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67 Cards in this Set

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Hodgkin lymphoma five types

Nodular sclerosing, mixed cellularity, lymphocyte depleted, lymphocyte rich, nodular lymphocyte-predominant

Hodgkin lymphoma signs

- Asymptomatic lymphad (painless)

- Unexplained weight loss, fever, night sweats

- hepatosplenomegaly

- Paraneoplastic syndromes

- Svc syndrome if massive mediastinal lymphad

Hodgkin's lymphoma sympts

- Chest pain, cough, sob

- Pruritis

- back/bone pain

- Fever

Type of lymphoma with strong family predominance

Nodular sclerosing hodge lymph

Causes microcytic anaemia


• Iron deficiency

• Thalassemia

• Anaemia of chronic disease

• Sideroblastic anemia

• Lead poisoning

Causes for megaloblastic anaemia

• B12 deficiency

• Folate deficiency

• Drugs that impair DNA synthesis (methotrexate, sulfa, chemotherapy)

Causes for macrocytic (non megaloblastic anaemias)


• Liver disease

• Alcoholism

• Reticulocytosis

• Hypothyroidism

• Myelodysplasia

Low Hb, normal MCV, low/high retic meaning

- Low: dec production

- High: increased destruction

Causes of normocytic anaemia with high retics

(Increased destruction)

- Bleeding

- Haemolysis:

- Inherited: Hemoglobinopathy (sickle cell disease,thalassemia, unstable Hb), Membrane (spherocytic), Metabolic (HMP shunt, glycolytic pathway)

- Acquired: • Immune (Coombs positive, drug-related, cold agglutinin), Infection (malaria), Microangiopathic hemolytic anaemias, Oxidative/drug-related

Causes of normocytic anaemia with low retics

Pancytopoenia: Aplastic anemia, MDSMyelofibrosis, Leukaemia, TB, Amyloidosis, sarcoidosis, Drugs (e.g. chemo)

Non pancytopoenia: Anaemia of chronic disease, renal/liver disease

Iron deficiency anaemia blood film

- Hypochromic microcytosis

- Pencil forms

- Target cells

- Anisocytosis (RBCs are not uniform in size)

a thalassaemia

- 1 gene defect: Clinically silent

- 2 defects:Normal Hb, also clinically silent, Low MCV

- 3 defects: Presents in adults, splenomegaly, Low Hb and MCV

4 defects: Not compatible with life

Sideroblastic anaemia s/s

- Same as Fe deficiency anaemia

- Hepatosplenomegaly

Anaemia of chronic disease aetiology RICEM

- Rheumatological disease

- Infection

- Chronic renal and liver disease

- Endocrine disease

- Malignancy

Anaemia of chronic disease patho

- Hepcidin increased in inflammatory conditions

- Traps iron in erythrocytes and MOs

- Less iron available for new RBC synthesis

Two types of macrocytic anaemia

- B12 (can be caused by inadequate intake or pernicious anaemia)

- Folate

Clinical features B12 def anaemia

- Cerebral




- Peripheral nerves


*Effects lower limbs > upper limbs

- Rare

*Optic atrophy

*Dorsal column and pyramidal tract damage

Folate deficiency anaemia s/s

- Stores only last 3 months (compare to 3 yrs for B12)

- Mild jaundice due to haemolysis

- Glossitis

- Angular stomatitis

- Melanin pigmentation

- No neuro signs

Causes of haemolytic anaemia

- Congenital

*Sickle cell anaemia

*G6PD deficiency


- Acquired


*transfusion reaction


*Normochromic, normocytic anaemia

* increased reticulocytes

Causes of polycythaemia


Polycythaemia vera


- Physiologic

*Carbon monoxide


*High altitude

*Pulmonary disease



*Pulmonary HTN

*Congenital heart defects

*HCC and RCC


* Post kidney transplant

Polycythaemia s/s

- Due to hyperviscosity




*Hypertensive symptoms



- Coagulopathy



*Gingival bleeding


*GI bleeding






Haemochromatosis patho, gene

- XS intestinal absorption

- Gene is C282Y

Thrombocythaemia aetiolpogy, def

- Sustained platelets >450

- BMBx showing proliferation of the megakaryocytic lineage

- Not PV, myelofibrosis, CML, MDS

- JAK2 mutation or calcereticulin

Thrombocythaemia s/s

- Asymptomatic

- Vasomotor symptoms:

