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Phase 2a > Haeotololology > Flashcards

Haeotololology Flashcards

1
Q

what is heprain induced thrombocytopenia and what heparin cuases it more

A

serious complication of taking the blood thinner heparin. With HIT, your immune system causes your platelets to clot in the presence of heparin, resulting in your platelet levels dropping.

it is caused more by unfractioned heparin

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2
Q

FE deficancy aneamia causes

A

Low iron diet
blood loss
Heavy periods- (menorrhagia)
GI bleeding
Hookworm
Malabsorption (celiac disease)
Pregnancy
Breastfeeding

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3
Q

FE deficancy aneamia key presintations

A

Brittle hair and nails
Atrophic glossitis (tongue inflammation and atrophy f papillea)
Spoon shaped nails
Inflammations of corners of the mouth

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4
Q

FE deficancy aneamia tests

A

FBC (microcytic)
Blood film
Serum ferratin - low
Reticulocyte count - reduced
Endoscopy/colonoscopy looking for GI bleed
`

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5
Q

FE deficancy aneamia manegemtne

A

Ferrous sulphate (oral iron tablets)
Ferrous fumarate

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6
Q

Alpha thalassemia aneamia defornition

A

Genetic anaemias caused by mutations which leads ot diffomed alpha chains

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7
Q

Alpha thalassemia aneamia epidemiology

A

South east asiea, africa, middle east. - provides some protection against malaria

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8
Q

Alpha thalassemia aneamia different types

A
  • Gene deletion
  • Level 1: silent carrier- the blood cells are smaller than normal but no disease
  • 2: Trait - genes are missing and there is mild anaemia
  • 3: HbH disease- genes missing, moderate to severe anaemia, blood transfusion are needed and also folic acid supplementation. Iron chelation therapy removes the excess iron from the blood.
  • 4: HbH more severe. All 4 genes are missing and the feuotis will die before birth
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9
Q

Alpha thalassemia aneamia key presintations

A

Hepatosplenomegaly
Family history
Symptoms of aneamia

People with both types of thalasseamia often end up with too much iron because there is increased gastorintesitinal absorption driven by the ineffective erethropoiess. This means there is too much iron and often atking iron tables

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10
Q

Alpha thalassemia aneamia tests

A
  • Haemoglobin
  • MCV
  • Mean corpuscular haemoglobin
  • Blood smear - shows stargert cells which are scrunched up red blood cells
  • Hemoglobulin electrophoresis - lab test to label haemoglobin types present
    Genetic testing
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11
Q

Alpha thalassemia aneamia manegement

A

Mild - don’t need treatment

Severe:
* blood transfusions
* Iron chelation therapy
* folic acid supplements
* Spelenectomy

There is also genetic screening available for pregnact women

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12
Q

beta thalassemia aneamia defornition

A

Genetic mutations leading to beta chain mutations. Not present in foetuses as they have gamma chains not beta!!!

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13
Q

beta thalassemia aneamia epidemiology

A

mediteranian

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14
Q

beta thalassemia aneamia types

A
  • Minor - there have a mutation which is only on 1 which leads to reduced or no beta chain. Asymptomatic.
  • Intermedia - 2 mutations which code for reduced beta globin chain synthesis. Symptomatic form 3-6 mnsths of life as the gamma chainss are replaced by the beta ones.
    Major - 2 mutted genes which leads to no beta chain synthesus
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15
Q

beta thalassemia aneamia symptoms

A

Intermediate- major:
Jaundice
Swollen abdomen
Aneamia smptoms
Growth retardation

Major:
Chipmunk facies

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16
Q

beta thalassemia aneamia tests

A

Hemoglobin
Low MCV
Heamoglobin electrophoresis ill show changes in the beta chain

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17
Q

beta thalassemia aneamia treatment

A

Intermedia:
Potentially transfusion
Iron monitering incase they become aneamic
Cheliation due to them becoming iron overloaded
Genetic counselling
Splenectomy
Stem cell transplantation
MAJOR:
* Regular transfusions
* Iron chelation
* Genetic counselling
* Spelenoctomy
Stem ell transplant

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18
Q

beta thalassemia aneamia complications

A

Arrhythmias
Pericarditis
Cirrhosis hypothyroidism
Diabetes mellitus

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19
Q

Sideroblastic aneamia defornition

A

The body has enough iron but is unable to make it into haemoglobin, causing aneaia and a build up of iron in the system

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20
Q

Sideroblastic aneamia causes

A

Genetic
Idiopathic
Exposure to alcohol led and drugs

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21
Q

Sideroblastic aneamia key presintations

A

Aneamia
Enlarged spleen and liver
Abnormal heart rhythem

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22
Q

Sideroblastic aneamia manegeeemtn

A

Blood transfusions
Vitamin B6 = pyridoxine
Iron chelation - deferoxamine

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23
Q

sickle cell aneamia defornition

A

Autosomal recessive condition. There is a point mutation in the B globulin gene which results in HbS protein. It produces destruction of blood cells and obstruction of microcirculation leading to tissue infarction.

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24
Q

sickle cell aneamia key presintations

A
  • Acute pain in hands and feet
  • Jaundice
  • Aneamia
  • Acute chest syndrome
  • Patiens don’t always have aneamia as they can produce the noraml red blood cells as well, however ethis can change is the spleen get overly cloged up, or there is BM aplasia and the precursors die,
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25
Q

test for sickle cell aneamia

A
  • Screen neonates with heel prick test
  • FBC - low Hb high reticulosiyte count due to compensatory mechanisms
  • Blood film - sickled erethrocytes
    Hb electrophoresis HbS confirms it
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26
Q

sickle cell aneamia tx

A

Folic acid
* Aggressive anaglsia for the pain
* Treat the causes (antibiotics if there is an infection)
* Fluids
* Hydroxycarbamide (incrases HbF concentrations)
* Blood transfusions
* Stem cell transplant

Pulmonary HTN and chronic lung disease are the most common cuases of death.

