Brainscape's Knowledge GenomeTM

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


See full index

FINALS > Haematology and Oncology > Flashcards

Haematology and Oncology Flashcards

1
Q

What are the causes of microcitic anaemia?

A

Iron deficiency anaemia of chronic disease thalassaemia lead poisoning

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

what are the two types of causes of Normocitic anaemia?

A

Haemolytic and non-haemolytic

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

what are haemolytic causes of Normocytic anaemia?

A

intrinsic: Hereditaries theory psychosis G6PD deficiency sickle-cell anaemia extrinsic: autoimmune

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

what are non-haemolytic causes of normocytic anaemia?

A

Iron deficiency anaemia of chronic disease chronic kidney disease aplastic anaemia acute bleeds

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

what are the two types of causes of macrocytic anaemia

A

megaloblastic and non-megaloblastic

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

what are the causes of megaloblastic macrocytic anaemia

A

folate being nine deficiency B12 deficiency drug induced such as allopurinol

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

what are the causes of non-megaloblastic macrocytic anaemia?

A

Alcohol use disease liver disease hypothyroidism

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

what is the MCV of Microcytic anaemia?

A

<80

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

What is the MCV of normocytic anaemia?

A

80-100

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

what is the MCV of macro cytic anaemia

A

> 100

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

what is the definition of anaemia?

A

Haemoglobin <120 (F) or < 140 (M)

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

what are the classic symptoms of anaemia?

A

Fatigue decreased exercise tolerance shortness of breath postural hypotension palpitations angina

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

what is a consequence of very severe anaemia?

A

heart failure

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

what are signs of anaemia?

A

Parlour tachycardia heart murmur

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

What does kolinichia indicates?

A

iron deficiency anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what does angular stomatitis and glossitis indicate?

A

vitamin B9 +/or B12 deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the symptoms of a major bleed?

A

Hypotension Pala clammy skin threaded pulse tachycardia dysnopear/air hunger altered mental status

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

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what does a full blood count include?

A

Haemoglobin haematocrit platelet count MCV CH MCHC red cell distribution width

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

what would a peripheral smear show in iron deficiency anaemia?

A

microcytic hypo-chromic

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

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

how is iron excreted?

A

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

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

what is the management of a women (menstruating) who is iron deficient?

A

Trial of iron supplements ferrous sulphate 200 mg if this doesn’t work go onto further investigations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is the management of male or postmenopausal female iron deficiency anaemia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what are some causes of iron deficiency anaemia which would require further testing and what testing is required?

A

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)

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

what investigation should you do in an individual over 60 with symptoms of iron deficiency?

A

OGD and colonoscopy

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

what further testing is required for iron deficiency anaemia in an individual younger than 60?

A

OGD

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

What is the management of iron deficiency anaemia if iron supplements do not work?

A

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

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

what does ascorbic acid do in terms of iron?

A

Enhances the absorption of iron

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

what is pernacious anaemia?

A

A megaloblastic anaemia without neuropathy caused by folate deficiency (B9)

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

what the typical causes of pernacious anaemia?

A

malabsorption increased demand poor dietary intake increased folate loss alcohol and drugs inborn errors of metabolic disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what diseases cause malabsorption?

A

Tropical sprue coeliac disease extensive intestinal resection/short bowel syndrome

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

what can cause increased demand for folate?

A

Pregnancy lactation prematurity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what can increase the loss of folate?

A

chronic dialysis and chronic haemolytic disease

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

what drugs cause increased folate use/loss?

A

sulphathiazine trimethoprim methotrexate and anticonvulsants

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

what is a classic symptom of megaloblastic anaemia

A

chronic headache

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

how do the symptoms of B12 deficiency in benign deficiency differ

A

they are very similar except for the fact that B12 deficiency causes neurological deficits such as peripheral neuropathy dementia subacute cord degeneration

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

apart from the usual anaemia tests what tests should you include in the diagnosis of pernacious anaemia?

A

Intrinsic factor antibody test (in B12 deficiency) and tests for IBD or coeliac disease

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

what is the management of folate deficiency?

A

Oral folic acid

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

what is the management of B12 deficiency?

A

B12 injections loading dose +3 monthly follow-up injections

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

describe the diffrerence in blood tests results between iron deficiency B12 deficiency and folate deficiency

A

insert picture pg 7

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

what drugs cause haemolytic anaemia?

A

Cephalosporins levodopa methyldops and penicillin

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

what are causes of haemolytic anaemia caused by abnormal haemoglobin production?

A

sickle cell and thalassaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what are the causes of autoantibody mediated haemolytic anaemia?

A

Autoimmune: SLE rheumatoid arthritis scleroderma lymphoproliferative: CLL or non-Hodgkin’s lymphoma

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

what is a more common enzyme deficient haemolytic anaemia?

A

Glucose six phosphate dehydrogenase deficiency

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

what type of anaemia does haemolytic disease of the newborn or transfusion reactions cause

A

alloimmune haemolytic anaemia

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

what other causes of infection or trauma mediated haemolytic anaemia?

A

DIC TTP haemolytic uraemia eclampsia

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

what are the characteristic features of haemolytic anaemia is?

A

pallor jaundice splenomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

as well as the usual investigations for anaemia what else should you include any haemolytic anaemia?

A

Coombs test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

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?

A

Haemolytic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what is the management of autoimmune haemolytic anaemia?

A

Folic acid corticosteroids plasma three’s (may provide temporary response)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what are the general principles of management of haemolytic anaemias?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is sickle-cell anaemia?

A

An autosomal recessive defect of the beta chain of haemoglobin causing the production of HBS sickle haemoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

describe the pathophysiology of sickle-cell anaemia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what are consequences of sickle-cell anaemia which can be fatal in children?

A

Splenic sequestration and bone marrow aplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what organs are most commonly damaged by sickle-cell anaemia?

A

kidneys retina spleen bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

how does splenic sequestration cause of morbidity and mortality?

