Haematology and Oncology Flashcards
(420 cards)
1
Q
What are the causes of microcitic anaemia?
A
Iron deficiency anaemia of chronic disease thalassaemia lead poisoning
2
Q
what are the two types of causes of Normocitic anaemia?
A
Haemolytic and non-haemolytic
3
Q
what are haemolytic causes of Normocytic anaemia?
A
intrinsic: Hereditaries theory psychosis G6PD deficiency sickle-cell anaemia extrinsic: autoimmune
4
Q
what are non-haemolytic causes of normocytic anaemia?
A
Iron deficiency anaemia of chronic disease chronic kidney disease aplastic anaemia acute bleeds
5
Q
what are the two types of causes of macrocytic anaemia
A
megaloblastic and non-megaloblastic
6
Q
what are the causes of megaloblastic macrocytic anaemia
A
folate being nine deficiency B12 deficiency drug induced such as allopurinol
7
Q
what are the causes of non-megaloblastic macrocytic anaemia?
A
Alcohol use disease liver disease hypothyroidism
8
Q
what is the MCV of Microcytic anaemia?
A
<80
9
Q
What is the MCV of normocytic anaemia?
A
80-100
10
Q
what is the MCV of macro cytic anaemia
A
> 100
11
Q
what is the definition of anaemia?
A
Haemoglobin <120 (F) or < 140 (M)
12
Q
what are the classic symptoms of anaemia?
A
Fatigue decreased exercise tolerance shortness of breath postural hypotension palpitations angina
13
Q
what is a consequence of very severe anaemia?
A
heart failure
14
Q
what are signs of anaemia?
A
Parlour tachycardia heart murmur
15
Q
What does kolinichia indicates?
A
iron deficiency anaemia
16
Q
what does angular stomatitis and glossitis indicate?
A
vitamin B9 +/or B12 deficiency
17
Q
what are the symptoms of a major bleed?
A
Hypotension Pala clammy skin threaded pulse tachycardia dysnopear/air hunger altered mental status
18
Q
when should you check ferritin levels?
A
If history is highly suggestive of iron deficiency anaemia or if on blood tests FBC comes back with low haemoglobin and MCV
19
Q
what is classed as anaemia in pregnancy?
A
Haemoglobin<110 and ferritin <30 - ferritin that low is the threshold for treatment in pregnancy
20
Q
why does pregnancy predispose to anaemia?
A
In pregnancy there is haemodilution and iron mobilisation meaning lower ferritin even if iron stores are normal
21
Q
what are the causes of iron deficiency anaemia?
A
Decreased iron intake either because of inadequate diets or impaired absorption increased iron loss from menstrual bleeding or other causes of bleeding increased iron requirements in young children pregnancy or lactation
22
Q
what does a full blood count include?
A
Haemoglobin haematocrit platelet count MCV CH MCHC red cell distribution width
23
Q
what would a peripheral smear show in iron deficiency anaemia?
A
microcytic hypo-chromic
24
Q
what is the iron used for in the body?
A
mainly red blood cell production. Iron is used in the formation of haemoglobin myoglobin and haem enzymes so it is essential for red blood cell production and cellular processes such as DNA replication repair and metabolism
25
how is iron excreted?
There is no pathway for iron excretion it is lost physiologically through use in the body the body replenishes iron stores through diet and maintains human stasis by recycling iron from destroyed red blood cells
26
what is the management of a women (menstruating) who is iron deficient?
Trial of iron supplements ferrous sulphate 200 mg if this doesn't work go onto further investigations
27
what is the management of male or postmenopausal female iron deficiency anaemia?
Go straight onto further testing, the further testing is decided by the symptoms which the individual presents with do not do trial of iron supplements
28
what are some causes of iron deficiency anaemia which would require further testing and what testing is required?
Coeliac – coeliac serology (transglutaminase (tTG) and deamidated gliadin peptide (DGP) antibody tests), renal tract malignancy (urinalysis), H. pylori (breath or stool test) GI bleed or positive serology (endoscopy or colonoscopy)
29
what investigation should you do in an individual over 60 with symptoms of iron deficiency?
OGD and colonoscopy
30
what further testing is required for iron deficiency anaemia in an individual younger than 60?
OGD
31
What is the management of iron deficiency anaemia if iron supplements do not work?
After finding and merging the underlying cause give oral iron replacement with ascorbic acid then IV iron and if there is cardiac compromise red cell transfusion
32
what does ascorbic acid do in terms of iron?
Enhances the absorption of iron
33
what is pernacious anaemia?
A megaloblastic anaemia without neuropathy caused by folate deficiency (B9)
34
what the typical causes of pernacious anaemia?
malabsorption increased demand poor dietary intake increased folate loss alcohol and drugs inborn errors of metabolic disease
35
what diseases cause malabsorption?
Tropical sprue coeliac disease extensive intestinal resection/short bowel syndrome
36
what can cause increased demand for folate?
Pregnancy lactation prematurity
37
what can increase the loss of folate?
chronic dialysis and chronic haemolytic disease
38
what drugs cause increased folate use/loss?
sulphathiazine trimethoprim methotrexate and anticonvulsants
39
what is a classic symptom of megaloblastic anaemia
chronic headache
40
how do the symptoms of B12 deficiency in benign deficiency differ
they are very similar except for the fact that B12 deficiency causes neurological deficits such as peripheral neuropathy dementia subacute cord degeneration
41
apart from the usual anaemia tests what tests should you include in the diagnosis of pernacious anaemia?
Intrinsic factor antibody test (in B12 deficiency) and tests for IBD or coeliac disease
42
what is the management of folate deficiency?
Oral folic acid
43
what is the management of B12 deficiency?
B12 injections loading dose +3 monthly follow-up injections
44
describe the diffrerence in blood tests results between iron deficiency B12 deficiency and folate deficiency
insert picture pg 7
45
what drugs cause haemolytic anaemia?
Cephalosporins levodopa methyldops and penicillin
46
what are causes of haemolytic anaemia caused by abnormal haemoglobin production?
sickle cell and thalassaemia
47
what are the causes of autoantibody mediated haemolytic anaemia?
Autoimmune: SLE rheumatoid arthritis scleroderma lymphoproliferative: CLL or non-Hodgkin's lymphoma
48
what is a more common enzyme deficient haemolytic anaemia?
Glucose six phosphate dehydrogenase deficiency
49
what type of anaemia does haemolytic disease of the newborn or transfusion reactions cause
alloimmune haemolytic anaemia
50
what other causes of infection or trauma mediated haemolytic anaemia?
DIC TTP haemolytic uraemia eclampsia
51
what are the characteristic features of haemolytic anaemia is?
pallor jaundice splenomegaly
52
as well as the usual investigations for anaemia what else should you include any haemolytic anaemia?
Coombs test
53
patient presents with anaemia and their peripheral smear shows abnormal forms of red blood cells their ridiculous is also raised what type of anaemia does this indicate?
Haemolytic
54
what is the management of autoimmune haemolytic anaemia?
Folic acid corticosteroids plasma three's (may provide temporary response)
55
what are the general principles of management of haemolytic anaemias?
