Revision Flashcards
1
Q
what is serum
A
clotted plasma
2
Q
what is the liquid in blood
A
plasma
3
Q
what is haematopoiesis
A
production of blood cells
4
Q
where does haematpoiesis occur
A
embryo- yolk sac then liver then marrow
birth- bone marrow, liver and spleen when needed
adult- bones in axial skeleton: skull, ribs, sternum, pelvis, proximal ends of femur
5
Q
what are the steps in the haematopoietic tree
A
stem cells multipotent progenitors (ones that proliferate the most) oligolineage progenitors (becomes the different types of these depending on the bodys needs) mature cells (RBC, platelets, granulocytes, macrophages, dendritic, T cells, B cells, NK cells)
6
Q
what is erythopoiesis
A
formation of mature red blood cells
7
Q
what are the stages in erythropoiesis
A
pronormoblast
(lots of others, all in bone marrow, cell and its nucleus gets smaller each differentiation)
reticulocyte (enters circulation)
mature red cell/ erythrocyte
8
Q
what is a reticulocyte
A
immediate precursor of red blood cell, has no nucleus but some RNA which makes it appear darker in colour
is in the circulation not bone marrow
9
Q
what do platelets originate from
A
bud off megakaryocytes (cytoplasm doesnt divide)
10
Q
what is the role of platelets
A
stop bleeding
11
Q
what are the types of granulocytes
A
eosinophils
basophils
neutrophils
12
Q
what are granulocytes
A
most common type of WBC, contains granule
13
Q
what are neutrophils
A
type of granulocyte
first white cell to respond in an infection (Q specific to bacterial infections)
14
Q
what are polymorphs
A
different name for neutrophils (called this because segmented lobular nucleus)
15
Q
what is the main phagocytosing cell
A
macrophage
16
Q
what are the roles of neutrophils
A
short life in circulation- goes to tissues where it:
phagocytoses invaders
kills with granule contents (dies in process)
attracts other cells
17
Q
what can increase neutrophils
A
body stress - infection, trauma, infarction
steroids (makes them unable to leave blood stream and get into tissues)
18
Q
what are eosinophils
A
type of granulocyte
are bilobed, granules makes them look red-orange
19
Q
what are the roles of eosinophils
A
fight parasitic infections
involved in hypersensitivity reactions/ allergic conditions
20
Q
what are basophils
A
type of granulocyte w/ purple- black granules
21
Q
what are the roles of basophils
A
mediates hypersensitivity reactions
granules contain histamine
FcReceptors bind IgE
22
Q
what are monocytes
A
largest type of white blood cell, pale, single nucleus
23
Q
what is the role of monocytes
A
circulate for a week then enter tissues to become macrophages
-phagocytose invaders (endocytosis, present antigen to lymphocytes)
-attract other cells
more long lived than neutrophils
24
Q
what is the structure of lymphocytes
A
mature- small
activated (aka atypical)- large open structure
25
what is the function of lymphocytes
lots of diff types: B, T, NK
| adaptive immune system
26
where are common sites for bone marrow aspiration/ biopsy
posterior iliac crests
27
what are target cells
In liver disease the red cell membrane is disrupted which causes change in shape of the red cell from pale bit in the middle (concave) --> dark part in the middle = target cells
28
what is the most common cause of macrocytic anaemia
liver disease (due to alcohol most commonly, then NAFLD)
29
what are the Hb levels below which probs means anaemia
```
children 6mnth-6yrs = 110
6-14 120
men 130
females 120
pregnant females 110
```
30
what are haematinics
MCV
| MCH (cell Hb content)
31
what does anaemia with increased reticulocyte mean
caused by haemolysis or blood loss
32
what does anaemia with reduced reticulocyte mean
maturation abornmalty or hypoproliferative
33
what will MCV be like in hypoproliferative anaemias
normocytic (and normochromic)
34
what can distinguish haemolysis from blood loss causing anaemia
(obvs Hx and clinical picture, blood film)
if bleeding then rbcs gone, nothing to breakdown
if haemolysing:
-increased unconjugated serum bilirubin
-increased urinary urobilinogen
