Arch HI exam answers Flashcards

1
Q

Two features of lymph node biopsy to distinguish Hodgkin’s and Non-Hodgkin’s lymphoma.

A

If a pathologist discovers Reed-Sternberg cells in the biopsy, the patient is diagnosed with Hodgkin lymphoma. T-cells and NKT cells in non-Hodgkins

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2
Q

Four investigations (other than lymph node biopsy and CXR) that would have been done to reach his NHL diagnosis.

A

Physical exam Blood and urine tests Imaging – CT scan , MRI, PET scan Bone marrow test Lumbar puncture/ spinal tap

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3
Q

2 x environmental risk factors for lymphoma

A

Benzene, radiation exposure, exposure to chemicals such as pesticides, tobacco

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4
Q

Stages of NHL.

A

Ann Arbor classification system Staging used for Hodgkin’s lymphoma in adults + children, and non-Hodgkin’s in adults

I - involvement of one group of lymph nodes

II - two groups of lymph nodes on the same side of the diaphragm

III - groups of lymph nodes on both sides of the diaphragm

IV - involvement of extralymphatic tissues

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5
Q

Explain lymphocyte differentiation

A
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6
Q

Explain B cell activation.

A
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7
Q

Two treatments you would suggest.

A

Chemotherapy = monoclonal antibodies

Bone marrow transplant

Radiation therapy

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8
Q

What is his likely prognosis for NHL?

A

The overall 5-year relative survival rate for people with NHL is 65-70%. But it’s important to keep in mind that survival rates can vary widely for different types and stages of lymphoma.

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9
Q

What are 3 indications of non-accidental bruising?

A
  • developing very large, painful bruises after minor injuries.
  • having many bruises without remembering their cause.
  • frequently developing bruises that take many weeks to heal.
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10
Q

Example & MOA of causes of vessel dysfunction, platelet abnormalities and coagulation abnormalities leading to bruising (1 each)

A

Vessel dysfunction – Ehler’s Danlos syndrome 🡪 connective tissue disorder -> vessel dysfunction

Platelet abnormality – VonWillebrand’s disease – deficiency of VWf 🡪 prevents platelet aggregation

Coagulation abnormality – Haemophilia A/B 🡪 deficiency of factor 8/9 🡪 affects coagulation cascade

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11
Q

How haematological malignancy leads to these symptoms: pallor, bleeding gums, splenomegaly, paraprotein, bone pain. (5 marks)

A

Pallor 🡪 displacement of blood precursors in bone marrow 🡪 reduce RBCs 🡪 anaemia 🡪 pallor

Bleeding gums 🡪 displacement of blood precursors in bone marrow 🡪 reduce platelets 🡪 reduction in coagulation ability 🡪 bleeding gums

Splenomegaly 🡪 neoplastic cells accumulate in lymph nodes and spleen 🡪 splenomegaly

Paraprotein 🡪 increased monoclonal plasma chains 🡪 increased immunoglobulins secreted 🡪Ig light chain paraproteins

Bone pain 🡪 expanding marrow pushing on bone 🡪 bone pain

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12
Q

What are the 3 examples of cells coming from myeloid lineage?

A

Megakaryocytes, erythrocytes, mast cells, neutrophils, basophils, eosinophils, monocytes

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13
Q

What does allogeneic mean?

A

Allogeneic – from another person of the same species, need to be HLA matched to limit graft rejection or GVHD, stem cells typically harvested from peripheral blood after dose of G-CSF

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14
Q

What is HLA protein II (MHC class II)?

A

APCs 🡪 The main function of major histocompatibility complex (MHC) class II molecules is to present processed antigens, which are derived primarily from exogenous sources, to CD4(+) T-lymphocytes. MHC class II molecules thereby are critical for the initiation of the antigen-specific immune response.

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15
Q

If there is no HLA matching, what are the serious of events that could lead to a complication?

A

GVHD - Condition that occurs following allogeneic haematopoietic stem cell transplant in which the donated blood cells will recognise the recipient’s body as foreign and initiate an immune response, can be acute (occurring within 100 days) or chronic (begins after 100 days) Requires three criteria: graft contains competent immune cells recipient is immunologically different to donor recipient is immunocompromised an unable to destroy the graft

Presentation – skin rash, diarrhoea, vomiting, weight loss, abdominal pain, dry eyes + mouth

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16
Q

other than fatigue what are 3 signs or symptoms of anaemia,

A

dizziness, alopecia, tachycardia, headaches, pale skin

17
Q

what are 2 possible conditions that can cause normocytic normochromic anaemia,

A

Occult GI blood loss, blood loss through trauma/surgery

18
Q

why might a patient with macrocytic anaemia have jaundice,

A

abnormal RBCS –> haemolysis 🡪 breakdown to Hb 🡪 elevated indirect bilirubin 🡪 sequesters to collagen rich areas like skin and conjunctiva of eyes 🡪 yellowing known as jaundice

19
Q

what is vitamin B12 used for/why is it important,

A

Erythroblasts require folate and vitamin B12 for proliferation during their differentiation. Deficiency of folate or vitamin B12 inhibits purine and thymidylate syntheses, impairs DNA synthesis, and causes erythroblast apoptosis, resulting in anemia from ineffective erythropoiesis. Vitamin B12 is needed to form red blood cells and DNA. It is also a key player in the function and development of brain and nerve cells.

