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MBChB Phase 3 > Week 2: General Pathology > Flashcards

Week 2: General Pathology Flashcards

1
Q

Name the main types of immune cells

A

Macrophage, neutrophil, eosinophil, basophil/mast cell, dendritic cell

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2
Q

What are the main functions of a macrophage and how is it identified in histology?

A

Clearance of micro-organism, getting help
A macrophage is a monocyte in the tissue.
The main FUNCTIONS are: phagocytosis, antigen presentation and cytokine production
HISTOLOGY: largest type of WBC, kidney bean shaped nucleus, abundant cytoplasm, some fine granules

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3
Q

What are the main functions of a neutrophil and how is it identified in histology?

A

Neutrophils make up most of the white cells. They’re the foot soldiers and provide a rapid response to infection. They also die locally.
The main FUNCTIONS are: chemotaxis, phagocytosis and degranulation
HISTOLOGY: bigger than RBC, single multilobed (2-5) nucleus

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4
Q

What are the main functions of an eosinophil and how is it identified in histology?

A

These respond to parasites and have a role in allergy.
FUNCTIONS: chemotaxis, degranulation, cytokine production
HISTOLOGY: 3x size of RBC, nucleus has 2 lobes, large acidophilic granules

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5
Q

What are the main functions of a basophil/mast cell and how is it identified in histology?

A

Basophil = blood; Mast Cell = tissue
FUNCTIONS: degranulation, cytokine release
HISTOLOGY: lots of deep blue staining granules, bilobed nucleus

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6
Q

What are the main functions of a dendritic cell and how is it identified in histology?

A

This is the sentinel of the immune system.
FUNCTIONS: antigen presentation, phagocytosis, migration
HISTOLOGY: branched shape, convoluted central nuclei, pale staining

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7
Q

What is the innate immune system?

A

A fast, non-specific response to pathogens. It consists of soluble factors (antibacterial factors, complement) and cellular factors (scavenger phagocytes). It activates the adaptive immune system through antigen presentation

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8
Q

What are the functions of complement?

A

recruitment of inflammatory cells, opsonisation of pathogens, killing of pathogens

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9
Q

Give examples of soluble antibacterial factors

A

A soluble factor is released into fluid. Examples are lysozyme and lactoferrin

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10
Q

What is the adaptive immune system?

A

This is created in response to a pathogen.
Functions: provide antibodies to innate system to enhance pathogen clearance, provide cytokines to innate system to upregulate activity finish clearing pathogens, develop memory.
Divisions: humoral, cellular

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11
Q

What do antibodies do?

A

Functions: opsonise for phagocytosis, activate complement, neutralise toxins.
Structure: have Fab region, Fc region, light chains and heavy chain
Isotype: IgM, IgA, IgD, IgG, IgE (all their Fc regions differ)

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12
Q

How do T cells help B cells?

A

This is part of adaptive humoral immunity. Optimal B cell response needs T cell help
This is done through: clonal expansion of specific B cells, progressio to antibody secreting cells, progression to memory B cells, isotype switching to IgG/A/E, affinity maturation

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13
Q

How does the body prevent autoimmunity?

A

If B cells bind strongly to ‘self’ in the marrow it dies by apoptosis.
If T cells bind strongly to ‘self’ in the thymus it dies by apoptosis

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14
Q

What is MHC?

A

Major histocompatibility complex. These are surface proteins essential. Main function: to bind to antigens from pathogens and display them on the cell surface.
MHC 1: presents to CD8 cells, is on all nucleated cells, presents intracellular antigen
MHC 2: presents to CD4, presents extra-cellular antigens (phagocytosed), found n APCs (dendritic cells, macrophage, B cell)

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15
Q

What are the functions of CD4 and CD8 T cells

A

antigen uptake, antigen processing, MHC biosynthesis.. CD4 = helper; CD8 = killer

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16
Q

What are the organs of adaptive immunity?

