
prophylactic supplementation are
at risk for bleeding complications.
Pts w/ CF are also at risk for vitK
defic due to poor absorption of fatsoluble
vits.
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7
Q

problems with antiphospholipid syndrome

A

Pts w/
antiphospholipid Abs are at risk
for venous and arterial TE and
unexplained, recurrent preg loss

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8
Q

what if we give a person B9 with a b12 deficiency how to differentiate between b12 and folate

A 
If megaloblastic
anaemia due to vitB12 defic is
mistakenly Tx w/ vitB9 alone, the
neuro dysfxn can worsen.
B12 def
• High MMA and homocysteine, peripheral
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9
Q

how do you diagnose multiple myeloma

A

system). A
bone marrow sample w/ >10%
plasma cells is strongly
suggestive of MM.

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10
Q

how does hypothyroid present with

A

Macrocytic RBC without hypersegmentel

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11
Q

what are the classic signs seen in hereditary spherocytosis how to diagnose it

A 
hemolytic anaemia, jaundice, and
splenomegaly
↑ osmotic fragility
on acidified glycerol lysis testing
confirms the Dx.
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12
Q

manifestations of g6pd deficiency

A

Infections, dapsone, antimalarials, TMp

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13
Q

explain mechanism of cachexia

A

TNF-a is thought to mediate PNP
cachexia in humans by
suppressing appetite and ↑ BMR

Anorexia, malaise, anemia, weight loss,
muscle wasting all driven by TNFalpha
(aka cachectin)
• Produced by macrophages
• Inhibits appetite in hypothalamus,
increases BMR
• Mediates symptoms of septic shock and
causes liver to release acute phase reactants
IFNalpha
• Antiviral and anti tumor
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14
Q

RAS oncogene
ERB1
ERB2

A

cholangiocarcinoma, pancreatic
adenocarcinoma
ERB1 (EGFR): lung adenocarcinoma
ERB2 (HER2): breast cancer

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15
Q

explain metalloproteinase

A 
Zn containing enzymes
• Degrades ECM and BM (laminin and
collagen type 3 and 7)
Cancer invasion
• Tumor cell detach by decreasing e
cadherins
• Tumor cell ahere to BM (facilitated by
laminin)
• Tumor cell produce metalloporteinase
and cathepsin D protease to invade
Random
Acid hydrolase: lysosomal enzyme
Alk Phos: bone or biliary process issue
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16
Q

what are leukoerythroblasts

A

Teardrop cells
• Nucleated RBC
• Marrow fibrosis and mets

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17
Q

funtion of tdt

A

Adds nucleotides to V,D and J region to

increase Ab diversity

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18
Q

AMl cuses anemia

A

• Myeloblast unable to differentiate >
suppress other cells
• Anemia, thrombocytopenia, neutropeni

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19
Q

which diseases have psitive coombs in autoimmune hemolytic anemia

A

SLE, Hodgkin, NHL, mycoplasma, EBV

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20
Q

heritditary spherocytosis

A

mchc over 36

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21
Q

how to compare LR with CML

A

LR LAP normal or Increased, in cml decreased

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22
Q

what are the complication of ebv in hiv

A 
Latent EBV can reactive > can cause B
cell lymphoma, burkitts and CNS
lymphoma
BK virus
• Typically post transplant nephropathy or
hemorrhagic cystitis
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23
Q

EBV

A

• CMV, HIV and Toxo:

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24
Q

what characterizes a tissue anaplastic

A
  • Loss of cell polarity and architecture
  • Variation in shape and size
  • High N:C ration
  • Many mitotic figures
  • Giant, multinucleated tumor cells
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25
Q

talk about kapsoki sarcoma

A 
s. This tumour arises from
primitive mesenchymal cells and
is strongly a/w HHV-8.
Late stage spread to lungs and GI tract
• Spindle and endothelial cell proliferation,
RBC extravasation and inflammation
• HHV8
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26
Q

aplasticanemia causes

A 
Autoimmune
• Parvo and EBV
• Carbamazepine, chloramphenical,
sulfonamides
• Benzene or radiation Dx
• Hypocellular bone marrow composed of
fat
•
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27
Q

pure red cell aplasia

A 
• IgG against erythropoietic precursors and
progenits
• Associated with thymomas and
lymphcytic leukemia and Parvo B19
• Thymectomy usually cures
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28
Q

fanconi anemia

A

Causes aplastic anemia
• Short stature
• Absent thumbs
• High risk of malignanc

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29
Q

myeodysplasia

A

Defect in stem cell maturation >

pancytopenia

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30
Q

why reticulocytes are blue

A 
↑ bone marrow EPO results in an
accelerated release of immature
RBCs (reticulocytes) into the
bloodstream. Reticulocytes
contain bluish cytoplasm and
reticular precipitates of residual
ribosomal RNA.
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31
Q

mediastinal mass

A

Large anterior mediastinal mass can
compress great vessels (SVC syndrome),
cause esophageal dysphagia, compress
trachea (stridor and dyspnea)

