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Clinic - Common Conditions Overview > Conditions of the Lymphatic System > Flashcards

Conditions of the Lymphatic System Flashcards

1
Q

Describe the condition of lymphadenopathy and lymphadenitis, including the classifications and aetiology

A

Lymphadenopathy:
- palpable enlargement (over 1cm) of lymph nodoes

Lymphadenitis:
- lymphadenopathy plus pain or symptoms (oedema, heat)

Localized:

  • most common 75%
  • present in one body area only
  • caused by pathology in region of drainage
  • common: cervical (from tonsillar / dental infection); axillary or inguinal (from infection in extremities)

Generalized:

  • less common 25%
  • present in 2 or more non-contiguous groups
  • caused by significant systemic disease (glandular fever, lymphoma, leukaemia, metastatic neoplasia, HIV, tuberculosi)
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2
Q

Which pathologies can cause generalized lymphadenopathy or lymphadenitis?

A

Significant systemic diseases including HIV, tuberculosi,s metastatic neoplasia, glandular fever

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3
Q

What are common sites of localized lymphadenopathy or lymphadenitis, and their causes?

A

Axillary - infection in upper extremity, breast neoplasia

Inguinal - infection in lower extremity

Cervical - infection in dental region/ tonsilitis

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4
Q

Describe the condition of splenomegaly, including the primary and secondary symptoms, and aetiology

A

Splenomegaly:
- enlargement of the spleen

Primary SSX:

  • palpable splenomegaly
  • dragging sensation in LUQ
  • sensation of fullness (especially after eating)

Secondary SSX:

  • anaemia (low RBCs)
  • leukopaenia (low WBCs)
  • thrombocytopenia (low platelets)

Aetiology:

  1. Infectious (glandular fever, HIV, TB, syphilis)
  2. Portal HTN (cirrhosis, hepatitis, liver failure)
  3. Lymphoid pathology (leukaemia, lymphoma, multiple myeloma)
  4. RBC disorders (thalassaemia)
  5. Inflammatory conditions (RA, lupus, erythematosus)
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5
Q

Describe the condition of glandular fever including the definition, the pathophysiology, the classic symptoms and complications, the disease progression, and management

A

Definition:
- acute infection of B lymphocytes with Epstein Barr Virus

Incidence:

  • most common in young adults
  • 90% of people have an EBV infection but doesn’t usually progress to glandular fever

Pathophysiology:

  • EBV contracted through saliva (most common) or mucous secretions
  • EBV incubates for 30-50 days

Progression of disease:

  1. infection of oropharynx, nasopharynx and salivary epithelial cells
  2. moves into lymphoid tissues and B cells
  3. generalized lymphadenopathy
  4. splenomegaly
  5. hepatomegaly

Complications:

  • secondary bacterial infections (strep pharyngitis in 20-30% of cases)
  • ocular, cardiac and CNS involvement (very rare)

Classic SSX:

  • fever
  • sore throat
  • Cx lymphadenopathy
  • fatigue

Management:

  • diagnosed by serologic testing
  • self limiting (recovery within weeks, fatigue can last months)
  • rest and SSX relief, treatment of secondary bacterial infections if present
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6
Q

Which virus causes glandular fever?

A

Epstein Barr Virus (EBV) -90% of adults have EBV but usually doesn’t progress to glandular fever

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7
Q

What are the 3 types of haemotological cancers?

A
  1. Leukaemia
    - proliferation of malignant leukocytes in blood stem cells being produced in bone marrow, causing malignant cells to overflow into bloodstream
    - classified by cell type origin (myeloid or lymphoid stem cells)
    (ALL acute lymphoblastic, AML acute myeloid; CML chronic lymphocytic; CML chronic myeloid)
  2. Lymphoma
    - proliferation of malignant lyphocytes in lymphatic system, formation of discrete tumours
    - Hodgkins: characteried by Reed-Sternberg neoplastic cells
    - non-Hodgkins: umbrella term for lymphomas without Reed-Sternberg neoplastic cells
  3. Multiple myelomas
    - proliferation of malignant plasma cells in bone marrow
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8
Q

In which parts of the body do leukaemia, lymphoma and multiple myeloma originate?