A 
Primary = thymus, bone marrow (T/B cell education)
Secondary = lymph nodes, spleen, MALT [mucosa associated lymphoid tissue], BALT [bronchus associated lymphoid tissue]
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17
Q

What is the importance of the spleen in immunology?

A

It filters blood of senescent cells & blood borne pathogens

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18
Q

What is the secondary immune response?

A

Occurs the 2nd time someone is exposed to the same antigen. So memory B/T cells are already present in high frequency, preformed IgA stops the pathogen binding and preformed IgG rapidly opsonises it.

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19
Q

What is an autoimmune disease?

A

harmful inflammatory response directed against ‘self’ tissue by the adaptive immune response

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20
Q

What are pattern recognition receptors:

A

these recognise molecules found commonly in microorganisms. They respons to bacteria, fungi and yeast.
They identify PAMPs (pattern associated molecular patterns) and DAMPs (damage associated molecular pattern).
These aren’t enough due to highly pathogenic bacteria and structural failure

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21
Q

What are the functions of antibody isotypes?

A

IgM: main ab of primary immune response, low affinity, activate complement
IgG: main ab of secondary response, activate complement
IgA: antiseptic pain - present in secretions and lines epithelial surface
IgE: high affinity to mast cells. Role in allergy

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22
Q

What are the types of hypersensitivity reactions (and describe them according to the Coombes and Gell classification)?

A

Type I: immediate, atopic, IgE mediated
Type II: cytotoxic, antibody dependent, IgM/G bound
Type III: immune complex, IgM or IgG bound to soluble Ag
Type IV: cell medaited, T cells
TYpe V: receptor mediated, IgM/G bound to receptors

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23
Q

What are the characteristics of Type I hypersensitivity?

A

Specific: immediate response, increased severity with immediate challenge, mediated by IgE bound to mast cells
Responsible for most ‘allergies’ (hayfever, eczema, asthma)

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24
Q

What are the main stages in an allergic reaction?

A
  1. sensitisation
  2. mast cells prime with IgE
  3. re-exposure to antigen
  4. antigen binds to IgE associated with mast cells
  5. mast cells degranulate releasing: toxins, tryptase, pro-inflammatory cytokines, chemokines, prostaglandins, leukotrienes
  6. pro-inflammatory process stimulates and amplifies future responses
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25
Q

What is anaphylaxis?

A

severe, systemic type I hypersensitivity.
Widespread mast cell degranulation caused by systemic exposure to antigen
Vascular permeability = immediate danger (soft tissue swelling threatens airway, loss of circulatory vol causes shock)
Can be rapidly fatal

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26
Q

What are the main characteristics of Type II hypersensitivity

A

caused by binding of antibodies against human cells. Common cause of autoimmune disease.
Can result in formation of bullous pemphigoid (IgG autoantibodies bind to basement membrane zone)

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27
Q

What are the main stages in a type I hypersensitivity reaction?

A
  1. Sensitisation
  2. Opsonisation of cells
  3. Cytotoxicity (complement activation, inflammation, tissue destruction)
    [4. direct biological activation w/ activation] – only in some cases
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28
Q

What are the main characteristics of type III hypersensitivity?

A

mediated by immune complexes bound to soluble antigen.
Cause of autoimmune disease and drug allergy
Aggregate in small blood vessels (direct occlusion, complement activation, perivascular inflammation)

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29
Q

What are the main characteristics of Type IV hypersensitivity?

A

aka delayed type hypersensitivity (presents days after exposure)
Mediated by action of lymphocytes infiltrating area

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30
Q

What are the main stages in a type IV hypersensitivity reaction?

A
  1. Contact sensitising agent penetrates the skin and binds to self proteins
  2. Taken up by Langerhans cells
  3. LC haptenate the self peptide with the antigen
  4. Presents to Th1 cells which secrete cytokines
  5. Keratinocyte secrete cytokines and chemokines
  6. Products pf Th1 and keratinocytes activate macrophages –> inflammation
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31
Q

Give examples of autoimmune diseases.