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32
Q

talk about different spleen patho

A 
Splenic hyperplasia/hypertrophy
• Infection
Splenic pressure atrophy
• Tumor
Splenic lipid accumulation
• Lysosomal lipid storage disorder
(Gaucher's)
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33
Q

b12 deficiency

A

Give B12 and will see
• Immediate rise and then fall in
reticulocyte coun

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34
Q

what does erythroid cells in spleen indicate

A 
The presence of erythroid
precursors in organs such as the
liver and spleen is indicative of
EMH, a condition characterised
by EPO-stim, hyperplastic
marrow cell invasion of EM
organs.
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35
Q

extramedullary hematopoeisis

A 
Caused by chronic hemolysis
• Can see "crew cut" on xray or chipmunk
facies
• Intrahepatic extramedullar
hematopoiesis can cause portal HTN
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36
Q

why normal serum fe in aplastic anemia

A

because absent HPO stem cells cant use iron

37
Q

what does lead poisoning do to rbc

A

• Basophilic stippling on hypochromic
microcytic anemia > abnormal degradation
of rRNA

38
Q

what does integrin bind to

A 
Adhesion of cells to the ECM
involves integrin-mediated
binding to fibronectin, collagen,
and laminin
s integrins, matric collagen, GAG
39
Q

function of GAGS

A 
GAG that contributes to
H2O retention in ECM and determines
stiffness of matric
Keraton sulfate: GAG in ECM that
maintains type 1 collagen fibrill
organization (like cornea)
40
Q

what are the causes of splenic infarction

A

• Sickle cell, infectious endocarditis and

myeloproliferative disorder

41
Q

explain peneerace of VWD

A

. It has
an AD pattern of inheritance and
variable penetrance.

42
Q

what is dysfibrongeimas

A

Abnormal fibrinogen causing excessing
bleeding or thrombophilia
• Normal bleeding time
• Abnormal TT, PT, and PTT

43
Q

transglutaminase crosslinking deficiency

A

=bleeding

44
Q

pathophys of itb

A 
Ab to GP2b/3a
• Low platelets
• Normal rest of labs
• Secondary ITP associated with HIV or
Hep C
45
Q

hypotyrodisim ffect on rbc

A

Fe deficiency anemia or pernicious

anemia

46
Q

whch bacteria sickle cell ppl get

A 
Bone necrosis leading to osteomyelitis
(Salmonella and Staph)
• Splenic infarction > scarring, fibrosis and
atrophy
• Infant: splenic sequestration crisis
(pooling of RBC) > low Hb, rapidly
enlarging spleen and hypovolemic shock
47
Q

what is sickle cell crisis

A

• Infant: splenic sequestration crisis
(pooling of RBC) > low Hb, rapidly
enlarging spleen and hypovolemic shock

48
Q

what sort f anemia is seen in sickel cell disease

A 
An MCV >110μm3 is highly
suggestive of megaloblastic
anaemia, such as that caused by
vitB9 or vitB12 defic. Pts w/
chronic hemolytic anaemia have ↑
vitb9 req due to ↑ erythrocyte
turnover and are predisposed to
devel macrocytosis.
49
Q

can extramedullary hemtoporisi cause macrocyic anemia

A

Extramedullary erythropoiesis in sickle
cell can cause macrocytic anemia BUT you
must check reticulocyte index (if elevated
retic index > adequate marrow response)

50
Q

exain her 2

A 
The HER2 oncogene encodes for
a transmembrane glycoprotein w/
intrinsic tyrosine kinase activity
and is a member of the family of
EGFRs. Overexpression of this
protein is a/w a worse prognosis
and ↑ risk of disease recurrence.
51
Q

explain pathogenessi of ebv

A 
Binds CD21 infecting B cells
• CD21 (CR2) binds C3d
• Atypical CD8 cells have abundant
cytoplasm, eccentrically placed nucleus,
and skirting
52
Q

active plasma cell

A

wagon wheel apperaence because of perinuclear clearing

53
Q

genetics of non small cell carcinoma

A

• Chromosome 2 fusion between EML4

and ALK >

54
Q

mutation in pcv

A

• V617F mutation involving JAK2 gene
resulting in more sensitive receptor to EPO
and TPO

55
Q

how does hypoxa present in copd and osa

A

COPD, OSA

• SaO2 < 92; PaO2 < 65

56
Q

which cancers present with EC epo

A

• RCC, HCC, pheo, hemangioblasoma,

leiomyoma

57
Q

in leukmoid reaction what des the peripheral smear look like

A 
peri smear can show
↑ bands, early mature neutrophil
precursors (e.g. myelocytes), and
granules (e.g. Dohle bodies) in
the neutroph
 Will also see increase bands, toxic
granulations and cytoplasmic vacuoles
58
Q