A

Splenic dysfunction increases the vulnerability to serious infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

How is sickle-cell anaemia diagnose?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what would a blood smear show in sickle-cell anaemia?

A

Nucleated red blood cells sickelling and howell jolly bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what causes symptoms in sickle-cell anaemia?

A

Vasoocclusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

a patient with a history of sickle cell anaemia presents with severe chest pain fever dysnopea tachyopnea and hypoxia what is happening?

A

acute chest syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What are some symptoms of sickle-cell anaemia?

A

Symptoms of acute chest syndrome bone pain floaters jaundice parlour lethargy Dactylitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what does the image below show and when does it usually occur?

A

Dactylitis - Usually occurring in sickle cell anaemia which is uncontrolled/undiagnosed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

what is the ongoing management of sickle-cell anaemia?

A

Hydroxicarbide = ongoing mainstay - simple analgesia, Pneumococcal immunisations and prophylactic penicillin if< 5y ( repeated transfusions may be needed)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

what is the management of sickle-cell anaemia in an acute crisis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

what would an x-ray show in acute chest syndrome?

A

Infiltrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

what other risk factors that predispose someone to a vaso occlusive crisis?

A

acidosis cold stress exercise infections dehydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

what are the absolute indications for blood transfusions in sickle cell anaemia?

A

Acute chest syndrome priapism and/

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

what is the management of red blood cell aplasia in sickle-cell anaemia?

A

transfusions steroids splenectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

what is thalassaemia?

A

An inherited blood disorder in which the body makes abnormal or inadequate amount of haemoglobin and there is increased haemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

what other two types of thalassaemia?

A

alpha and beta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

describe alpha thalassaemia?

A

A reduction in the functioning levels of alpha haemoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

described beta thalassaemia?

A

a reduction in the functioning levels of beta haemoglobin?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What are the subcategories of alpha and beta thalassaemia and what does that mean?

A

major – severe symptoms intermedia – mild/moderate symptoms trait – mostly asymptomatic but a carrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

what is the presentation of alpha thalassaemia major?

A

The most severe cases of alpha thalassaemia presentation is of stillbirth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what is the presentation of alpha thalassaemia intermedia?

A

Anaemia neonatal jaundice failure to thrive shortness of breath

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

what is the management of alpha thalassaemia?

A

Regular monthly blood transfusions bone marrow transplantation if possible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

what is the presentation of beta thalassaemia major?

A

prolonged new natal jaundice severe anaemia failure to thrive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

what is the presentation of beta thalassaemia intermedia?

A

The same as beta thalassaemia major: prolong innate jaundice severe anaemia failure to thrive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

how do you treat beta thalassaemia?

A

Bone marrow transplants only treat beta thalassaemia when or if Burton is low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

what does the image below show and when does it occur?

A

maxillary overgrowth this is a complication of alpha and beta thalassaemia if untreated (a bony deformity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

why do you not use iron supplements in anagement of thalassaemia

A

because iron supplements are not as good as blood transfusions, and if used in conjunction with blood transfusion they cause iron overload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

what is a complication of regular blood transfusions?

A

iron overload so to Laois in therapy is used - Desferrioxamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

what is a glucose six phosphate deficiency

A

and inherited enzyme deficiency in which patients are accessibly susceptible to the development of haemolytic anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

what is the mechanism of inheritance of glucose-6-phosphate deficiency?

A

X-linked

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

describe the pathophysiology of glucose-6-phosphate deficiency

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

what is an advantage of G6PD?

A

protective against malaria so it is commonly found in populations such as: African Asian Mediterranean

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

what is the presentation of G6PD?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

what is the management of G6PD?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

what is polycythaemia?

A

erythrocytosis: concentration of red blood cells in your blood making your blood more viscous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

what is polycythaemia characterised by?

A

erythrocytosis thrombocytosis leukocytosis and splenomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

what is polycythaemia characterised as?

A

a myeloproliferative neoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

what are the consequences of polycythaemia?

A

increased risk of thrombosis and haemorrhage - MI PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

what are the symptoms of polycythaemia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

how is polycythaemia diagnosed?

A

usually Patients will not present because of polycythaemia and will often be found by accident when elevated haemoglobin is seen on routine blood tests

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

what does an FBC show in polycythaemia?

A

includes haemoglobin normal haematocrit leucocytosis thrombocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

what gene mutation is polycythaemia commonly associated with?

A

JA K2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

what is the management of polycythaemia?

A

Phlebotomy plus low-dose aspirin and management of cardiovascular risk factors ie hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

A patient presents with a left leg oedema, call swelling redness and you notice soe prominent superficial veins - what is the most likely diagnosis?

A

deep vein thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

what may you notice on palpation of a leg affected by DVT?

A

It is tender especially along the venous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

described the Wells score?

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What are risk factors for developing DVT?

A

Major surgery hospitalisation immobile Cancer smoking obesity pregnancy increased age COCP/HRT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

what part of the physical examination is significant in the diagnosis of DVT?

A

measuring the calf circumference if the difference is greater than 3 cm then the chances of a DVT raises significantly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

what further investigations are required in patient with a Wells score of less than two and no significant clinical symptoms of DVT?

A

None

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What further investigations are required in a patient with a Wells score of less than two with significant clinical symptoms of DVT?

A

require a D dimer test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

when would you perform a venous duplex ultrasound in a patient with ? DVT?

A

anyone who scores over two and a Wells score or if their D dimer is positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Why is D dimer not diagnostic for DVT?

A

It is not specific and frequently is positive in patients who are older are acutely ill pregnant or have underlying hepatic disease or infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

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?

A

Either whole leg ultrasound or a proximal Doppler ultrasound scan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

you perform proximal Doppler ultrasound scan patient with? DVT are further investigations are required?

A

yes, Repeat ultrasound in five – seven days if it is negative again then DVT is excluded

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

what drug class is used to treat DVT and why?