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27
Q

sickle cell aneamia complications

A
  • Painful crisis
  • Mesenteric ischemia
  • Renal impairment
    Pulmonary hypertension
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28
Q

Hereditary spherocytosis aneamia defornition

A

Inherited abnormality that causes structural defects in the membrane proteins which makes them spherical in sha

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29
Q

Hereditary spherocytosis aneamia cause

A

Genetic - dominant inheritance

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30
Q

Hereditary spherocytosis aneamia key presintations

A
  • Prescence of risk factors
  • Pallor
  • Splenectomy
  • Jaundice
  • Fatigue
  • Gall stones caused by excess bilirubin
    Leg ulcers
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31
Q

Hereditary spherocytosis aneamia first line test

A

FBC
Reticulocyte
Blood smear - spherocytes and reticulocytes
Serum bilirubin

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32
Q

Hereditary spherocytosis aneamia treatments

A

Neonates:
* Rbc transfusion
* Folic acid supplementation

Infants:
* Folic acid
* RBC transfusion
* Cholecystectomy (there can be gall stones)
Splenectomy

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33
Q

G6PDH deficiency aneamia defornition

A

Glucose-6-phosphate dehydrogenase (G6PD) deficiency

Inherited x linked deficancy which cuases a lack of ability to tolerate biochemical oxidative stress, with heamolysis as the result.

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34
Q

G6PDH deficiency aneamia risk fctor

A
  • Subsaharan africa
    • Asia
    • Middle east
  • Male
  • Neonate
    Family history
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35
Q

G6PDH deficiency aneamia key presintations

A

Usually asympotmatic but can get the anaemia if they take certain drugs (quinine) or eat broad beans

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36
Q

G6PDH deficiency aneamia tests

A
  • FBC
  • Reticulocyte count
  • Urinalysis
  • Unconjugated bilirubin
  • G6PD fluroescent spot test

Heinz bodies show

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37
Q

G6PDH deficiency aneamia treatmetn

A

Avoid broad beans

* Supportive care 
* Folic acid
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38
Q

malaria aneamia causes

A
  • Protozoa plasmodia falciparum
    Transmitted by the female mosquito
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39
Q

malaria aneamia life cycle

A

here are three stages;

* Exoerythrocytic 
* Endoerthrocytic 
* Hypnozoite stage 

* The parasites traves in the blood to the liver in the form of a sporozoite  
* Multiply inside hepatocytes as merozoites
* The infected hepatocytes rupture and release the merozoites into the blood where they are take up by RBCs 
* They develop further and then rupture out causing aneamia
*
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40
Q

malaria aneamia symptoms

A
  • Fever
  • Chills and sweats
  • Jaundice
  • Hepatos[lenomegally
  • Aneami
  • Fatuigue
    Black urine (black ater fever)
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41
Q

malaria aneamia tests

A
  • Thick and thisn blood film: thick shows parasite prescence, thin sshows which types of parasite
  • Rapid diagnotic test to detet plasmodium in the blood
  • Pregnancy test
  • Rule out meningitis
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42
Q

treatetn for malaria aneamia

A
  • Quinine
    Doxycycline
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43
Q

autoimmune aneamia defornition

A

The red blood cells are destroyed by the immune system

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44
Q

autoimmune aneamia causes

A
  • Drugs
  • Lymphoma or leukaemia
    Idiopathic
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45
Q

autoimmune aneamia symptoms

A
  • Galllsotnes from excess billiruin
  • Jeandice
  • Dark urine
  • Fever tiredness
  • SOB
    This is amking me want to sob
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46
Q

autoimmune aneamia test

A

Coombs test - looks for Igs which are oncoleved in destorying red blood cells

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47
Q

autoimmune aneamia tx

A
  • Steroids - surpress the immune system
  • Folic acid
  • Blood transfusions if severe
    Splenoctomy
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48
Q

aneamia of chronic disease causes

A

Chrons
Rheumatoid arithritus
TB
Systematic lupus erythematousus
CKD

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49
Q

aneamia of chronic disease pathophysiology

A

they ether reduce RBC production or lifespan or some other mechanisms:

* Less iron released 
* Less erythropoetin form kideys 
* Higher levels of hepcidin expression which inhibits duodenal iron absorbtion  Inflamation mediated reduction in RBC
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50
Q

aneamia of chronic disease test

A
  • Fbc and blood film
  • Low serum iron
    Increased serum ferratin
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51
Q

aneamia of chronic disease treatemtn

A
  • Treat underlying cause
    Recombinant erythropoietin
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52
Q

anaplastic aneamia defornition

A

Bone marrow faliure

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53
Q

anaplastic aneamia causes

A

Congenital
Chemotherapy
Infections - HIV, EBV,TB,hepatitis
Pregnancy

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54
Q

anaplastic aneamia pathophysiology

A

There is a reduction in the number of pulripotent stem cells causgin a lack of heamopoisesis - production of blood cells and patelets

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55
Q

anaplastic aneamia symptoms

A

Anaemia
Increased infection
Increased bleeding/bruising

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56
Q

anaplastic aneamia test

A

FBC
Reticulocyte count - low or absent
BM biopsy - hypocellular marrow with increased fat spaces

