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Yr 3 Sem 1 > Week 5 Common Conditions > Flashcards

Week 5 Common Conditions Flashcards

1
Q

What is lymphadenopathy?

A

DEFINITION: the palpable enlargement (>1cm) of lymph nodes

Lymphadenitis: lymphadenopathy with pain +/- other signs of inflammation (redness, warmth)

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2
Q

What is the classification of lymphadenopathy?

A

Localised = present in 1 body area
75% of lymphadenopathies are localised
Usually reflect pathology in region of drainage

e. g. dental or tonsillar infection  cervical lymphadenitis
e. g. infections in the extremities axillary or inguinal node involvement

Generalised = present in 2 (or more) non-contiguous nodal groups
25% are generalised
Generally due to significant underlying disease

e.g. glandular fever, lymphoma, leukaemia, metastatic neoplasia, HIV infection, tuberculosis

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3
Q

What is splenomegaly?

A

An important diagnostic clue
If large enough: dragging sensation in the LUQ, sensation of fullness (esp. after eating)

The storage function of the spleen is enhanced in splenomegaly

Sequestration of cellular components can lead to anaemia, leukopenia &/or thrombocytopenia

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4
Q

What are associated disorders of spenomegaly? (5)

A

Associated disorders include:

INFECTIONS
e.g. glandular fever, TB, syphilis , HIV

PORTAL HYPERTENSION
e.g. cirrhosis, cardiac failure

LYMPHOID DISORDERS
e.g. leukaemia, lymphoma, multiple myeloma

RBC DISORDERS
e.g. thalassaemia (haemolytic anaemia)

INFLAMMATORY CONDITIONS
e.g. rheumatoid arthritis, systemic lupus erythematosus

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5
Q

What is glandular fever?

A

Acute infection of B lymphocytes with Epstein-Barr Virus (EBV)
Also referred to as infectious mononucleosis

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6
Q

What is the incidence of glandular fever?

A 
Most people (~90%) have had an EBV infection by the time they are adults
Infection usually occurs in childhood, but is rarely symptomatic

Glandular fever (acute symptomatic infection) is common in young adults (15-35 years)

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7
Q

What is the transmission of glandular fever?

A

Usually through close personal contact - most commonly saliva
Mucosal secretions of the respiratory tract, genital tract, blood

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8
Q

What is the pathophysiology of glandular fever?

A

EBV initially infects the oropharynx, nasopharynx and salivary epithelial cells

Later extends into lymphoid tissues and B cells

ADAPTIVE IMMUNE RESPONSE
Unaffected B cells produce antibodies against EBV

Cytotoxic T cells attack virus-infected B-cells directly

Enlargement of lymphoid tissue occurs due to:

Proliferation of lymphocytes
Removal of dead and damaged B cells

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9
Q

What are the clinical features of glandular fever?

A

Long incubation period: 30-50 days

Classical symptoms: fever, sore throat, cervical lymphadenopathy, fatigue

Progression of disease: generalised lymphadenopathy, splenomegaly, hepatomegaly

Rare complications (~5%): ocular, cardiac, CNS involvement

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10
Q

What is the management of glandular fever?

A

Diagnosis of EBV infection is through serologic testing

The disease is usually self-limiting: recovery commences in a few weeks
Fatigue may last 1-2 months

Rest

Symptom relief: analgesics, antipyretics

Treatment of secondary bacterial infections
Streptococcal pharyngitis occurs in 20-30% of cases
Antibiotics required (penicillin or erythromycin)
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11
Q

What are the types of haematological cancer? (3)

A

Leukaemia
Proliferation of malignant leucocytes in the bone marrow
Overcrowding causes malignant cells to spill into blood

Lymphoma
Proliferation of malignant lymphocytes in lymphatic system
Formation of discrete tumours

Multiple Myeloma
Proliferation of malignant plasma cells in the bone marrow

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12
Q

What is the classification of leukaemia?