A

Leukaemia:
- in the stem cells (lymphoid or myeloid) of blood stem cells in bone marrow

Lymphoma:
- in the lymphatic system

Multiple myelomas:
- plasma cells in the bone marrow

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9
Q

What are the classifications for leukaemia?

A
  • classified based on cell type of origin (lymphoid or myeloid blood stem cells) and rate of progression (acute or chronic)
  • AML: acute myeloid
  • CML: chronic myeloid
  • ALL: acute lymphoblastic
  • CML: chronic lymphocytic
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10
Q

What are the risk factors for the development of leukaemia?

A

(exact aetiology unclear: interplay between genetic and environmental factors)

  1. genetic
    - including Philadelphia chromosome
  2. exposure:
    - tobacco
    - benzene
    - ionizing radiation
    - chemotherapy
  3. Infections:
    - HIV
    - Hep C
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11
Q

Describe the conditions of lymphoid leukaemia (acute and chronic) including the incidence, prognosis, symptoms and management

A
  • arise from lymphoid stem cells in red bone marrow (blood stem cells)

Incidence:

  • ALL: most common cancer in children (60% of cases <14)
  • CLL: most common form of adult leukaemia (90% of cases >50)

Prognosis:

  • ALL: great prognosis, 90% complete remission and 2/3rd cured
  • CLL: good, early stage diagnosis has a 10-15 year median survival rate

Symptoms:

  1. ALL:
    - rapid onset of SSX (3/12)
    - bone pain
    - systemic (anorexia, weight loss, atrophy)
    - nervous system (HA, vomiting, palsies, visual / auditory change)
    - RBC inadequacy (anaemia, fatigue, pallor)
    - WBC inadequacy (decreased immunity, fever, mouth ulcers, recurrent infections)
    - platelet inadequacy (bleeding)
    - splenomegaly, hepatomegaly, lymphadenopathy
  2. CLL:
    - insidious onset of SSX
    - systemic (weight loss, extreme fatigue, night sweats, fever)
    - splenomegaly

Management:

  1. ALL:
    - combination chemotherapy (goal: remission)
    - post remission radiotherapy and bone marrow transplant
  2. CLL:
    - no treatment in early stages (can worsen outcomes); treatment begins when SSX progress
    - chemotherapy and antibody therapy
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12
Q

Describe the conditions of myeloid leukaemia (acute and chronic) including incidence, prognosis, symptoms and management

A
  • originate from myeloid stem cells in red bone marrow (blood stem cells)

Incidence:
- can occur at any age, but incidence increases with age

Aetiology:
- philadelphia chromosome present in 95% of CML cases

Prognosis:

  • AML: less good than ALL; 60% achieve remission but 70-85% recurrence within 5 years
  • CML: poor prognosis; chronic phase 2-5 yr survival; accelerated phases 6-18 mth survivial; acute blast crisis 3-6 mth survival

Symptoms:

  1. AML:
    - acute onset (3/12)
    - bone pain
    - systemic (anorexia, weight loss, atrophy)
    - nervous (HA, vomiting, palsies, visual / auditory changes)
    - decreased RBCs (anaemia, fatigue, pallor)
    - decreased WBCs (decreased immunity, recurrent infections, mouth ulcers, fever)
    - decreased platelets (bleeding)
    - splenomegaly, hepatomegaly, lymphadenopathy
  2. CML:
    - insidious onset
    a. chronic phase (2-5 yrs) asymptomatic
    b. accelerated (6-18 mths) primary SSX
    b. acute blast crisis (3-6 mths) SSX of acute leukaemia

Management:

  1. AML:
    - combination chemotherapy to achieve remission
    - radiotherapy and bone marrow transplant post remission
  2. CML:
    - tyrosine kinase inhibtors (imatinib) can prolong survival
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13
Q

What are the incidence and prognosis rates for different types of leukaemia?

A

ALL:

  • most common childlhood cancer
  • great prognosis: 90% remission, 2/3 cure

CLL:

  • most common adult leukaemia
  • good prognosis: 10-15 yr survival rate

AML:
- 60% remission but a 70-85% recurrence within 5 years

CML:
- terminal: 3-6 month survival once in acute blast crisis

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14
Q

Which of the leukaemias is terminal?