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57
Q

anaplastic aneamia tx

A
  • Remove causative agens
  • Blood/platelet transfusion
  • BM transplant
    Immunosuppressive therapy
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58
Q

what aneamias are microcytic

A

Fe deficiency, Alpha & Beta Thalassemia, Sideroblastic

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59
Q

wat aneamias are normocytic heamolytic

A

Haemolytic – Sickle cell, Hereditary spherocytosis, G6PDH deficiency, Malaria, Autoimmune Haemolytic,

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60
Q

what aneamias are normocytic non heamolytic

A

Chronic disease

Anplastic

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61
Q

what aneamias are macrocytic megoblastic

A

Megaloblastic – B12 deficiency, Folate deficiency,

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62
Q

what aneamias are macrocytic non megoblastic

A

Non-megaloblastic – Hypothyroidism, Alcohol excess, Liver disease

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63
Q

B12 aneamia causes

A
  • Autoimmune (this is pernicious)
  • Atrophic gastritis
  • Gastrectomy
  • Chrons disease
  • Coeliac disease
    Malabsorption
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64
Q

B12 aneamia pathophysiology

A

Parietal cells produce intrinsic factor which binds to B12 for it to be absorbed. There is an autoimmune condition where the parietal cells are destroyed, or poeplc can just be deficant.

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65
Q

B12 aneamia signs

A

Glossitis - tounge inflamation
Angular stomatitis - inflamed corners of the mouth
Janunduce - excess bilirubin
Neurologcal symptoms - polyneuropathy

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66
Q

B12 aneamia symptoms

A
  • Fatuihue
  • Dyspnea
  • Palpitations
  • Heasaches
    Legarthy
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67
Q

B12 aneamia tests

A

FBC
Blood film
Autoantibody screen
Serum B12 - low

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68
Q

B12 aneamia treatmetns

A

Vitamin B12 injection/ tablets
Not folic acid - causes neurologial deficancys

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69
Q

B12 aneamia complicatios

A

Heart faliure
Angina
Neuropathy

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70
Q

folic acid aneamia causes

A
  • Poor dies (elederly, alcholoics, poverty)
  • Malabsoption - chrons
  • Pregnancy n
    Antifolate drugs - methotrexate and trimethoprim
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71
Q

folic acid aneamia pathophysiology

A

Absorbed n the jejunum, it is needed for DNA synthesis , it is foud in green vedgetables.

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72
Q

key pesintation of folic acid aneamia

A

There is no neuropathy so its distuinguidahbel from B12 defiecancy

Glossitis - tounge inflamation
Angular stomatitis - inflamed corners of the mouth
Janunduce - excess bilirubin

  • Fatuihue
  • Dyspnea
  • Palpitations
  • Heasaches
  • Legarthy
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73
Q

folic acid aneamia tests

A

FBC
Blood film
Serum ad erythrocyte folate levels

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74
Q

folic acid aneamia tx

A

Folic acid supplementation

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75
Q

hypohyrpodosm aneamia pathophysiology

A

The hypothyrpidims cuases bone marrow depletion, deceaed EPO production, and B12 and folate deficancies. It may alos linkt to othe rautoimmune disesases which lead to aneamia such as cealiac disease

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76
Q

alcohol excess aneama patthophysology

A

Gastrointestinal bleeding causes aneamia and this is a result of alcoho

Heavy alcohol consumption can cause generalized
suppression of blood cell production and the production of structurally abnormal
blood cell precursors that cannot mature into functional cells. Alcoholics frequently
have defective red blood cells that are destroyed prematurely, possibly resulting in
Anemia.

Alcohol is toxic to bone marrow

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77
Q

liver desase aneama pathophysology aneam

A

Gastrointestinal bleeding can causes it.

Hemolysis also plays a part

Iron deficany aneamia

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78
Q

liver aneama tx

A

iron tablems

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79
Q

HIV

A

Most people present with a flu lie illness which occurs 2-6 weeks after infection

Then there are no symptoms for a long time and then people start to get ill as the immune system is very damaged.

It attacks the CD4+ cells which leaves the immune system undefended

80
Q

HIV

A

Most people present with a flu lie illness which occurs 2-6 weeks after infection

Then there are no symptoms for a long time and then people start to get ill as the immune system is very damaged.

It attacks the CD4+ cells which leaves the immune system undefended

A retrovirus that replicate=s n human lymphocytes and cuases immune deficancy and suseptability to infections.

81
Q

risk factors for HIV

A

Unprotected sex
IV drug users
Higher risk areas

82
Q

HIV symptoms initial and chronic

A

Initial:
Fever
Sore throat
Rash
Tiredness
Joint pai
Muscle pain
Swollen glands

Chronic:
* Weight loss
* Diahorhea
* Night sweats
* Skin problems
Reoccurring infections

83
Q

test for HIV

A

ELISA: enzyme linked immunosrobernt assay
Serum HIV Rapid test - blood from finger prick

84
Q

HIV differenal diagnosis

A

Infections mononucleosis
Influnza infectoin

85
Q

HIV manegement

A

Pre exposure prophylaxis - taken before

Antiretroviral therapy - decreases diseases progression.
Another selectve antiviral.
Supportive care - reduce further transmission

86
Q

glandular fever deforniton

A

An infectio causd by the epsien barr virus whish is passed thrligh saliva

87
Q

glandular fever pathophysology

A

Epstien barr virus (human herpesvirus 4), it is also called infectious mononucleosis.
It is spread though saliva.