A

Based on the predominant cell of origin:

Lymphoid leukaemia
Myeloid leukaemia

Based on the degree of differentiation before the cells became malignant:

Acute leukaemia – rapid growth of immature cells (referred to as ‘blasts’)
Chronic leukaemia – slow growth of more differentiated cells

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13
Q

What are the types of leukaemia?

A

Acute lymphoblastic leukaemia (ALL)
Acute myeloid leukaemia (AML)

Chronic lymphocytic leukaemia (CLL)
Chronic myeloid leukaemia (CML)

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14
Q

What is the aetiology/risk factors of leukaemia (5)?

A

Exact cause unknown - likely a complex interplay between environmental & genetic factors

RISK FACTORS INCLUDE:

Genetic factors
Tendency to reappear in families

Specific chromosomal abnormalities
e.g. Philadelphia Chromosome

Exposure to cigarette smoke, benzene, ionising radiation

Certain infections e.g. HIV, HCV

Chemotherapy for the treatment of lymphoma, multiple myeloma, ovarian and breast cancer

Chronic myeloid leukaemia: can develop into an acute leukaemia (‘blast crisis’) in its end-stage

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15
Q

What age does acute lymphoblastic leukaemia occur in? What is the prognosis?

A

Most common cancer of children
60% cases arise in children <14 years

PROGNOSIS
90% of children achieve complete remission

> 2/3 can be considered cured

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16
Q

What age does acute myeloid leukaemia occur in? What is the prognosis?

A

Occurs at all ages, although incidence increases w. age (>60 years)

PROGNOSIS
AML = more difficult to treat than ALL
60% of patients achieve remission

Only 15 - 30% remain free of disease at 5yrs

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17
Q

What are the clinical features of acute leukaemia?

A

Rapid onset of symptoms (Pts usually present within 3/12)

Proliferation of blast cells overcrowd bone marrow (suppresses formation of other blood cells):

Anaemia (↓ RBCs): fatigue, pallor, weakness
Decreased immunity (↓ normal WBCs): fever, mouth ulcers, recurrent infections
Bleeding tendencies (↓ platelets): epistaxis, purpurae, gum bleeding
Bone pain (marrow expansion) 
Splenomegaly, hepatomegaly, lymphadenopathy (sequestration of blasts)

Non-specific features: anorexia, weight loss, m. wasting
Nervous system infiltration: HA, vomiting, palsies, visual/auditory changes

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18
Q

What is the management of acute leukaemia?

A

DIAGNOSIS: blood marrow biopsy + blood film + clinical features

Primary aim is to achieve remission
Defined as normal bone marrow + blood + clinical status

First line: combination chemotherapy
Cytaribine – inhibits DNA synthesis
Daunorubicin – inhibits mRNA synthesis, induce DNA breakage
Vincristine – inhibits mitosis

“Curative” measures taken post-remission
Radiotherapy, prior to bone marrow transplant
Autologous vs. allogenic

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19
Q

What age does chronic myeloid leukaemia occur in? What is the prognosis?

A

Can occur at any age
Peak age for diagnosis is 50-70 yrs

Philadelphia Chromosome (BCR-ABL oncogene) present in 95% of cases

Chronic phase (2 -5 yrs): asymptomatic
Accelerated phase (6-18 mth): primary symptoms
Acute Blast Crisis: 3-6 mth survival
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20
Q

What age does chronic lymphocytic leukaemia occur in? What is the prognosis?

A

Most common form of adult leukaemia

90% of cases occur > 50 yrs

Usually follows an indolent course (does not require treatment in its early stages)

PROGNOSIS
Pts with early stage disease at diagnosis have a median survival of 10-15 yrs

21
Q

What are the clinical features of chronic leukaemia?