A

Type 1 diabetes, myasthenia gravis, systemic autoimmune disease (RA, SLE, IBD, CTD, vasculitis)

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32
Q

Explain T1DM in an immunology context

A

selective, autoimmune destruction of pancreatic b cells
Causes profound insulin deficiency
Inflammation of islets of Langerhans precedes symptoms by years

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33
Q

Explain myasthenia gravis in an immunology context

A

A syndrome of fatigable muscle weakness

Caused by IgG against ACh receptor. The antibody blocks the receptor and prevents signal transduction

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34
Q

Explain Rheumatoid Arthritis in an immunology context

A

Multisystem autoimmune disease, chronic auto-inflammatory condition.
Symptoms: pulmonary nodules and fibrosis, pericarditis & valvular inflammation, small vessel vasculitis, soft tissue nodules, skin inflammation, weight loss, anaemia
Pathophysiology: rheumatoid factor (IgM/A against IgG Fc region - forms large immune complexes). Inflammation leads to release of PAD from inflammatory cells. Alters variety of proteins by converting alanine to citruline. Anti-citrullinated protein/peptide antibodies common

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35
Q

Give methods of treating autoimmunity

A

Steroids, inhibitors of metabolism, inhibitors of T cell function, biologic therapy

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36
Q

What is the pathogenesis of autoimmune disease?

A

genetic predisposition + environmental factors (eg infection, geographical factors, smoking).
Recognition of self antigens as foreign
Persistence of inflammatory response to develop chronic disease

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37
Q

What is the link between smoking and rheumatoid arthritis?

A

The presence of antibodies of citrullinated proteins strongly predicts RA
Citrullinated proteins develop due to action of enzymes induced during inflammation
Associated with conversion of alanine to citrulline

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38
Q

What are the broad tissue types?

A

epithelial (squamous, glandular, solid organs), connective tissue (fibrous, blood vessel, fat, muscle, bone, cartilage), haemato-lymphoid, neuro-glial, melanocytic, germ cell

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39
Q

Why might cell injury occur?

A

If the stress is too intense, long lasting or of a specific type. Cells directly affected may undergo sub-lethal cell injury or cell death. The body may respond with inflammation

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40
Q

What are some physical agents which cause cell injury/death?

A

Mechanical trauma: stricture, adhesions, hernia, criminal
Temperature extremes
Ionising radiation: causing DNA damage
Electric shock

41
Q

Discuss ischaemia

A

=reduction in blood supply to tissue
Caused by blockage of arterial supply or venous drainage
Depletion of oxygen and nutrients

42
Q

What are some mechanisms of cell injury?

A

Damage to:
Mitochondria (disrupted aerobic respiration)
Cell membrane (disrupted ion concentration)
Cytoplasm/ribosomes (disrupted enzyme/protein synthesis)
Nucleus (disrupted DNA maintenance)
Oxidative stress (from ROS)

43
Q

Discuss reversible cell injury

A

Reversible are less severe than irreversible.
They include:
Cloud swelling - osmotic disturbance
Cytoplasmic blebs, disrupted microvilli, swollen mitochondria
Fatty change - accumulation of lipid vacuoules in cytoplasm caused by disruption of fatty acid metabolism

44
Q

Discuss cell death

A

usually uncontrolled necrosis due to external stimuli (pathological, cell contents leak out)
Apoptosis = controllable cell death (cell contents don’t leak out)

45
Q

What is necrosis?

A

Unprogrammed cell death.
Histological changes: cell swelling, disruption of cell membrane, cell lysis (release of cell contents), acute inflammation

46
Q

What are the types of necrosis?

A

Coagulative: firm, tissue outline retained
Colliquitive: tissue becomes liquid, structrue lost
Caseous: combination of coagulative and colliquitive

47
Q

What are the effects of necrosis?