The virus first replicates in sie the nasopharynx cuasing a sore throat nt then go onto infect the b lymphocytes which circulate through the body and reticular endothelial system

88
Q

glandular fever signs and symptoms

A

Splenomegally
Rash
Signs of hepatitis
Jeanundice

There are three hallmark symptoms:
Fever
Lymphadenpathy (swelling of the lymph nodes)
Tonsillar pharyngitis (swelling of throat)

Malaise
Hepatosplenomegaly

89
Q

glandular fever 1st lne then gold standard tet

A

FBC -
Heterophil antibodies - these are antibodies found in humas which are produced from certai infection which will agglutinate the RBCs form other species (such as bovine or horse)

Epstien Barr virus specific antibodies

90
Q

glandular fever dfferential

A

Group a strepp throat infection, Hepatitis A, HIV, adenovirus, Influenza.

91
Q

glandular fever complicatons

A

Splenic rupture
Increase risk of hodkins
Neurological syndromes (guillian barre, meningocephalitis)
Hepatitis
Myocarditis
Pancreatitis

Ineffecitve T cell response has been linked to Hodgkins Lymphoma in later life.

92
Q

glandular fever tx

A

SUPPORTIVE CARE: Paracetamol and ibruprofen
* Antipyretics - reduce fever
* Anelgesics

If there is upperairwat obsutruction or heamolytic aneami agive cotricosteriods.

93
Q

what are the 4 types of leuema and whch cell do each of them affect

A
  • Acute myloid - myloblast cell
    • Chronic myloid - neutrphil basophil, eosinophl
    • Acute lymphoblastic - lymphoblast
    • Chrnoic lymphatic - B lymphoblast
94
Q

what are risk factros for acute leauemas

A
  • Exposure to radiation (for exmaple for treating a previous cnacer)
  • Exposure to formalyhyded ad benzene
    Congenital disorder for example down syndrome
95
Q

in which age groups are the 2 acute leukeamias more common

A

aml - older people
all - childhoood, this is the most common type of childhood canacer and has a good prognosis

96
Q

what is the pathophusiology of leaukemia

A

here is clonal proliferation of myloid or lymphoid precursours
Thet loose the abbility to differenctiate and are stuck in the blst stage and malfunction

They crowsd out the other cells and causes cytopenia

It can also causes low platelets (thrombocytopenia)

97
Q

what are teh symptoms of leueamiia

A
  • B symptoms = weight loss, appetite loss, night sewats
  • Fatigue due to the aneamia
  • Easier bleeding and brusing sue to thrombocytopenia
  • Infection - leukopenia
  • Bone pain - incrased cell production and BM expansion
  • Fever

Acute
* Lymphadenopathy - pain in lymph nodes
* Heaptosplenomegally - abdominal fullness

98
Q

tests for acute leukemia

A

FBC - aneamia and thrombocytemia. WBC can be raised

Blood film - characteristic myeloblasts and lymphoblasts, depending on which cancer
- myeloblasts - large cells with fine chromatin and prominent nuculoi
- lymphoblasts - smaller cells with coarse chromatin and small nucuoli

BM biopsy - increased cellularity with high percentage of abnormal lymphoid/myeloid cells

Immunophenotyping

99
Q

treatments for acute leukaemia’s

A

AML and ALL:
* Supportive treatment - blood, platelts, fluid
* Correction of the -penias such as aneamia,, throombocytopenia and coagulation abnormalaties
* Allopurinol - prevention of acute tumour lysis syndrome
* cHemo
BM transplant

100
Q

chronic lymphoblastic leukemia epidemiology and risk factors

A

More commen in men
Increases with age

Family history of it
More common in white people

101
Q

chronic lymphoblastic leukemia pathophysiology

A

Malignancy of the B cells

Uncontrolled proliferation and accumulation o mature B lymphocytes that have escaped apoptosis. Accumulate in the bone marrow and causes cytopenia and anaemia by crowing put the healthy cells

102
Q

chronic lymphoblastic leukemia key presintations

A
  • Normally asymptomatic
  • Fatigue - due ot aneamia
  • Easier bleeding
  • More infections
  • Lymphadenopathy
    Hepatosplenomegaly
103
Q

chronic lymphoblastic leukemia tests

A

first line test* FBC - shows lots of lymphocytes, no plassma cells and so no antibodies, aneamia, thrombocytopenia.
* Should be WBC cound and there will be elevated WBC
* Blood film - small lymphocytes with mature appearance with smudge cells whoch are an artefact produced during preperation
Immunophenotyping is needed to explode reactive lymphocytosis with other lymphoid neoplasms

104
Q

chronic lymphoblastic leukemia Tx

A

Radiotherapy to shrink lymphadenopathy
Splenectomy
BM transplant
Stem cell transplant
Chemo

105
Q

chronic myloid leukemia risk fators

A
  • Middle age
    Ionising radiation
106
Q

chronic myloid leukemia pathophysiology

A

Mutation in the philidelphia chromosone which leads to the activation of tyrosine kinase, this leads to granulocyted to divide too quickl leadsing to an accumulation I the BM

107
Q

chronic myloid leukemia symptoms

A
  • Asympomatic
  • Fever
  • Weight loss
  • Sweating
  • Aneamia
  • B symptoms
  • Bone pain
    Splenomegally
108
Q

chronic myloid leukemia tests

A
  • FBC - leucocytosis, aneamia, high platelets, Hb low
  • BM biopsy - hypercellular marrow with increase in myloid prognitors
    Genetic testing for Philadelphia chromosome - fluorescents in situ hybridisation (FISH)
109
Q

chronic myloid leukemia treatment

A

Imatinib - if philidelphia chromosome positive, this si a cancer cell growth blocker.
Watchfu waiting
Chmo
Stem cell transplant
BM transplant

110
Q

lymphoma pathophysiology

A

Genetic mutation in the lymphocyte which proliferates

Metastasis to the spinal cord which causes compression

Malignant proliferation of lymphocytes which accumulated into the lymph nodes. B and T cell malignancy’s.