A

anticoagulants are used because of venous clots is fibrin rich

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

describe the management of a DVT?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

what drugs are classed as anticoagulants?

A

DOAC warfarin low molecular weight heparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

when would a DVT be required to be treated in hospital?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

what usually causes arterial thrombosis?

A

atherosclerotic plaques which predispose platelet aggregation if it ruptures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

what do arterial thrombotic events lead to?

A

Heart attacks and strokes or TIA as well as limb ischaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

what are risk factors for arterial thrombosis?

A

Increasing age smoking century lifestyle being overweight exes alcohol high cholesterol diabetes atherosclerosis arterial fibrillation antiphospholipid syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

what is the treatment of arterial thrombosis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

what are the common methods to diagnose arterial thrombosis?

A

CT angiography however if peripheral something like a Doppler ultrasound can be used

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

you suspect a patient has been over anticoagulated - what bloods should you order?

A

FBC PT APTT fibrinogen concentration creatinine and LFT (can do type and cross too) + INR if on Warfrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

what should you do if you suspect the patient has been over anti coagulated?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

what is the management of haemorrhage caused by over anticoagulating?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

do DOACs have a reversal agent?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

what is the management of a minor bleed caused by over anticoagulating?

A

DOAC: delayed or discontinued depending on severity Warfrin: INR < 4.5 = withhold warfarin INR > 4.5 withhold warfarin and give vitamin K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

what type of inheritance is haemophilia?

A

X-linked recessive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

what clotting factor is haemophilia A deficient in?

A

factor 8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

what clotting factor is haemophilia B deficient in?

A

factor 9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

what are symptoms of haemophilia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

what would bleeding into muscles present as in haemophilia?

A

Pain and swelling usually in the extremities decreased range of motion erythema and warmth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

what is Haemarthrosis?

A

recurrent leads over the years caused severe joint damage causing total cartilage erosion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

describe the X-linked inheritance in haemophilia?

A

insert picture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

what levels of clotting factor are regarded as mild haemophilia?

A

> 5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

What levels of clotting factor are regarded as moderate haemophilia?

A

1-5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

what levels of clotting factor are regarded as severe haemophilia?

A

<1%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

what bloods are required in haemophilia?

A

FBC PT APTT VWF studies LFT Coag factor asseys genetric testing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

What imaging may be required in haemophilia?

A

X-rays for joints CT for intracranial bleed CT or ultrasound the gastrointestinal bleeds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

what is the management of haemophilia?

A

Give factor concentrate!! analgesia and physiotherapy for complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

what drugs apart from factor concentrates can be used in severe haemophilia?

A

Bypassing agents which are special blood products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

what drugs should be used acute management of haemophilia with a life-threatening bleed?

A

factor concentrates or bypassing agents and antifibrinolytics (tranexamic acid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

what causes abnormalities in prothrombin time?

A

abnormalities of the extrinsic pathway such as warfarin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

what causes abnormalities in APTT?

A

abnormalities in the intrinsic pathway such as factor 8, 9 heparin and some DOAC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

what is Von Willebrand Disease?

A

the most common inherited bleeding disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

what type of inheritance is Von Willebrand Disease?

A

autosomal inheritance with variable penetrance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

what is the pathophysiology of Von Willebrand Disease?

A

VWF provides the critical link between platelets and exposed vascular epithelium whilst also binding in stabilising the coagulation factor 8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

how does Von Willebrand Disease present?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

which type of Von Willebrand Disease is most common?

A

type I it is also the least severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

what bloods should you investigate in Von Willebrand Disease?

A

PT (normal) and APTT (prolonged) FBC VWF antigen and VWF function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

which test is diagnostic for Von Willebrand Disease?

A

Von Willebrand factor function is best but antigen can also be used

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

describe PT and APTT in VWF and why the results are as such?

A

PT = normal APTT = prolonged because VWD causes a decrase in functonal factor 8 which affects the intrinsic pathway which prolongs APTT (PT is extrinsic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

what is the management of Von Willebrand Disease?

A

Von Willebrand factor concentrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

what is tDIC?

A

and acquired syndrome characterised by the activation of coagulation pathways resulting in the formation of intravascular thrombi and depletion of platelets and coagulation factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

what are features of DIC?

A

generalised bleeding evidenced at three unrelated sites signs of circulatory collapse purpura fulminans + gangrene Delerium or coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

gave examples of bleeding at three unrelated sites which may be found in DIC?

A

nosebleed gingival bleeding haematuria blood in the cannula

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

what causes the purpura fulminans and gangrene in DIC?

A

micro-or microvascular thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

How do you diagnose DIC?

A

abnormal coagulation tests and one known underlying condition which predisposes to DIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

what’s conditions predispose to developing DIC?

A

sepsis major trauma bans malignanciesObstetric disorders severe organ destruction of vascular disorders and transfusion reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

what obstetric disorders predispose to the development of DIC?

A

amniotic fluid embolism eclampsia placental abruption retained fatal products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

which organs if severely injured most commonly predisposed to DIC?

A

pancreas and liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

describe the coagulation tests results that you would find in DIC?

A

platelets (-) PT (+) d dimer (+) fibrinogen (-)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

what is the management of DIC?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

what are indications for replacement therapy in DIC?

A

active bleeding/ requiring an invasive procedure /at risk for bleeding complications/ with a documented deficiency of platelets/coagulation factors/inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

what is immune thrombocytopenia purpura?

A

and autoimmune haematological disorder characterised by isolated thrombocytopenia in the absence of an identifiable cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

what risk factors predispose to ITP?

A

children with proceeding viral illness with abrupt onset / young adult females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

what is the presentation of ITP?

A

Bruising / petichiea / haemorrhagic bullae / bleeding gums/ amaemia + Sx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

what is the diagnostic criteria for ITP?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

how would you diagnose thrombocytopenia?

