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Clinical Haematology 2 Flashcards

(45 cards)

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1
Q

White Cell Abnormalities

A

Leukaemia (effects any white blood cell)
Lymphoma (only lymphocytes)
Quantity of cells vary in each
Malignant (cancer) non malignant (just infection)

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2
Q

Non Malignant cell count change

A

Destruction or production of poly clonal cells

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3
Q

Haematological Malignancies cell count change

A

Uncontrolled clonal proliferation of haemopoietic cells (precursors from bone marrow)

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4
Q

Neutrophilia (too much neutrophils)

A

-released from bone marrow or spleen
-above 7x10^9
-pseudo neutrophilia possible or pathological

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5
Q

Pseudo neutrophilia (non pathological) Causes

A

-Pregnancy end of 3rd trimester prepare for birth risk of infection
-diurnal variation
-exercise (running)

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6
Q

True Neutrophilia

A

-infection, inflammation (sepsis)
-left-shift of neutrophil lobes (lots of immature ones, less nuclear lobes) [1-2 lobes instead of 3-5]
-toxic granulation [too much cytoplasmic granules caused by cytokines]
-Dohle bodies (aggregation of degraded ribosomes trying to finish maturation)

[3 signs not seen in pseudo]

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7
Q

Sepsis

A

Inappropriate inflammation response, local infection gets into circulation. Organs shut down, blood pressure drops.
-kills 48,500 per year UK

Predisposition - elderly, acutely unwell patients (ITU), recent surgery

Common infection site that causes - GI, Respiratory, Renal/GU (UTIs)

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8
Q

Sepsis Causative Bacteria

A

Staph Aureus
pseudomonas spp (aeruginosa) [Common in cystic fibrosis, pneumonia] [skin organism opportunistic infection]
Escherichia coli (UTI)
[Causative bacteria not identified in 30% of cases]

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9
Q

Sepsis Diagnosis

A

-Inflammatory symptoms
- Systolic BP under 90
-Heart rate over 130 beats per min
-Respiratory rate over 25 per min
-Non blanching rash
-Recent chemo
-not passed urine in 18hrs
(low BP and O2 kills nephrons)

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10
Q

Treatment of Sepsis

A

Oxygen
Fluid
Treat underlying infection (broad spectrum antibiotics)

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11
Q

Haematology in Sepsis diagnosis

A

-observe true neutrophilia
-Reactive thrombocytosis (platelets increase) (acute phase reactant)
[thrombocytopenia, decrease in platelets sign of coagulation]
-Red cell changes? (caused by infection not sepsis]

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12
Q

Neutropenia

A

Less than 1.5x10^9
Genetic (most common) [micronutrient deficiencies, folate, B12]
Drugs
Infections - Malaria suppresses immune system IL-10
-Inflammatory response

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13
Q

Chronic granulomatous Disease

A

-inherited neutropenia
-mutation in NADPH oxidase, x-linked, no respiratory burst
-Reoccurring atypical bacteria and fungal infection (pneumonia)
-Ineffective immune response=granulomas
[balls of tissue, benign, often in lungs(key bacteria entry area)]
-treat with antibiotics

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14
Q

Eosinophilia

A

-non malignant = idiopathic reactive or organ-eosinophilic syndromes
-Reactive eosinophilia transient= acute inflammation
chronic= persistent parasitic infection, autoimmune disease, not-haematological malignancy (helminths common cause)
-activated T-cells secrete eosinopoietic growth factors (IL-4,5,13)

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15
Q

Signs and Symptoms of parasitic infection

A

-gradual weight loss unexplained
-gastric distress
-worms in faeces

diagnosis: faeces sample, microscopic eggs, clinical history

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16
Q

Organ Associated Eosinophilia Syndromes (allergic reactions)

A

-persistent eosinophilia in tissues (more than 6 months)
-systemic or organ restricted
-asymptomatic until damage
-eosinophilic gastroenteritis can take 4 years to become symptomatic [e. oesophagitis common too, difficulty swallowing]

Caused by ingested allergens, tissue damage, clonal proliferation, infiltration (release cytoplasmic granules, similar to inflammation)

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17
Q

Lymphocytosis (too many)

A

-non malignant - sign of immune response
-Viral infections inflammation (Epstein Barr Virus)
-morphological changes possible

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18
Q

Epstein Barr Virus

A

-Herpesviridae family, dsDNA virus
-infects epithelial cells and B-lymphocytes (persistent infection)
-90% of adults infected, saliva spread
-usually asymptomatic, unless glandular fever (IMN) develops
-EBV associated with auto immune disease and cancer

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19
Q

Infectious Mononucleosis (IMN) (glandular fever)

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A

-EBV, 6 week incubation
-lymphocytosis and morphological change to cells
[abnormal mononuclear cells (lymphocytes)]
-Common in children and young adults (upper respiratory tract infections, 10% of all)
-self limiting, supportive therapy, symptoms can last months (post viral syndrome)

20
Q

Infectious Mononucleosis (IMN) (glandular fever) symptoms

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A

Tiredness, sore joints and throat, fatigue, reddening, swollen lymph nodes, cough

21
Q

Diagnosis of IMN

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A

-rapid diagnostic test (immunoassay)
-antibodies react with antigens to form coloured line
-antigens=heterophile antibodies (agglutinates virus)
-pan reactive antibody which binds red blood cells
- might not detect early (acute) infection as antibodies may not have been produced yet (test twice)

22
Q

Epstein Barr Virus and Future Malignancies

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A

Linked to multiple sclerosis
200,000 cancer per year linked

23
Q

Lymphopenia

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A

-Non malignant
-caused by drugs, viral infections and malaria

24
Q

Human immunodeficiency virus (HIV)