111
Q

lymphoma causes

A

Primary immunodeficiency
Secondary immunodeficiency (HIV)
Infection - ebv, h pylori
Autoimmune

112
Q

lymphoma symptoms

A
  • Painless LN enlargement
  • Hepatosplenomegaly
  • Compression syndromes:
  • Illaic vessels cause deep vein thrombosis
  • Pressure on spinal cord
  • Pres on neck causes superior vena cava compression
  • Lymphadenopathy - swollen lymph nodes
  • SVC obstruction
  • B symptoms are what show up when the diseas sint asymptomatic, and the progression can be staged from this (weight loss apatite loss, night sweats)
113
Q

lymphoma test

A

FBC
Lymph node biopsy and histology
PET scan

114
Q

lymphoma complications

A

Metastasis to the spinal cord which causes compression

Metastasis to the bone marrow which causes the levels of the healthy cells to decrease and leads to decraed levels of RBCs, leukocytes and platelets

115
Q

hodkins lymphoma epidemiology and rick factors

A

Typically in young adults

Has been linked to having glandular fever (which effects the B cells)

116
Q

hodkins lymphoma pathophysiology

A

It has the presence of the reed-Sternberg lymphocyte and hodkins cells. It is spread contigously so the cancer spreads from one lymph node to the next in a chain fashion

Reed sterberg cells are large mononucleur neoplastic cells that looks like two cells fused (owl eyes)

There are tow classifications:
* Classical Hodgkin’s lymphoma - reed Steinberg cells
* Nodular lymphocyte predominant Hodgkin’s lymphoma

117
Q

what syptom can non hodkins have that hodkins doesnt

A

extraonoadl involvemnt :

* Bone marrow - fatuigue and easy bruising 
* GI tract - bowel obstruction  Spinal cord - loss of sensation
118
Q

hodkins lymphoma symptoms

A

Painless lymphadenopathy - cervical lymph nodes which a rubbery consistency on examination

B symptoms (night sweats, weight loss, loss of appetite, fever)

119
Q

hodkins lymphoma tests

A
  • CT/MRI of chest abdomen and pelvis
  • Lymph node byopsy showing reed-Sternberg cells
  • FBC
  • CXR
    PET scan
120
Q

hodkins lymphoma staging system

A

Staged using the ANN Arbor system:
1. Involvement of the nodes in 1 region
2. 2 or more node regions
3. Lymoh nodes both sides of eth diaphragm
4. Widespread over the body
There is also type A and b f each of these, B being the presence of B symptoms and A being the absence of B symptoms.

121
Q

where is teh most common place for non hodkins extranodla lymphoma to develop

A

GI tract

122
Q

hodkins lymphoma tx

A
  • ABVD chemotherapy
  • Stage 1-2a - chemo followed by radiotherapy
  • Stage 2b-4 - longer course of ABVD
    Relapse responds well to bone marrow transplant
123
Q

hodkins lymphoma complications

A

Chemo:
* Infertility
* Alopecia
* Vomiting
* Rash
Radiotherapy:
* IHD
* Second malignancies
* Hypothyroidism

Psychological issues

124
Q

non hodgkins lymphoma pathophysioogy

A

No special cell presence and doesn’t spread contiguously and so is harder to treat as it spreads extra-nodaly.

Majority of the cells are B cells (90%)

Tow classifciatio :
* Aggressive
* indolent (for exampke follicular, it is slow growin, incurable, live for 10 years sih, maintinaince treatment

125
Q

non hodgkins lymphoma tests

A
  • CT for stagin
  • Lymph node biopsy, you need wither a core needle biopsy or excision node biopsy
  • FBC
  • CXR
  • PET scan
  • Liver biochemisty
126
Q

non hodgkins lymphoma tx

A

R-CHOP chemo:
Rituximab
Cyclophosphamide
Hydroxy-daunorubicin
O – Vincristine (oncovin is brand name)
Prednisolone

* Low grade:
* Observation 
* Purine analouge 
* Readiotherapy 
* BM transplant 
* Monoclonal antibodies 
* Combination chmo 

* High grade;
* R-CHOP + radio therapy  Advanced - RCHOP and monoclonal antibodies
127
Q

non hodgkins lymphoma complications

A
  • Secondary malignancies
  • IHD
  • Infertility
    nausea
128
Q

multiple myeloma defornitio

A

Cancer of plasma cells which produce antibodies (plasma cells)

129
Q

Multiple Myeloma epidemiology and risk factors

A

Men
Age 60 is peak
More common is afro Caribbean

Family history
Radiation exposure

130
Q

Multiple Myeloma pathophysiology

A

Normally there is clonal proliferation of the plasma cells into all the antibodies
In myeloma, the plasma cells produce excess antibodies (mainly IgG and IgA), these build up and causes damage to the kidneys. This produces Bence jones protein deposits in the urine.

The plasma cells also release cytokines which increased osteoclast activity causing a lot of calcium to be reabsorbed form bone into the blood and the bones to become weak and holes and lesions.

There can also be plasmacytomas which are plasma cells build ups causing tumours which can occur in the bones or soft tissues.