-work hypertrophy (splenomegaly)
35
what causes hypochromic microcytic anaemia
problems with haemoglobin formation:
- iron deficiency
- haem defects (rare, lead poisoning, congenital sideroblastic anaemia)
- globin defects (thalassaemias)
36
what causes macrocytic anaemias
nuclear maturation defects (failure of cell division)
- diet: B12, folate (megaloblastic)
- myelodysplasia
- drugs e.g. chemo
37
what can cause macrocytosis without significant anaemia
hypothyroidism
alcohol
liver disease
38
what can cause normochromic normocytic anaemia
hypoproliferative:
-marrow failure :drug induced, aplastic anaemia (can be mactocytic)
hypometabolic (can be macro)
marrow infiltration (mets, fibrosis)
renal impairment
chronic disease (infective. inflammatory, malignant= anaemia of chronic disease) (can be micro)
39
what is renal anaemia
an anaemia of chronic disease due to failure of erythropoietin production
40
what is the second most common cause of anaemia after iron deficiency
anaemia of chronic disease
41
what causes anaemia of chronic disease
inflammatory stimulus activates monocytes and T cells which releases inflammatory cytokines:
- inhibits erythropoietin release
- inhibits erythroid proliferation
- augments haemophagocytosis = reduced red cell survival
- increases hepatic syntheses of hepcidin (negative regulator of iron absorption, decreasing iron)
42
why might anaemia of chronic disease by microcytic
If the predominant mechanism is through hepcidin stimulation
reduced release of iron from macrophages ie failure of haemoglobin synthesis
Explains low transferrin saturation despite normal/raised ferritin
Explains why it may respond to IV iron
43
are iron def anaemias always microcytic
no- relative measure so many normocytic (in normal range just not normal for the individual)
44
how do you differentiate anaemia of chronic
serum iron:
- ID: reduced
- ACD: reduced
transferrin:
- ID: normal/ increased
- ACD: normal/ reduced
% transferrin sat:
- ID: reduced
- ACD: reduced
Ferritin:
- ID: reduced
- ACD: normal/ increased
MCV:
- ID: reduced (can be normal)
- ACD: normal (can be reduced)
45
what are the implications of the biconcave shape of ebcs
needed for increased gas exchange
| need more room for Hb so why nucleus removed
46
what is needed to make the rbc flexible
lipid bi layer membrane with protein spars and anchors
47
what is enucleation
when the nucleus is budded off with other organelles and functional fibrous proteins (absorbed by the macrophage)
48
In what circumstances might nucleated red cells appear in the blood?
bone marrow damage or severe stress
- severe anaemia
- thalassaemia
- hypoxia
- myelomas
- leukemias
- lymphomas
- myelofibrosis
removal of spleen can make immature cells more apparent in the blood
49
is Fe2+ or Fe3+ oxygenated- which one is blue or red
Fe2+ deoxygenated- blue
| Fe3+ oxygenated- red
50
what does free iron cause
is toxic- causes inflammation
51
what can free Hb cause in the blood
can be life threatening
| can cause DIC and other dysfunctional responses
52
what different mechanisms can cause red cell membrane damage
Mutations in cytoskeletal proteins resulting in the cell membrane not working well:
- Hereditary spherocytosis (this is usually autosomal dominant)
- RARE! Zieve’s syndrome: haemolysis related to alcoholic liver disease. Abnormalities of lipid metabolism results in red cell membrane damage
Autoimmune haemolytic anaemia: autoantibodies against red cells damage the red cell membrane
Infection
- DIC(disseminating intravascular coagulopathy)
- Sepsis
Mechanical damage
- Severe burns: capillaries are damaged and as blood vessels squeeze through these they get sheared resulting in microspherocytes
- Heart valve
- Haemolytic Uraemic Syndrome (E.Coli)
- Thrombotic Thrombocytopenic Purpura (TTP)
53
what virus might cause a decompensation in HS
parovirus
| virus enters bone marrow and stops erythroid precursors from dividing
54
What are the sources of energy and reducing powers which protect the red blood cell against oxidative damage?