A

Insidious onset of symptoms
Many Pts are asymptomatic & diagnosed incidentally via routine blood test (leukocytosis)

Common initial symptoms: splenomegaly, extreme fatigue, weight loss, night sweats, fever

CLL – suppression of normal antibody production is often fatal in the later stages

CML - acute blast crisis: features associated with acute leukaemia

22
Q

What is the management of chronic leukaemia?

A

Bone marrow transplantation (usually only suitable for Pts <55 yrs)
Biological response modifiers & combination chemotherapy

Chronic Lymphocytic Leukaemia
Observation in early stages
Premature treatment can lead to poorer outcomes

Indications for treatment: progressive fatigue, symptomatic lymphadenopathy, anaemia or thrombocytopaenia

First line therapies include:
Chemotherapy – fludarabine: inhibits DNA synthesis
Antibody therapy – rituximab: destroys B lymphocytes (pictured right)

Chronic Myeloid Leukaemia
Tyrosine kinase inhibitors (e.g. imatinib) can prolong survival significantly
Tyrosine kinases are intracellular enzymes required for cellular proliferation

23
Q

What is the definition of lymphoma?

A

discrete, malignant tumours arising in the lymphatic system

Most lymphomas arise in lymph nodes, but recall that lymphoid tissue is virtually ubiquitous in the body

Depending on the type of lymphoma, malignant cells may be found in other organs e.g. spleen, thymus, gastrointestinal tract, skin

Spread to bone marrow can occur

24
Q

What is the classification of lymphoma?

A

Hodgkin’s lymphoma

Non-Hodgkin’s lymphoma

25
Q

What are the risk factors of lymphoma?

A

Family history

Certain infections
Epstein-Barr Virus, HIV, HCV, HTLV, Herpes Virus-8, H. pylori

Obesity
Adipose tissue possesses endocrine & metabolic properties

Iatrogenic immunosuppression e.g. anti-rejection therapy

Autoimmune conditions: RA, SLE

Exposure to ionizing radiation or mutagenic chemicals

26
Q

What is hodgkins lymphoma?

A

One of the most common cancers in young adults

Usually arises in a single node or chain of related nodes

Spreads to nodes in close anatomical proximity.

Characterised by a distinctive neoplastic cell, the Reed-Sternberg (RS) cell

RS cells are large and binucleate; their presence is necessary for the diagnosis of HL

Cytokines secreted by RS cells promote tumour growth

27
Q

What are the clinical features of Hodgkins lymphoma? (4)

A

Lymphadenopathy
Single or related group of superficial lymph nodes
Nodes are typically painless, discrete and rubbery

Cervical nodes usually affected first
Spread: occurs to adjacent nodes (esp. mediastinal)

Extranodal lymphoid involvement: uncommon

Compressive features
Occur secondary to nodal enlargement
Dysphagia, dyspnoea, engorged neck veins, neural compression

“B” symptoms
Have prognostic significance
Unexplained fever (>38C), drenching night sweats, unexplained wt loss (>10%) in preceding 6/12

Other constitutional symptoms: persistent fatigue, pruritis, anorexia

28
Q

What is Non-Hodgkins lymphoma?

A

6th most common type of cancer in Australia

increased incidence of NHLs: attributed to increased HIV infections

Average age for diagnosis: 65
Although the disease can present at any age

The term ‘ NHL’ refers to a diverse group of disorders
B cell neoplasms (85% of tumours)
T cell & NK cell neoplasms

All types feature the neoplastic proliferation of lymphoid cells, but NOT the Reed-Sternberg form.