131
Q

Multiple Myeloma key presintations

A

CRAB -
* Calcium levels raised
* Renal failure
* Anaemia
bone disease

132
Q

Multiple Myeloma signs and symptoms

A

Raised calcium
Renal failure
Anaemia
Bone pain causes by osteoclast bone eating - this can causes lesions and spinal cord compression

Fatigue
Infections

133
Q

Multiple Myeloma tests

A

Serum and blood electrolytes - B2 macroglobulin
Blood film- rouleaux formation
Bence jones protein in urine
BM aspiration shows plasma cells abnormal
X ray shows pepper pot skull and yes in the long bones
FBC
Serum and urinary electrophoresis to look for immunoglobulins
Full body MRI or CT
Creatine to look at kidney function

134
Q

multiple myloma treatmetn

A

Chemo - thalidomide and bortezomid.
BM transplant
Bisphosphonates - surpress ocsteoclast activity t stop bone degeneration
Correction of anaemia
Dexamethasone
Radiotherapy to bone lesions
Orthapedic surgery to stabalise bones
Cement augmentaiton - injecting cemens into vertebreal fractures to improve spine stability

135
Q

polycythaemia causes

A

Primary causes:
Increased sensitivity of BM cells to erythropoietin which leads to incrased RBC production. There are 2 main causes:
1. polycythaemia rubra vera - genetic mutaion in JAK2 gene
2. Primary familial and congenital polycythaemia - mutation on eh EPO gene

Secondary causes:
There are more RBCs due to more circulating EPO
- Chronic hypoxia
- EPO producing tumours

136
Q

polycythaemia causes

A

Primary causes:
Increased sensitivity of BM cells to erythropoietin which leads to incrased RBC production. There are 2 main causes:
1. polycythaemia rubra vera - genetic mutaion in JAK2 gene
2. Primary familial and congenital polycythaemia - mutation on eh EPO gene

Secondary causes:
There are more RBCs due to more circulating EPO
- Chronic hypoxia
- EPO producing tumours

137
Q

polycythaemia risk factors

A

Obesity, smoking, chronic alcoholism, diabeties, hyoertension, male, over 50.

138
Q

polycythaemia defornition

A

Increases in haemoglobin, packed cell volume and RBCs.

139
Q

polycythaemia symptoms

A
  • May be asymptomatic
  • Easy bruising/bleeding
  • Fatuigue
  • Diziness
  • Headaches
  • Hypertension

Symptoms of rubra vera - plethroic complextion (red cheeks or dark brown cheeks, also facila swelling), hepatospelnomegally

Syptoms of secondary: plethoric complexoin, no splenomegaly

140
Q

polycythaemia tests

A

FBC - in rubra vera there is raised plateletsand low serum EPO
- in secondary there is normal white blood cells and platelet but low epo

Bone marrow biopsy
Genetic testing for JAK2 gene

141
Q

polycythaemia treatmetn

A

Blood letting (venesection of 400-500ml of blood)
Asprin

If it is secondary treat the causes

142
Q

which type of thrombocytopenia is more commone

A

Immune throbocytopenia purpura

143
Q

Immune throbocytopenia purpura p[athophysiology

A

Pathophysiology

Autoimmue destruction of platlets by IgG antibodies. It is often triggerd by a viral infection or a malignancy.

IgG bind to the plateltes and are then removed by the Fc receptos on macropgages

144
Q

Immune throbocytopenia purpura signs and symptoms

A

Signs

Purpura - red or purple spots under the skin

Symptoms

Easy bruising
Nose bleeds (epistaxis)
Menorrhagia
Gum bleeding

145
Q

Immune throbocytopenia purpura fist line tests

A

1st line test

FBC - thrombocytopenia
Increased megakaryocytes on BM investigation
Detectino of platelt autoantibodies

146
Q

Immune throbocytopenia purpura treatment

A

Management
Initial
Secondary

Corticosteroids - prednislone

Splenectomy
IV immunoglobulin

147
Q

thrombotic thrombocytopenia purpura epidemiology

A

Women, black ethnicity, obesity, pregnancy.

148
Q

Immune throbocytopenia purpura epidemiology

A

Epidemiology

ITP is more common that TTP!!!

In children it is ofen actue and self limiting

In adults less acute and seen in young women

149
Q

thrombotic thrombocytopenia purpura pathophysiology

A

extensive microvascular clots form in small vessle in the body whihc results in lowered overall platelet counts and organ damage

It is usually due to the absence of the von willebrand factor cleaving enzyme (responsible for breaking down VWF) which leads to unsusually large von willebrand multimers.

150
Q

thrombotic thrombocytopenia purpura key presintations

A

Easy bruising
Purpura

Fever

Renal faliure, heamolytic aneamia, neurological changes

There is usually SEVERE neurologicl symptoms such as coma, and seizures)

151
Q

thrombotic thrombocytopenia purpura tests

A

FBC - reduced platelets but normal/increased magakaryocytes

Coagulation screen - lactate dehydrogenate is raised due to haemolysis

152
Q

thrombotic thrombocytopenia purpura manegement

A

Plasma exchange to remove the ADAMTS 13 antibody
IV Methylprednisolone (corticosteriodi)
Immunosuppression - IV Rituximab (corticosteroid)

153
Q

Von Willebrand factor disease causes and risk factors

A

Autosomal inheritance with variable penetrance

Positive family history
Consangeous relationships

154
Q

Von Willebrand factor disease pathophysiology

A

Ther are quantitative or qualitative issue with the VWF which is the critical link between pltetls and exposed vascular endothelium

There are three types of the disease:
1. Most common, they have a reduced level, which leads to bleeding
2. The VWF doesn’t work preoperly, its more severe
The most severe, they have very low levels or none at all, thsiciases bleeding fomr ehmouth and gums aand there can be muscle and joint bleeds after injury.

