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Steep 2 CK hematology > hema 1 > Flashcards

hema 1 Flashcards

1
Q

asplenia and infection?

A

loss of splenic macrophage and Ab production–Increase the risk of encapsulated organism sepsis

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2
Q

what is the fun? of splenic macrophage and Ab production?

A 
splenic macrophage(found in red pulp around cord and sinusoid--engulf blood microbes and aged RBC
 Ab production--From white bulb after Ag presentation?
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3
Q

acquired complement deficiency causes?

A

SLE and antiphospholipid syndrome

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4
Q

Androgen abuse drugs?

A

exogenios(Testostrone replacment)
systemic(stanozolol and nandronolol)
precursor(DHEA)

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5
Q

CM?

A

Reproductive/CVS/Psychiatric and haematologic

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6
Q

Reproductive?

A

Men-testicular atrophy. decrease sperm production and mild gynecomastia..
Female:acne, voice depning,hirtuism and AUB

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7
Q

CVS?

A

left ventricular hypertrophy
decrease HDL
Increase LDL

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8
Q

Psychiatric?

A

aggressive behavior

mood disturbance

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9
Q

haematologic

A

polycythemia

hypercoagulability

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10
Q

Differentials?

A

autologous B/D transfusion
erythropoietin injection
polycythemia vera
strenuous exersise

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11
Q

autologous B/D transfusion?

A

blood removed some week before and replace blood near competition.
have only polycythemia

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12
Q

erythropoietin injection?

A

only polycythemia

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13
Q

Multiple myeloma?

A

plasma cell disorder

common in elderly

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14
Q

CM?

A

symptom of anemia
Bone pain
punched out a lesion on an x-ray

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15
Q

Diagnosis?

A

> 10% plasma cell in BM biopsy(clock face nuclei cell with intracytoplasmic IgG)

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16
Q

Laboratory?

A

serum protein gap
RF
rouleaux forming RBC in pheripherial morphology
Hypercalcemia
normocytic anemia
urinalysis–Increase light chain(BJP) with the negative dipstick.
Anemia (normocytic, normochromic)

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17
Q

what is the serum protein gap?

A

total protin and albumin gap >=4g/dl

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18
Q

causes?

A

Multiple myeloma
Wanderstorm Macroglobulinemia
Connective tissue disease
Infection

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19
Q

How to D/T?

A

Plasma electrophoresis

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20
Q

How?

A

polyclonal/monoclonal

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21
Q

Polyclonal?

A

Connective tissue disease

Infection

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22
Q

Monoclonal(M spike)?

A

Multiple myeloma

Wanderstorm Macroglobulinemia

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23
Q

How to d/tMultiple myeloma from Wanderstorm Macroglobulinemia?

A

clinical
PEEP
Bone marrow biopsy
Complication

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24
Q

clinical?

A 
WM has cx by
-Peripheral neuropathy
-No CRAB findings
-Hyperviscosity syndrome:
ƒ Headache
ƒ Blurry vision
ƒ Raynaud phenomenon
ƒ Retinal hemorrhage
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25
Q

PEEP?

A

WM–IgM

MM-IgG.IgA

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26
Q

Bone marrow biopsy?

A

IN WM

>10% small lymphocytes with intranuclear pseudoinclusions containing IgM (lymphoplasmacytic lymphoma).

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27
Q

Complication?

A

MM-infection and amilodosis

WM-thrombosis

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28
Q

CRAB?

A

HyperCalcemia
ƒ Renal involvement
ƒ Anemia
ƒ Bone lytic lesions

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29
Q

The normal range os srum albumin?

A

3.4 to 5.4 g/dL (34 to 54 g/L).

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30
Q

The normal serum protein level?

A

6 to 8 g/dl.

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31
Q

Clinical future of paroxysmal nocturnal hemoglobinuria?

A

Fatigue
Dark urine(hemoglobinuria)
Jaundice
VTE(cerebral and abdominal)

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32
Q

Pathophysiology?

A

Loss of anchor proteins (GPI)–CD55 and DC59) absence – Cell enables to inhibit complement activation—Hemolysis

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33
Q

workup?

A 
Coombs ⊝ hemolytic anemia(High LDH and Low haptoglobin)
Pancytopenia
Venous thrombosis
CD55/59 negative RBCs on flow cytometry
Hyperbilirubinemia
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34
Q

Treatment?

A

Eculizumab (targets terminal complement protein C5)

Iron and folate suplementation

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35
Q

CM of Budd-chiari syndrome?

A

acute/subacute/chronic

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36
Q

acute?

A 
Jaundice
Elevated transaminase
Hepatic encephalophaty
Varicial bleeding
Elevated INR/PTT
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37
Q

subacute/chronic?

A 
Progresive abdominal pain
Hepatomegaly
Spleenomegaly
Ascitis
Elevated bilirubin and transaminase
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38
Q

DIagnosis?

