PBL 1 Flashcards

1
Q

What does anaphylaxis present as?

A

oedema to lips and neck, hypotension, severe bronchoconstricton, tachycardia

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2
Q

what are the 2 types of histamine blockers?

A

first generation (have high lipid solubility so can cross blood-brain barriers) or second generation (have far less lipid solubility so have less cognitive and antimuscarinic side effects)

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3
Q

how do histamine antagonists work?

where are histamine receptors mostly found?

A

they reversibly inhibit H1 receptors

predominantly found on endothelial cells, smooth muscle cells, sensory nerve endings and the brain.

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4
Q

what is an example of the natural glucocorticoid we produce at the adrenal gland?

A

cortisol

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5
Q

how are steroid hormones transported around in the blood?

A

by transcortin

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6
Q

what are indications for glucocorticoids?

A

autoimmune diseases, allergies, asthma, adrenal insufficiency, cancer, heart failure and skin conditions

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7
Q

what is the problem with long-term use of glucocorticoids?

A

it can cause immunosuppression and can lead to Cushing’s syndrome, it can also cause osteoporosis, weight gain, fluid retention

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8
Q

how can long term use of glucocorticoids cause osteoporosis?

A

it inhibits osteoblast activity and promotes osteoclast activity so more bone is broken down than made

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9
Q

how do we treat anaphylaxis?

A

Epinephrine (adrenaline) to reduce your body’s allergic response.
Oxygen, to help you breathe.
Intravenous (IV) antihistamines and cortisone to reduce inflammation of your air passages and improve breathing.
A beta-agonist (such as albuterol) to relieve breathing symptoms.

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10
Q

what is self-tolerance?

A

the ability of the immune system to recognise self-produced antigens as a non-threat.

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11
Q

why do we not normally develop immune responses to self-antigens?

A

in the bone marrow, B cells randomly get their antibody as its encoded by random re-arrangement of pre-existing gene segments. if it reacts to a self-protein then it will cause changes to the cell which will lead to cell death.

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12
Q

what are Autoreactive lymphocytes?

A

lymphocytes which have receptors against self-antigens

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13
Q

what is central tolerance?

A

also known as negative selection- the process of eliminating any developing T or B lymphocytes that are reactive to self within the primary lymphoid organs

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14
Q

what is peripheral tolerance?

A

ensure that self-reactive T and B cells which escaped central tolerance do not cause autoimmune disease. - this negative selection occurs at the site of antigen-recognition sites

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15
Q

why could failure of central tolerance occur?

A

some weakly self-reactive clones survive the negative selection
molecular mimicry
inappropriate expression of MHC 2 molecule can sensitise auto-reactive T cells
self-antigens not being expressed where negative selection occurs

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16
Q

describe the process of hyposensitisation?

A

administration of gradually increasing quantities of specific allergens to patients until a dose is reached that is effective in reducing severity from natural exposure. it does this by directing the immune response away from humeral immunity and towards cellular immunity

17
Q

describe how B and T cells can also develop self-tolerance via positive selection?

A

pre-cells express receptors that interact with self-MHC proteins on epithelial cells. these cells survive, those that cannot recognise it will undergo apoptosis

18
Q

what is anergy?

A

absence of the normal immune response to a particular antigen or allergen

19
Q

what is an autoantibody?

A

an antibody produced by the immune system that is directed against one or more of the individual’s own proteins

20
Q

outline some of the ways that autoantibodies can cause disease?

A
mimic hormone stimulation of receptor
blockade of neural transmission 
induction of altered signalling
cell lysis
uncontrolled neutrophil action
induction of inflammation at site of autoantibody binding
21
Q

what does urticaria (hives) look like?

A

red spots or raised red patches. it is often itchy and can feel like a sting or burn

22
Q

what happens in Graves disease?

A

autoantibodies mimic thyroid stimulating hormone and stimulate secretion of thyroid hormones

23
Q

what happens in myasthenia gravis?

A

autoantibodies bind to and block ACh receptors causing muscle weakness

24
Q

what happens in type 1 diabetes mellitus?

A

T cells attack the insulin-producing pancreatic beta cells

25
Q

what happens in multiple sclerosis?

A

T cells attack myelin sheaths around axons of neurones

26
Q

what are the 2 ways in which autoimmune disease can come about?

A

autoantibodies

mis-directed T cells