how to treat ttp how o dy/dx from dic

A

Need hemolytic anemia to dx Tx:
plasmapheresis
pt and ptt

59
Q

classic triad of HSP

A

• Palpabale purpura, abdominal pain,
arthralgia
• Normal platelet count

60
Q

bone lytic cancers

A

MM, non small cell of lung, NHL,

RCC and melanom

61
Q

bone blastic cancer

A

: prostate (blacks at higher risk),

small cell of lung, Hodgki

62
Q

how does pnh destroy nephron

A

• Chronic hemolysis > Fe deposits in

nephron (especially PCT) > hemosiderosis

63
Q

explain process f cancer cahcexia leading to mucle loss

A 
In carelated cachexia, high lvls of proinflammatory cytokines lead to ↑
ubiquitination of sarcomeric
muscle proteins, which in turn
leads to extensive skeletal muscle
loss.
64
Q

most likely caus of opc cnacner

A

hpv

65
Q

explain histopath of melanoam

A 
s. Dx is gen made when a
histopath sample shows cellular
atypia w/ cells containing brown
pigment (melanin granules);
immunostaining for
melanin/melanoma markers (e.g.
S-100, HMB-45) is gen (+).
66
Q

histopath f mm

A

Histopath will show
replacement of the normal bone
marrow w/ plasma cells and
blasts.

67
Q

diagnosis of cll based on

A 
en CBC reveals dramatic
leukocytosis, and FC
subsequently shows a clonal
population of leukocytes w/
typical B-cell markers such as
CD19, CD20, and CD23.
68
Q

what is the histopath in parvo virus infection of cell

A

pronormoblasts w/ glassy,

intranuclear viral inclusions.

69
Q

histopath of ewin sarcoma

A 
It most
commonly involves the lower
extremity and pelvis and often
metastasizes to the lungs.
Histopathology is Chx by
uniform, small, round, cells;
fibrous septae; and patches of
necrosis and hemorrhage.
70
Q

difference between band neutrophil vs segmented

A

Band neutrophils are slightly less mature than segmented neutrophils and have indented, unsegmented “C” or “S” shaped nuclei. Band neutrophils normally account for approximately 5-10% of peripheral blood leukocytes. An increased proportion of band neutrophils can be seen in infectious and inflammatory conditions.

71
Q

monocyes morph

A

Here is a monocyte. It is slightly larger than a lymphocyte and has a folded nucleus. Monocytes can migrate out of the bloodstream and become tissue macrophages under the influence of cytokines. Note the many small smudgy blue platelets between the RBC’s.

72
Q

what is left shift

A

A very high WBC count (>50,000) with pronounced left shift that is not a leukemia is known as a “leukemoid reaction”.

73
Q

lead posionng basophilic stippling

A

Basophilic stippling due to inhibition of

5’ nucleotidase resulting in retained RNA

74
Q

what is hoell olly odies

A

DNA remnant in RBC with asplenic pt

75
Q

explain pathogensis of warfin induced necrosis

A

thrombotic occlusion of the

microvasc w/ skin necrosis.

76
Q

antitrombin3 deficiency

A

AD
• Presents with venous thrombosis
• No change in PTT with hep > blast with
hep until you can bridge to warfarin

77
Q

pathophys of beta thalessemia

A

transcription, processing, and

translation of beta-globin mRNA

78
Q

how are target cells gformed

A

erythrocytes decrease volme and excessive membrane

79
Q

why do pts with splenectomy develop target cells

A 
Pts
who undergo splenectomy usually
develop target cells b/c the spleen
is the 1ary organ that prunes
excessive RBC membrane.
80
Q

molecular pathogenesis of MM

A 
Myeloma
cells stim osteoclast devel by
secreting RANKL and destroying
OPG, which incr RANK activity
and results in osteoclast diff.
81
Q

when do rbc sickle

A

• RBC sickle when deoxygenated or
dehydrated (causing chain polymerization
via hydrophobic bonds)

82
Q

gardos

A

Gardos (Ca dependent) K channel
blockers prevent dehydration by prevent K
efflux

83
Q

opiods tolerance symtoms

A
  • Pruritis is mild and tolerance develops
  • Nausea develops tolerance
  • Can decrease micturation reflex
84
Q

explain the MDR 1

A

ATp dependent
efflux pump (normal in nephron and BBB)
• Verapamil, diltiazem, ketoconazole:
reduce action of pump

he human MDR1 gene codes for
P-gp, a transmembrane ATPdependent efflux pump protein
that has a broad specificity for
hydrophobic compounds. This
protein can both ↓ the influx of
drugs into the cytosol and can ↑
efflux from the cytosol, thereby
85
Q

why never give leuovorin

A

5• Fluoruracil
• Inhibits thymidylate synthetase
• Leucovorin potentiates the cytotoxic
effect

86
Q

how to cancer cells avoid imune suppression

A

Ca cells avoid immune
recognition by overexpression PDL1, which binds to the PD-1
receptor on Tc cells and inhibs
their response (T-cell
exhaustion). mAbs that block PDL1 and PD-1 are effective against
ca that express high lvls of neoAgs on their surface b/c these
tumours are particularly
susceptible to immune
recognition by Tc cell

87
Q

cdks 4/6

A

g1-s

88
Q

what is Emicizumab

A 
hemophilia A is an XL disorder
a/w a defic of FVIII. Emicizumab
— a bispecific, mAb — mimics
the activity of FVIII by binding to
both FIXa and FX, bringing them
into close proximity to allow for
FX activation.

usmle (38 decks)

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