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A

-retrovirus targeting T-helper cells
-primary infection flu like symptoms
- then asymptomatic (10 years)
-severely immunocompromised when CD4+ count falls below 200 cells per uL
-bodily fluids transmit (sex ,blood, needles)
-Kaposi sarcoma and pneumocystis association
-Zoonotic disease (from eating monkey)
-GRID originally

25
HIV Diagnosis and Management
Serological (ELISA) Viral antigen Host antibody response -molecular methods (RT-PCR) antiretroviral drugs reduce viral load until its untransmittable. Combination therapies (mutates rapidly)
26
HIV Classes of Antiretrovirals (expensive)
-Entry Inhibitor [stop CCRS interaction] -nucleotide (side) reverse transcriptase inhibitor [chain terminating analogues] -Non-nucleotide RT inhibitors [Non competitive inhibitor of RT enzyme] -protease inhibitor [viron budding prevention] -integrase inhibitor [prevent viral DNA integration]
27
Acquired Immunodeficiency Disorder (AIDS)
- infection of T-helper cells collapse immune system -atypical infections occur numosyscyt -atypical malignancies
28
Haematological Malignancies
Classified based on lineage of cell leukaemia or lymphoma and speed of progression. (often advanced age but varies) 25k per year UK -14k Non-Hodgkin's lymphoma -2K Hodgkin's Lymphoma -9K leukaemia
29
Acute Myeloid Leukaemia (any myeloid derived cell)
100s of subtypes -1/3rd of all adult leukaemias -poor prognosis (elderly)(acute fast progression, fatal in 2 weeks) -aetiology liftetime exposure to solvents, ionizing radiation. -failure of bone marrow -invasion of vital organs -metabolic imbalance
30
Acute Promyelocytic Leukaemia
-Identified underlying genetic factor -retinoid mutation -give transretinioic acid -prognosis went from 5 days to best
31
Acute Lymphocytic Leukaemia
-children -lymphocyte precursors little cytoplasm and stains deep blue -monoclonal antibodies, tyrosine kinase inhibitors prevent action of oncogenic protein, prognosis went from 40 to 100% survival -easy bruising, impaired blood cell production bone marrow taken over, rapid progression
32
Chronic Myeloid Leukaemia
-watch and wait, takes years to develop -elderly -Philadelphia chromosome (9,22) understood -in disease tyrosine kinase produces BCR-ABL, tyrosine kinase inhibitor binds and prevents -chronic vs acute can be seen under microscope acute=white blood cells will be immature chronic=white blood cells will be terminally differentiated
33
Chronic Lymphocytic Leukaemia
-slow, watch and wait -accumulation of incompetent B cells (accidental diagnosis) -genetic cause? -most prevalent adult leukaemia (monoclonal antibodies treat, rituximab)
34
Hodgkin Lymphoma Disease
(B Cell origin) -5 subtypes -15% of all lymphoma cases (2000 per year) -Reed Sternberg Cells (large 50 microns, no antibody secretion, derived from B cells, bilobed, multinucleated cells, CD30 and 15 positive)
35
Location of Lymphomas
Lymph nodes then metastasise to bone marrow, spleen, brain, other organs. -thought to be TB to begin with
36
Reed Sternberg Cells Development
-from germinal centres (VOJ recombination, somatic hypermutation) -hypersomatic mutations cripple RS cells to express typical lymphocyte genes (proliferate uncontrollably) -Hyperactive proinflammatory cascades, NF-KB JaK and STAT -CT cells and functional lymphocytes effect, they mutate eventually
37
Clinical Presentation of Hodgkin's Lymphoma
-lymphadenopathy (swollen lymph nodes) -Night sweats from inflammation -weight loss(10% of body weight in month) -localised infiltration of tumour causes symptoms
38
Epidemiology of Hodgkin's Lymphoma
1/200 cancer cases in UK -3rd most common for 15-29 -Rare in East Asia common in West
39
Aetiology of Hodgkin's Lymphoma
-EBV DNA found in 90% of cases (all HIV HL cases are EPV positive) -EBV (VDJ recombination) -EBV genes associated with malignancy = LMP1, LMP2a, EBNA1 drive for vaccine to prevent
40
non-Hodgkins Lymphoma
Various heterogenous lymphomas -not HL 85% of cases Cytogenetics most recent way of classifying (WHO System)
41
WHO System for Classification of NHL
Use flow cytometry to class to class as : -precursor cell NHL (2 recognised lymphoblastic lymphoma -B cell NHL (10 -T cell NHL (10 more than 60? prognosis varies throughout
42
Management of Haematological Malignancies
-targeted therapy - monoclonal ABs, RTK inhibitors -combination therapy (multiple drugs reduces resistance risk) -ABVD regime (Adriamycin, bleomycin, vinblastine, dacarbazine) -BEACOPP (bleomycin, etoposide, adriamycin) -surgery (remove tumour) -Radiotherapy
43
ABVD Therapy
IV, 1 to 15 days - 6 cycles -adriamycin=inhibits topoisomerase 11 -bleomycin=induces dsDNA breaks -vinblastine=disrupts microtubule formation -Dacarbazine=alkylating agent Remission rates 70-90%
44
BEACOPP Therapy
Stage 2 and above HL -21 days 4 cycles in first instance -etoposide - topoisomerase 2 non interrelating poison -procarbazine and cyclophosphamide: alkylating agent -prednisone: steroid Remission in 80% of patients
45
Supportive therapies for Haematological Malignancies
(protect from immunocompromising) -prophylactic antimicrobials -acyclovir =anti viral -fluconazole - antifungal -Quinolone -antibiotic Blood products = RBCs, platelets Antiemetic drugs

Clinical Physiology (8 decks)

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