(Anaerobic) NADH and NADPH are important molecules generated by the cycle (direct or hexose monophosphate shunt)
G6PD contributes to formation of glutathione which is required for NADPH formation
55
what does a G6PD deficiency result in
reduced protection from oxidative damage
56
what is dapsone
antibiotic previously used in the treatment of leprosy
| can induce oxidative stress
57
what drugs induce oxidative stress
dapsone, quinines, anti-malarials, fava beans
| can lead to splenomegaly
58
what are the clinical manifestations of increased oxidative damage
tiredness, lethargy, pale gums, pallor, jaundice
59
what are heinz bodies
Red cells with haemoglobin exposed to oxidative stress-->Hb has been oxidised + damaged-->clumped together in a ball (Heinz body)-->red cells are contracted-->heinz body anaemia
this seen in G6PD deficiency causing haemolytic anaemia
60
what can cause a problem with Hb synthesis
Haem production
- Iron deficiency
- Porphyrin synthesis
Globin production
-Thalassaemia
61
what are the symptoms and signs of microcytic hypochromic anaemia
Signs: Tachycardia, tachypnoea, rising pulse or even extra heart sound, pallor
Symptoms: Palpitations, lethargic, fatigue, TATT, tinnitus, somnolence
62
how does the red cell try and improve oxygen delivery in microcytic anaemia
increase 2,3-DPG to increase oxygen dissociation
63
what codes for beta chains
1 gene on each chromo 11
64
what are the affects of beta thalassaemia major
Failure to thrive
General Sx of anaemia
Splenomegaly
Chronically - permanent bone marrow changes. Frontal bossing, skeletal deformities, spinal cord compression
65
what is B12 important for the production of
thiamine
66
what are agranulocytes
leukocytes and monocytes
67
what are the symptoms of megaloblastic anaemia
Pallor, mild jaundice (lemony tinged), red beefy tongue, reduced vibration and proprioception sense (dorsal columns): rely on proprioception in the dark (falling over in the night), lemony tinged/mild jaundice
68
what causes sickle cell anaemia
substitution of valine for glutamic acid at codon 6 of beta glogin gene
homozygotes produce only haemoglobin S and variable amount of haemoglobin F
sickled red cells produces microvascular obstruction and ischaemia
69
```
Pale patient
Mildly jaundiced
No obvious bleeding
Dark urine
suspect what?
```
haemolysis
70
what tests to confirm haemolysis
Blood film: polychromasia, spherocytes
Reticulocytosis
Unconjugated hyperbilirubinaemia
if intravascular : haemoglobinuria haemosiderinuria methaemalbuminaemia
71
what are the acuired immune causes of haemolysis
Autoimmune: spherocytic
Alloimmune: haemolytic disease
of the newborn (non-spherocytic)
ABO mismatch transfusion
72
what are the non immune acquired causes of haemolysis
Mechanical: prosthetic heart valve,
disseminated intravascular coagulation
Infection: malaria, Clostridium welchii
Chemical/ physical: oxidative stress
(aspirin, dapsone, anti-malarials), burns
Membrane: liver disease
73
what are the inherited causes of haemolysis
red cell enzyme defects: G6PD def
red cell membrane defects: HS, hereditary elliptocytosis
74
what diagnostic tests for haemolysis
Direct Coombs test: detects antibody coated red cells using antisera to immunoglobulins; end point is red cell agglutination
Osmotic fragility test: incubate red cells in increasingly hypotonic solutions and measure release of haemoglobin from lysed cells. Increased fragility in hereditary spherocytosis.