Treat any underlying cause give supportive care and foaling acid once daily plasma exchanges used if there are antibodies, DIC or TTC and splenectomy is used if there is splenomegaly without portal hypertension
56
What is sickle-cell anaemia?
An autosomal recessive defect of the beta chain of haemoglobin causing the production of HBS sickle haemoglobin
57
describe the pathophysiology of sickle-cell anaemia?
Sickle cells are an abnormal shape meaning they obstruct blood flow and also they breakdown prematurely causing varying degrees of normocytic anaemia. Obstruction of small capillaries (caused by aggregation of sickle cells to one another) causes painful crises and can lead to organ damage
58
what are consequences of sickle-cell anaemia which can be fatal in children?
Splenic sequestration and bone marrow aplasia
59
what organs are most commonly damaged by sickle-cell anaemia?
kidneys retina spleen bone marrow
60
how does splenic sequestration cause of morbidity and mortality?
Splenic dysfunction increases the vulnerability to serious infections
61
How is sickle-cell anaemia diagnose?
all infants are screened for sickle cell anaemia and then diagnosis is confirmed by a haemoglobin electrophoresis full blood count reticulocyte count (-) and blood smear
62
what would a blood smear show in sickle-cell anaemia?
Nucleated red blood cells sickelling and howell jolly bodies
63
what causes symptoms in sickle-cell anaemia?
Vasoocclusion
64
a patient with a history of sickle cell anaemia presents with severe chest pain fever dysnopea tachyopnea and hypoxia what is happening?
acute chest syndrome
65
What are some symptoms of sickle-cell anaemia?
Symptoms of acute chest syndrome bone pain floaters jaundice parlour lethargy Dactylitis
66
what does the image below show and when does it usually occur?
Dactylitis - Usually occurring in sickle cell anaemia which is uncontrolled/undiagnosed
67
what is the ongoing management of sickle-cell anaemia?
Hydroxicarbide = ongoing mainstay - simple analgesia, Pneumococcal immunisations and prophylactic penicillin if< 5y ( repeated transfusions may be needed)
68
what is the management of sickle-cell anaemia in an acute crisis?
analgesia up the pain ladder 02 if hypoxic IV hydration blood transfusions if life-threatening cover with antibiotics if there is any suspicion of infection
69
what would an x-ray show in acute chest syndrome?
Infiltrates
70
what other risk factors that predispose someone to a vaso occlusive crisis?
acidosis cold stress exercise infections dehydration
71
what are the absolute indications for blood transfusions in sickle cell anaemia?
Acute chest syndrome priapism and/
72
what is the management of red blood cell aplasia in sickle-cell anaemia?
transfusions steroids splenectomy
73
what is thalassaemia?
An inherited blood disorder in which the body makes abnormal or inadequate amount of haemoglobin and there is increased haemolysis
74
what other two types of thalassaemia?
alpha and beta
75
describe alpha thalassaemia?
A reduction in the functioning levels of alpha haemoglobin
76
described beta thalassaemia?
a reduction in the functioning levels of beta haemoglobin?
77
What are the subcategories of alpha and beta thalassaemia and what does that mean?
major – severe symptoms intermedia – mild/moderate symptoms trait – mostly asymptomatic but a carrier
78
what is the presentation of alpha thalassaemia major?
The most severe cases of alpha thalassaemia presentation is of stillbirth
79
what is the presentation of alpha thalassaemia intermedia?
Anaemia neonatal jaundice failure to thrive shortness of breath
80
what is the management of alpha thalassaemia?
Regular monthly blood transfusions bone marrow transplantation if possible
81
what is the presentation of beta thalassaemia major?
prolonged new natal jaundice severe anaemia failure to thrive
82
what is the presentation of beta thalassaemia intermedia?
The same as beta thalassaemia major: prolong innate jaundice severe anaemia failure to thrive
83
how do you treat beta thalassaemia?
Bone marrow transplants only treat beta thalassaemia when or if Burton is low
84
what does the image below show and when does it occur?
maxillary overgrowth this is a complication of alpha and beta thalassaemia if untreated (a bony deformity)
85
why do you not use iron supplements in anagement of thalassaemia
because iron supplements are not as good as blood transfusions, and if used in conjunction with blood transfusion they cause iron overload
86
what is a complication of regular blood transfusions?
iron overload so to Laois in therapy is used - Desferrioxamine
87
what is a glucose six phosphate deficiency
and inherited enzyme deficiency in which patients are accessibly susceptible to the development of haemolytic anaemia
88
what is the mechanism of inheritance of glucose-6-phosphate deficiency?
X-linked
89
describe the pathophysiology of glucose-6-phosphate deficiency
the inability to tolerate biochemical oxidative stress resulting in blood cell haemolysis due to G6PD catalysing the first step in the pathway which protects cells from oxidation
90
what is an advantage of G6PD?
protective against malaria so it is commonly found in populations such as: African Asian Mediterranean
91
what is the presentation of G6PD?
it's mainly asymptomatic however presents in neonates through prolonged/severe neonatal jaundice and in non-neonates can appear as jaundice parlour and dark urine symptoms are usually precipitated by infections drugs and ingesting broad beans
92
what is the management of G6PD?
neonatal – phototherapy and if levels of bilirubin are very high then exchange transfusions in older patients folate acid supplements and in severe anaemia blood transfusions may be required and splenectomy be considered
93
what is polycythaemia?
erythrocytosis: concentration of red blood cells in your blood making your blood more viscous
94
what is polycythaemia characterised by?
erythrocytosis thrombocytosis leukocytosis and splenomegaly
95
what is polycythaemia characterised as?
a myeloproliferative neoplasm
96
what are the consequences of polycythaemia?
increased risk of thrombosis and haemorrhage - MI PE
97
what are the symptoms of polycythaemia?
Headache blurred vision red skin at the peripheries weakness and fatigue Itching operate by contact with warm water may have symptoms of anaemia easy bruising and nosebleeds
98
how is polycythaemia diagnosed?
usually Patients will not present because of polycythaemia and will often be found by accident when elevated haemoglobin is seen on routine blood tests
99
what does an FBC show in polycythaemia?
includes haemoglobin normal haematocrit leucocytosis thrombocytosis
100
what gene mutation is polycythaemia commonly associated with?
JA K2
101
what is the management of polycythaemia?
Phlebotomy plus low-dose aspirin and management of cardiovascular risk factors ie hypertension
102
A patient presents with a left leg oedema, call swelling redness and you notice soe prominent superficial veins - what is the most likely diagnosis?
deep vein thrombosis
103
what may you notice on palpation of a leg affected by DVT?
It is tender especially along the venous system
104
described the Wells score?