A

FBC + peripheral blood smear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

what is the management of ITP?

A

satisfactory platelet count: observation / corticosteroids or IVIG or Anti- D Ig

170
Q

what is the criteria for treatments of ITP?

A

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
Q

what are the causes of secondary ITP?

A

H. pylori hepatitis C HIV immunodeficiency autoimmune disorders drug induced

172
Q

what drugs can cause secondary ITP?

A

frusemide or NSAIDs

173
Q

what autoimmune disorders can cause secondary ITP?

A

SLE antiphospholipid syndrome autoimmune thyroid disease

174
Q

what is thrombotic thrombocytopenic purpura?

A

in a clinical syndrome characterised by haemolytic anaemia and thrombocytopenic purpura - if untreated is almost always fatal

175
Q

what does this triad describe: haemolytic anaemia thrombocytopenic purpura neurological symptoms?

A

thrombotic thrombocytopenic purpura

176
Q

what is the pathophysiology behind thrombotic thrombocytopenic purpura?

A

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
Q

what symptoms does thrombotic thrombocytopenic purpura cause?

A

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
Q

what art schystocytesand when might they be found

A

in haemolytic diseases for example TTP - they are broken down red blood cells see image below

179
Q

how would you diagnose thrombotic thrombocytopenic purpura?

A

full blood counts showing thrombocytopenia anaemia leukopenia reticulocytes (+) Coombs test (-ve). Peripheral smear showing: schystocytes and micro-angiographic haemolysis

180
Q

why might you want to check renal function in thrombotic thrombocytopenic purpura?

A

thrombotic thrombocytopenic purpura effects microvascular system and can cause renal failure is a good indicator of the severity of the disease

181
Q

how do you manage thrombotic thrombocytopenic purpura?

A

plasma exchange/ corticosteroids/ after resolution use long-term aspirin – adjunct to initial therapy are aspirin folic acid blood transfusions immunotherapy and splenectomy

182
Q

what is thrombocytopenia?

A

to a few platelets

183
Q

what are the different methods in which thrombocytopenia can occur?

A

bone marrow making too few platelets, increase platelet destruction, increase platelet use

184
Q

what are some causes of thrombocytopenia in which the bone marrow makes too few platelets?

A

B9 or B12 deficiency leukaemia or other causes of bone marrow infiltration radiation or cytotoxic therapy

185
Q

what are some causes of thrombocytopenia caused by increased obstruction or use of platelets?

A

hypersplenism ITP DIC

186
Q

what is thrombocytosis?

A

too many platelets

187
Q

What are the two types of thrombocytosis?

A

primary and secondary

188
Q

what causes primary thrombocytosis?

A

essential thrombocythaemia - a rare blood disorder that causes a high number of blood cells called platelets to form

189
Q

what causes secondary thrombocytosis?

A 
Malignancy 
inflammation such as IBD 
infection 
removal of spleen 
iron deficiency 
haemolytic anaemias
190
Q

what are platelets?

A

non-nucleated cells made from megakaryocytes created inside the bone marrow

191
Q

what is the lifespan of a platelet?

A

Eight – 10 days

192
Q

what is the main function of platelets?

A

Forming primary haemostatic plugs

193
Q

what happens if your platelet count drops below 20?

A

you develop spontaneous breathing

194
Q

what our red blood cells?

A

oval by concave discs lacking a cell nucleus which contain haemoglobin and made in the bone marrow

195
Q

what is the lifespan of red blood cell??

A

100 to 120 days

196
Q

what breaks down red blood cells?

A

macrophages

197
Q

what is the process by which red blood cells made?

A

erythropoesis stimulated by the hormone EPO which is synthesised by the kidney

198
Q

describe the maturation of a red blood cell?

A

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
Q

what are the different types of white blood cell?

A

Neutrophil eosinophil basophil lymphocyte monosites

200
Q

what is the appearance of a neutrophil?

A

multilobar nucleus

201
Q

what is the function of a neutrophil?

A

specifically targets bacteria and fungi

202
Q

what is the appearance of an Eosinophil?

A

Bi lobar nucleus

203
Q

what is the function of an eosinophil?

A

targeting larger parasites and mediating allergic responses

204
Q

what is the appearance of a basophil?

A

Bi or Tri lobar

205
Q

what is the function of a basophil?

A

Releases histamine for inflammatory processes

206
Q

what are the types of lymphocytes?

A

B cells and T cells

207
Q

what is the function of B lymphocytes?

A

release antibodies which cause the activation of T cells

208
Q

what is the function of T lymphocytes?

A

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
Q

what are monocytes and whats their appearance?

A

kidney -shaped nucleus which migrate from the bloodstream and differentiate into macrophages

210
Q

describe the differentiation of blood stem cells?

A

insert image page 22

211
Q

what is acute myeloid leukaemia?

A

clonal expansion of myeloid blasst in the: bone marrow and peripheral blood or the extra medullary tissues

212
Q

who does AML typically affect

A

older adults

213
Q

what is the presentation of AML

A

symptoms of anaemia, ecchymoses or petechia frequent infections with fever lymphadenopathy hepatosplenomegaly mucosal bleeding

214
Q

what causes the ecchymoses or petechia in AML?

A

thrombocytopenia

215
Q

what are risk factors of AML?

A

over 65 previous treatment with chemo or radio

216
Q

what blood tests do you perform in AML?

A

Full blood count with differential shows: leucocytosis neutropenia and thrombocytopenia but an increased white cell counts / peripheral blood smear / Coag Panel

217
Q

how do you diagnose AML?

A

bone marrow biopsy

218
Q

what would a peripheral blood smear show in AML?

A

blasts and Auer Rods

219
Q

what is a complication of AML which is serious??

A

Coagulopathy which may be life-threatening so coag panel should be performed

220
Q

what is chronic myeloid leukaemia?

A

A malignant clonal disorder of haemopoietic stem cells (or Myeloid in older people)

221
Q

what is the presentation of CML?

