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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
What is anaphylaxis?
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
26
What are the main characteristics of Type II hypersensitivity
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)
27
What are the main stages in a type I hypersensitivity reaction?
1. Sensitisation 2. Opsonisation of cells 3. Cytotoxicity (complement activation, inflammation, tissue destruction) [4. direct biological activation w/ activation] -- only in some cases
28
What are the main characteristics of type III hypersensitivity?
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)
29
What are the main characteristics of Type IV hypersensitivity?
aka delayed type hypersensitivity (presents days after exposure) Mediated by action of lymphocytes infiltrating area
30
What are the main stages in a type IV hypersensitivity reaction?
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
31
Give examples of autoimmune diseases.
Type 1 diabetes, myasthenia gravis, systemic autoimmune disease (RA, SLE, IBD, CTD, vasculitis)
32
Explain T1DM in an immunology context
selective, autoimmune destruction of pancreatic b cells Causes profound insulin deficiency Inflammation of islets of Langerhans precedes symptoms by years
33
Explain myasthenia gravis in an immunology context
A syndrome of fatigable muscle weakness | Caused by IgG against ACh receptor. The antibody blocks the receptor and prevents signal transduction
34
Explain Rheumatoid Arthritis in an immunology context
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
35
Give methods of treating autoimmunity
Steroids, inhibitors of metabolism, inhibitors of T cell function, biologic therapy
36
What is the pathogenesis of autoimmune disease?
genetic predisposition + environmental factors (eg infection, geographical factors, smoking). Recognition of self antigens as foreign Persistence of inflammatory response to develop chronic disease
37
What is the link between smoking and rheumatoid arthritis?
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
38
What are the broad tissue types?
epithelial (squamous, glandular, solid organs), connective tissue (fibrous, blood vessel, fat, muscle, bone, cartilage), haemato-lymphoid, neuro-glial, melanocytic, germ cell
39
Why might cell injury occur?
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
40
What are some physical agents which cause cell injury/death?
Mechanical trauma: stricture, adhesions, hernia, criminal Temperature extremes Ionising radiation: causing DNA damage Electric shock
41
Discuss ischaemia
=reduction in blood supply to tissue Caused by blockage of arterial supply or venous drainage Depletion of oxygen and nutrients
42
What are some mechanisms of cell injury?
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
Discuss reversible cell injury
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
Discuss cell death
usually uncontrolled necrosis due to external stimuli (pathological, cell contents leak out) Apoptosis = controllable cell death (cell contents don't leak out)
45
What is necrosis?
Unprogrammed cell death. Histological changes: cell swelling, disruption of cell membrane, cell lysis (release of cell contents), acute inflammation
46
What are the types of necrosis?
Coagulative: firm, tissue outline retained Colliquitive: tissue becomes liquid, structrue lost Caseous: combination of coagulative and colliquitive
47
What are the effects of necrosis?
Functional - depends on tissue/organ | Inflammation: release of cell contents activates inflammation and causes damage
48
What is apoptosis?
= Programmed cell death Doesn't cause inflammation but may be caused by immunological mechanisms Morphology: cell shrinkage, chromatin condensation, membrane remains intact
49
What are depositions?
= Abnormal accumulation of substances Location: intracellular, extracellular, in connective tissue Composition: endogenous, exogenous
50
Explain how inflammatory changed in the vasculature and cells occur?
``` Vascular dilation (histamine, arteriole dilation, blood flow stasis) Neutrophil activation Endocthelial activation ```
51
What are the clinical signs of inflammation?
Redness, Swelling, Loss of Function, Heat, Pain
52
What are the sequelae of acute inflammation?
Abscess, resolution, healing by repair, chronic inflammation
53
Define chronic inflammation
Results from persistent tissue damage, associated with chronic inflammatory cell infiltrate, often leads to fibrosis or scarring
54
What is granulomatous inflammation?
= presence of granulomas, collections of epithelioid macrophages and multinucleate giant cells Types: necrotising, non-necrotising, foreign body
55
What are the important stages in a post mortem?
``` External exam Evisceration Organ Dissection Return Organs into body Issue Death Certificate Body Reconstruction Release of Body ```
56
What does Virchow's triad involve?