A

Chronic myeloid leukaemia:

  • tyrosine kinase inhibitors can prolong survival
  • once in acute blast crisis, survival only 3-6 months
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15
Q

Which drugs are used to treat leukaemia?

A

Chemotherapy drugs for acute leukaemia:

  • cytarabine (inhibits DNA synthesis)
  • daunorubicin (inhibits mRNA synthesis)
  • vincristine (inhibits mitosis)

Chemotherapy drugs for CLL:
- fludarabine (inhibits DNA synthesis)

Antibody drugs for CLL:
- rituximab (destroys B lymphocytes)

For CML:
- imatinib (tyrosine kinase inhibitor, tyrosine kinase is an intracellular enzyme required for intracellular communication)

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16
Q

Describe the condition of lymphoma (Hodgins and non-Hodgkins) including risk factors, definition, incidence and prognosis, and symptoms

A

Definition:

  • neoplastic proliferation of lymphatic cells causing discrete malignant tumours in lymphatic system
  • usually in lymph nodes but can occur in any lymphoid tissue
  • tumours can spread to bone marrow and other organs

Hodgkins:

  • characterized by Reed-Sternberg (RS) neoplastic cells (secrete cytokines that promote tumour growth)
  • usually a single node or chain of nodes

Non-Hodgkins:

  • umbrella term for lymphomas not involving RS cells
  • usually in multiple sites and non-contiguous nodes

Incidence:

  • Hodgkins: one of the most common cancers in young adults
  • non Hodgkins: 6th most common cancer in Aus, average age 65

Prognosis:

  • Hodgkins: good, 75% cured
  • non Hodgkins: variable

Risk factors:

  1. Infectious (HIV, EBV, HCV, herpes, H pylori)
  2. autoimmune (RA, SLE)
  3. Exposure (chemicals, radiation)
  4. Obesity (adipose tissue has endocrine properties)

SSX:

  1. Lymphadenopathy
    - Hodgkins: single or contiguous, usually begins in Cx and spreads to mediastinal nodes, extranodal lymphoid spread rare
    - non Hodgkins: multiple sites esp Cx, axillary, inguinal, femoral, spread to non-contigous nodes, extranodal lymphoid spread common
  2. Compressive SSX
    - dysphagia
    - dyspnoea
    - engorged neck veins
    - neural compression
  3. B symptoms:
    - unexplained high fever
    - drenching night sweats
    - unexplained weight loss
  4. Other:
    - persistent fatigue
    - pruritis
    - anorexia
17
Q

What are the key differences between Hodgkins and non-Hodgkins lymphoma?

A

Age of prognosis:

  • Hodgkins: young adults
  • non Hodgkins: peak diagnosis 65 y.o.

Site:

  • Hodgkins: single or contiguous nodes, rarely spreads to other lymphoid organs
  • non Hodgkins: multiple and non-contigous nodes, commonly spreads to other lymphoid organs

Prognosis:

  • Hodkins: good prognosis, 75% cured
  • non Hodgkins: variable

Reed-Sternberg (RS) cells:

  • present in Hodgkins
  • not present in non Hodgkins
18
Q

What are the similarities and differences between lymphoid leukaemia and lymphoma?

A

Simliarities:
- both involve proliferation of neoplastic B cells

Differences:

  • if most cancer cells are in lymph nodes: classified as lymphoma
  • if most cancer cells are in bone marrow and blood stream: classified as lymphoid leukaemia
19
Q

Describe the condition of multiple myeloma, including the incidence, pathophysiology, symptoms and management

A

Definition:
- uncontrolled replication of malignant plasma cells in bone marrow

Incidence:

  • rare (1.3% of cancers)
  • peak age diagnosis 65 y.o.