* Headache



*Erythromelalgia (burning hands and feet)



*Pregnancy complications

Primary haemostasis definition, mech, ix, tx

- Initial, rapid cessation of bleeding

- Vessel injury=>collagen/subendothelial matrix exposure=>release of vasoconstrictors=>platelets come into contact w damaged vessel wall=> platelets adhere to subendothelium via vWFActivation=> platelets activated=> change shape=>release of ADP, thromboxane A2=> recruitment + aggregation of more platelets=>platelet plug

- Test with platelet count

- Inhibit with aspirin, clopidogrel, ticagrelor, abciximab, dipyridamole

Secondary haemostasis definition, inhibition, ix, mech

Platelet plug reinforced by fibrin clot

Extrinsic pathway - initiation of coagulation

Test with PT/INR (measures extrinsic (fact 7) and common pathway)

Intrinsic pathway - amplification once coagulation has started

Test with aPTT (measures intrinsic 8,9,11,12, monitor heparin therapy, increased in antiphospholipid syndrome)

- Inhibit with warfarin, NOACs, heparin

Clinical features primary coagulopathy

- Platelet prob

- Excessive prolonged bleeding with cuts

- Bleeding immediately after injury

- Mucosal/skin bleeds


- Gingival

- GI

- Uterine

- Petichiae and ecchymoses

Clinical features secondary coagulopathy

Secondary (coagulation)

- Slightly prolonged bleeding with cuts

- Delayed onset haemorrhage

- Deep structure bleeding







Immune thrombocytopenic purpura

- Primary disorder

- Most common cause of isolated thrombocytopoenia

- Antiplatelet antibodies: immune mediated splenic clearance and reduced prod of platelets

- F:M

- Onset 20s-40


- Asymptomatic, minimal bruising

- Rarely causes serious bleed

Heparin induced thrombocytopenia

- Primary

- Immune mediated rxn following heparin=>platelet activation

- Diagnosis: 50% reduction in platelets with on heparin w/i 5-15 weeks

- 30% thrombosis risk (venous and arterial)

Von willebrand disease

- Most common inheritable coag abnormality (usually autosomal dominant)

- vWF is required for platelet adhesion and is a carrier for factor 8. This is a prob with vWF

- Presents: long hx bleeding probs, bruising, 10min epistaxis, XS menstrual bleeding

Haemophilia A (factor 8 deficiency A sounds like 8)

- X linked recessive (1/5000 males)

- Rarely severe

- S/s:





*Head haemorrhage

Haemophilia B (factor IX def)

- X-linked recessive (1/30,000 males)

- Clinical: 5Hs??

Factor 11 deficiency (Rosenthal syndrome/haemophilia C)

- Autosomal recessive (ashkenazi jews)- Usually mild, diagnosed in adulthood- factor 11 levels do not correlate with risk

Liver induced coagulopathy

- Deficiency in all factors except 8

- Liver doesn't clear pro-coagulants and other blood bits

Vitamin K deficiency, aetiology

- Aetiology:

*oral anticoagulants inhib fact 2, 7, 9, 10, proteins C&S

*antibiotics that eradicate GI flora - alter vit K uptake

* poor diet (alcoholics)

*Biliary obstruction

*chronic liver disease (dec stores)

*malabsorption (coeliac)

DIC definition

- Uncontrolled release of plasmin and thrombin =>IV coagulation=>depletion of plt, coag factors and fibrinogen=> risk of life threatening haemorrhage

DIC aetiology

- Activation of procoagulant activity

*Antiphospholipid syndrome

*Intravascular haemolysis (incompatible blood, malaria)

*Tissue injury (trauma, burns)


- Endothelial injury



*Metastatic adenocarcinoma

- Reticuloendothelial injury

*Liver disease


- Vascular stasis *Hypotension/hypovolaemia



* hypoxia/acidosis

*Extracorporeal circulation

DIC presentation

- Presents w both haemorrhage and clotting

Hypercoagulable states; activated protein C resistance and prothrombin gene mutation

- Activated protein C resistance (factor 5 leiden)

*most common hereditary thrombophilia

*Resistance to inactivation of 5a by activated protein C=>hypercoag

- Prothrombin gene mutation=>inc. levels prothrombin=>increased thrombin generation

Hypercoagulable states - Antithrombin def

*slowly inactivated thrombin (fast in the presence of heparin)

*Causes: autosomal dominant, urinary losses in nephrotic, low synthesis in liver disease

Hypercoagulable states; protein C&S def

*C inactivates 5a with S as a cofactor

*Deficiency can be congenital or acquired

Hypercoagulable states; antiphospholipid syndrome

- Diagnoses with at least 1 clinical and 1 lab finding

- Clinical:



*Premature birth

- Lab

*Anticardiolipin ab

*Anti-B2 glycoprotein I

*Lupus anticoagulant

CLL definition and epi

- Clonal malignancy of mature B cells

- Common in western world and old people

Clinical features CLL

- 25% incidental finding of CBE

- 10% present with B sx

- Lymphadenopathy

- Hepatosplenomegaly

- 50% s/s anaemia

- Can have inc. infections

CLL prognosis

- Depends on stage

- Overall median survival 4-6 years

- Small minority present with aggressive disease,usually associated with chromosomal abnormalities (p53 deletion)

CLL patho

-Genetic mutations=>B lymphocytes do not undergo normal process of apoptosis=> accumulation in lymphoid organs

Lymphocytes are morphological mature butimmunologically incompetent=>impaired lymphocyte function, hypogammaglobulinaemia => inc infections

CML patho

Translocation b/w chromosomes 9 & 22=> formation new BRC-ABL fusion protein =>Tyrosine kinase defective + overactive=>proliferative advantage of malignant haemopoeitic cells over normal haematopoeisis =>prominent neutrophilic leukocytosis

- Neoplastic extramedullary hematopoiesis w/i splenic red pulp=>marked splenomegaly

- Cells look morphologically normal but aregenetically unstable

CML age of onset and natural hx

- 45-55 years

- Many are assymptomatic in chronic phase: *Fatigue, weakness, weight loss

* Splenomegaly/LUQ pain

- Accelerated Phase:

* Increase severity of symptoms

- Blastic phase >30% blasts

- Usually found in chronic phase

ALL ((smallpeople, small blasts, small granules, small mortality rate). Definition, ss

- Early lymphoid precursors proliferate - can be B cell or T cell

- s/s:

- Anaemia: fatigue, raccoon eyes

- Thrombocytopenia: bruising, bleeding gums

- Neutropenia: infections (often pharyngitis)

- Lympad/organomeg

- Bony tenderness

- Testicular enlargement

- CNS involvement (headache, vomiting)

ALL onset and RFs

- Abrupt, stormy onset (days- weeks)

- Risk factors:

§ Environmental: radiation, cytotoxic chemotherapy, smoking

§ Congenital disorders: Down Syndrome

§ High birth weight

§ Infectious agent in pregnancy

Tumour lysis syndrome

Tumour lysis syndrome - 48-72 hrs after starting treatment in rapidlydividing cancers (chemo)

- Rapid cell lysis =>hyperphosphataemia +hyperkalaemia + hyocalcaemia (after hyperphosphataemia causes precipitation ofcalcium phosphate in soft tissues) + hyperuricaemia + acute renal failure fromtrying to fix all this

- Allopurinol used to ensure that hyperuricaemia isavoided with chemo.

AML (big people, big blasts (cytoplasm), lots of granules, big mortality rate)

- Rapidly progressive

- Abrupt onset (weeks to months)

- Middle aged people (65 yrs)

- Can arise de novo or secondary to preexisting haem disorder like MDS, myelofibrosis

- Same RFs as ALL

Clinical features AML

- Anaemia

- Thrombocytopoenia

- Neutropoenia

- Accumulation of blasts in marrow=>bone pain

- Organ infiltration=>gingival hypertrophy, hepatosplenomegaly


Myelodysplasia definition

- group of malignant stem cell disorders

- causes dysplastic and ineffective blood cell prod

- Preleukaemic=>30% transform

- Dysplasia w no hyperplasia (this is what distinguishes it from leukaemia

Myelodysplasia s/s

- Infections and bleeding out of proportion with blood count

- Insidious onset

- Often preceeded by a few years of unexplained macrocytic anaemia (not megaloblastic) + mild htrombocytopoenia/neutorpoenia

- Infections

- s/s anaemia

- Pancytopoenia

Myelofibrosis definition and patho

XS bone marrow fibrosis=>failure

- abnormal myeloid precursosr produces dysplastic megakaryocytes which secrete fibroblast GFs

- Deposition of collagen in BM

Myelofibrosis s/s

- Anaemia; severe fatigue

- Hypermetabolic state; weight loss, fever, night sweats

- Organomegaly (extramedullary haematopo)

- bone and joint pain

Complications myelofibrosis

- Portal HTN in 7%

- Splenic infarct

- Osteosclerosis

Left shift meaning

lots of blasts/immature cells (almost always refers to WBCs)

TTP patho

- vWF synthesized in endothelial cells and assembled in larger multiples than those in plasma (ultralarge vWF)

- Rapidly degraded to normal sized multimers in plasma by protease ADAMTS13

- In TTP there is either conginital lack or ADAMTS13 or autoantibodies against ADAMTS13

=> accumulation of ULvWF=>plt aggregation/clumping=>extensive microthrombi formation w haemolysis (MAHA), end organ effects

- May be triggered by intercurrent event eg. surgery, pancreatitis, sepsis, preg that tirggers endothelial activation

TTP preso (FAT RN), classic pentad

- Fever

- Anaemia (microangiopathic haemolytic anaemia; inc. uncongugated bilirubin, scleral icterus, schistocytes)

- Thrombocytopenia

- Renal problems (88% have renal probs, 15% haematuria - this is more likely in HUS than TTP)

- Neurological probs (headaches, confusion, seizures, intra-cranial haemorrhage, focal deficits - this is more common in TTP than HUS)

RF for TTP

- E. Coli specific strain (classically HUS)

- Calcineurin inhibitors, clopidrogrel, cyclosporin other drugs

- Pregnancy

- Graft vs host disease

- CT disorders

- Malignancy

Acute haemolytic transfusion rxn

- Mostly due to ABO incompatibility

- Causes haemolysis, fever, nausea, flushing, pruritis, urticaria, flank pain, dyspnoea, burning at IV site

=> renal failure, DIC, jaundice

- Rapid onset during transfusion

Non haemolytic, febrile transfusion rxn

- Occurs in ~3% of transfusions

- If blood has been sitting around for a while it can release cytokines=>inflamm response in host. Hosts pre-formed abs to WBCs in transfusion contribute to this

- Fever, malaise, chills

- Onset 1-6hrs


- Antibodies + other junk in donor blood activates recipient granulocytes=>ARDs-like picture

- Happens w/i 6hrs of transfusion w rapid onset

- <0.1% of transfusions

- Mortality <20%

X-linked agammaglobulinaemia (Bruton's)

- Boys only

- Onset >4mnths (when maternal Ig has run out)

- Complete lack of B cells, T cells normal, diagnose on flow cytometry

- Tonsilar and other lymphoid tissue hypoplasia

- Recurrent infections, esp. w encapsulated organisms

- Give IV Ig to treat