A

one third of patients are asymptomatic however if symptoms are present they are: systemic features splenomegaly - abdominal discomfort and night sweats

222
Q

what is CML associated with?

A

the Philadelphia chromosome

223
Q

what bloods should be performed in CML?

A

Full blood count with differential showing anaemia with thrombocytosis or thrombocytopenia peripheral blood smear

224
Q

what would a peripheral blood smear show in CML?

A

almost all white blood cells are mature or maturing myeloid cells

225
Q

what test is diagnostic for CML?

A

bone marrow biopsy (showing granulocytic hyperplasia ) and cytogenetics which may show the Philadelphia chromosome

226
Q

what is the management of CML?

A

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
Q

what is acute lymphocytic leukaemia?

A

Malignant clonal disease that develops when a lymphoid progenitor cell becomes genetically altered and undergoes uncontrolled proliferation

228
Q

who does ALL usually affect?

A

children

229
Q

what is the most common presenting symptom of ALL?

A

lymphadenopathy

230
Q

what symptoms does ALL cause

A

lymphadenopathy pallor eccymoses petichea splenomegaly

231
Q

what are symptoms of tissue infiltration which occur in ALL and when they occur?

A

in more severe disease and include bone pain and symptoms of anaemia and testicular enlargement and cranial nerve palsy

232
Q

what blood tests would you perform for ALL?

A

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
Q

what would show on a peripheral blood smear in ALL?

A

leukaemic lymphoblastic

234
Q

How do you diagnose ALL and what is the result?

A

bone marrow aspiration and biopsy showing hyper cellularity and infiltration by lymphoblastic

235
Q

what is the management of ALL?

A

intensive chemotherapy and early stem cell transplantation should be considered

236
Q

what is a chronic lymphocytic leukaemia?

A

Lymphoproliferative disorder in which monoclonal B lymphocytes are elevated

237
Q

who is most at risk of CLL?

A

elderly

238
Q

what is a presentation of CLL?

A

typically doesn’t cause very many symptoms usually presents with absolute lymphocytosis as an incidental finding or with asymptomatic lymphadenopathy

239
Q

what blood test would you want to perform in CLL?

A

full blood count with differential showing lymphocytosis and a blood smear

240
Q

what Tessa diagnostic for CLL?

A

blood smear and flow cytometry

241
Q

what is a finding on blood smear with CLL?

A

smudge cells

242
Q

what is the management of CLL?

A

watch and wait or active management but typically since elderly and slow progressing it’s not used

243
Q

what is Hodgkins lymphoma?

A

haematological malignancy arising from mature B cells

244
Q

who does a Hodgkins lymphoma typically affect?

A

young adults and adults over 55 years

245
Q

what is the presentation of Hodgkin’s lymphoma?

A

painless cervical or supra-cervical lymphadenopathy in more advanced presentation will have red flag symptoms

246
Q

what do respiratory symptoms such as shortness of breath dysnopea and chest pain indicating Hodgkin’s lymphoma

A

mediastinal adenopathy

247
Q

how do you diagnose Hodgkin’s lymphoma and what is the result?

A

bone marrow biopsy showing Hodgkin and Reid Steinberg cell

248
Q

after diagnosis of Hodgkin’s lymphoma what other tests would you want to perform?

A

PET CT shows organs involved in the extent of the disease classic three might be ordered if presenting with respiratory symptoms

249
Q

Hodgkin’s lymphoma and how successful is this?

A

is a good response to chemotherapy with a median survival of 90%

250
Q

what is non-Hodgkin’s lymphoma?

A

an umbrella term of 60 different types of non-Hodgkin lymphoma effecting mature B cells however they can also cause T cell proliferation

251
Q

what are the types of non-Hodgkin lymphoma?

A

low-grade and high-grade

252
Q

what is a presentational non-Hodgkin’s lymphoma?

A

lymphadenopathy and splenomegaly however each subtype is specific set of symptoms

253
Q

who does non-Hodgkin’s lymphoma usually affect?

A

typically only ever in those over 50 years old

254
Q

what is the progression of low-grade non-Hodgkin’s lymphoma?

A

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
Q

what is the progression of high-grade lymphoma?

A

rapid and without treatment you can be dead within weeks but with treatment you can be cured

256
Q

do you see Reed Steinberg cells in non-Hodgkin’s lymphoma?

A

no

257
Q

what is myeloma?

A

A blood cancer characterised by the clonal proliferation of plasma cells in the bone marrow

258
Q

what cells does multiple myeloma usually consist of?

A

terminally differentiated plasma cells

259
Q

What is multiple myeloma usually associated with?

A

osteolytic bone disease anaemia and renal failure

260
Q

what other characteristic features of multiple myeloma?

A

terminally differentiated plasma cells infiltration of the bone marrow by plasma cells present on monoclonal immunoglobulin is in serum or urine

261
Q

what is the usual presentation of multiple myeloma?

A

anaemia bone pain infections fatigue renal impairment

262
Q

what is the most important prognostic factor in multiple myeloma?

A

serum albumin (which is a feature of renal impairment) and serum beta microglobulin

263
Q

How do you diagnose multiple myeloma?

A

Serum or urine electrophoresis showing increased light chain immunoglobulins or serum-free lighting say or bone marrow aspiration and biopsy

264
Q

why is a bone marrow aspirate and biopsy useful in multiple myeloma apart from diagnosis?

A

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
Q

what imaging might you want to perform in multiple myeloma? And why?

A

Whole-body CT or MRI to diagnose osteopenia + pathogenic fractures or osteolytic lesions

266
Q

what bloods would you want to perform in multiple myeloma?

A

serum calcium – hypocalcaemia can occur in osteolytic lesions FBC U+E - for renal impairment

267
Q

what is MGUS?

A

an asymptomatic premalignant disorder associated with a relatively low risk of progression to multiple myeloma or another plasma cell proliferative malignancy

268
Q

how does MGUS usually present?