Prognosis and management:

  • terminal
  • palliative care
  • chemotherapy and radiotherapy to prolong life

Pathophysiology:

  1. neoplastic plasma cells (myeloma cells) produce excessive amounts of abnormal antibodies (M proteins) in bone marrow
    - causes decreased immunity
    - causes overcrowding of bone marrow
  2. Antibody fragments (light chains) are produced and accumulate in tissues and organs
    - amyloidosis causes renal failure
  3. myeloma cells form discrete tumours (plassmacytomas) in bone
    - release osteolytic cytokines that destroy overlying cortical bone
    - show up as punched out lesions on X ray

SSX:

  1. intraosseous plasmacytomas (tumours)
    - usually in vertebrae, ribs, skull, femur, clavicle, scapula
    - high risk of fracture
    - high risk of metastatic spread
  2. extraosseous plasmacytomas
    - in eye, tongue, skin, vocal cords
  3. bone destruction
    - bone pain
    - pathological fractures
    - hypercalcaemia (confusion, weakness, lethargy, polyuria, thirst, constipation)
  4. marrow overcrowding
    - decreased immunity (recurrent infections, fever)
    - anaemia
  5. overproduction of light chains
    - deposited in kidneys as toxic amyloid protein
    - Bence Jones proteinuria in 99% of patients
20
Q

What are the 3 stages of infection in HIV / AIDS?

A
  1. Acute infection
    - acute infection with HIV
    - 50% experience acute illness soon after exposure
    - SSX subside within 1-3 weeks but chronic lethargy and depression can persist
  2. chronic infection / clinical latency
    - relatively SSX free
    - virus multiplies but is only released sporadically, CD4 lymphocytes gradually decrease
    - months to 20 years before onset of AIDs
  3. AIDS
    - when CD4 lymphocyte count is less than 200 cells per mcL
21
Q

What is the pathophysiology of HIV / AIDS?

A

(HIV is the pathogen that causes AIDS)

  1. Entry into cell
    - HIV binds to CD4 receptor and chemokine co-receptor on host cell
    - viral envelope and cell membrane fuse
    - HIV RNA injected into host cell’s cytoplasm
  2. Conversion of viral DNA
    - viral DNA integrated into host cell by viral enzyme integrase
  3. Dormancy
    - if host cell is not activated, viral DNA remains dormant
  4. Activation
    - when host cell is activated by cytokines, virus proliferates
    - viral enzyme protease modifies new virions
  5. Host cell death
    - release of new virions causes host cell necrosis
    - new virions infect other CD4 bearing cells

(AIDS diagnosed when CD4 lymphocyte count less than 200 cells per mdL)

22
Q

What are the symptoms of HIV / AIDS?

A
  1. Acute infection:
    - flu like SX
    - fever, night sweats, fatigue
    - myalgia, arthralgia, sore throat, HA, photophobia
    - diarrhea, rash
    - lymphadenopathy
  2. Chronic infection / clinical latency:
    - very few SSX
    - maybe lymphadenopathy
  3. AIDS
    - fatigue, night sweats, fever
    - weight loss, atrophy
    - nausea
    - generalized lymphadenopathy
    - neurological (AIDS dementia complex with cognitive, behavioural and motor changes)
    - opportunistic infections (TB, herpes)
    - neoplasia (non Hodgkins lymphooma, Kaposi’s sarcoma)
23
Q

Describe the condition of HIV / AIDS including transmission and incidence, brief pathophysiology, stages, and management

A

Definition:
- HIV virus infects and depletes immune cells that possess the CD4 glycoprotein (mostly T helper lymphocoytes); AIDS is diagnosed when CD4 count is less than 200 per mcL

Transmission:
- blood and semen

Incidence:

  • 37 million cases globally
  • 25,000 Australians
  • notification rates highest 25-44 y.o.

Pathophysiology:

  • HIV viral cell enters immune cell that possesses CD4 glycoprotein (usually T helper lymphocytes)
  • virus converts DNA of cell to proliferate viral cells
  • virus lies dormant until cell is activated, and then proliferates virions
  • virions cause host cell necrosis

Stages:

  1. Acute infection (1-3 weeks)
  2. Chronic infection / clinical latency (months to 20 years)
  3. AIDS (when CD4 cell count less than 200 per mcL)

Management:

  1. anti-retroviral medication (inhibits viral replication)
  2. post-exposure prophylaxis (within 72 hours of exposure, 28 days of anti-retroviral treatment, reduces risk by up to 80%)
  3. pre-exposure prophylaxis
  4. maintenance (including notification of past partners)

Clinic - Common Conditions Overview (26 decks)

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