A

Functional - depends on tissue/organ

Inflammation: release of cell contents activates inflammation and causes damage

48
Q

What is apoptosis?

A

= Programmed cell death
Doesn’t cause inflammation but may be caused by immunological mechanisms
Morphology: cell shrinkage, chromatin condensation, membrane remains intact

49
Q

What are depositions?

A

= Abnormal accumulation of substances
Location: intracellular, extracellular, in connective tissue
Composition: endogenous, exogenous

50
Q

Explain how inflammatory changed in the vasculature and cells occur?

A 
Vascular dilation (histamine, arteriole dilation, blood flow stasis)
Neutrophil activation
Endocthelial activation
51
Q

What are the clinical signs of inflammation?

A

Redness, Swelling, Loss of Function, Heat, Pain

52
Q

What are the sequelae of acute inflammation?

A

Abscess, resolution, healing by repair, chronic inflammation

53
Q

Define chronic inflammation

A

Results from persistent tissue damage, associated with chronic inflammatory cell infiltrate, often leads to fibrosis or scarring

54
Q

What is granulomatous inflammation?

A

= presence of granulomas, collections of epithelioid macrophages and multinucleate giant cells
Types: necrotising, non-necrotising, foreign body

55
Q

What are the important stages in a post mortem?

A 
External exam
Evisceration
Organ Dissection
Return Organs into body 
Issue Death Certificate
Body Reconstruction
Release of Body
56
Q

What does Virchow’s triad involve?

A

Blood composition, vessel wall, blood flow

57
Q

What are the differences between an arterial and venous thrombus

A

ARTERIAL: white thrombus, many platelets, small amount of fibrin (reflects high flow)
VENOUS: red thrombus, many fibrin with trapped red cells (reflects indolent flow)

58
Q

What is the pathophysiology of coronary heart disease?

A

Development of atheroma - progressive narrowing & stenosis of artery - plaque rupture - acute thrombus - vascular occlusion - downstream ischaemia and infarction

59
Q

What are the differences between an AP and PA view on x rays?

A

PA: x rays penetrate through back of patient onto film. Standard projection. Heart closer to film and so less magnified
AP: x rays penetrate through front of patient onto film. Heart looks enlarged

60
Q

What are 2 types of cytology?

A

exfoliative, fine needle aspiration

61
Q

What are the stages of tissue processing?

A

formalin (fixes tissue) - alcohol (enables mixing with xylene) - xylene (clears tissue in preparation) - wax (when cooled enables structure of cellular material)

62
Q

What does FISH do?

A

Determines the presence/absence of DNA or RNA sequences.
Can localise these to specific sites.
Labelled probes hybridise to specific areas of interest following denaturation
Annealed hybrids then visualised using fluorescence microscopy

63
Q

What is a developmental anomaly?

A

A congenital defect that occurs when normal growth and differentiation of the foetus is disturbed

64
Q

What is a congenital anomaly?

A

Anomaly that exists at or before birth, regardless of the cause. Are either functional/metabolic or structural

65
Q

What is a ventricular septal defect?

A

An acyanotic congenital heart defect. It’s a left to right shunt so there’s initially no cyanosis. If left untreated pulmonary resistance may develop leading to reversal of the shunt (this would cause cyanosis)

66
Q

What is spina bifida?

A

A neural tube defect where there’s failure of the neural tube to develop or close properly

67
Q

What are some symptoms of spina bifida?

A

Muscle weakness/paralysis
Seizures
Hydrocephalus

68
Q

What is a hamartoma?

A

A malformation resulting from faulty growth of an organ (may resemble a neoplasm)
Composed of mature tissue that would normally grow at that site

69
Q

What is a chondroid hamartoma?