A

found incidentally in serum or urine by detection of monoclonal M proteins

269
Q

what are the symptoms of MGUS?

A

by definition it cannot have symptoms it requires absence of anaemia hypercalcaemia renal failure and osteolytic lesions

270
Q

how do you diagnose MGUS?

A

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
Q

when would a biopsy be required in MGUS?

A

only if M protein levels are very high

272
Q

what is the management of MGUS?

A

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
Q

what are the principles of cancer management?

A

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
Q

when word cancer management not be given in regards to performance status?

A

anyone with performance status three or more will not receive cancer treatment very rarely do people with level III received radical treatment

275
Q

define radical treatment of cancer?

A

curative intent usually surgical or radiotherapy

276
Q

define neoadjuvant cancer treatment?

A

given before the curative treatments either to reduce the size or make the survival rate higher

277
Q

what is the definition of adjuvant/ adjunct treatments in cancer?

A

given after curative treatments

278
Q

define palliative cancer treatment?

A

improves quality of life and the length of survival with cancer also decreases the need for analesia reducing sedative effects

279
Q

describe the ECOG performance status?

A

insert picture

280
Q

how does chemotherapy work?

A

directly by binding to cell DNA and changing it resulting in cell death indirectly affecting DNA cell replication or by causing apoptosis

281
Q

what are common side effects of chemotherapy?

A

fatigue hair loss constipation diarrhoea mucosal sores peripheral neuropathy weight changes neutropenia anaemia which can lead to success

282
Q

how does radiotherapy work?

A

high energy x-rays are used to destroy cancer cells can be delivered externally or internally

283
Q

what are side effects of radiotherapy?

A

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
Q

how does immunotherapy work in cancer treatment?

A

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
Q

what are side effects of immunotherapy?

A

allergies nausea vomiting diarrhoea skin rashes labour pressure and flulike symptoms

286
Q

what are targeted agents?

A

inhibits specific targets involved in cell replication

287
Q

described endocrine therapies in cancer treatment?

A

Generally use for breast prostate and endometrial cancers inhibit the action of various hormones on hormone responsive cancer cells

288
Q

what are side effects of endocrine therapies

A

menopausal EDC they are usually in relation to hormone depletion

289
Q

describe the TNM stages?

A

insert picture - other letters are S: serum some cancers are staged by serum markers G: histological grade L: lymphatic involvement V: veins

290
Q

described the 1 – 4 staging patients may ask for?

A

insert picture page 28

291
Q

Describe breast cancer in situ?

A

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
Q

what is the presentation of breast cancer in situ?

A

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
Q

what would you see on mammography of breast cancer in tissue and what would be the next step?

A

calcifications next step would be an ultrasound/MRI to assess likelihood of it being cancerous however sometimes go straight to biopsy

294
Q

what biopsy is required for breast cancer in situ?

A

fine needle or core biopsy

295
Q

What would you find on biopsy in breast cancer in situ?

A

necrosis and a high nuclear grade

296
Q

what is the treatment of breast cancer in situ?

A

lumpectomy followed by radiotherapy but chemoprophylaxis can be used in high-risk patients

297
Q

what should you offer to high-risk patients that have had their breast cancer in situ treated?

A

preventative bilateral total mastectomy or chemoprophylaxis

298
Q

what is a primary invasive breast cancer?

A

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
Q

what genetic mutations are associated with primary invasive breast cancer?

A

BRCA1 or 2

300
Q

what are risk factors for primary invasive breast cancer?

A

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
Q

what is the usual presentation of primary invasive breast cancer?

A

usually are asymptomatic and found on screening however some patients may present with a lump

302
Q

if primary invasive breast cancer is symptomatic what the symptoms are present?

A

a firm breast mass nipple discharge axillary lymphadenopathy skin thickening skin discolouration retraction or scaling of the nipple

303
Q

who should you refer to the two-week wait pathway of breast cancer?

A

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
Q

what would a mammogram show in primary invasive breast cancer?

A

a regulated speculated mass clustered microcalcifications linear branching calcifications

305
Q

whatever biopsy is required for primary invasive breast cancer?

A

core needle biopsy

306
Q

once primary invasive breast cancers diagnosed what must also be histologically confirmed?

A

determination of oestrogen or progesterone receptors as well as her two receptors and Jean expression assays

307
Q

what adjuvant treatment is used for primary invasive breast cancer if HER 2 positive

A

monoclonal antibodies such as trasbtuzamab

308
Q

what I do when treatment is used for primary invasive breast cancers if hormone receptor positive ?

A

premenopausal: Tamoxifen postmenopausal: aromatase inhibitors

309
Q

what other drug should you include in the management of primary invasive breast cancer if it’s been treated with aromatase inhibitors?

A

bisphosphonates

310
Q

what is metastatic breast cancer?

A

considered metastatic if it is spread beyond the breast and its ipsilateral lymph nodes

311
Q

what counts as ipsilateral lymph nodes Of the breast?

A

axilla internal mammary infra and supraclavicular

312
Q

where is breast cancer likely to metastasise to?

A

bone lungs brain liver

313
Q

how do you investigate metastatic breast cancer?

A

FBC LFT Serum Calcium PET scan can be used, CXR Head CT (also abdo)

314
Q

described breast cancer screening?

A

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
Q

What features of a prostate exam would indicate prostate cancer?

A

an asymmetrical nodular prostate

316
Q

if a man presents with symptoms of L UTS what is the next step?

A

prostate exam and PSA blood test

317
Q

when should you refer a man for the two-week wait in prostate cancer?

A

if their prostate feels malignant on DR E or if their PSA is elevated above the age specific range

318
Q

what investigations are offered during the two-week wait appointment for prostate cancer?

A
  1. MRI offered before biopsy in order to limit invasive tests 2. biopsy
319
Q

what is the management of prostate cancer?

