Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2a > Haematology (blood stuff) > Flashcards

Haematology (blood stuff) Flashcards

1
Q

describe clots formed in arterial circulation

A

high pressure system = platelet rich

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

describe clots formed in venous circulation

A

low pressure system = fibrin rich

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the risk factors for venous thrombus formation

A 
surgery
immobility
leg fracture/cast
oral contraceptive
pregnancy
HRT 
long haul flight
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is a DVT

A

clot within venous system, usually in area between knee and hip

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what investigations are carried out to diagnose a DVT

A

D-dimer test

ultrasound compression test/doppler USS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is a D dimer test

A

measure of levels of degrading fibrin which is present in clotting
if positive = may be DVT/PE but not specific
if negative you can exclude DVT/PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

when is d dimer raised

A

infection
malignancy
inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how is DVT treated

A

immediate:
DOAC
LWMH in pregnancy

long term:
DOAC
warfarin in antiphospholipid (INR 2-3)
LWMH in pregnancy

compression stockings
treat/seek for underlying cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is a PE

A

clot breaks off in leg/pelvis

embolus breaks off travels through venous system to right side of heart = stuck in pulmonary circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what investigations for suspected PE

A

ECG = sinustachy + S1Q3T3
CXR = usually normal
ABG = T1 resp failure/decreased O2 and CO2
D dimer = raised
V/Q scan = shows mismatch
CT pulmonary angiogram = inject dye allows visualisation of major segmental thrombi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how is PE treated

A

Immeadiate:
DOAC or LWMH
Massive:
unfractionated heparin + thrombolysis (alteplase)

Long term = same as DVT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is myeloma

A

malignant neoplastic proliferation of bone marrow plasma cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is monoclonal gammopathy of unknown significance

A

the process of abnormal myeloma protein being found in standard blood tests
can lead to formation of multiple myeloma but doesnt necessarily mean myeloma is present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is amyloidosis

A

group of symptoms caused by amyloid protein build up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the symptoms of amyloidosis

A 
raccoon eye
enlarged tongue
HF
hepatosplenomegaly
nephrotic syndrome
AKI
peripheral neuropathy
carpal tunnel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what can cause a lump in the neck

A
  1. reactive lymph node - infection/inflammation
  2. malignant - lymphoma, metastases, head/neck cancer
  3. underlying structure - thyroid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is leukemia

A

malignant neoplasm of blood or bone marrow

classified into lymphoid or myeloid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is rituximab

A

drug that targets CD20 on surface of lymphoma/leukemia B cells = marks them out for killing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the usual symptoms of bone marrow failure

A

anaemia
infection
bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are auer rods

A

red staining, needle like bodies found in cytoplasm of myeloblasts in certain leukemias (acute myeloid leukemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how is leukemia diagnosed

A
  1. bone marrow sample = more than 20% increase in blast cells
  2. bloods = decreased Plts, low Hb, low neutrophil, myelofibrosis with circulating blasts
  3. lymph node biopsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are the complications of leukemia

A

death
infection
haemorrhage - pulmonary or intercranial
depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are the complications of chemotherapy

A 
anaemia
neutropenia
thrombocytopenia
bystander organ damage
hair loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is chemotherapy

A

combination of drugs that cause damage to rapidly diving cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is anaemia

A

reduced RBC mass with or without decreased haemoglobin concentration
mmicrocytic, macrocytic, normocytic based on RBC size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what are the complications of lymphoma

A 
increased risk infection
recurrence and mets
increased risk CVS disease
complications of chemo
neurological complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what are the normal Hb concentrations

A 
male = 130-180g/L
female = 115-160 g/L
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

describe the pathological changes in anaemia

A

heart/liver fat change
skin/nail atrophy
ischaemia
CNS death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

describe the physiological changes in anaemia

A

reduced O2 transport = hypoxia = compensatory mechanism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what are the symptoms of general anaemia

A

fatigue/lethargy/tiredness
dyspnoea
headaches
faintness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what are the signs of general anaemia

A

conjunctival pallor
hyperdynamic circulation
palpitations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is microcytic anaemia

A

RBCs have a low mean cell volume MCV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is macrocytic anaemia

A

RBCs have a high MCV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

name some microcytic anaemias

A 
iron deficient = most common
thalassemia
chronic disease (late phase)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

name some normocytic anaemias

A

haemolytic anaemia = sickle cell
acute blood loss
chronic kidney disease
chronic disease (early phase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

name some macrocytic anaemias

A 
B12 deficiency (pernicious anaemia) = most common
folate deficiency anaemia
excess alcohol = liver disease
hypothyroidism
chemotherapy
BM failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is epidemiologically significant about sickle cell disease