A

Abdominal dopler U/S

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39
Q

causes?

A

myloproliferative disease
malignancy(HCC)
OCP
PNH

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40
Q

Polycytemia vera?

A

Primary polycythemia. Disorder of  RBCs, usually due to acquired JAK2 mutation.

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41
Q

CM?

A 
aquaporic pruritis
erythromelagia
facial plutora
transient vision disturbance
thrombosis/heamorage
HTN
High RBC turnover(gouty arteritis)
42
Q

aquaporic pruritis?

A

iching during shower

43
Q

erythromelalgia?

A

Rare but classic symptom
(severe, burning pain and red-blue coloration)
due to episodic blood clots in vessels of the
extremities A .

44
Q

Transient vision disturbance?

A

due to hyperviscosity

45
Q

Treatment?

A

Phlebotomy
Hydroxyurea
Ruxolitinib (JAK1/2 inhibitor)

46
Q

Blood transfusion related anaphlaxis?

A

Bronchospasm(RD)
Angioedema
Hypotension
Shock and respiratory failure

47
Q

Managment?

A

epiniphrne
antihistamin and bronchodilator co administration
respiratory support/MV if RF developed
future transfusion–IgA deficient plasma and wahed RBC

48
Q

How lymphoploliferative disease cause anemia?

A

Replacment of BM cell by cancerous cell

49
Q

Hodgkin lymphoma?

A

Is a type of lymphoma, which is a cancer originating from white blood cells called lymphocyte
Epstein–Barr virus (EBV) may have an increased risk
Painless LDP

50
Q

age affected?

A

early adulthood and >60

51
Q

LN affected?

A

contagious
cervical
supraclaviculaar
mediasternal

52
Q

CM?

A 
Itchy skin
Night sweats
fever
Unexplained weight loss
Hepatosplenomegaly
Pain following alcohol consumption(specific)
Back pain
Nephrotic syndrome(MCD)
pruritis
53
Q

managment?

A

Patients of any stage with a large mass in the chest are usually treated with combined chemotherapy and radiation therapy.
Generaly have good prognosis

54
Q

poor prognosis sighn?

A 
Age ≥ 45 years
    Stage IV disease
    Hemoglobin < 10.5 g/dl
    Lymphocyte count < 600/µl or < 8%
    Male
    Albumin < 4.0 g/dl
    White blood count ≥ 15,000/µl
55
Q

Diagnosis?

A

biopsy–reed stunberg cell
PET scan with florodeoxy glucose
eosinophilia.elevated LDH

56
Q

PET scan with florodeoxy glucose?

A

Uptake by high metabolic cell(tumour,brain,liver) and urinary tract due to excretion

57
Q

The Reed–Sternberg cells are?

A

identified as large often bi-nucleated cells with prominent nucleoli and an unusual CD45-, CD30+, CD15+/- immunophenotype
abundant, amphophilic, finely granular/homogeneous cytoplasm

58
Q

risk factor?

A

Sex: male
Ages: 15–40 and over 55
Family history
History of infectious mononucleosis or infection with Epstein–Barr virus, a causative agent of mononucleosis[
Weakened immune system, including infection with HIV or the presence of AIDS[23]
Prolonged use of human growth hormone
Exposure to exotoxins, such as Agent Orange

59
Q

Risk factor for non hodgkin lymphoma?

A

Infection
Some chemicals, like polychlorinated biphenyls (PCBs),diphenylhydantoin, dioxin, and phenoxy herbicides.
Medical treatments, like radiation therapy and chemotherapy
Genetic diseases, like Klinefelter’s syndrome, Chédiak-Higashi syndrome, ataxia telangiectasia syndrome
Autoimmune diseases, like Sjögren’s syndrome, celiac sprue, rheumatoid arthritis, and systemic lupus erythematosu

60
Q

Infection?

A

Epstein-Barr virus – associated with Burkitt’s lymphoma, Hodgkin’s lymphoma, follicular dendritic cell sarcoma, extranodal NK-T-cell lymphoma
Human T-cell leukemia virus – associated with adult T-cell lymphoma
Helicobacter pylori – associated with gastric lymphoma
HHV-8 – associated with primary effusion lymphoma, multicentric Castleman disease
Hepatitis C virus – associated with splenic marginal zone lymphoma, lymphoplasmacytic lymphoma and diffuse large B-cell lymphoma
HIV infection[6]

61
Q

symptome?

A

Progresive,painless LDP
B-Symptome
Elevated LDH

62
Q

How to d/t from TB?

A

TB LDP have rarely sytemic symptom unlike HLwhich have B symptome

63
Q

Superior vena cava syndrome pathogenesis?

A

An obstruction of the SVC that impairs blood
drainage from the head (“facial plethora”;
note blanching after fingertip pressure in A ),
neck (jugular venous distention), and upper
extremities (edema). .

64
Q

Commonly caused by?

A

Commonly caused by malignancy (eg, mediastinal mass, Pancoast tumor)
Thrombosis from indwelling catheters
fibrosing mediasternitis(TB and fungal infection)

65
Q

whyit is Medical emergency?

A

Can raise intracranial pressure (if obstruction is severe)
Ž headaches, dizziness, 
risk of aneurysm/
rupture of intracranial arteries

66
Q

adjuvant therapy?

A

Treatment given adition to standard therapy

67
Q

consolidation therapy?

A

Given after induction therapy with multiple drug to reduce tumour burden

68
Q

Induction therapy?

A

Intial treatment given rapideley to reduce tumour burden

69
Q

maaintainance therapy?

A

given after initial and consolidation treatment to kill residual tumour cell

70
Q

neoadjuvant therapy?

A

treatment given bevore standard treatment

71
Q

salvage therapy?

A

Given after failure of primary regimen(in recurence)

To prevent long term disease progress and localize

72
Q

risk of erethropoitin treatment?

A

moderate/sever HTN

73
Q

nutrisional folate deficiency CM?

A

pancytopnia

macrocytic anemia

74
Q

alcohol deficiency?

A

Increase excretion
Decreased absorbtion
Defct in storage

75
Q

cause of anemia in SLE?

A

IDA
Animia of chronic disease
Heamolysis

76
Q

other future?

A

lukopnia

thrombocytopnia

77
Q

symptom of drug induced hemolytic anemia?

A

hemolysis
hyperbilirubinimia
reticulocytocis
splenomegaly

78
Q

hemocystin uria and TE?

A

vascular damage
activation of cloting factor
inhibition of anticoagulation

79
Q

Treatment?

A

pyridoxin
folic acid
documented deficoiency

80
Q

TTP pathophysiology?

A

Decrease ADMAS level–uncleaved VWF–platelet activation.

Acquired or hereditary

81
Q

clinical future?

A 
Hemolytic anemia
Thrombocytopenia
Renal failure
Neurologic symptom
Fever
82
Q

management?

A

Plasma exchange
Glucorticosteroid
Rituximab

83
Q

mortality w/o plasma exchange?

A

90 %

84
Q

HIV and NHL?

A

10 % risk

By leading EBV reactivation

85
Q

Cause of macrocytosis?

A

megaloblastic

Non-megaloblastic

86
Q

megaloblastic?

A 
Folate deficiency
B-12 deficiency
orotic aciduria
Drugs
Fanconi
87
Q

Drugs?

A 
Hydroxyurea
zidovudine
phenytoin
methotrexate
sulfa drug
88
Q

characteristics?

A

Hypersegmented neutrophil
low reticulocytosis
Anikocytosis and poikilocytosis

89
Q

characteristics?

A

Hypersegmented neutrophil
low reticulocyte
Anikocytosis and poikilocytosis
Macroovalocyte(enlarged, oval-shaped erythrocytes)

90
Q

Cxs?

A

non-hypersegmented neutrophil

low/normal/increased reticulocyte count

91
Q

management?

A

First, do B12 and folate level then consider BM aspiration.

92
Q

How to D/T lukomoid rxn from CML?

A

WBC count
Cause
LAP score
DOminant neutrophil precursor

93
Q

WBC count?

A

LR=>50,000

CML=elevated (useualy > 100,00

94
Q

Cause?

A

LR=Infection

CML=BCR-ABL mutation

95
Q

LAP score?

A

LR=High

CML=Low

96
Q

Dominant neutrophil precursor?

A

LR=more mature (metamyelocytes) dominate

CML=More immature(promyelocyte and myelocyte)

97
Q

absolute basophilia?

A

LR=not present

CML=present

98
Q

sign and symptom of CML?

A

blast stage
accelerated stage
chronic stage

99
Q

blast stage?

A

symptoms are most likely fever, bone pain, and an increase in bone marrow fibrosis

100
Q

accelerated stage?

A 
Some (<10%) are diagnosed in this stage 
 bleeding
petechiae 
ecchymosis
 In these patients, fevers are most commonly the result of opportunistic infections
101
Q

chronic?

A

Most patients (~90%) are diagnosed during this stage which is most often asymptomatic.
diagnosed incidentally with an elevated white blood cell count on a routine laboratory test.
enlarged spleen and liver and the resulting upper quadrant pain this causes.
The enlarged spleen may put pressure on the stomach causing a loss of appetite and resulting in weight loss.
It may also present with mild fever and night sweats due to an elevated basal level of metabolism

102
Q

Risk factor?

A

age of 65 years

Exposure to ionizing radiation ( about 10 years after the exposure

Steep 2 CK hematology (4 decks)

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