```
Active cancer
Treatment or palliation within 6 months
No0
Yes+1
Bedridden recently >3 days or major surgery within 12 weeks
No0
Yes+1
Calf swelling >3 cm compared to the other leg
Measured 10 cm below tibial tuberosity
No0
Yes+1
Collateral (nonvaricose) superficial veins present
No0
Yes+1
Entire leg swollen
No0
Yes+1
Localized tenderness along the deep venous system
No0
Yes+1
Pitting edema, confined to symptomatic leg
No0
Yes+1
Paralysis, paresis, or recent plaster immobilization of the lower extremity
No0
Yes+1
Previously documented DVT
No0
Yes+1
Alternative diagnosis to DVT as likely or more likely
```
105
What are risk factors for developing DVT?
Major surgery hospitalisation immobile Cancer smoking obesity pregnancy increased age COCP/HRT
106
what part of the physical examination is significant in the diagnosis of DVT?
measuring the calf circumference if the difference is greater than 3 cm then the chances of a DVT raises significantly
107
what further investigations are required in patient with a Wells score of less than two and no significant clinical symptoms of DVT?
None
108
What further investigations are required in a patient with a Wells score of less than two with significant clinical symptoms of DVT?
require a D dimer test
109
when would you perform a venous duplex ultrasound in a patient with ? DVT?
anyone who scores over two and a Wells score or if their D dimer is positive
110
Why is D dimer not diagnostic for DVT?
It is not specific and frequently is positive in patients who are older are acutely ill pregnant or have underlying hepatic disease or infection
111
you suspect DVT and WELLS score is high.
You perform a venous duplex ultrasound which shows signs of DVT
what is the next step in the diagnosis of DVT?
Either whole leg ultrasound or a proximal Doppler ultrasound scan
112
you perform proximal Doppler ultrasound scan patient with? DVT are further investigations are required?
yes, Repeat ultrasound in five – seven days if it is negative again then DVT is excluded
113
what drug class is used to treat DVT and why?
anticoagulants are used because of venous clots is fibrin rich
114
describe the management of a DVT?
Initial treatment is 5 to 21 days: it arrests the active pro thrombotic events and inhibit thrombus propagation and embolisation then there is long-term treatments up to 3 months: prevents new thrombus whilst the original plot has stabilised and is subsequently thrombolysed after long-term treatment secondary prevention may be required if the initial cause of DVT has not resolved (an acute event such as short-term immobilisation from surgery would not require long-term treatment)
115
what drugs are classed as anticoagulants?
DOAC warfarin low molecular weight heparin
116
when would a DVT be required to be treated in hospital?
If requiring IV unfractionated heparin if there is a suspected or confirmed PE if the DVT requires interventional therapy if the DVT is highly symptomatic if there is poor patient education and they would not be able to be compliant with treatment if there are coexisting comorbidities requiring hospital management if there are presence of risk factors for bleeding whilst on Tx - such as chronic liver disease
117
what usually causes arterial thrombosis?
atherosclerotic plaques which predispose platelet aggregation if it ruptures
118
what do arterial thrombotic events lead to?
Heart attacks and strokes or TIA as well as limb ischaemia
119
what are risk factors for arterial thrombosis?
Increasing age smoking century lifestyle being overweight exes alcohol high cholesterol diabetes atherosclerosis arterial fibrillation antiphospholipid syndrome
120
what is the treatment of arterial thrombosis?
Thrombolysis or embolectomy followed by antiplatelet (clopidogrel) followed by statins and low-dose aspirin in long-term management in certain conditions such as atrial fibrillation warfarin may be used
121
what are the common methods to diagnose arterial thrombosis?
CT angiography however if peripheral something like a Doppler ultrasound can be used
122
you suspect a patient has been over anticoagulated - what bloods should you order?
FBC PT APTT fibrinogen concentration creatinine and LFT (can do type and cross too) + INR if on Warfrin
123
what should you do if you suspect the patient has been over anti coagulated?
stop the drug document the timing and the amount of the last dose and any presence of pre-existing renal or hepatic impairment assesses source of bleeding order bloods begin fluids
124
what is the management of haemorrhage caused by over anticoagulating?
AB CDE and steps of initial assessment if on warfarin give it vitamin K based on INR. In general give human plasma with coagulation factors (a.k.a. FFP) and consider Ivy tranexamic acid. To not restart anticoagulation until the patient is haemodynamically stable and there has been stabilisation of haemoglobin
125
do DOACs have a reversal agent?
no
126
what is the management of a minor bleed caused by over anticoagulating?
DOAC: delayed or discontinued depending on severity Warfrin: INR < 4.5 = withhold warfarin INR > 4.5 withhold warfarin and give vitamin K
127
what type of inheritance is haemophilia?
X-linked recessive
128
what clotting factor is haemophilia A deficient in?
factor 8
129
what clotting factor is haemophilia B deficient in?
factor 9
130
what are symptoms of haemophilia?
History of recurrent or severe bleeding bleeding into muscles prolonged bleeding following heel prick examination or circumcision mucocutaneous bleeding i.e. nosebleeds or from dental procedures haemarthrosis muscle wasting from inability to move from pain fatigue from iron deficiency anaemia
131
what would bleeding into muscles present as in haemophilia?
Pain and swelling usually in the extremities decreased range of motion erythema and warmth
132
what is Haemarthrosis?
recurrent leads over the years caused severe joint damage causing total cartilage erosion
133
describe the X-linked inheritance in haemophilia?
insert picture
134
what levels of clotting factor are regarded as mild haemophilia?
>5%
135
What levels of clotting factor are regarded as moderate haemophilia?
1-5%
136
what levels of clotting factor are regarded as severe haemophilia?
<1%
137
what bloods are required in haemophilia?
FBC PT APTT VWF studies LFT Coag factor asseys genetric testing
138
What imaging may be required in haemophilia?
X-rays for joints CT for intracranial bleed CT or ultrasound the gastrointestinal bleeds
139
what is the management of haemophilia?
Give factor concentrate!! analgesia and physiotherapy for complications
140
what drugs apart from factor concentrates can be used in severe haemophilia?
Bypassing agents which are special blood products
141
what drugs should be used acute management of haemophilia with a life-threatening bleed?
factor concentrates or bypassing agents and antifibrinolytics (tranexamic acid)
142
what causes abnormalities in prothrombin time?
abnormalities of the extrinsic pathway such as warfarin
143
what causes abnormalities in APTT?
abnormalities in the intrinsic pathway such as factor 8, 9 heparin and some DOAC
144
what is Von Willebrand Disease?
the most common inherited bleeding disorder
145
what type of inheritance is Von Willebrand Disease?
autosomal inheritance with variable penetrance
146
what is the pathophysiology of Von Willebrand Disease?
VWF provides the critical link between platelets and exposed vascular epithelium whilst also binding in stabilising the coagulation factor 8
147
how does Von Willebrand Disease present?
mucocutaneous bleeding or menorrhagia or postnatal haemorrhage - spontaneous bleeding into the joint is seen but is rare and is only seen in more severe disease
148
which type of Von Willebrand Disease is most common?
type I it is also the least severe
149
what bloods should you investigate in Von Willebrand Disease?
PT (normal) and APTT (prolonged) FBC VWF antigen and VWF function
150
which test is diagnostic for Von Willebrand Disease?
Von Willebrand factor function is best but antigen can also be used
151
describe PT and APTT in VWF and why the results are as such?