A

A lung lesion, benign, can mimic malignancy if endobronchial
Composed of: epithelium, cartilage, fat, smooth muscle

70
Q

Describe ectopia and give some examples

A

Abnormal location/position of an organ or tissue.
May be congenital or due to injury
EXAMPLES: ectopia cordis (heart outside body), ectopic pregnancy (implantation in wrong site), ectopic thyroid tissue

71
Q

What is diverticulum?

A

A circumscribed pouch/sac formed by herniation of lining mucosa through of an organ defect in muscular coat

72
Q

What are the effects of diverticular disease?

A

Inflammation, bleeding, perforation, fistulation.
Fibrosis (due to chronic inflammation and healing) may cause hypertrophy which may eventually lead to stenosis and then large bowel obstruction

73
Q

What is homeostasis?

A

Normal cells in a steady state

74
Q

Explain cellular adaptations to stress

A

Adaptations = reversible changes in number/size/type of cells in response to changes in the environment
Physiological adaptation = response of cells to normal stimulation
Pathological adaptations = response to stress that allow cells to modulate their structure/function and avoid injury

75
Q

What is hypertrophy?

A

Increase in the size of cells and so size of an organ

Cause: increased functional demand, hormonal stimulation

76
Q

What is hyperplasia?

A

Increase in number of cells in an organ/tissue

77
Q

What is atrophy?

A

Shrinkage in size/number of cells by loss of cell substance

Results from decreased protein synthesis and increased protein degradation

78
Q

What are some causes of atrophy?

A

loss of innervation, diminished blood supply, inadequate nutrition, ageing

79
Q

What is metaplasia?

A

Reversible change from one fully differentiated cell type into another

80
Q

What is neoplasia?

A

Abnormal tissue mass with excessive/uncoordinated growth compared to adjacent normal tissue

81
Q

What are the differences between benign and malignant neoplasms?

A 
Benign = doesn't invade adjacent tissue/spread, well circumscribed 
Malignant = invades surrounding tissue, metastasises, not well circumscribed
82
Q

What is the importance of grading differentiation?

A

Figuring out site of origin in metastatic disease, prognosis and treatment

83
Q

What is tumour stage based on?

A

Size of primary tumour, extent of invasion into surrounding tissue, spread to regional lymph nodes, presence of metastases

84
Q

What is carcinoma in situ?

A

Full thickness epithelial dysplasia extending from basement membrane to surface of epithelium

85
Q

What is local invasion?

A

Growth into surrounding tissues by direct extension/expansion

86
Q

How can a tumour metastasis?

A

Lymphatic, haematogenous, transcoelomic

87
Q

What are some possible local effects of a neoplasm?

A

Space occupying, ulceration, pain, induce fibrosis

88
Q

How do you diagnose a neoplasm?

A

history, imaging (XR, US, CT, MRI), tumour markers, biopsy, bloods

89
Q

What does suppurative mean?

A

The discharge or formation of pus

90
Q

What is an abscess?

A

A collection of inflammatory cells

91
Q

What are some complications of acute (suppurative) appendicitis?

A

Gangrenous appendicitis, appendiceal perforation, abscess formation, acute purulent peritonitis

92
Q

What is an ulcer?

A

Loss of integrity of epithelial surface/mucosa

93
Q

What is a polyp?

A

Simple area of mucosa raised above adjacent surface

94
Q

What pathological process are granulomas a sign of?

A

Chronic inflammation

95
Q

What are some complications of Crohn’s disease?

A 
Chronic terminal ileal inflammation
Ulceration
Haemorrhage 
Perforation 
Fistula 
Fibrosis 
Obstruction 
Adhesions
96
Q

How are immune cells organised within the structure of a lymph node?

A

Immune cells do not tend to stick to each other and so are usually well spread out

97
Q

What is the most common tumour in neck lymph nodes?

A

metastatic squamous cell carcinoma

98
Q

What does normal breast tissue look like in histology?

A

asipose tissue, epithelial ducts, acini, fibrous connective tissue in background

MBChB Phase 3 (15 decks)

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