G-6-PD enzyme activity screening test: quantitate fluorescence of NADPH generation by G-6-PD. Detects enzyme activity <20%
75
what are causes of macrocytosis not related to B12 or folate deficiency
Drugs: methotrexate/ AZT/ metformin
Alcohol abuse/ liver disease/ myelodysplasia (stem cell dysfunction) /myeloma/anaplastic anaemia/ hypothyroidism
pregnancy, neonatal, reticulocytosis
76
why would hypothyroidism be relevant in a Hx of macrocytic anaemia
as can cause macrocytosis but also is associated with pernicious anaemia
77
what is pernicious anaemia
autoimmune condition that results from atrophic gastritis and destruction of the gastric parietal cells ultimately leading to a reduction in intrinsic factor.
IF is required to bind to vitamin B12 to allow absorption in the terminal ileum.
Pernicious anaemia is also linked with other autoimmune conditions such as hypothyroidism, vitiligo and addison’s disease.
78
is macrocytosis always associated with anaemia
no
79
what is the most common cause of macrocytosis
alcohol consumption
80
what does a MCV >120 mean
macrocytosis usually caused by def of B12 or folate
81
what does macrocytosis with anaemia and also low neutrophils or platelets
Megaloblastic or myelodysplasia more likely
82
macrocytosis blood film:
| hypersegmented neutrophils, oval macrocytes
megaloblastic
83
macrocytosis blood film:
| uniform macrocytosis
alcohol
84
macrocytosis blood film:
| dysplastic neutrophils
myelodysplasia
85
macrocytosis blood film:
| polychromasia
reticulocytosis
86
macrocytosis blood film:
| agglutinates
artefacts with cold agglutins
87
what are the causes of microcytic anaemias
iron deficiency
anaemia of chronic disease
thalassaemia
sideroblastic anaemia
88
what is the best test for diagnosing iron deficiency anaemia
serum ferritin (should be low showing lack of iron stores)
FBC
if symptomless: GI endoscopy, barium enema/ colonoscopy
89
what happens to reticulocytes in iron deficiency
reduced
| raised if bleeding
90
how else can you measure storage iron
bone marrow biopsy with perls stain
91
which iron in body is depleted first
storage iron
| then transport iron
92
what are the causes of iron deficiency
```
Reduced dietary iron
Increased physiological requirements
Blood loss (menstruation, GI)
Malabsorption
jejunum
need gastric acid
```
93
why in acute bleeding might the Hb underestimate any blood loss
as redistribution of body water has not yet fully allowed dilution of the remaining red cells
94
what fluid is 1st line in the acutely shocked patient
synthetic colloids
95
when is reticulocytosis maximal after a bleed
8-10 days after (begins days 1-2)
96
what is an appropriate marrow response to marked anaemia
6-8 fold increase in reticulocyte count
(3-4 fold increase in amount of erythropoiesis +
earlier release of reticulocytes into blood)
97
what are the signs of shock
```
Tachycardia
Hypotension (postural)
Tachypnoea
Peripheral vasoconstriction (pallor, delayed capillary refill)
Oliguria
```
98
what are the causes of vasogenic shock
anaphylaxis
| sepsis
99
how is blood cross matched
ABO and RhD antigen grouping of patient
Screen for alloantibodies in patient:
-Antibodies in the patient to antigens that might be on the donor red cells
-If alloantibody identified in patient check donor unit is negative for that antigen
Mix donor cells and recipient plasma as a final check in wet crossmatch
Confirm historical records for an electronic crossmatch
quickest test ABO group
100
what types of blood are available (maybe if not time to do all tests)
O RhD negative
ABO type specific
Fully crossmatched
Electronic crossmatched (if historical group and negative allo antibody screen)
101
what can ABO transfusion reactions cause
DIC and death
102
when and why do delayed transfusion reactions occur
IgG alloantibody to red cells antigen
Acquired following previous transfusion or pregnancy
at low level but secondary response 10 days later
103
what are the immune complications of transfusion
febrile non-haemolytic reactions (white cell antibodies/ hypersensitivity to donor plasma proteins)
immediate (intravascular- acute haemolytic- ABO) or delayed (extravascular- IgG- red cell antigen) haemolytic reactions
urticarial reactions
taGVHD, PTP, IgA deficiency, TRALI
104
what is the role of VWf
helps platelets stick together and to collagen in the endothelium
also binds to factor 8 to protect it from destruction, increasing its half life
105
how do you screen for problems in primary haemostasis
```
(usually results in mucosal bleeds)
platelet count (within FBC)
```
106
what is the extrinsic, intrinsic and final common pathway
parts of secondary haemostasis
Extrinsic factors= Tissue factor released first in tissue damage, this activates factor 7 (becomes CF VIIa)- when activates has a negative charge, binds to positive (calcium) platelets
TF and CF 7 activate factors 5 and 10, which then activate prothrombin to thrombin (prothrombin is CF II)
Thrombin converts the protein fibrinogen to fibrin which forms stable blood clot.