155
Q

Von Willebrand factor disease key presintations

A

Family history
Postoperative bleeding
Bleeding from minor wounds
Epistaxis
GI bleeding
Mehhonragia
Bleeding gums

156
Q

Von Willebrand factor disease tests

A

Prothrombin time - clotting test for the extrinsic and common pathwya

Activated partial thromboplastic time - clotting est for intrinsic athway which will rule our heamophillia

FBC - asses platelet number

Von Willebrand factor antigen

VWF function assay

Women can be put on the oral contraceptive to reduce heavy periods

157
Q

Von Willebrand factor disease tx

A

Desmpressioin (ADH analouge) - this increases the amounf of VWF and factor 8 and also improvs platelet function).

VWF concentrate - in injection

Avoid asprin, and NSAID as they can make the bleeding worse
Avoid IM ijection, and tell any healthcare before aby prdcdure or operation

158
Q

Haemophilia A and b factor feficnecy

A

Definition

A -Factor 8 deficiency
B - facor 9 deficency

159
Q

Haemophilia A , Haemophilia B epidemiology and cuases

A

X linked recessive disorder that mainly effects men

Haemophilia type A is more common

160
Q

Haemophilia A , Haemophilia B classing levels

A
  • Level < 1 frequent spontansou bleeding into muscles and joint which can cases crippling arthropathy
  • Levels 1-5 are associated with severe bleeding follwing injury and occasional aparently spoetanosu episodes
    >5 mild diseases with bleeding increased after trama or surgery
161
Q

Haemophilia A , Haemophilia B signs and symptoms

A
  • Cereberal hemmorage
  • Eady bruising
  • Heamatomas
  • Prolonged bleeding after cut
  • GI bleeding
  • Heamaturia (blood in the urine)
  • Epistaxis (nose bleed)
    Heamarthrosis (bleeding into joint spaces)
162
Q

Haemophilia A , Haemophilia B tests

A

PTT -Partial thromboplastin time: this measure the extrinsic pathway

APTT - Activated partial thromboplastin time: measures the intrinsic pathway (the one that contains 8 and 9) takes to clot the blood after the addition of reagents tp the plasma. The time taken will be longer than normal because there is les factr 8 and 9. The way the test works its that initially the plasmsa is stopped from blotting, and tehn platlet substitutes are added, nd fator 12 activators and Ca2+, this should cuases a stable clot to form.

Factor 8 and 9 assay - Reduced plasma factor 8 and 9 when measured

163
Q

Haemophilia A , Haemophilia B differential

A

Von Willebrand’s disease (tis is ruled out by the prothrombin time test)

164
Q

Haemophilia A , Haemophilia B tx

A
  • Recombient factor 8/9 concentrate given as a prophalaxyis before and after surgery or to trat a bledding eisode
  • Syntetic vasporession - to raise facor of 8/9
  • Hep a/b vax
    Encouragement to join exercise reigeme and avoid contact soprts and asprin!
165
Q

Haemophilia A , Haemophilia B complications

A

joint deformities and arteritis
Increased risk of bleeding and hemmoaring

166
Q

Disseminated Intravascular Coagulopathy pathophysiology

A

Widespread clotting and bleeding which involves the widespread generation of fibrin in the blood vessels and initiation of coagulation pathway which leads to multiple small thrombosis which causes organ damage.

This also causes consumption of the clotting factors and secondary activation of fibrinolytics which will leasd to bleeding happening more in other part of the body.

167
Q

Disseminated Intravascular Coagulopathy causes

A

Malignancy - leukemia is a obestrics - amniotic fluid emobolism
Speticeia
Trauma
Infections - meningitis
Heamolysic tranfusion
Liver disease

168
Q

Disseminated Intravascular Coagulopathy key presintations

A

Varies from no bleeding to complete haemostatic failure
Form venepuncture sights and Nose and mouth
Bruising
Dyspona
Haemoptysis

169
Q

Disseminated Intravascular Coagulopathy tests

A

Diagnosis suggested by history such as sepsis, trauma, malignancy

Prolonged PTT,APTT, TT
- PT - prothrombin time: extrinsic and common pathways
- Activated partial throbroplastn time: intrinsic and common
- thrrombin tome - dibrinogen to fibrin

D dimer test - should be elevated
Platelet count - decreased
Fibrinogen - decreased
Facotr5, 8, 10, 13 - all decreased

Blood film - fragmented red cells

170
Q

Disseminated Intravascular Coagulopathy tx

A

Treat underlying cuases - maintin blood volume and tissue perforation
May need transfusion platelets, RBCs nd fresh frozen plasma
Activate protien C - an inactive enzyme that regulates anticoaggulation

171
Q

Tumour lysis syndrome defornition

A

Oncologicla emergcanyc cause y the metabolic and electrolyte emergencies caused by the initation of cancer treatment.

172
Q

Tumour lysis syndrome pathophysiology

A

There is a rapid breakdown o the cancer cells whihc releases lage amounts of intracellular content into the bloodstream which overwhelms normal homeostatic mechanisms

This can lead to acute kidney damage, cardiac arrhythmias, seizure, neuromuscular dysfunction. It is heavily associated with high grade B cell lymphoid, and leukaemia.

There are cryctals produced which damage the kidneys and get deposited n small blood vessles

173
Q

Tumour lysis syndrome ost common cancer that cuses it

A

high-grade non-Hodgkin’s lymphoma

174
Q

Tumour lysis syndrome key presintations

A

There is hyperuricaemia, hyperphosphatemia, hyperkalaemia or hypocalcaemia. And Prescence of a clinical manifestation such as kidney injury, cardiac arrhythmias, seizure or sudden death.

Seizures
Chest pain
Syncope
Dyspnoea
N&V
Anorexia
Diarrhoea
Muscle weakness
Recent chemotherapy!!!

175
Q

Tumour lysis syndrome tests

A

Serum uric acid
Serum phosphate
Serum potassium
Serum calcium

Lactate dehydrogenase
FBC
ECG

176
Q

Tumour lysis syndrome treatment and prevention

A
  • IV hydration
  • Loop diuretic
  • Allopurinol - decreases uric acid
    Rasburicase - decreases uric acid as a prevention of TLS
177
Q

what are teh normal values for neutophils, lymphocyes and platelets in teh blood

A

Neutrophils ( x10^9/L) - 1.7-6.6
Lymphocytes (x10^9/L) - 1-3
Platelets ( x10^9/L) - 150-400

178
Q

What does PT stand for, what does it mean, what does INR stand for, what does it mean.

A
  • Prothrobin time is how long it takes for a clot to form down the extrinsic pathwya
    • The INR is the international Normalised Ratio - this is the normal time it should take to clot. This si especialy usefu if the person is one warfrin as it can help them to change the dde.
    • In healthy people it is 1.1 or below os normal
    • In warfin 2-3 is normal
    • When the INR is higher it means that the blood clots slower
    • INR= patient PT / Controll PT
179
Q

what does aptt stand for

A

Activated partial thromboplastin time - how long it takes the blood to clot down the intrinsic pathway - 8 9 10 11 12 clotting factors

180
Q

what are teh 5 heamotologival emergancies

A
  • Tumour Lysis Syndrome
    ○ Chemotherapy given→ Cancer cell broken down → Release contents (Hyperkalaemia, Nucleic acid) → Produce crystals and get deposited in the kidneys → damage/ loss of function.
    ○ To prevent give Allopurinol (Xanthine oxidase inhibitor)
    ○ To treat IV fluid and correct electrolytes
    • Neutropenic Sepsis (Temp >38℃ and absolute neutrophil count >1x109)
      ○ Antibiotics immediately!
    • Acute Sickle Cell Crisis
      ○ Pain relief and IV fluid.
    • Chest Crisis
      ○ IV Fluid, Abx, Closely monitor.
    • Spinal Cord Compression
      ○ Steroid e.g. high dose dexamethasone and MRI
181
Q

what are teh 5 mian microcytic aneamias

A

TAILS

Thalesseamia
Aneamia of chronic disease
Iron deficency
Lead poisening
Sidroblastic

182
Q

what is transferrin

A

moves the iron around

183
Q

what do people who have had a splenoctomy have ot be careful of

A

If you’ve had a splecetomy you cant have live vaccines!!! The immune system is copramised.

184
Q

what are teh test for someone with suspected multiple myeloma

A

Suspect myeloma in anyone over 60 with bone pain.
The initial investigations are:
* FBC- low white blood count
* Camcium - raised
* ESR - raised
* Plasma viscosity - raised die to incrase immunglobulins
If these ae suspected perform a serum protein electrophoresis and a urine Bence-jones protein test.

BLIP

* Bence jones protein in urine (request urine electrophoresis) 
* Light - Serum frees LIGHT chain
* IMUNOGLOBULINS in the serum 
* PROTIEN in serum  electrophoresis

Bone marrow biopsy is needed for diagnosis .
Imaging is required to asses for bone lesions -MRI, then CT, then skeletal survey, an x-ray of the full skeleton, you only need to do one of these

185
Q

what is Monoclonal gammopathy of undetermined significance (MGUS)

A

MGUS - an excess of a single type of antibody wotoug the features of myelom or cance. It may presnt in a healthy person and may preognress of myelmoa.

186
Q

what is MAHA

A

microangiopathic haemolytic anaemia - anaemia from damage of red blood cells due the occlusion of arterioles and capillaries due to fibrin and platelet deposition

187
Q

what is teh differnce bwteeen biopsy and aspiration

A

An aspiration takes a sample of the liquid part of your bone marrow. A biopsy takes a sample of the solid, spongy part of your bone marrow

188
Q

what are teh most common ages of onset for teh leukeamias

A

ALL CELLMATES HAVE COMMON AMBITIONS

Under 5 and over 45 – acute lymphoblastic leukaemia (ALL)
Over 55 – chronic lymphocytic leukaemia (CeLLmates)
Over 65 – chronic myeloid leukaemia (CoMmon)
Over 75 – acute myeloid leukaemia (AMbitions)

189
Q

what are teh most common featues of ALL

A

Acute lymphoblastic leukaemia: Most common leukaemia in children. Associated with Down syndrome.

190
Q

most common features of AML

A

Acute myeloid leukaemia: Most common acute adult leukaemia. It can be the result of a transformation from a myeloproliferative disorder. Associated with Auer rods.

191
Q

most common features of CLL

A

Chronic lymphocytic leukaemia: Most common leukaemia in adults overall. Associated with warm haemolytic anaemia, Richter’s transformation into lymphoma and smudge / smear cells.

192
Q

most common features of CML

A

Chronic myeloid leukaemia: Has three phases including a 5 year “asymptomatic chronic phase”. Associated with the Philadelphia chromosome

193
Q

wha is teh precursor condition to myeloma

A

MGUS - mammyloid gammopathy of undertemined significance is the precursor condition to multiple myeloma

194
Q

what would you see on a blood smear for multiple myeloma

A

roulex formation - blood cells stacked ontop of eachother

195
Q

wht is teh gold standard test for multiple myeloma

A

bone marrow bioppsy - would show >10% plasma cells

196
Q

what are teh drugs in ABVD chemo and what is it for

A

hydrochloride (Adriamycin), bleomycin sulfate, vinblastine sulfate, and dacarbazine.

hodkins lymphoma

Phase 2a (18 decks)

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