20
Q

what metabolic pathway is affected by vit B12 deficiency?

A

Vitamin B12 influences folate-dependant reactions and mitochondrial energy and lipid metabolic pathways.

21
Q

What is in the IM injection used during an anaphylactic fit (1 mark)

A

epinephrine

22
Q

What type of hypersensitivity reaction is this - anaphylaxis (1 mark)

A

IgE mediated Type 1 hypersensitivity

23
Q

Describe the pathophysiology of anaphylaxis

A
24
Q

What other disease is a type 1 hypersensitivity reaction and is similar? Explain the two phases it is characterised by (3 marks)

A

Asthma, atopic dermatitis and allergic rhinitis – acute and chronic

25
Q

Two meds that aren’t adrenaline which could be used in the management of a patient with anaphylaxis (4 marks)

A

Corticosteroids, beta-2 agonists

26
Q

What are 2 epidemiological factors effecting the development of autoimmune disease (2 marks)

A

Genetic factors (family hX of autoimmune or predisposed)

Environmental = smoking, stress, air pollution in urban environments, workers that work with chemicals

27
Q

Explain how each contributes to a diagnosis of SLE (3 marks)

A

Genetic factors 🡪 thought to reduced the clearance rate of apoptotic cell body fragments 🡪 leads in increase chances of being recognised as foreign bodies with the body generating autoantibodies towards it 🡪 type 3 hypersensitivity reaction 🡪 SLE UV damage 🡪 DNA metylation 🡪 recognition as foreign -> antibody complex formation 🡪 type 3 hypersensitivity reaction 🡪 SLE

28
Q

Explain the thermoregulatory set point (3 marks)

A
29
Q

What is the pathophysiology of anti-phospholipid syndrome, and what pathology does it cause (3 marks)

A

anti-phospholipid antibodies - usually targets proteins bound to phospholipid can lead to antiphospholipid syndrome which causes a hypercoagulable state leading to stroke, DVT and other clotting issues

30
Q

MOA of NSAIDs & hydroxychloroquine (2 marks - table)

A

NSAIDs 🡪 Cox inhibitor 🡪 Prostaglandin synthesis inhibitions

Hydroxychloroquine 🡪 toll-like receptor inhibitor 🡪 reduced innate immune response

31
Q

Describe the 4 types of hypersensitivity reactions (8 marks )

A
32
Q

SLE What antibodies are you looking for on serology?

A

ANA – low spec

SLE specific - Anti-Smith, Anti-dsDNA

Cardiolupin

Antiphospholipid Lupus antibody/anticoagulant

Anti- B2-Glycoprotein1

note ** anti-phospholipid antibodies - usually targets proteins bound to phospholipid can lead to antiphospholipid syndrome which causes a hypercoagulable state leading to stroke, DVT and other clotting issues

33
Q

How is joint pain caused in SLE?

A

Type 3 hypersensitivity reaction 🡪 antibody against self antigen 🡪 systemic inflammation 🡪 immune complex sequesters in joint spaces leading to increased immune infiltrate in synovial joints🡪 lead to activation of inflammation cascade, swelling and bursitis 🡪 will activate nociceptors 🡪 +++ pain signals to brain SLE is a type III hypersensitivity reaction that forms Ab/Ag complexes -> it travels in the blood and deposits in joints -> inflammation of the joint -> inc neutrophils -+ vasodilation + cytokines + extravasation of WBCs -> swelling, redness, heat and joint pain. - Nociceptors -> pain signal to brain Arthritis or synovitis (sequestration of immune complexes in joint spaces -> inc immune infiltrate in synovial joints -> leads to activation of inflammation cascade)

34
Q

2 ways to confirm an enlarged spleen

A

Ultrasound or CT scan to help determine the size of your spleen and whether it’s crowding other organs.

Physical examination

35
Q

What is the normal function of the spleen? (3 marks)

A

It filters the blood and removes abnormal cells (such as old and defective red blood cells), and it makes disease-fighting components of the immune system (including antibodies and lymphocytes).

36
Q

platelet adhesion, release, aggregation, stabilisation of plug

A
37
Q

Drugs for haemostasis

A