A

highly prevalent in malarial countries as carriers = increased protection to falciparum malaria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what are the chains of normal Hb

A

2 x alpha, 2 x beta

each chain has haem group which binds to O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what are the chains of foetal Hb

A

2 x alpha, 2 x gamma (y)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

how many genes control alpha and beta Hb

A

4 genes control alpha

2 genes control beta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what is alpha thalassemia

A

caused by depletion of alpha chains
number of faulty genes = severity of disease
highly prevalent in african/asian populations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what is beta thalassemia

A

caused by depletion of beta chains
number of faulty genes = NOT associated with severity
highly prevalent in european communities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what is hydrops fatalis

A

fatal condition not compatible with life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what are membranopathies

A

condition that causes destabilised RBC membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what is hereditary sperocytosis

A

autosomal dominant condition
caused by structural protein loss within RBC membrane
= RBCs abnormally shaped and spherical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what are the 2 types of hereditary spherocytosis

A 
MILD 
= compensated haemolysis
= haemolytic anaemia
= asymptomatic
MODERATE 
= severe anaemia
= splenomegaly during childhood due to RBC lysis
= gallstones often occur due to increased bilirubin levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

how is hereditary spherocytosis treated

A

splenectomy in cases of severe anaemia

no spleen? = needs vaccinating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what are enzymopathies

A

RBCs have nucleus = Enbden-Meyerhof pathway created
enzymopathies = deficiency in enzymes controlling this pathway which results in abnormal RBCs = spleen acts to lysis these

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what is pyruvate kinase deficiency

A

autosomal recessive condition
clinical features of chronic haemolysis
late life presentation
those with disease = prone to aplastic crisis, no RBC production, lysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

define haemolysis

A

rupture or destruction of RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

define reticulocytopenia

A

abnormal decrease of reticulocytes in the body

52
Q

define aplastic crises

A

decrease in Hb
with reticulocytopenia
without evidence of haemolysis

53
Q

how are enzymopathies treated

A

folic acid
transfusion in severe crises
consider splenectomy if recurrent crises to prevent lysis

54
Q

what is polycythaemia

A

increase in RBC mass/haemocrit

55
Q

what is relative polycythaemia

A

an apparent rise in RBC mass, however underlying cause is reduced plasma levels
e.g. dehydration

56
Q

what is erythropoietin

A

hormone released from kidneys

stimulates stem cells in bone marrow to produce RBCs

57
Q

how are platelets produced

A

fragments of megakaryocytes

process regulated by thrombopoietin = produced in the liver

58
Q

what are the normal features of platelets

A

anucleate cells
life span 7-10 days
normal count of 15 to 400x10^9/L
have surface glycoproteins

59
Q

what are platelets activated by

A

adhesion to collagen via GP1a
OR
adhesion to vWF via GP1b and IIb/IIIa

60
Q

what does platelet activation lead to

A
  1. release of alpha granules containing fibrinogen, PDGF, vWF, PF4
  2. release of dense granules containing nucleotides, calcium ions, seratonin
  3. membrane bound phospholipids activating clotting factors 2,5,10
61
Q

describe the process of clotting

A
  1. patelets adhere to vascular endothelium via colagen and vWF
  2. stimulates cytoskeleton shape change w/n platelets
  3. increases SA = platelet activation = release granules to facilitate clotting cascade
  4. platelets aggregate due to cross linking by fibrin
  5. activated Plts provide neg charge phospholipid surface = allows coagulation factors to bind and enhance clotting cascade
62
Q

how is platelet function assessed

A

FBC = number
blood film = appearance
flow cytometry = surface proteins
platelet function analyser PFA = can see response to aggregating agents like collagen/ADP to be seen
bleeding times = small cut in forearm to see how long clotting takes - dont often do this anymore

63
Q

what causes bleeding disorders (4)

A
  1. vascular disorders
  2. low platelet count
  3. abnormal platelet function
  4. defective coagulation
64
Q

what are the clinical features of bleeding disorders

A 
mucosal bleeding
gum bleeding
epistaxis (nose bleed)
menorrhoea
easy bruising
petechiae/purpura (dotty rash)
traumatic haematomas
65
Q

name 3 congenital causes of impaired platelet function

A

von Willebrand disease
Bernard soulier
Glanzmann’s thrombasthenia

66
Q

name 2 acquired causes of impaired platelet function

A

uraemia

drugs = clopidogrel, aspirin

67
Q

what is Bernard-Soulier syndrome

A

autosomal recessive disease leads to deficiency in glycoprotein Ib =
prolonged bleeding time
low (or norma) platelet count

treat with desmopressin to decrease bleeding time and recombinant activated factor VII