Blood composition, vessel wall, blood flow
57
What are the differences between an arterial and venous thrombus
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
What is the pathophysiology of coronary heart disease?
Development of atheroma - progressive narrowing & stenosis of artery - plaque rupture - acute thrombus - vascular occlusion - downstream ischaemia and infarction
59
What are the differences between an AP and PA view on x rays?
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
What are 2 types of cytology?
exfoliative, fine needle aspiration
61
What are the stages of tissue processing?
formalin (fixes tissue) - alcohol (enables mixing with xylene) - xylene (clears tissue in preparation) - wax (when cooled enables structure of cellular material)
62
What does FISH do?
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
What is a developmental anomaly?
A congenital defect that occurs when normal growth and differentiation of the foetus is disturbed
64
What is a congenital anomaly?
Anomaly that exists at or before birth, regardless of the cause. Are either functional/metabolic or structural
65
What is a ventricular septal defect?
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
What is spina bifida?
A neural tube defect where there's failure of the neural tube to develop or close properly
67
What are some symptoms of spina bifida?
Muscle weakness/paralysis Seizures Hydrocephalus
68
What is a hamartoma?
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
What is a chondroid hamartoma?
A lung lesion, benign, can mimic malignancy if endobronchial Composed of: epithelium, cartilage, fat, smooth muscle
70
Describe ectopia and give some examples
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
What is diverticulum?
A circumscribed pouch/sac formed by herniation of lining mucosa through of an organ defect in muscular coat
72
What are the effects of diverticular disease?
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
What is homeostasis?
Normal cells in a steady state
74
Explain cellular adaptations to stress
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
What is hypertrophy?
Increase in the size of cells and so size of an organ | Cause: increased functional demand, hormonal stimulation
76
What is hyperplasia?
Increase in number of cells in an organ/tissue
77
What is atrophy?
Shrinkage in size/number of cells by loss of cell substance | Results from decreased protein synthesis and increased protein degradation
78
What are some causes of atrophy?
loss of innervation, diminished blood supply, inadequate nutrition, ageing
79
What is metaplasia?
Reversible change from one fully differentiated cell type into another
80
What is neoplasia?
Abnormal tissue mass with excessive/uncoordinated growth compared to adjacent normal tissue
81
What are the differences between benign and malignant neoplasms?
``` Benign = doesn't invade adjacent tissue/spread, well circumscribed Malignant = invades surrounding tissue, metastasises, not well circumscribed ```
82
What is the importance of grading differentiation?
Figuring out site of origin in metastatic disease, prognosis and treatment
83
What is tumour stage based on?
Size of primary tumour, extent of invasion into surrounding tissue, spread to regional lymph nodes, presence of metastases
84
What is carcinoma in situ?
Full thickness epithelial dysplasia extending from basement membrane to surface of epithelium
85
What is local invasion?
Growth into surrounding tissues by direct extension/expansion
86
How can a tumour metastasis?
Lymphatic, haematogenous, transcoelomic
87
What are some possible local effects of a neoplasm?
Space occupying, ulceration, pain, induce fibrosis
88
How do you diagnose a neoplasm?
history, imaging (XR, US, CT, MRI), tumour markers, biopsy, bloods
89
What does suppurative mean?
The discharge or formation of pus
90
What is an abscess?
A collection of inflammatory cells
91
What are some complications of acute (suppurative) appendicitis?
Gangrenous appendicitis, appendiceal perforation, abscess formation, acute purulent peritonitis
92
What is an ulcer?
Loss of integrity of epithelial surface/mucosa
93
What is a polyp?
Simple area of mucosa raised above adjacent surface
94
What pathological process are granulomas a sign of?
Chronic inflammation
95
What are some complications of Crohn's disease?
``` Chronic terminal ileal inflammation Ulceration Haemorrhage Perforation Fistula Fibrosis Obstruction Adhesions ```
96
How are immune cells organised within the structure of a lymph node?
Immune cells do not tend to stick to each other and so are usually well spread out
97
What is the most common tumour in neck lymph nodes?
metastatic squamous cell carcinoma
98
What does normal breast tissue look like in histology?
asipose tissue, epithelial ducts, acini, fibrous connective tissue in background

MBChB Phase 3 (15 decks)

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