Intrinsic pathway= thrombin activating factors 8 and 9 which in turn activates factors 5 and 10, allows rapid response and quick formation of a fibrin clot
Also have factors 11 and 12 (if 12 missing no clinical consequences) (if 11 missing can get bleeding problems but not as significant as other CF)
Final common pathway= prothrombin -> thrombin and fibrinogen -> firbrin
107
what tests make up a coagulation screen
prothrombin time
activated partial thromboplastin time
(additional tests sometimes done inc. fibrinogen assay, thrombin time (surrogate marker for fibrinogen), heparin
108
what coagulation tests assess the extrinsic and intrinsic pathways
```
extrinsic= PT
intrinsic= APTT
```
109
what is a normal platelet range
150-400
110
19 year old with menorrhagia and easy bruising
Isolated prolonged APTT
normal platelets
VWF deficiency
111
what can cause an isolated prolonged APTT
factor 8 or 9 deficiency (haemophilia)
heparin
APS
112
what are the features of APS
autoimmune condition, that causes increased blood clots (arterial and venous and miscarriage)
113
why do you get prolonged APTT in APS
lupus anticoagulants interfere with assay and prolong APTT. Anti body binds to antiphophospholipid which are used in tests
114
why do people with VWf deficiency have a prolonged APTT
VWf binds to factor 8 to protect it from destruction prolonging its half life. Those with VWf def will have low factor 8 (not as much as in haemophilia) but enough to cause increase in APTT
115
59 year old male with past history of thromboembolic disease
prolonged PT and APTT
normal platelets
warfarin therapy
116
what can cause prolongation of PT and APTT
multiple factor deficiency, DIC, liver disease (don’t make clotting factors and increased platelet destruction due to hypersplenism), warfarin (affects 2,7,9,10 as antagonises vit K which is required for the carboxylation of these clotting factors), vit k deficiency (diet- leaf green veg, intestinal synthesis- haemorrhagic disease of the newborn (no vit k in breast milk and no gut bacterial), obstructive jaundice (is a fat soluble vitamin and bile salts are needed to absorb it)
117
what is the placenta v rich in
tissue factor and phopsholipids- why DIC happens in placental abruption
118
what is the target range for INR
2-3
119
what is the target APTT for those on heparin
1.5-2
120
what do NOACs target
CF Xa
thrombin
(more direct action so dont need monitoring)
121
what does thrombin clotting time show
fibrinogen levels
122
what tests can confirm DIC
```
low platelets, markedly prolonged APTT and PT
D dimers (fibrin degradation products, will be high)
```
123
what are the differentials for an acute onset red swollen leg
```
DVT
cellulitis
lymphoedema
trauma
ruptured bakers cyst
```
124
what tests for a DVTT
doppler USS
| D-dimer (can exclude if low, high can be caused by lots of things)
125
is smoking a risk factor for arterial or venous clots
arterial (provokes atherosclerosis pathophysiology)
126
what can decrease anticoagulant defences
hereditary deficiency in proteins C and S (factor 5 leiden or heretary deficiency), antithrombin
127
why does the COCP increase clot risk
makes body think its pregnant by increasing oestrogen
| this causes increased CFs and fibrinogen
128
what type of vessel damage increases the risk of a VTE