68
Q

what is Glanzmann’s thrombasthenia

A

autosomal recessive or acquired autoimmune condition = platelets are deficient of GPIIb/IIIa
bleeding time is prolonged
treat with desmopressin + recombinant activated factor VII

69
Q

what is von Willebrand disease

A 
caused by defect in vWF
causes:
increase activated partial thromboplastin time
increased bleeding time
normal prothrombin time (PT)
decreased vWF
decreased factor VIIIc
70
Q

what is haemophilia

A

inherited condition that causes lack of factor VIII (type A) or lack of factor IX (type B)
PT time normal
increased partial thromboplastin time
X LINKED RECESSIVE

71
Q

how do you treat haemophilia

A

replace missing clotting factors with regular transfusions

72
Q

define thrombocytopenia

A

low platelet count (due to increased platelet usage or decreased platelet formation)

73
Q

what causes SIRS

A 
systemic inflammatory response syndrome
trauma(inluding surgery)
sepsis
septic shock
pancreatitis
malignancy
74
Q

what is bone marrow failure

A

reduction in number of pluripotential stem cells together with a fault in those remaining/immune reaction against them
= unable to repopulate
can occur in only 1 cell line = isolated deficiencies

75
Q

what are the investigations in BM failure

A

FBC = pancytopenia with low reticulocytes

BM biopsy = hypocellular marrow with increased fat spaces

76
Q

how would you treat bone marrow failure

A

removal of causative agent
cautious blood/platelet transfusion
if worse = BMT or immunosuppressive therapy

77
Q

which age group is characteristically affected by hodgkins lymphoma

A

children and YA

78
Q

what type of drug is ondansetron

A

anti-emetic

79
Q

what is the mechanism of action of ondansetron

A

5HT3 antagonist = for chemo induced nausea

80
Q

where are RBCs removed

A

spleen
liver
BM
blood loss

81
Q

what types of infection see raised lymphocytes

A

viral

82
Q

what types of infection see raised neutrophils

A

bacterial

83
Q

what is febrile neutropenia

A

haematologic emergency
ABC
perform cultures
broad spec IV Ab within 1r e.g. tazosin and gentamicin

84
Q

what does malignant spinal cord compression present with

A

back pain

spastic paresis and sensory level

85
Q

how to manage malignant spinal cord compression

A 
emergency
urgent MRI
bed rest + pressure care area
steroids
analgesia
chemo/radiotherapy
86
Q

how does aspirin exert antiplatelet effect

A

cyclooxygenase inhibitor

87
Q

how does clopidogrel exert antipplatelet effect

A

P2Y12 inhibitor

88
Q

how does tirofiban exert antiplatelet effect

A

GPIIb/IIIa inhibitor

89
Q

what is the reticulocyte count expected to be in sickle cell anaemia

A

raised

90
Q

what is alendronic acid and what is it usually taken with

A

bisphosphonate drug reduces rate of bone turnover to prevent osteoporosis
taken with vitamin D/calcium supplement

91
Q

what advice is given to people taking alendronic acid and why

A

regular dental checkups because can cause osteonecrosis of jaw

92
Q

what is letrazole

A

aromatase inhibitor that stops androgens conversion to oestrogen = lower oestrogen levels to prevent cancer growth

93
Q

what group of women is letrazole used in

A

ONLY works in post-menopausal women

94
Q

what is the difference between acute and chronic leukemias

A

acute leukemia = cells dont mature at all, rapid progression with no treatment
chronic leukemia = cells partially mature

95
Q

describe the pathophysiology of chronic myeloid leukemia

A
  1. chromosomal translocation = philadelphia chromosome (BCR-ABL protein)
  2. myeloid leucocytes (granulocytes/monocytes)
  3. stop maturing and divide too fast
  4. buildup and cause hepatosplenomegaly (MASSIVE SPLENOMEGALY)
96
Q

describe the pathophysiology of chronic lymphoid leukemia

A
  1. chromosomal abnormality = interfere with B receptor
  2. lymphoid leucocytes (B cells)
  3. stop maturing and die too slowly
  4. buildup and cause lymphadenopathy (rubbery lymph nodes)
97
Q

how does a chromosomal mutation cause AML/ALL

A

cells lose ability to differentiate = dont function properly
cells undergo uncontrollable division = crowd out other cells in BM and cause cytopenias e.g. anaemia/thrombocytopenia/leucopenia = symptoms