PT = normal APTT = prolonged because VWD causes a decrase in functonal factor 8 which affects the intrinsic pathway which prolongs APTT (PT is extrinsic)
152
what is the management of Von Willebrand Disease?
Von Willebrand factor concentrate
153
what is tDIC?
and acquired syndrome characterised by the activation of coagulation pathways resulting in the formation of intravascular thrombi and depletion of platelets and coagulation factors
154
what are features of DIC?
generalised bleeding evidenced at three unrelated sites signs of circulatory collapse purpura fulminans + gangrene Delerium or coma
155
gave examples of bleeding at three unrelated sites which may be found in DIC?
nosebleed gingival bleeding haematuria blood in the cannula
156
what causes the purpura fulminans and gangrene in DIC?
micro-or microvascular thrombosis
157
How do you diagnose DIC?
abnormal coagulation tests and one known underlying condition which predisposes to DIC
158
what's conditions predispose to developing DIC?
sepsis major trauma bans malignanciesObstetric disorders severe organ destruction of vascular disorders and transfusion reactions
159
what obstetric disorders predispose to the development of DIC?
amniotic fluid embolism eclampsia placental abruption retained fatal products
160
which organs if severely injured most commonly predisposed to DIC?
pancreas and liver
161
describe the coagulation tests results that you would find in DIC?
platelets (-) PT (+) d dimer (+) fibrinogen (-)
162
what is the management of DIC?
active treatment of the underlying cause will stop The triggering process. Mainstay of treatment is replacement therapy and treatment with FFP and platelet concentrates however if there is a dominant presentation of thrombosis without significant bleeding heparin can be used ( be careful of this as DIC can cause haemorrhage)
163
what are indications for replacement therapy in DIC?
active bleeding/ requiring an invasive procedure /at risk for bleeding complications/ with a documented deficiency of platelets/coagulation factors/inhibitors
164
what is immune thrombocytopenia purpura?
and autoimmune haematological disorder characterised by isolated thrombocytopenia in the absence of an identifiable cause
165
what risk factors predispose to ITP?
children with proceeding viral illness with abrupt onset / young adult females
166
what is the presentation of ITP?
Bruising / petichiea / haemorrhagic bullae / bleeding gums/ amaemia + Sx
167
what is the diagnostic criteria for ITP?
Thrombocytopenia In the absence of systemic symptoms absence of splenomegaly or hepatomegaly absence of any causes of secondary thrombocytopenia and absence of lymphadenopathy (this is an indication for secondary ITP)
168
how would you diagnose thrombocytopenia?
FBC + peripheral blood smear
169
what is the management of ITP?
satisfactory platelet count: observation / corticosteroids or IVIG or Anti- D Ig
170
what is the criteria for treatments of ITP?
adults who have bleeding gums but satisfactory platelet counts asymptomatic but have additional risk factors of: anti-thrombolytic treatment undergoing interventions are high risk job adults who have a very low platelet count
171
what are the causes of secondary ITP?
H. pylori hepatitis C HIV immunodeficiency autoimmune disorders drug induced
172
what drugs can cause secondary ITP?
frusemide or NSAIDs
173
what autoimmune disorders can cause secondary ITP?
SLE antiphospholipid syndrome autoimmune thyroid disease
174
what is thrombotic thrombocytopenic purpura?
in a clinical syndrome characterised by haemolytic anaemia and thrombocytopenic purpura - if untreated is almost always fatal
175
what does this triad describe: haemolytic anaemia thrombocytopenic purpura neurological symptoms?
thrombotic thrombocytopenic purpura
176
what is the pathophysiology behind thrombotic thrombocytopenic purpura?
VWF is not played because the enzyme which does this is either deficient or inactive. The unusually large VWF interacts of platelet membranes causing aggregation of circulating platelets especially at sites of high intravascular stress resulting in thrombi in the microvascular system
177
what symptoms does thrombotic thrombocytopenic purpura cause?
neurological symptoms ranging from severe to mild: home at focal abnormalities seizures headaches confusion digestive symptoms from clots in the GI system: nausea vomiting diarrhoea abdominal pain although in the name purpura is relatively uncommon as well as any other bleeding symptoms
178
what art schystocytesand when might they be found
in haemolytic diseases for example TTP - they are broken down red blood cells see image below
179
how would you diagnose thrombotic thrombocytopenic purpura?
full blood counts showing thrombocytopenia anaemia leukopenia reticulocytes (+) Coombs test (-ve). Peripheral smear showing: schystocytes and micro-angiographic haemolysis
180
why might you want to check renal function in thrombotic thrombocytopenic purpura?
thrombotic thrombocytopenic purpura effects microvascular system and can cause renal failure is a good indicator of the severity of the disease
181
how do you manage thrombotic thrombocytopenic purpura?
plasma exchange/ corticosteroids/ after resolution use long-term aspirin -- adjunct to initial therapy are aspirin folic acid blood transfusions immunotherapy and splenectomy
182
what is thrombocytopenia?
to a few platelets
183
what are the different methods in which thrombocytopenia can occur?
bone marrow making too few platelets, increase platelet destruction, increase platelet use
184
what are some causes of thrombocytopenia in which the bone marrow makes too few platelets?
B9 or B12 deficiency leukaemia or other causes of bone marrow infiltration radiation or cytotoxic therapy
185
what are some causes of thrombocytopenia caused by increased obstruction or use of platelets?
hypersplenism ITP DIC
186
what is thrombocytosis?
too many platelets
187
What are the two types of thrombocytosis?
primary and secondary
188
what causes primary thrombocytosis?
essential thrombocythaemia - a rare blood disorder that causes a high number of blood cells called platelets to form
189
what causes secondary thrombocytosis?
```
Malignancy
inflammation such as IBD
infection
removal of spleen
iron deficiency
haemolytic anaemias
```
190
what are platelets?
non-nucleated cells made from megakaryocytes created inside the bone marrow
191
what is the lifespan of a platelet?
Eight – 10 days
192
what is the main function of platelets?
Forming primary haemostatic plugs
193
what happens if your platelet count drops below 20?
you develop spontaneous breathing
194
what our red blood cells?
oval by concave discs lacking a cell nucleus which contain haemoglobin and made in the bone marrow
195
what is the lifespan of red blood cell??
100 to 120 days
196
what breaks down red blood cells?
macrophages
197
what is the process by which red blood cells made?
erythropoesis stimulated by the hormone EPO which is synthesised by the kidney
198
describe the maturation of a red blood cell?
Blood stem cells differentiate to myeloid stem cells EPO then causes the formation of an erythroid blast which still has a nucleus the nucleus is then exposed and it becomes a reticulocyte which is a newly formed red blood cell
199
what are the different types of white blood cell?
Neutrophil eosinophil basophil lymphocyte monosites
200
what is the appearance of a neutrophil?
multilobar nucleus
201
what is the function of a neutrophil?
specifically targets bacteria and fungi
202
what is the appearance of an Eosinophil?
Bi lobar nucleus
203
what is the function of an eosinophil?
targeting larger parasites and mediating allergic responses
204
what is the appearance of a basophil?
Bi or Tri lobar
205
what is the function of a basophil?
Releases histamine for inflammatory processes
206
what are the types of lymphocytes?
B cells and T cells
207
what is the function of B lymphocytes?
release antibodies which cause the activation of T cells
208
what is the function of T lymphocytes?
CD4 + activates and regulates T killer cells and B cells and CD8+ a.k.a. killer T cells are cytotoxic cells which induce apoptosis
209
what are monocytes and whats their appearance?
kidney -shaped nucleus which migrate from the bloodstream and differentiate into macrophages
210
describe the differentiation of blood stem cells?
insert image page 22
211
what is acute myeloid leukaemia?
clonal expansion of myeloid blasst in the: bone marrow and peripheral blood or the extra medullary tissues
212
who does AML typically affect
older adults
213
what is the presentation of AML
symptoms of anaemia, ecchymoses or petechia frequent infections with fever lymphadenopathy hepatosplenomegaly mucosal bleeding
214
what causes the ecchymoses or petechia in AML?
thrombocytopenia
215
what are risk factors of AML?
over 65 previous treatment with chemo or radio
216
what blood tests do you perform in AML?
Full blood count with differential shows: leucocytosis neutropenia and thrombocytopenia but an increased white cell counts / peripheral blood smear / Coag Panel
217
how do you diagnose AML?
bone marrow biopsy
218
what would a peripheral blood smear show in AML?
blasts and Auer Rods
219
what is a complication of AML which is serious??
Coagulopathy which may be life-threatening so coag panel should be performed
220
what is chronic myeloid leukaemia?
A malignant clonal disorder of haemopoietic stem cells (or Myeloid in older people)
221
what is the presentation of CML?
one third of patients are asymptomatic however if symptoms are present they are: systemic features splenomegaly - abdominal discomfort and night sweats
222
what is CML associated with?
the Philadelphia chromosome
223
what bloods should be performed in CML?
Full blood count with differential showing anaemia with thrombocytosis or thrombocytopenia peripheral blood smear
224
what would a peripheral blood smear show in CML?
almost all white blood cells are mature or maturing myeloid cells
225
what test is diagnostic for CML?
bone marrow biopsy (showing granulocytic hyperplasia ) and cytogenetics which may show the Philadelphia chromosome
226
what is the management of CML?
biological enzyme inhibitors and monitoring with bone marrow biopsy and cytogenetics at 3, 6 and 12 months until there is remission and then yearly thereafter
227
what is acute lymphocytic leukaemia?
Malignant clonal disease that develops when a lymphoid progenitor cell becomes genetically altered and undergoes uncontrolled proliferation
228
who does ALL usually affect?
children
229
what is the most common presenting symptom of ALL?
lymphadenopathy
230
what symptoms does ALL cause
lymphadenopathy pallor eccymoses petichea splenomegaly
231
what are symptoms of tissue infiltration which occur in ALL and when they occur?
in more severe disease and include bone pain and symptoms of anaemia and testicular enlargement and cranial nerve palsy
232
what blood tests would you perform for ALL?
full blood count with differential showing on the Citic anaemia with leucocytosis neutropenia and possibly thrombocytopenia but an increased white cell count and peripheral blood smear and Coag Screen
233
what would show on a peripheral blood smear in ALL?
leukaemic lymphoblastic
234
How do you diagnose ALL and what is the result?
bone marrow aspiration and biopsy showing hyper cellularity and infiltration by lymphoblastic
235
what is the management of ALL?
intensive chemotherapy and early stem cell transplantation should be considered
236
what is a chronic lymphocytic leukaemia?
Lymphoproliferative disorder in which monoclonal B lymphocytes are elevated
237
who is most at risk of CLL?
elderly
238
what is a presentation of CLL?
typically doesn't cause very many symptoms usually presents with absolute lymphocytosis as an incidental finding or with asymptomatic lymphadenopathy
239
what blood test would you want to perform in CLL?
full blood count with differential showing lymphocytosis and a blood smear
240
what Tessa diagnostic for CLL?
blood smear and flow cytometry
241
what is a finding on blood smear with CLL?
smudge cells
242
what is the management of CLL?
watch and wait or active management but typically since elderly and slow progressing it's not used
243
what is Hodgkins lymphoma?
haematological malignancy arising from mature B cells
244
who does a Hodgkins lymphoma typically affect?
young adults and adults over 55 years
245
what is the presentation of Hodgkin's lymphoma?
painless cervical or supra-cervical lymphadenopathy in more advanced presentation will have red flag symptoms
246
what do respiratory symptoms such as shortness of breath dysnopea and chest pain indicating Hodgkin's lymphoma
mediastinal adenopathy
247
how do you diagnose Hodgkin's lymphoma and what is the result?
bone marrow biopsy showing Hodgkin and Reid Steinberg cell
248
after diagnosis of Hodgkin's lymphoma what other tests would you want to perform?
PET CT shows organs involved in the extent of the disease classic three might be ordered if presenting with respiratory symptoms
249
Hodgkin's lymphoma and how successful is this?
is a good response to chemotherapy with a median survival of 90%
250
what is non-Hodgkin's lymphoma?
an umbrella term of 60 different types of non-Hodgkin lymphoma effecting mature B cells however they can also cause T cell proliferation
251
what are the types of non-Hodgkin lymphoma?
low-grade and high-grade
252
what is a presentational non-Hodgkin's lymphoma?
lymphadenopathy and splenomegaly however each subtype is specific set of symptoms
253
who does non-Hodgkin's lymphoma usually affect?
typically only ever in those over 50 years old
254
what is the progression of low-grade non-Hodgkin's lymphoma?
slow progress of lymphoma considered indolent which is asymptomatic for many years and it is not curable however you can live many years with it
255
what is the progression of high-grade lymphoma?
rapid and without treatment you can be dead within weeks but with treatment you can be cured
256
do you see Reed Steinberg cells in non-Hodgkin's lymphoma?
no
257
what is myeloma?
A blood cancer characterised by the clonal proliferation of plasma cells in the bone marrow
258
what cells does multiple myeloma usually consist of?
terminally differentiated plasma cells
259
What is multiple myeloma usually associated with?
osteolytic bone disease anaemia and renal failure
260
what other characteristic features of multiple myeloma?
terminally differentiated plasma cells infiltration of the bone marrow by plasma cells present on monoclonal immunoglobulin is in serum or urine
261
what is the usual presentation of multiple myeloma?
anaemia bone pain infections fatigue renal impairment
262
what is the most important prognostic factor in multiple myeloma?
serum albumin (which is a feature of renal impairment) and serum beta microglobulin
263
How do you diagnose multiple myeloma?
Serum or urine electrophoresis showing increased light chain immunoglobulins or serum-free lighting say or bone marrow aspiration and biopsy
264
why is a bone marrow aspirate and biopsy useful in multiple myeloma apart from diagnosis?
helps differentiate from MGUS and shows if there is monoclonal plasma cell infiltration into the bone marrow which is a characteristic feature of multiple myeloma
265
what imaging might you want to perform in multiple myeloma? And why?
Whole-body CT or MRI to diagnose osteopenia + pathogenic fractures or osteolytic lesions
266
what bloods would you want to perform in multiple myeloma?
serum calcium – hypocalcaemia can occur in osteolytic lesions FBC U+E - for renal impairment
267
what is MGUS?
an asymptomatic premalignant disorder associated with a relatively low risk of progression to multiple myeloma or another plasma cell proliferative malignancy
268
how does MGUS usually present?
found incidentally in serum or urine by detection of monoclonal M proteins
269
what are the symptoms of MGUS?
by definition it cannot have symptoms it requires absence of anaemia hypercalcaemia renal failure and osteolytic lesions
270
how do you diagnose MGUS?
after initial detection do electrophoresis and immuno fixation to identify and measure the protein. To complete diagnosis you have to exclude multiple myeloma by performing U+E (Calcium+ Creatinine) FBC complete bone survay with imagine
271
when would a biopsy be required in MGUS?
only if M protein levels are very high
272
what is the management of MGUS?
intermediate and high risk patients should be followed up six months after diagnosis and then yearly thereafter all other patients should only present if there is a development of symptoms
273
what are the principles of cancer management?
deciding : what is the type of cancer what stages the cancer is incurable or not what the patient wishes what is a patient's performance status
274
when word cancer management not be given in regards to performance status?
anyone with performance status three or more will not receive cancer treatment very rarely do people with level III received radical treatment
275
define radical treatment of cancer?
curative intent usually surgical or radiotherapy
276
define neoadjuvant cancer treatment?
given before the curative treatments either to reduce the size or make the survival rate higher
277
what is the definition of adjuvant/ adjunct treatments in cancer?
given after curative treatments
278
define palliative cancer treatment?
improves quality of life and the length of survival with cancer also decreases the need for analesia reducing sedative effects
279
describe the ECOG performance status?
insert picture
280
how does chemotherapy work?
directly by binding to cell DNA and changing it resulting in cell death indirectly affecting DNA cell replication or by causing apoptosis
281
what are common side effects of chemotherapy?
fatigue hair loss constipation diarrhoea mucosal sores peripheral neuropathy weight changes neutropenia anaemia which can lead to success
282
how does radiotherapy work?
high energy x-rays are used to destroy cancer cells can be delivered externally or internally
283
what are side effects of radiotherapy?
they are site-specific but generally include skin changes: itchiness drowning blistering. Fatigue if on the head: tooth decay and stiffness of the jaw with difficulty swallowing even the lands: radiation fibrosis GI: diarrhoea and rectal bleeding pelvic: infertility
284
how does immunotherapy work in cancer treatment?
systemic agents that aim to stimulate a patient's own immune system to attack the cancer cells also stimulates the immune system componentsto help improve or restore the system
285
what are side effects of immunotherapy?
allergies nausea vomiting diarrhoea skin rashes labour pressure and flulike symptoms
286
what are targeted agents?
inhibits specific targets involved in cell replication
287
described endocrine therapies in cancer treatment?
Generally use for breast prostate and endometrial cancers inhibit the action of various hormones on hormone responsive cancer cells
288
what are side effects of endocrine therapies
menopausal EDC they are usually in relation to hormone depletion
289
describe the TNM stages?
insert picture - other letters are S: serum some cancers are staged by serum markers G: histological grade L: lymphatic involvement V: veins
290
described the 1 – 4 staging patients may ask for?
insert picture page 28
291
Describe breast cancer in situ?
and non-invasive breast cancer that is confined to the duct or lobules in which it originated and it does not extend beyond the basement membrane however it is a potential precursor to invasive carcinoma
292
what is the presentation of breast cancer in situ?
typically asymptomatic and is diagnosed at screening however can present with: nipple discharge that is unilateral which can bloody breast lump is not common presentation
293
what would you see on mammography of breast cancer in tissue and what would be the next step?
calcifications next step would be an ultrasound/MRI to assess likelihood of it being cancerous however sometimes go straight to biopsy
294
what biopsy is required for breast cancer in situ?
fine needle or core biopsy
295
What would you find on biopsy in breast cancer in situ?
necrosis and a high nuclear grade
296
what is the treatment of breast cancer in situ?
lumpectomy followed by radiotherapy but chemoprophylaxis can be used in high-risk patients
297
what should you offer to high-risk patients that have had their breast cancer in situ treated?
preventative bilateral total mastectomy or chemoprophylaxis
298
what is a primary invasive breast cancer?
malignancy originating in the breast and nodal basins which has penetrated past the basement membrane of the doctor/globe and is spreading to surrounding tissues but has not yet spread to other organs
299
what genetic mutations are associated with primary invasive breast cancer?
BRCA1 or 2
300
what are risk factors for primary invasive breast cancer?
higher age high socio-economic class family history of Brecker prolonged oestrogen or progesterone exposure high levels of alcohol consumption family history of breast cancer radiation exposure existing benign breast disease increased breast density
301
what is the usual presentation of primary invasive breast cancer?
usually are asymptomatic and found on screening however some patients may present with a lump
302
if primary invasive breast cancer is symptomatic what the symptoms are present?
a firm breast mass nipple discharge axillary lymphadenopathy skin thickening skin discolouration retraction or scaling of the nipple
303
who should you refer to the two-week wait pathway of breast cancer?
over 30 and have unexplained breast lump with or without pain or over 50 with discharge, retraction, any other skin changes of concern in one breast/nipple. Nonurgent referral is considered for those under 30 with unexplained breast lump with or without pain. you can consider to equate pathway for anyone with skin changes that suggest breast cancer or anyone aged > 30 with unexplained lump in axilla
304
what would a mammogram show in primary invasive breast cancer?
a regulated speculated mass clustered microcalcifications linear branching calcifications
305
whatever biopsy is required for primary invasive breast cancer?
core needle biopsy
306
once primary invasive breast cancers diagnosed what must also be histologically confirmed?
determination of oestrogen or progesterone receptors as well as her two receptors and Jean expression assays
307
what adjuvant treatment is used for primary invasive breast cancer if HER 2 positive
monoclonal antibodies such as trasbtuzamab
308
what I do when treatment is used for primary invasive breast cancers if hormone receptor positive ?
premenopausal: Tamoxifen postmenopausal: aromatase inhibitors
309
what other drug should you include in the management of primary invasive breast cancer if it's been treated with aromatase inhibitors?
bisphosphonates
310
what is metastatic breast cancer?
considered metastatic if it is spread beyond the breast and its ipsilateral lymph nodes
311
what counts as ipsilateral lymph nodes Of the breast?
axilla internal mammary infra and supraclavicular
312
where is breast cancer likely to metastasise to?
bone lungs brain liver
313
how do you investigate metastatic breast cancer?
FBC LFT Serum Calcium PET scan can be used, CXR Head CT (also abdo)
314
described breast cancer screening?
annual mammography to: women aged 40 – 49 at moderate risk of breast cancer women aged 40 – 59 at high risk of breast cancer standard breast screening is offered to women aged 50 – 71 every three years
315
What features of a prostate exam would indicate prostate cancer?
an asymmetrical nodular prostate
316
if a man presents with symptoms of L UTS what is the next step?
prostate exam and PSA blood test
317
when should you refer a man for the two-week wait in prostate cancer?
if their prostate feels malignant on DR E or if their PSA is elevated above the age specific range
318
what investigations are offered during the two-week wait appointment for prostate cancer?
1. MRI offered before biopsy in order to limit invasive tests 2. biopsy
319
what is the management of prostate cancer?
low-risk: observation active surveillance with routine PSA tests >20 years projected survival: radioactive treatments or radical prostatectomy with lymph-node dissection Intermediate risk and high risk: Surgery + androgen deprivation therapy
320
what is neutropenic sepsis?
are potentially life-threatening complication of anti-cancer/Immunosuppressive drug treatment
321
what is the criteria for neutropenic sepsis?
and absolute neutrophil count of 0.5x10^9 with any signs of sepsis (usually fever over 38'c)
322
what is febrile neutropenia?
neutropenia with a fever is an indication of neutropenic sepsis
323
what are the causes of neutropenia?
drugs and treatments infection autoimmune bone marrow failure nutritional deficiencies
324
what drugs can cause neutropenia?
cytotoxic therapy immunosuppressive i.e. methotrexate haemopoietic stem cell transplant penicillin carbimazole valproic acid clozapine olanzapine allopurinol NSAIDs
325
which infections can cause neutropenia?
Viral causes: HIV hepatitis B RSV CMV EBV – all cause transient bone marrow suppression and neutropenia bacterial causes: TB and Shigella
326
what autoimmune diseases can cause neutropenia?
Crohn's disease rheumatoid arthritis SLE
327
what nutritional deficiencies can cause neutropenia?
B12 and folate
328
why should absence of fever not exclude neutropenic sepsis?
can present with hypothermia, drugs such as corticosteroids can mask pyrexia, atypical presentations may include mental state changes or general malaise
329
how do you diagnose neutropenic sepsis?
FBC and Sepsis 6
330
how do you manage neutropenic sepsis?
empirical antibiotics and a high risk of MRSA cover with Vancomycin
331
what should you do if after 3 – 5 days of treatment with antibiotics there no imporement in Neutropenic Sepsis?
evaluate for occult infections specifically fungal organisms and viral organisms if these were not found earlier
332
what is the treatment of fungal induced neutropenic sepsis?
IV fluconazole
333
what is the management of viral induced neutropenic sepsis?
IV Ganglocyclovir
334
what is tumour lysis syndrome?
a combination of metabolic and electrolyte abnormalities that occur in a patient with cancer usually after the initiation of cytotoxic treatment but can also occur spontaneously which causes excessive cell lysis
335
what electrolyte abnormalities are associated with tumour lysis syndrome?
hyperuricaemia hypophosphataemia hyperkalaemia hypocalcaemia
336
which cancers is tumour lysis syndrome most commonly associated with?
lymphomas and leukaemias as they are highly proliferative bulky and chemo sensitive
337
what is the presentation of tumour lysis syndrome?
nausea vomiting diarrhoea/anorexia/muscle weakness and muscle cramps/lethargy and paraesthesia/lymphadenopathy and splenomegaly/hyper- or hypotension/oliguria or an Aurea or haematuria
338
why is renal compromise specifically monitored for when starting chemotherapy ?
Because renal compromise and dehydration can predispose to tumour lysis syndrome
339
what is the diagnostic criteria of tumour erosive syndrome?
abnormality in two of the following electrolytes: uric acid potassium phosphate calcium occurring three days before or seven days after chemotherapy
340
what tests must be performed in order to detect tumour lysis syndrome?
renal function (urea and electrolytes + Creatinine) lactate dehydrogenase urinary pH
341
what are some severe complications of tumour lysis syndrome and how would you monitor for this?
Cardiac arrhythmias ECG – hypokalaemia and hypocalcaemia of electrolytes just specifically dangerous for this + EEG or increased awareness for seizures
342
what is the mainstay of management for tumour lysis syndrome?
prevention
343
how would you manage a patient is at low risk for tumour lysis syndrome?
regular monitoring of blood biochemistry and regular assessment of fluid balance and vital signs
344
how would you manage intermediate or high risk patients tumour lysis syndrome?
two days before systemic therapy: IV hydration with isotonic NaCl maintaining urine output 200 miles an hour to maintain high GFR 's phosphate binding agents (aluminium antacid) reducing excess absorption of phosphate / allopurinol (if intermediate) rasburicase (high) - all metabolites should be assessed before treatment and once or twice daily for the first few days of treatment and then once daily their fourth
345
if urine output drops to below a hundred mph in an intermediate risk patients for tumour lysis syndrome what can you do?
Add a loop diuretic
346
what are the risks of adding a loop diuretic to a patient who is at risk of tumour lysis syndrome?
this can predispose to uric acid increase as well as calcium and phosphate abnormalities so be careful
347
if tumour lysis syndrome occurs what do you do?
Optimise renal function with aggressive hydration plus minus loop diuretics/serum phosphate reduced by using phosphate binding agents/Uric acid reduction using rasvuricase/ managers hyperkalaemia and dialysis if abnormalities are resistant
348
when is tumour lysis syndrome considered clinical?
if there are cardiac abnormalities seizures or renal failure
349
how do you merge hyperkalaemia?
levels under six: hydration loop diuretics and sodium polystyrene sulphate. Over six calcium gluconate with insulin and glucose infusion followed by sodium polystyrene sulphonate
350
how does vomiting occur physiologically what is it stimulated by?
Nerves in the stomach chemo receptors in the trigger zone senses and emotions
351
what conditions may cause vomiting?
hypercalcaemia raised intracranial pressure liver failure constipation bowel obstruction
352
What cancer treatments can cause nausea and vomiting?
chemo radio hormonal targeted therapies morphine-based medicines
353
how do 5 HT 3 inhibitors work to reduce nausea and vomiting?
work by blocking the effects of serotonin on the internecine
354
what type of nausea do 5 HT 3 inhibitors work best for?
sickness caused by chemotherapy and radiotherapy
355
what's is an example of a 5 HT 3 inhibitor?
ondesetron
356
how do metoclopramide and domperidone work to reduce nausea and vomiting?
help them to the stoic and relieved feelings of sickness
357
when would you use Chlorporamazine ?
used in advanced cancer and one other anti-sickness drugs do not work
358
what drug class does cyclazine belong to?
antihistamine
359
what drugs are usually given alongside 5 HT 3 inhibitors?
steroids and NK1 inhibitors
360
when would haloperidol be given to treat nausea vomiting?
low-dose to treat sickness caused by morphine
361
apart from 5 HT 3 what other drugs can help control nausea caused by chemotherapy?
Lorazepam when used in conjunction with other anti-sickness drugs
362
what are some side effects of 5 HT 3 inhibitors?
constipation and headaches
363
what are common side effects to all anti- emetic?
weakness tiredness
364
what is a side effect that metoclopramide causes?
twitching
365
what can cause diarrhoea in treatment of cancer?
chemo – immunotherapy – radiotherapy especially of the pancreas and pelvis or abdomen – removal of a portion of bowel – graft-versus-host disease which is a side-effect of transplantation
366
what are some lifestyle methods of preventing diarrhoea?
Avoid caffeine alcohol dairy fat fibres orange juice prune juice and spicy food. More frequent small meals ensuring plenty of water has been drunk
367
what medicines can cause diarrhoea?
metoclopramide or laxatives
368
what is the management of diarrhoea?
loperamide and anti-secretory agents such as corticosteroids and acreotide can be used plus IV hydration if necessary
369
what is superior veno cava obstruction?
syndrome that occurs as a result of obstruction to the superior vena cava resulting in interrupted venous return from the head door rights and upper extremities to the right atrium
370
what is the presentation of SVC obstruction?
facial swelling Dysnopea arm swelling facial plethora chest pain hoarseness of voice stridor symptoms worsening when lying down or bending forwards
371
what signs may be present in SVC obstruction?
enlarged veins of the neck and upper chest wall at the extremity oedema papilloedema mental changes
372
what cancer is most commonly cause SVC obstruction?
lung cancer and lymphoma
373
why is Dysnopea a particularly worrying symptom in SVC obstruction?
can have a very sudden onset and worsening progression due to laryngeal oedema which can be fatal
374
how do you diagnose SVC obstruction?
IV contrast CT
375
what is the management of SVC obstruction ?
airway obstruction: corticosteroids and radiotherapy - if airway obstruction seems imminently dangerous give percutaneous stenting instead of radiotherapy And treat underlying cancer
376
how do you manage benign SVC obstruction?
Thrombolysis grafting and anticoagulation
377
what are causes of benign SVC obstruction?
less frequent than malignant causes usually caused by thrombosis from central venous catheter or pacemaker
378
what are the benign causes of chronic airways obstruction?
tuberculosis sarcoidosis of Wagner's granulomatosis
379
what are the most common malignant causes of chronic upper airway obstruction?
laryngeal cancer and tracheal cancer
380
what cancers commonly metastasised to the brain?
lung cancer breast Cancer Colon Cancer kidney cancer melanoma
381
How do cencers metastasise to the brain?
bloodstream or lymphatic system
382
what are symptoms of brain metastases?
headaches with or without nausea and vomiting mental changes dizziness
383
how do you diagnose brain metastases?
imaging with MRI CT or PET biopsy is required
384
how do you treat brain metastases?
if diagnosed early they usually respond to therapy treatment includes surgery/radiosurgery radiation chemotherapy or immunotherapy high-dose corticosteroids used to ease swelling and decrease neurological symptoms
385
at what age does the ABO blood grouping system develop?
six months - new start to develop naturally occurring antibodies (IgM)
386
before six months does the child have any blood antibodies?
yes IgG from transplacental passage- rhesus antibodies (significant if theses rhesus incompatibility)
387
why are anti-D antibodies significant in women who are rhesus negative?
if their baby is rhesus positive then Anti-D antibodies can cross the presenter and cause haemolysis of fatal red blood cells
388
how is resource disease of the newborn avoided in pregnancy?
thorough testing and Anti- D Ig is given to the woman
389
what does a group and save determine?
ABO blood group and Rhesus state
390
what is a cross match?
when donor blood is tested against patient's blood to test for coagulation - if this occurs then there has been antibody interaction
391
what are the risks associated transfusion occuring early in the process?
HBO incompatibility allergic reactions pirate generate reactions bacterial contamination coagulopathy after massive transfusion circulatory overload T ACO transfusion -related acute lung injury TRA LI post-transfusion purpura
392
What value of platelets should you aim for?
over 10 unless the patient is septic (or other serious pathology) in which case over 20
393
What are indications for platelet transfusion?
thrombocytopenia or active bleeding with disordered platelet count
394
what does FFP contain?
coagulation proteins and inhibitors
395
what are indications for the use of FFP?
massive transfusion disordered coagulopathy liver disease DIC
396
what is cryoprecipitate? And when is it used?
rich in fibrinogen and used in massive transfusions and DIC
397
What human albumin solution used for?
increase on public pressure in limited areas and nephrotic syndrome can help reduce oedema
398
what are the components of blood?
red blood cells platelets cryopreserved and FFP
399
describe the pathophysiology of ABO incompatibility?
anti-H and anti-D are naturally occurring IgM antibodies capable of activating the complement system. If there is incompatibility of the protein complement activation results in lysis of the antibody coated red blood cells. Causing haemolysis. This results in shops and organ failure which can be fatal
400
how do you avoid ABO incompatibility?
by doing two independent checks of two separate group and saves performed by different staff members at different times
401
what is TACO?
the most frequent cause of morbidity and mortality associated with transfusions it is circulatory overload
402
what are risk factors that predispose to TACO?
```
congestive cardiac failure
severe aortic stenosis
moderate -severe left ventricular dysfunction
diuretics use (indicating predisposition to fluid overload)
pulmonary oedema
peripheral oedema
hypoalbuminaemia
renal impairment
```
403
what are the signs and symptoms of TA CO?
dysnopea wheezing the tightness of chest cough cyanosis tachyopnea rapid increase in blood pressure distended neck veins peripheral and pulmonary oedema within 24-hour of a blood transfusion
404
what investigation should you run if you suspect T ACO?
chest x-ray to check for pulmonary oedema and heart involvement
405
what signs may you see on chest x-ray for TACO?
bilateral infiltrates and possibly an enlarged heart
406
what anticoagulant would you give Iv?
unfractionated heparin
407
what anticoagulant would you give sub cut?
low molecular weight heparin
408
what anticoagulant would you give orally?
DOACS or warfarin
409
how does warfarin work?
binds to plasma proteins and inhibits the production of clotting factors 2 7 9 and 10
410
do you expect to notice changes in INR immediately after giving warfarin or immediately after stopping?
nerve because it's peak effect is 3 to 4 days after starting and warfarin is usually still present 4 to 5 days after stopping
411
what are the side effects associated with warfarin?
bleeding and is highly teratogenic
412
how do you monitor warfarin?
measure INR
413
what is the target for warfarin in the first DVT/PE?
2 – 3
414
do DOACS require monitoring?
now they also are given as a standard dose
415
why are DOA C good?
however rapid onset of action have fixed dowsing with predictable anticoagulant effect have a low potential for food or alcohol interactions have a low potential for drug interactions require no drug monitoring
416
what are the cons associated with DOAC?
renal elimination no specific antidotes are currently licensed for specific indications
417
in a patient with cancer you notice a right hilar mass what is most common cause of this?
hilar lymph nodes being enlarged in this case because of cancer
418
in a patient with cancer who has undergone lots of chemotherapy you notice that they have kidney failure however the albumin is low what does this indicate?
low albumin usually occurs in deteriorating chronic kidney failure/disease
419
is hypertension a risk factor for thrombosis?
no
420
what is the most appropriate management for cancer associated thrombosis?
dalteparin or rivaroxiban not warfarin