A

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
Q

what is neutropenic sepsis?

A

are potentially life-threatening complication of anti-cancer/Immunosuppressive drug treatment

321
Q

what is the criteria for neutropenic sepsis?

A

and absolute neutrophil count of 0.5x10^9 with any signs of sepsis (usually fever over 38’c)

322
Q

what is febrile neutropenia?

A

neutropenia with a fever is an indication of neutropenic sepsis

323
Q

what are the causes of neutropenia?

A

drugs and treatments infection autoimmune bone marrow failure nutritional deficiencies

324
Q

what drugs can cause neutropenia?

A

cytotoxic therapy immunosuppressive i.e. methotrexate haemopoietic stem cell transplant penicillin carbimazole valproic acid clozapine olanzapine allopurinol NSAIDs

325
Q

which infections can cause neutropenia?

A

Viral causes: HIV hepatitis B RSV CMV EBV – all cause transient bone marrow suppression and neutropenia bacterial causes: TB and Shigella

326
Q

what autoimmune diseases can cause neutropenia?

A

Crohn’s disease rheumatoid arthritis SLE

327
Q

what nutritional deficiencies can cause neutropenia?

A

B12 and folate

328
Q

why should absence of fever not exclude neutropenic sepsis?

A

can present with hypothermia, drugs such as corticosteroids can mask pyrexia, atypical presentations may include mental state changes or general malaise

329
Q

how do you diagnose neutropenic sepsis?

A

FBC and Sepsis 6

330
Q

how do you manage neutropenic sepsis?

A

empirical antibiotics and a high risk of MRSA cover with Vancomycin

331
Q

what should you do if after 3 – 5 days of treatment with antibiotics there no imporement in Neutropenic Sepsis?

A

evaluate for occult infections specifically fungal organisms and viral organisms if these were not found earlier

332
Q

what is the treatment of fungal induced neutropenic sepsis?

A

IV fluconazole

333
Q

what is the management of viral induced neutropenic sepsis?

A

IV Ganglocyclovir

334
Q

what is tumour lysis syndrome?

A

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
Q

what electrolyte abnormalities are associated with tumour lysis syndrome?

A

hyperuricaemia hypophosphataemia hyperkalaemia hypocalcaemia

336
Q

which cancers is tumour lysis syndrome most commonly associated with?

A

lymphomas and leukaemias as they are highly proliferative bulky and chemo sensitive

337
Q

what is the presentation of tumour lysis syndrome?

A

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
Q

why is renal compromise specifically monitored for when starting chemotherapy ?

A

Because renal compromise and dehydration can predispose to tumour lysis syndrome

339
Q

what is the diagnostic criteria of tumour erosive syndrome?

A

abnormality in two of the following electrolytes: uric acid potassium phosphate calcium occurring three days before or seven days after chemotherapy

340
Q

what tests must be performed in order to detect tumour lysis syndrome?

A

renal function (urea and electrolytes + Creatinine) lactate dehydrogenase urinary pH

341
Q

what are some severe complications of tumour lysis syndrome and how would you monitor for this?

A

Cardiac arrhythmias ECG – hypokalaemia and hypocalcaemia of electrolytes just specifically dangerous for this + EEG or increased awareness for seizures

342
Q

what is the mainstay of management for tumour lysis syndrome?

A

prevention

343
Q

how would you manage a patient is at low risk for tumour lysis syndrome?

A

regular monitoring of blood biochemistry and regular assessment of fluid balance and vital signs

344
Q

how would you manage intermediate or high risk patients tumour lysis syndrome?

A

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
Q

if urine output drops to below a hundred mph in an intermediate risk patients for tumour lysis syndrome what can you do?

A

Add a loop diuretic

346
Q

what are the risks of adding a loop diuretic to a patient who is at risk of tumour lysis syndrome?

A

this can predispose to uric acid increase as well as calcium and phosphate abnormalities so be careful

347
Q

if tumour lysis syndrome occurs what do you do?

A

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
Q

when is tumour lysis syndrome considered clinical?

A

if there are cardiac abnormalities seizures or renal failure

349
Q

how do you merge hyperkalaemia?

A

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
Q

how does vomiting occur physiologically what is it stimulated by?

A

Nerves in the stomach chemo receptors in the trigger zone senses and emotions

351
Q

what conditions may cause vomiting?

A

hypercalcaemia raised intracranial pressure liver failure constipation bowel obstruction

352
Q

What cancer treatments can cause nausea and vomiting?

A

chemo radio hormonal targeted therapies morphine-based medicines

353
Q

how do 5 HT 3 inhibitors work to reduce nausea and vomiting?

A

work by blocking the effects of serotonin on the internecine

354
Q

what type of nausea do 5 HT 3 inhibitors work best for?

A

sickness caused by chemotherapy and radiotherapy

355
Q

what’s is an example of a 5 HT 3 inhibitor?

A

ondesetron

356
Q

how do metoclopramide and domperidone work to reduce nausea and vomiting?

A

help them to the stoic and relieved feelings of sickness

357
Q

when would you use Chlorporamazine ?

A

used in advanced cancer and one other anti-sickness drugs do not work

358
Q

what drug class does cyclazine belong to?

A

antihistamine

359
Q

what drugs are usually given alongside 5 HT 3 inhibitors?

A

steroids and NK1 inhibitors

360
Q

when would haloperidol be given to treat nausea vomiting?

A

low-dose to treat sickness caused by morphine

361
Q

apart from 5 HT 3 what other drugs can help control nausea caused by chemotherapy?

A

Lorazepam when used in conjunction with other anti-sickness drugs

362
Q

what are some side effects of 5 HT 3 inhibitors?

A

constipation and headaches

363
Q

what are common side effects to all anti- emetic?

A

weakness tiredness

364
Q

what is a side effect that metoclopramide causes?

A

twitching

365
Q

what can cause diarrhoea in treatment of cancer?