98
Q

what cells are characteristic of hodgkins lymphoma

A

reed-sternberg cells

99
Q

which lymphoma is more common

A

nonhodgkins is more common

100
Q

what type of cancer does epstein-barre virus most commonly cause

A

non hodgkin lymphoma

101
Q

describe reed-sternberg cells

A 
large lymphoid cell of B cell origin
2 nuclei
eosinophilic nucleolus 
= owl eye appearance
FOUND IN HODGKINS LYMPHOMA
102
Q

describe ABVD chemo

A

adriamycin
bleomycin
vinblastine
dacarbazine

103
Q

describe the mneumonic for presentation of myeloma

A

CRAB

  1. Calcium = increased due to increased osteoclast activity = dehydration, constipation, confusion
  2. Renal impairment = increased Ca and dehydration
  3. Anaemia = low BM RBC production = anaemia symptoms
  4. Bone lesions = high osteoclast activity = pepper pot skill, bone pain, hypercalcaemia
104
Q

what is antiwarfarin

A

phytomenadione (vitamin K)

105
Q

what is antiheparin

A

protamine sulphate

106
Q

what is glucose-6-phosphate dehydrogenase deficiency

A 
X linked recessive disorder
G6PD = enzyme protects against oxidant injury in RBC
deficiency = increased haemolysis
= haemolytic anaemia
precipitated by fava beans!!!!!!
107
Q

what is immune thrombocytopenia purpura ITP

A

AI platelet destruction = antibodies form against platelets and destroy
caused by virus in children/SLE in adults
cause increased bleeding symptoms
prednisalone to treat

108
Q

what is thrombotic thrombocytopenic purpura TTP

A

can be congenital/AI
ADAMTS13 = degrade vWF
lack of ADAMTS13 = no vWF degradation = widespread aggregation of platelets = microvascular thrombosis in heart/lungs/brain

cause increased bleeding symptoms + cerebral dysfunction + renal failure
bloods = raised lactate dehydrogenase
requires plasma exchange

109
Q

what is disseminated intravascular coagulation DIC

A

cytokine response to SIRS = systemic activation of clotting cascade = excess diffuse clotting which then depletes platelets/clotting factors = uncontrolled bleeding
cause bleeding at unrelated sights
positive D dimer
platelet transfusion needed

110
Q

what age group does non-hodgkins lymphoma usually present in

A

rare before 40 = disease of older age

111
Q

describe ann arbour staging of hodgkins lymphoma AND non-hodgkins

A 
1 = only 1 lymph node affected
2 = 1+ lymph node on same side of diaphragm
3 = lymph nodes on both sides of diaphragm
4 = spread to organs - liver/BM
A = absence of B symptoms
B = B symptoms
112
Q

what are B symptoms in the presentation of hodgkins lymphoma

A 
= systemic
fever
weight loss
night sweats
lethargy
113
Q

what is the difference between hodgkins and non-hodgkins lymphoma

A 
hodgkins:
= B + T cell involved
= Ann arbour staging
= Reed-Sternberg cells
= more treatable/survivable
= NO rituximab given (CD20 NOT present)
non-hodgkins:
= 70% B cell 30% T cell involvement
= extranodal involvement more common (MALT cells)
= worse prognosis 
= rituximab Tx
114
Q

which anaemia should you NOT treat with folic acid

A

B12 deficiency/pernicious anaemia

115
Q

what is the most common cancer in children

A

acute lymphoblastic leukemia

116
Q

what cancer shows smudge cells on a blood film

A

chronic lymphoblastic leukemia

117
Q

what drugs are used to treat AML

A

chemo - cytarabine + anthracycline

118
Q

what drugs are used to treat ALL

A

chemo = vincristine
with prednisolone
intrathecal methotrexate

119
Q

what drugs are used to treat CML

A 
imatinib
sibling SCT (not v reliable)
can transform to acute leukemia = bad prognosis
120
Q

what drugs are used to treat CLL

A

fludarabine = lowers blood count and decreases lymphadenopathy /organmegaly
cyclophophamide
prednisolone
possible monoclonal Ab

121
Q

what is a burkitts lymphoma

A

very high grade non-hodgkins lymphoma

122
Q

what does the presence of bence jones proteins in the urine suggest the diagnosis is

A

multiple myeloma

123
Q

what is a rare but classic complication of polycythaemia

A

can progress to acute myeloid leukemia

124
Q

what blood cancer shows blast cells on blood film

A

ALL

125
Q

which blood cancer is most likely to present with gum hypertrophy

A

acute myeloid leukemia

Phase 2a (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions