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3rd Year > Case 14 > Flashcards

Case 14 Flashcards

0
Q

What are component causes?

A

Factors that work together with the necessary cause to produce disease.

Overcrowding and TB

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1
Q

What is a necessary cause?

A

A factor that must be present for a disease to occur.

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2
Q

What is a sufficient cause?

A

A combination of factors that is sufficient to cause disease in at least some people

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3
Q

Levels of causation: upstream factors

A

Social - gender, race, SES

Population: income inequality, lack of social cohesion, inadequate medical services

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4
Q

Levels of causation: downstream factors

A

Physiological: genetics, sex, age

Behavioural: smoking, diet, exercise, alcohol

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5
Q

Ecological model: levels of causation

A

Biological
Behavioural
Societal
Structural

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6
Q

Evidence based practice

A 
Assess your patient
Ask the right question
Access the evidence
Appraise the evidence
Apply the evidence
Audit your clinical practice
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7
Q

Which study designs are best for evaluating potential harms?

A

Case reports can’t draw generalisable conclusions

Case control prone to bias and confounding

Trials not useful for long term effects

Cohort studies with a large representative sample, objective measures of exposure and outcome and good long term follow up are good

Systematic reviews of all the good evidence are best

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8
Q

Is an apparent association real?

A

Bias?
Confounding?
Chance?
Is the association causal? Bradford Hill

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9
Q

Bradford hill criteria

A 
Does cause precede effect?
What is the strength of the effect?
Is there a dose-response effect?
Is there biological plausibility?
Has the effect been consistently shown in similar studies in different populations?
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10
Q

Acute leukaemia non-specific presenting features

A 
Unwell
Tired
Aches and pains
Fever
Often little to find on exam but may have bleeding, sepsis, pallor

NB if symptoms persist/get worse

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11
Q

Acute leukaemia specific features

A

Bone marrow infiltration: anaemia, bleeding, infections

Tissue infiltration: gum hypertrophy, lymphadenopathy, splenomegaly, CNS disease (ALL)

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12
Q

Tests used toc lassify acute leukaemia

A 
Morphology (peripheral blood and bone marrow)
Cytochemistry
Immunophenotype ( flow cytometry)
Genetic abnormalities (FISH, PCR)
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13
Q

Leukaemia initial diagnosis

A

FBC
Differential count
Morphological review of peripheral blood slide

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14
Q

Leukaemia definitive diagnosis

A

Bone marrow aspirate/trephine biopsy

Aspirate provides cells for cytogentic/molecular studies

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15
Q

Leukaemia additional non-diagnostic tests

A

LP to exclude CNS disease
HIV test
DIC screen
Electrolytes and renal function

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16
Q

Supportive therapy

A

Packed red cell transfusion for anaemia
Platelet transfusion for thrombocytopaenia
Hydration and allopurinol for tumour lysis syndrome
Prevention and treatment of infections
Anti emetics to prevent chemo-associated nausea

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17
Q

Primary lymphoid organs

A

Bone marrow

Thymus

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18
Q

Main Th1 cytokines

A

IL-2, TNF beta, IFN gamma

Cell mediated response

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19
Q

Main Th2 cytokines

A

IL-4, IL-10

Antibody response

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20
Q

A chromosomal translocation may result in

A

Fusion protein product

Aberrant expression of normal protein

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21
Q

Karyotype analysis

A

Direct morphological observation of chromosomes under a microscope
Requires cells to be in metaphase
Therefore cell culture is performed before analysis

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22
Q

FISH

A

Uses fluorecent-labelled genetic probes which hybridize to different parts of the genome and allow visualization of karyotype abnormalities

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23
Q

How is acute leukaemia defined?

A

> 20% blasts in blood or BM at presentation

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24
Q

Abnormalities leading to build up of leukaemic cells

A

Increased rate of proliferation
Avoidance of apoptosis
Block in differentiation

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25
Q

Modes of action of antibodies

A

Neutralisation
Opsonisation
Agglutination
Activation of classical complement pathway

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26
Q

General properties of immunity

A

Specificity
Versatility
Memory
Tolerance

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27
Q

Secondary lymphoid tissues

A 
Lymph nodes
Spleen
Tonsils
MALT
BALT
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28
Q

T cell mediated killing

A

Perforin release
Release of granzyme proteases
Fas ligand

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29
Q

NK cell killing

A

NK cells are inhibited by class 1 MHC which are not expressed at normal levels on cancer or virally infected cells

Perforin release
Macrophage activation

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30
Q

Structure of the lymph node

A

Dense connective tissue capsule pierced by afferent lymphatics with valves.

Fibrous trabeculae

Subcapsular space flows into paratrabecular sinuses - lined with macrophages.

Outer cortex with follicles, inner cortex, medulla

Medullary sinuses surrounded by medullary cords.

One efferent lymphatic vessel

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31
Q

Where do most lymphocytes enter the lymph node?

A

High endothelial venules in the inner cortex

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32
Q

Where in the lymph node are plasma cells found?

A

In the medullary cords where they can secret antibodies directly into the medullary sinusoids without leaving the lymph node

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33
Q

What is the function of follicular dendritic cells?

A

Mature activated B cells migrate to the germinal centre where they must interact strongly with whole antigen presented by FDCs in order to proliferate or else they accumulate in the mantle zone and undergo apoptosis and phagocytosis by macrophages.

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34
Q

Structure of the thymus

A

Fibrous capsule

Two lobes, divided into incomplete lobules by fibrous trabeculae containing trabecular arterioles

Cortex contains thymic epithelial cells organised in a 3D network supported by collagen fibres

Thymic epithelial cells populate the medulla. Some form Hassal’s corpuscles which produce thymic stromal lymphopoeitin which optimises negative selection

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35
Q

Blood thymus barrier

A

Double basal lamina
Endothelial cells linked by tight junctions
Thymic epithelial cells surround capillaries and are linked tightly by desmosomes
Macrophages engulf foreign antigen

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36
Q

General organisation of the spleen

A

Surrounded by a fibrous capsule. Capsule-derived trabeculae penetrate the stroma carrying trabecular arteries and veins
No cortex/medulla. No afferent lymphatics
Stroma consists of reticular fibres supporting the red and white pulp

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37
Q

Component of the splenic white pulp

A

Central arteriole
PALS
Corona containing B cells and APCs
Germinal centre

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38
Q

Red pulp

A

Interconnected network of splenic sinusoids lined by elongated endothelial cells.

Splenic cords separate splenic sinusoids.

Splenic cords contain plasma cells, macrophages and blood cells.

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39
Q

Vascularisation of the spleen

A 
Splenic artery enters at the hilum
Trabecular arteries
Central arteriole + radial arterioles + marginal sinus
Penicillar artery
Macrophage sheathed capillaries
Splenic sinusoids or red pulp stroma
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40
Q

How is the classical complement pathway activated?

A

Binding of C1 to an antigen bound antibody

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41
Q

B cell development

A

Occurs in bone marrow niche environment created by stromal nurse cells in the presence of IL-7

As the cell matures from pro-B to pre-B to immature B, heavy chain VDJ rearrangement occurs followed by light chain VJ rearrangement

As the cell matures it migrates from the subendosteum towards the central axis

Negative selection takes place in the BM and self-reactive cells undergo apoptosis

42
Q

T cell development

A

Immature T cells must migrate from the BM to thymus to complete development

Arriving T cells are double negative.

They become double positive and express both CD4 and CD8

Positive selection allows cells that bind self MHC but not self antigen to continue and the rest undergo apoptosis

Negative selection eliminates self reactive cells and they are phagocytosed by macrophages

Single positive mature cells migrate to the periphery

43
Q

5 periods of psychosocial support

A 
At diagnosis
At remission
At relapse
At terminal phase
At death
44
Q

Hypersplenism

A

Association between peripheral blood pancytopaenia and splenic enlargement

Primary idiopathic form causes massive splenomegaly requiring splenectomy

45
Q

Causes of gross splenomegaly

A

Chronic myeloid leukaemia
Myelofibrosis
Malaria
Gaucher’s disease

46
Q

Causes of moderate splenomegaly

A

Amyloidosis
Haemolytic anaemia
Chronic lymphocytic anaemia
Congestion

47
Q

Causes of mild splenomegaly

A

Infection
Autoimmune disease
Felty’s disease

48
Q

Anat path reader general causes of splenomegaly

A 
Congestion
Infection
Immune disorders
Red blood cell abnormalities
Primary or metastatic neoplasms
Storage disorders
Amyloidosis
49
Q

Reactive lymph node hyperplasia

A

Usually mixed response in nodes draining sites of infection

50
Q

Granulomatous lymphadenitis

A

Mycobacterial: caseous necrosis with Langhans giant cells

Toxoplasma: follicular hyperplasia with adjacent granulomas and marginal zone B cell hyperplasia

Sarcoidosis
Crohn’s disease
Reaction to tumour antigen
Foreign body reaction

51
Q

Necrotising lymphadenitis

A

Stellate abcesses within lymph nodes surrounded by pallisades histiocytes

Lymphogranuloma venereum and cats scratch disease

Kikuchi’s disease
SLE

52
Q

Follicular hyperplasia

A

Syphilis, any stage
Marked follicular hyperplasia with many interfollicular plasma cells

Rheumatoid arthritis

53
Q

Paracortical hyperplasia

A

EBV
Paracortical hyperplasia with numerous large transformed T cells

Dermatopathic lymphadenopathy. Brown yellow cut surface. Histiocytes contain melanin

54
Q

HIV lymphadenopathy

A

AIDS related complex or persistant generalised lymphadenopathy syndrome

Initial hyperplasia
Mantle zone implosion/follicular lysis
Loss of germinal centre B cells and paracortical T cells

55
Q

Hodgkins lymphoma distinguishing features

A

Almost never involves tonsils, skin, stomach, ileum

Reed-Sternberg cells

56
Q

Classic Reed Sternberg cell

A

Large cell with large multilobated nucleus, very large eosinophilic nucleolus and slight acidophilic cytoplasm

57
Q

Classifying HD

A

Use WHO classification

Divided into lymphocyte predominant and classic HD

Classic HD is further divided into 4 types. Lymphocyte rich, nodular sclerosing, mixed cellularity and lymphocyte depleted

58
Q

Spread of disease in HD

A

Spreads predominantly through contiguous lymphatics

59
Q

HD complications

A

Infection
Cachexia
Iatrogenic
Second malignancy

60
Q

NHL risk factors

A

Viruses: EBV, HTLV1
Immunodeficiency: x-linked, AIDS, transplantation

61
Q

NHL presentation

A

Painless rubbery nodes
More likely to be multicentric
May be no systemic symptoms
May involve extralymphoid tissue like skin, GIT etc

62
Q

List the human herpes viruses

A 
HSV 1 and 2
VZV
CMV
EBV
HHV 6 and 7
HHV8
63
Q

Herpes virus morphology

A

Double stranded RNA
Icosahedral capsid
Envelope

64
Q

Which anatomical sites are affected by HSV 1 and 2?

A

1: orofacial
2: genital

65
Q

How does HSV maintain latent infection?

A

Persists in episomal form in the sensory ganglia supplying the area of primary infection - generally the trigeminal or sacral ganglia.

66
Q

Rare life threatening HSV syndromes

A

Acute necrotising encephalitis
Neonatal infection
Disseminated infection

67
Q

HSV reactivation may be provoked by

A 
Sunlight 
Stress
Febrile illness
Menstruation
Immunosuppression
68
Q

HSV primary infection syndromes

A 
Gingivostomatitis
Exzema herpeticum
Traumatic inoculation 
Conjunctivitis, keratitis
Genital herpes
69
Q

Recurrent HSV syndromes

A

Cold sores
Recurrent genital herpes
Recurrent kertitis

70
Q

HSV diagnosis

A

IgG indicates past infection. Igm unreliable
Microscopy
PCR
Culture

71
Q

Progression of VZV lesions

A 
Macule
Papule
Vesicle
Pustule
Scab
72
Q

Chicken pox

A

Mild febrile illness
Generalised vesicular rash
Highly infectious via respiratory droplets and vesicle secretions

73
Q

Chicken pox complications

A 
Secondary skin infections
Post infectious encephalomyelitis
Stroke (vasculitis)
Pneumonia
Haemorrhagic varicella
74
Q

Congenital VZV

A

Infection before 20 weeks teratogenic

75
Q

Zoster complications

A

Post herpetic neuralgia
Encephalitis, myelitis
Stroke

76
Q

Preciptating factors for zoster

A

Immunosuppression
HIV
Old age
Cancer

77
Q

VZV diagnosis

A

Clinically apparent
IgG for past infection. IgM unreliable
PCR

78
Q

Treatment of HSV and VZV

A

Acyclovir

79
Q

PEP for varicella

A

Immunosuppressed, baby less than 6 months or pregnant: zoster immune globulin or avyclovir

Low risk patient: varicella vaccine or acyclovir

80
Q

CMV transmission

A

70-90% of adults have antibodies. Infection in first few years of life

Spread in saliva, urine, breast milk, semen, blood. Therefore close contact, kissing, sexual contact, iatrogenic

81
Q

CMV clinical syndromes

A

Primary infection in adulthood gives an infectious mononucleosis-like illness

Congenital: severe disease only follows primary infection in pregnancy

Immunosuppressed patients: interstitial pneumonia, retinitis, GIT ulceration neurological disorders

82
Q

CMV treatment

A

Gancyclovir

83
Q

CMV diagnosis

A

IgG
Viral antigen in diseased tissue
PCR
Viral load

84
Q

EBV transmission

A

Saliva, kissing

As for CMV

90-100% of adults have antibodies

85
Q

Infectious mononucleosis symptoms

A 
Fever, malaise
Rash
Lymphadenopathy
Sore throat
HSM
Atypical lymphocytosis

Self limiting

86
Q

Infectious mononucleosis differential diagnosis

A

EBV
CMV
HIV
HHV6

87
Q

EBV diagnosis

A

Mono spot heterophile antibodies

IgG and IgM to viral capsid antigen

88
Q

Complications of EBV latency

A

Lymphoproliferative disorders
NHL
HD
Nasopharyngeal carcinoma

89
Q

Neonatal HHV6 infection

A

Roseola infantum: febrile illness, rash, febrile convulsions

90
Q

HHV8 disease associations

A

Kaposi’s sarcoma
Primary effusion lymphomas
Multicentric castleman’s disease

91
Q

Gout

A

Recurrent inflamatory disorder caused by deposition of urate crystals in synovial fluid

92
Q

Gout pathogenesis

A

Hyperuricaemia
Crystal deposition
Macrophage phagocytosis
Inflammatory cascade

93
Q

Causes of hyperuricaemia

A 
Overproduction: 
Inherited enzyme defects
Ethanol
Obesity
Malignancy
Myeloproliferative, lymphoproliferative, heamatological disorders

Underexcretion:
Clinical disease- renal insufficiency, ketoacidosis, hypothyroidism etc
Diuretics

Overconsumption of meat, seafood, beer

94
Q

Gout prevention

A 
Diet
Drugs:
Increase excretion- probenecid
Decrease production - allopurinol
Increase metabolism - rasburicase
95
Q

Tumour lysis syndrome

A

Life threatening oncological emergency caused by rapid lysis of malignant cells.

Hyperuricaemia
Hyperkalaemia
Hypocalcaemia
Hyperphosphataemia

GIT disturbances
Muscle weakness, cramps
Parasthaesia
Tetany
Lethargy
96
Q

Tumour lysis syndrome treatment

A

Kayexalate
Calcium replacement
Phosphate binders
Dialysis

97
Q

Tumour lysis syndrome prevention

A

IV hydration
Urine alkalinisation
Hypouricaemic agents

98
Q

Multiple myeloma clinical features

A

Bone marrow infiltration:
Bone pain, fractures, lytic lesions
Hypercalcaemia
Anaemia, infections

Monoclonal protein production:
Renal failure
Hyper viscosity syndrome
Peripheral neuropathy

99
Q

Receptor mediated apoptotic pathway

A

Ligand binding to the Fas or TNF receptors triggers an intracellular caspase cascade resulting in cell shrinkage, DNA cleavage, nuclear fragmentation and phagocytosis of apoptotic bodies by macrophages

100
Q

Mitochondrial apoptosis pathway

A

Damage to cellular components triggers release of cytochrome C from the mitochondria which then activates caspase proteases. Mitochondrial membrane permeability controlled by Bcl proteins. p53 activates apoptosis by raising the level of BAX which overrides Bcl2 and triggers Cytochrome c release

101
Q

Specific treatment of acute leukaemia

A

Induction
Consolidation
High dose intesification (requires BM transplant)
Maintenance

102
Q

Mechanisms of action of chemotherapeutic drugs

A 
Damage to mitotic spindle
Bind DNA and interfere with mitosis
Deprive cells of asparaginine
Lysis of lymphoblasts
Cross-link DNA, impede RNA formation

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