A

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
Q

what are some lifestyle methods of preventing diarrhoea?

A

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
Q

what medicines can cause diarrhoea?

A

metoclopramide or laxatives

368
Q

what is the management of diarrhoea?

A

loperamide and anti-secretory agents such as corticosteroids and acreotide can be used plus IV hydration if necessary

369
Q

what is superior veno cava obstruction?

A

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
Q

what is the presentation of SVC obstruction?

A

facial swelling Dysnopea arm swelling facial plethora chest pain hoarseness of voice stridor symptoms worsening when lying down or bending forwards

371
Q

what signs may be present in SVC obstruction?

A

enlarged veins of the neck and upper chest wall at the extremity oedema papilloedema mental changes

372
Q

what cancer is most commonly cause SVC obstruction?

A

lung cancer and lymphoma

373
Q

why is Dysnopea a particularly worrying symptom in SVC obstruction?

A

can have a very sudden onset and worsening progression due to laryngeal oedema which can be fatal

374
Q

how do you diagnose SVC obstruction?

A

IV contrast CT

375
Q

what is the management of SVC obstruction ?

A

airway obstruction: corticosteroids and radiotherapy - if airway obstruction seems imminently dangerous give percutaneous stenting instead of radiotherapy And treat underlying cancer

376
Q

how do you manage benign SVC obstruction?

A

Thrombolysis grafting and anticoagulation

377
Q

what are causes of benign SVC obstruction?

A

less frequent than malignant causes usually caused by thrombosis from central venous catheter or pacemaker

378
Q

what are the benign causes of chronic airways obstruction?

A

tuberculosis sarcoidosis of Wagner’s granulomatosis

379
Q

what are the most common malignant causes of chronic upper airway obstruction?

A

laryngeal cancer and tracheal cancer

380
Q

what cancers commonly metastasised to the brain?

A

lung cancer breast Cancer Colon Cancer kidney cancer melanoma

381
Q

How do cencers metastasise to the brain?

A

bloodstream or lymphatic system

382
Q

what are symptoms of brain metastases?

A

headaches with or without nausea and vomiting mental changes dizziness

383
Q

how do you diagnose brain metastases?

A

imaging with MRI CT or PET biopsy is required

384
Q

how do you treat brain metastases?

A

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
Q

at what age does the ABO blood grouping system develop?

A

six months - new start to develop naturally occurring antibodies (IgM)

386
Q

before six months does the child have any blood antibodies?

A

yes IgG from transplacental passage- rhesus antibodies (significant if theses rhesus incompatibility)

387
Q

why are anti-D antibodies significant in women who are rhesus negative?

A

if their baby is rhesus positive then Anti-D antibodies can cross the presenter and cause haemolysis of fatal red blood cells

388
Q

how is resource disease of the newborn avoided in pregnancy?

A

thorough testing and Anti- D Ig is given to the woman

389
Q

what does a group and save determine?

A

ABO blood group and Rhesus state

390
Q

what is a cross match?

A

when donor blood is tested against patient’s blood to test for coagulation - if this occurs then there has been antibody interaction

391
Q

what are the risks associated transfusion occuring early in the process?

A

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
Q

What value of platelets should you aim for?

A

over 10 unless the patient is septic (or other serious pathology) in which case over 20

393
Q

What are indications for platelet transfusion?

A

thrombocytopenia or active bleeding with disordered platelet count

394
Q

what does FFP contain?

A

coagulation proteins and inhibitors

395
Q

what are indications for the use of FFP?

A

massive transfusion disordered coagulopathy liver disease DIC

396
Q

what is cryoprecipitate? And when is it used?

A

rich in fibrinogen and used in massive transfusions and DIC

397
Q

What human albumin solution used for?

A

increase on public pressure in limited areas and nephrotic syndrome can help reduce oedema

398
Q

what are the components of blood?

A

red blood cells platelets cryopreserved and FFP

399
Q

describe the pathophysiology of ABO incompatibility?

A

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
Q

how do you avoid ABO incompatibility?

A

by doing two independent checks of two separate group and saves performed by different staff members at different times

401
Q

what is TACO?

A

the most frequent cause of morbidity and mortality associated with transfusions it is circulatory overload

402
Q

what are risk factors that predispose to TACO?

A 
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
Q

what are the signs and symptoms of TA CO?

A

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
Q

what investigation should you run if you suspect T ACO?

A

chest x-ray to check for pulmonary oedema and heart involvement

405
Q

what signs may you see on chest x-ray for TACO?

A

bilateral infiltrates and possibly an enlarged heart

406
Q

what anticoagulant would you give Iv?

A

unfractionated heparin

407
Q

what anticoagulant would you give sub cut?

A

low molecular weight heparin

408
Q

what anticoagulant would you give orally?

A

DOACS or warfarin

409
Q

how does warfarin work?

A

binds to plasma proteins and inhibits the production of clotting factors 2 7 9 and 10

410
Q

do you expect to notice changes in INR immediately after giving warfarin or immediately after stopping?

A

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
Q

what are the side effects associated with warfarin?

A

bleeding and is highly teratogenic

412
Q

how do you monitor warfarin?

A

measure INR

413
Q

what is the target for warfarin in the first DVT/PE?

A

2 – 3

414
Q

do DOACS require monitoring?

A

now they also are given as a standard dose

415
Q

why are DOA C good?

A

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
Q

what are the cons associated with DOAC?

A

renal elimination no specific antidotes are currently licensed for specific indications

417
Q

in a patient with cancer you notice a right hilar mass what is most common cause of this?

A

hilar lymph nodes being enlarged in this case because of cancer

418
Q

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?

A

low albumin usually occurs in deteriorating chronic kidney failure/disease

419
Q

is hypertension a risk factor for thrombosis?

A

no

420
Q

what is the most appropriate management for cancer associated thrombosis?

A

dalteparin or rivaroxiban not warfarin

FINALS (24 decks)

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