29
Q

What are the clinical features of non-hodgkins lymphoma? (3)

A

Lymphadenopathy
Nodes are typically painless and discrete

Usually originate in multiple sites: cervical, axillary, inguinal and femoral nodes commonly affected first

Spread: occurs to non-contiguous nodes

Extranodal lymphoid involvement: common
Features reflect affected organs e.g. nasopharynx, GIT, bone, thyroid, testes, skin

Compressive features
Occur secondary to nodal enlargement

”B” symptoms & constitutional symptoms
Can also exist in NHL

30
Q

Lymphoma vs Lymphoid Leukaemia

A

Used to beconsidered distinct entities, current knowledge suggests the distinction is vague

Example: chronic lymphocytic leukaemia & small lymphocytic lymphoma
Considered to have the same underlying disease process (neoplastic B cell proliferation)

Current convention is to classify the disease based upon clinical presentation:

If most cancer cells are in bone marrow + bloodstream = chronic lymphocytic leukaemia

If most cancer cells are in lymph nodes, the disease is termed small lymphocytic lymphoma

31
Q

What is the management of lymphoma?

A

Depends on the type of lymphoma and intent of treatment (curative vs. palliative)

TREATMENTS INCLUDE
Chemotherapy

Radiotherapy

Antibody therapy

Corticosteroids

Stem cell transplant

PROGNOSIS
~75% of HL Pts can be cured
NHL: prognosis depends greatly on subtype

32
Q

What is multiple myeloma?

A

Lymphoid malignancy of the bone marrow, characterised by the uncontrolled replication of plasma (immunoglobulin-secreting) cells

33
Q

What is the incidence of multiple myeloma?

A

Accounts for 1.3% of all cancers in Australia

Rarely occurs before 40 yrs – peak age for diagnosis is 65

34
Q

What is the aetiology of multiple myeloma?

A

Chromosomal mutations play a key role
Exact aetiology unknown

Risk assoc. w/ radiation exposure

Familial predisposition?

35
Q

What is the pathophysiology of multiple myeloma?

A

Myeloma cells: neoplastic plasma cells that produce excessive amounts of abnormal antibodies (M proteins)

Result: decreased immunity, overcrowded marrow

Antibody fragments (light-chains) are also produced and accumulate in tissues and organs

Result: amyloidosis leads to renal failure

Myeloma cells form discrete tumours (plasmacytomas) within bone
Release of osteolytic cytokines destroys overlying cortical bone

Result: radiographic ‘punched-out’ lesions (1-4cm in diameter)

36
Q

What are interosseous plasmacytomas? Where do they affect?

A

Most commonly affects the vertebral column, ribs, skull, pelvis, femur, clavicle, scapula
Risk for pathologic #

Bone marrow biopsy: abundant myeloma cells
Can comprise between 10 -90% of cells

Large potential for spread:
Lymph nodes
Other bones
Spleen, liver, kidneys lungs

37
Q

What are the clinical features of multiple myeloma? (4)

A

Often insidious for years

Bone destruction
Bony pain, pathological #
Hypercalcaemia - confusion, weakness, lethargy, polyuria, thirst, constipation

Marrow overcrowding
Decreased immunity - recurrent infections, fever
Anaemia

Overproduction of light-chains
Deposited in kidneys as amyloid protein (toxic)
Bence-Jones proteinuria in 99% of Pts

Extraosseous plasmacytomas

38
Q

What is the management of multiple myeloma?

A

Palliation: radiotherapy, chemotherapy

39
Q

What is human immunodeficiency virus?

A

HIV is the pathogen responsible for acquired immunodeficiency syndrome (AIDS)

It is a retrovirus and carries its genetic material as RNA (not DNA)

The disease arose in Africa in the 1950s and has now spread throughout the world

40
Q

What is the incidence of HIV?

A

At the end of 2016: 37 million people living with HIV worldwide, including 25, 000 Australians

HIV notification rates are highest in the 25-44 age group

Australian deaths from AIDS peaked in 1994 (953 deaths)

It has now become a chronic disease due to the advent of anti-retroviral drugs

41
Q

What are the modes of transmission of HIV?