valve damage- age (collagen loss), previous VTE (risk massive is previous VTE was spontaneous without provoking factor)
(NOT atherosclerosis= arterial)
129
factor V leiden patient (X5 risk) goes on COCP (X6 risk)
what is there new risk of a VTE
x30 (risks times each other dont add up= synergistic)
130
what are the non inherited risk factors for VTE
Age: vessel damage, stasis
Marked obesity: stasis, hypercoagulable (fat cells secrete cytokines e.g. IL 6 that increase coagulation)
Pregnancy (hypercoagulability, stasis)
Puerperium (hypercoagulability, stasis)
Oestrogen therapy (hypercoagulability)
Previous DVT/PE (vessel damage)
Trauma/Surgery: (highest risk surgery lower limb orthopaedic surgery) stasis and hypercoagulability
Malignancy: tissue damages releases TF increases coagulation, immobility
Paralysis: Immobility - stasis
Infection (hypercoagulability)
Thrombophilia (hypercoagulablility)
131
what measures can be taken to reduce risk of VTE after surgery
```
early mobilisation
compression stockings
flowtron boots
LMWH
fonaparinux sodium (inhibits CF Xa)
```
132
what must you ensure the patient doesnt have before firring compression stockings
arterial disease - ensure peripheral pulses good
133
what does LMWH predonminantly target
activated factor 10
134
why would you choose LMWH over warfarin in clot prevention after surgery
immediate action
warfarin antagonises vit K so takes a while for CFs to decrease, however in first few days it decreases proteins c and s making the patient hypercoagulable
warfarin needs to be monitored by APTT
135
why would you choose LWMH over unfractionated heparin
unfractionated needs to be given IV and needs more monitoring (APTT)
136
what does unfractionates heparin predominantly target
antithrombin (protentiates it action) and then CF Xa binds to this complex
137
what are acanthocytes
spicules (spikes) on RBCs caused by unstable membrane due to splenctomy, alcoholic liver disease, spherocytosis
138
what are blasts
nucleated precursor cells, appear in myelofibrosis or malignancy
139
what are cabot rings
seen in pernicious anaemia, lead poisoning and bad infections
140
what are howell jolly bodies
DNA nuclear remnants in RBCs, normally removed by spleen, seen post splenectomy, hyposplenism (e.g. sickle cell, coeliac, crohns/uc, myeloproliferative, amyloid)
141
what is rouleaux
stacking of red cells (chronic inflammation, myeloma)
142
what are spherocytes
spherical cells seen in HS and autoimmune haemolytic anaemia
143
what are target cells
RBCs with central staining, a ring of pallor and outer ring of staining
seen in liver disease, hyposplenism, thalassaemia
144
what are pappenheimer bodies
granules of siderocytes containing iron, seen post splenectomy
145
when should you vaccinate beofre splenectomy
2 weeks before (can give all types)
| may also need lifelone Abx prophylaxis
146
what is the test for EBV
IgM response
| if this negative test for HIV
147
what are pencil cells a sign of
iron deficiency
148
what should mature red cells be the same size as
lymphocyte nucleus
149
what do you see macrovalocytes and hypersemented (more than 5 segments) neutrophils in
B12 and folate def
150
where do you get haemolysis in macrosytosis
in bone marrow as cells too big to leave
151
lacking central pallor + spherical = ?
spherocytes
152
what is the test for autoimmune haemolytic anaemia
direct coombs test
153
what are schistocytes
fragmented RBCs: look for microangiopathic anaemia (anything that fragments RBCs- mechanical damage, DIC, HUS, TTP, pre-eclampsia)
154
what are the signs of hyposplenism on a blood film
howell jolly bodies
| target cells
155
should you normall ahve more neutrophils or lymphcytes
neutrophils
156
what causes lympcytosis
acute viral infections, chronic infections, leukaemias and lymphomas (esp chronic lymphcytic anaemia)
157
62 yr old woman visiting GP generally under the weather. Feels exhausted all the time, everything is an effort the last few months. Gets very short of breath even just walking up a flight of stairs and everyone says how pale and gaunt she is looking. Has lost a fair bit of weight over the last 3 months too
blood tests: hypochromic microcytic anaemia
what test would you do to confirm the cause of the anaemia
serum ferritin
158
62 yr old woman visiting GP generally under the weather. Feels exhausted all the time, everything is an effort the last few months. Gets very short of breath even just walking up a flight of stairs and everyone says how pale and gaunt she is looking. Has lost a fair bit of weight over the last 3 months too
blood tests: hypochromic microcytic anaemia
she also has neutrophilia and thrombocytosis- why might this be
reactive changes to underlying inflammatory problem
159
62 yr old woman visiting GP generally under the weather. Feels exhausted all the time, everything is an effort the last few months. Gets very short of breath even just walking up a flight of stairs and everyone says how pale and gaunt she is looking. Has lost a fair bit of weight over the last 3 months too
blood tests: hypochromic microcytic anaemia
what is the most likely cause
malignancy of the GI tract causing occult blood loss/ anaemia of chronic disease resulting in iron deficiency anaemia
160
A 52 year old woman with a past history of graves disease presented with a six month history of increasing fatigue. Family members thought she was looking jaundiced and sent her to the GP. He checked her bloods and sent her into the medical admissions ward for an urgent transfusion.
FBC: pancytopenia, macrocytic anaemia, oval macrocytes, circulating megaloblasts, macrocytic normochromic anaemia
what test would you do to establish the diagnosis
serum B12 and folate
161
what would bone marrow look like in megaloblastic anaemia
hypercellular
| lots of output activity but ineffective erythropoesis so increases apoptosis - jaundice
162
Patient is B12 deficient and has intrinsic factor auto antibodies confirming the diagnosis of pernicious anaemia (PA).
Why is she jaundiced?
B12 deficiency causes premature red cell destruction in the marrow resulting in excess bilirubin production
163
A 23 year old male found wandering the streets confused and aggressive. Was thought to be smelling of drink. On admission febrile, tachycardic and hypotensive.
reactive features on FBC- neutrophilia and monocytosis
what might be the causes of this
sepsis
| alcohol wouldnt increase white cells that much
164
what does it mean if a neutrophil has vacuoles
is angry- immune response has been initiated
165
This man was seen in the haematology clinic for annual review. He is of short stature and jaundiced. His gallbladder was removed when he was 12 years old. His father is similarly affected. he has splenomegaly
blood film: polychromasia, spherocytes
what blood test would confirm haemolysis
reticulocyte count
166
what is the test for autoimmune haemolysis
coombs test (direct antiglobulin)
167
This man was seen in the haematology clinic for annual review. He is of short stature and jaundiced. His gallbladder was removed when he was 12 years old. His father is similarly affected. he has splenomegaly
blood film: polychromasia, spherocytes
hereditary spherocytosis
168
do you use genetic tests to diagnose spherocytosis
no as not caused by one single gene
169
what treatment for hereditary spherocytosis
if have compensated haemolysis and are fully grown= folate supplements
if still growing/ decompensated haemolysis= splenectomy
170
why might someone with HS be short
chronic marrow hyperplasia- when growing all energy was put into making red cells
171
This 59 year old woman presented two weeks following a valve replacement for bacterial endocarditis with a history of increasing shortness of breath.
normocytoic normochromic anaemic (has some large and some small cells on blood film)
why is the MCV normal
there are both large and small cells and the mean is normal as a result
172
This 59 year old woman presented two weeks following a valve replacement for bacterial endocarditis with a history of increasing shortness of breath.
normocytoic normochromic anaemic (has some large and some small cells on blood film)
what will the small and large cell be
small- spherocytes
| large- reticulocytes
173
This 59 year old woman presented two weeks following a valve replacement for bacterial endocarditis with a history of increasing shortness of breath.
normocytoic normochromic anaemic (has some large and some small cells on blood film)
what is the diagnosis
microangiopathic haemolytic anaemia
(conditions that cause red cell fragmentation resulting in haemolytic anaemia- in this case mechanical damage to cells form valves)
174
what tests make up a coagulation screen
```
PT
APTT
INT
FBC
depending on NHS region- fibrinogen assay and thrombin time
```
175
what are the causes of a low platelet count
hereditary: inherited thrombocytopenia
acquired: increased destruction (heparin induced thrombocytopenia, ITP, SLE, TTP, DIC, HELLP, HUS), reduced production (diet (b12 and folate def), myelosuppression from chemo, myeloma/ leukemia/lymphoma, aplastic anaemia, viral infection, hep A/B/C, long term alcohol use)
176
what are the common causes of shock
```
o Hypovolaemic
Haemorrhage
Burns
Renal disease
o Cardiogenic
MI
Arrhythmias
o Distributive
Anaphylactic
Sepsis
Neurogenic
o Obstructive
Tension pneumothorax
Cardiac tamponade
```
177
how is shock treated
```
o Fluids
o Oxygen
o Treat the cause of shock; antibiotics, blood, adrenaline, stabilisation (C-spine), ionotropes, pacing, steroids (addisonian crisis, myxoedema coma)
o Sepsis 6
o Stop bleeding
```
178
when does the bone marrow start blood production
16 weeks, before this liver and yolk sac
179
how is venous thrombosis treated
DOAC/ low molecular weight heparin
180
which works quicker heparin or warfarin
heparin
181
what factor influence warfarin control
drinking, drugs, liver enzymes
182
what is the screening test for primary haemostasis
platelet count
183
what can cause thrombocytopenia
hereditary (rare)
acquired:
- reduced production (bone marrow failure: leukaemia, lymphoma, parovirus B19 (aplastic anaemia)
- increased destruction (DIC, ITP, hypersplenism)
- drugs (aspirin, NSAIDS)
- renal failure
184
what can cause failure of fibrin clot formation
multiple factor deficiency: DIC, liver failure, vit K def, warfarin therapy
(will have prolonged PT and APTT)
single CF deficiency: haemophilua
185
what is a 'rub' seen in
PE
186
why is an abdo/pelvic mass a risk factor for VTE
might compress IVC/ causes stasis
187
can you do a V/Q scan in pregnancy
yes
188
are D dimer sensitive or specific
sensitive
189
who should you not request D dimers in
people with malignancy, pregnancy, sepsis, post op (will be raised in all of these)
190
what can a D dimer definitively tell you
(want to reduce need for imaging)
| patients that are low from from a clinical scoring system and have a negative d imers = no VTE
191
what is the wells score
calculates risk factor for a VTE
192
where are vit k dependent factors synthesised
(CF 2,7,9,10, proteins C and S)
| liver
193
which work quicker to reverse warfarin vit k or clotting factors
clotting factors
| vit k takes 6 hours
194
what inheritance is haemophilia
X linked (usually inherited, 1/3rd spontaneous mutation)
195
when does haemophilia usually present
as toddlers start to mobilise
196
what are the bleeds link in haemophilia
bleeding into joints (haemoarthrosis) and muscle
197
what blood test for haemophilia
APTT
| then CF 8 and 9 assays
198
why would alcohol affect blood production
toxic to bone marrow
liver disease
spleno and hepatomegaly
199
why does liver disease affect coagulation
liver produces all procoagulant proteins expect VWf
will have reduced levels or naturally occuring anticoagulants
impaired utilisation of vit K
200
what cell type do monocytes share a precursor with
granulocytes
201
what is infective mononucleosis
when T cells are activated (usually in response to EBV but can be HIV, CMV, viral hepatitis and toxoplasma) and gain blue cytoplasm that wraps around neighbouring cells