A

Predominantly through the exchange of body fluids (blood, semen)
Not transmitted by fomites i.e. plates, cutlery, phones, drinking fountains

Children can be infected: transplacental spread, blood spread during birth, via breast milk
Occupational exposures e.g. nurses, pathology lab technicians

Before rigorous screening measures were introduced, some contracted HIV from receiving blood transfusions or blood products

42
Q

What is the pathophysiology of HIV? (Key viral enzymes & steps (5))

A

HIV infects and depletes immune cells which possess the CD4 glycoprotein

Predisposes life-threatening infections and malignancies

CD4 is found predominantly on T Helper (TH) lymphocytes
Other CD4+ cells: some Tc lymphocytes, NK cells, macrophages, DCs

Key viral enzymes:
protease, reverse transcriptase

Entry into cell
HIV binds to CD4 receptor and chemokine co-receptor on the host cell
Viral envelope and cell membrane fuse
HIV RNA injected into the host cell’s cytoplasm

Conversion of viral RNA
HIV RNA converted to double-stranded DNA by the viral enzyme reverse transcriptase
Viral DNA is integrated into the host cell’s DNA by the viral enzyme integrase

Dormancy
If host cell is NOT activated, viral DNA remains dormant (can be years)

Activation
If host cell is activated (by cytokines) the virus proliferates
The viral enzyme protease modifies new virions

Host cell death
Release of new virions results in host cell lysis (necrosis)
New virions free to infect other CD4-bearing (CD4+) cells

43
Q

What are the stages of HIV infection?

A
  1. Acute infection
  2. Chronic infection
  3. Acquired immune deficiency syndrome
44
Q

Describe stage 1 HIV (acute)

A

~50% of infected people experience acute illness soon after the initial exposure

Due to the sudden increase of viruses in the host

CLINICAL FEATURES
Nonspecific flu-like symptoms, including:

Fever, night sweats, fatigue, lymphadenopathy

Sore throat, headache, photophobia, myalgia, arthralgia

Diarrhoea, generalised maculopapular rash

Most symptoms subside in 1-3 weeks, although chronic lethargy, depression & irritability can persist

HIV antibodies may not be detectable for some months, however viral transmission is still possible

45
Q

Describe stage 2 HIV (chronic- clinical latency)

A

Relatively symptom-free +/- lymphadenopathy

Can be 2 months  20 years before the onset of AIDS
The median period is 10 years

Virus multiplies but is only released sporadically
CD4+ lymphocytes gradually decrease

46
Q

Describe stage 3 HIV (acquired immune deficiency syndrome)

A

AIDS can be diagnosed when various criteria are fulfilled

Most common diagnostic criterion met: CD4+ lymphocyte count of <200 cells/mcL

47
Q

What are the clinical features of AIDS? (4)

A

Non-specific features
Generalised lymphadenopathy
Weight loss, wasting, nausea, fatigue, night sweats, fevers

Neurological symptoms
CNS affected more than PNS

HIV encephalopathy (AIDS dementia complex)
Cognitive, behavioural, motor changes

Opportunistic infections
Candidiasis, tuberculosis, widespread herpes simplex
Rare infections

Neoplasia
e.g. non-Hodgkin’s lymphoma, Kaposi’s sarcoma

Kaposi’s sarcoma: painless, red-purple lesions (can be on any part of the body)

48
Q

What is the pharmacology of HIV?

A

ANTI-RETROVIRAL MEDICATIONS

Used in combination to inhibit viral replication and prevent progression to AIDS

49
Q

What is the management of HIV?

A 
MAINTAIN PHYSICAL &amp; MENTAL HEALTH:
Exercise, nutritional support
Cessation of nicotine, alcohol &amp; drug use
Counselling
Trace past partners

POST-EXPOSURE PROPHYLAXIS
Must be implemented within 72 hours of potential exposure to HIV
Short-term (28-day course) anti-retroviral treatment

Reduces risk of seroconversion by up to 80%
Available from sexual health clinics, hospital EDs

PRE-EXPOSURE PROPHYLAXIS
Approved by Therapeutic Goods Administration, but currently not on PBS

Yr 3 Sem 1 (7 decks)

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