Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2 > Pathology > Flashcards

Pathology Flashcards

1
Q

What is the role of the autopsy?

A

Who was the deceased?
When did they die?
Where did they die?
How did they come about their death?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the structure of an autopsy?

A
  1. History
  2. External examination
  3. Evisceration
  4. Internal examination
  5. Reconstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Name the three types of death referred to the coroner?

A

Presumed Natural (Cause not known
Presumed Iatrogenic
(Caused by care or surgery)
Presumed Unnatural

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Define acute inflammation

A

Initial and transient series of tissue reactions to injury of short duration that normally resolves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Define chronic inflammation

A

Subsequent and prolonged tissue reactions following initial response (Sequel to acute that may never resolve)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 5 cells involved in inflammation?

A 
Neutrophil polymorphs 
Macrophages 
Lymphocytes 
Endothelial cells 
Fibroblasts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the roles of neutrophil in inflammation

A
  1. Short lived - first cells on scene
  2. Cytoplasmic granules full of bacteria killing enzymes
  3. Die at the scene of inflammation
  4. Release chemicals that attract other inflammatory cells (Macrophages)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the role of macrophages in inflammation

A
  1. Long lived (Weeks to months)
  2. Phagocytic
  3. Ingest bacteria and debris
  4. May carry debris away
  5. Present antigens to lymphocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the role of lymphocytes in inflammation

A
  1. long lived
  2. Produce chemicals that attract other inflammatory cells
  3. Immunological memory for past infections and antigens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the role of endothelial cell in inflammation

A
  1. Line capillary blood vessels in areas of inflammation
  2. Become sticky in areas of inflammation so inflammatory cells adhere to them
  3. Become porous to allow inflammatory cells to pass into tissues
  4. Grow into areas of damage to form new capillary vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the role of fibroblasts in inflammation

A

Long lived cells that form collagen in areas of chronic inflammation and repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Name the 6 causes of acute inflammation

A
  1. Microbial Infections
  2. Hypersensitivity reactions
  3. Physical agents (Trauma, ionising radiation, heat and cold)
  4. Chemicals (Corrosive, acids, alkalis and reducing agents)
  5. Bacterial toxins
  6. Tissue necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Define hypersensitivity Reactions

A

Reaction which occurs when an altered state of immunological responsiveness causes an inappropriate or excessive immune reaction that damages tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the 5 characteristic of acute inflammation

A
  1. Redness (Dilation of small blood vessels) Rubber
  2. Heat (Due to increased blood flow) Calor
  3. Swelling (oedema from accumulation of fluid in the extravascular space) Tumor
  4. Pain (Due to tissue distortion, pus under pressure in abscess cavity and chemical mediators that induce pain (Bradykinin, serotonin and prostaglandins) Dolor
  5. Loss of function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Name the three processes involved in the acute inflammatory response

A
  1. Change in vessel calibre (width) and increased flow
    - precapillary sphincters regulate flow through the capillary bed
  2. Increased vascular permeability and fluid exudate formation
  3. Formation of cellular exudate due to increased capillary hydrostatic pressure and escape of plasma proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Name the 4 outcomes of acute inflammation

A 
1. Resolution 
= complete restoration of tissue to normal 
2. Suppuration
= formation of pus 
3. Organisation
= tissue replaced by granulation tissue 
4. Progression to chronic inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the 4 causes of chronic inflammation?

A
  1. Primary chronic inflammation
  2. Transplant rejection
  3. Progression from acute inflammation
  4. Recurrent episodes of acute inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the features of chronic inflammation?

A
  • Cellular infiltrate consists of lymphocytes, plasma cells and macrophages
  • Macrophages may form multinucleate giant cells
  • Neutrophils are scarce
  • Continued tissue destruction - necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is a granuloma?

A

Aggregate of epithelioid histiocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Name some examples of granulomatous inflammation?

A
  1. Tuberculosis
  2. Leprosy
  3. Crohns disese
  4. Sarcoidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What causes histolytic giant cells to form?

A

Accumulation of particulate matter that is indigestible by macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What do fibroblasts produce?

A

Collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Name 6 types of cell that are capable of regeneration

A 
Hepatocytes 
Pneumocytes 
All blood cells 
Gut epithelium 
Skin epithelium 
Osteocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Name 2 types of cell that do not regenerate

A

Myocardial cells

Neurones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Define thrombus

A

Solid mass of blood constituents formed within an intact vascular system during life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Name 3 factors that pre-dispose thrombosis?

A

Change in the vessel wall = endothelial damage
Change in the constituents of blood = more platelets
Change in the blood flow = laminar to turbulent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe the formation of thrombus in veins

A

Slow blood flow in veins as not pulsatile so blood in stasis - if endothelial wall becomes sticky then thrombus forms but more slowly - most likely to form at valves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the 4 potential outcomes once a thrombus has formed

A
  1. lysis and resolution
  2. Organisation = scar tissue by invasion of macrophages which clear away the thrombus and fibroblasts and replane it with collagen
  3. Recanalise = intimal cells of vessel on which the thrombus lies proliferate, capillaries grow through it and fuse to form larger vessels
  4. Embolism = bit breaks off
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Why does aspirin prevent thrombus formation

A

Because it is an anti platelet drug so prevents platelets binding to exposed collagen in endothelial wall and prevents further collagen aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Define Embolus

A

Mass of material in the vascular system that is able to become lodged within a vessel and block its lumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Define ischaemia

A

Reduction in blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Define infarction

A

Death of cells due to reduced blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Describe what happens in reperfusion injury

A

Limited blood supply has caused cells to become damaged but they have not died. If blood flow is restored to the cells then they may start to produce superoxide ions that cause damage to the cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Are macrophages associated with acute or chronic infection?

A

Chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Are plasma cells associated with acute or chronic infection?

A

Chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Are neutrophil polymorphs associated with acute or chronic infection?

A

Acute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Are lymphocytes associated with acute or chronic infection

A

Chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Are giant cells associated with acute or chronic infection

A

Chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Define organisation

A

The repair of specialised tissues by the formation of a fibrous scar which forms due to the production of granulation tissue and removal of dead tissue by phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is granulation tissue made of?

A

Capillary loops and myofibroblasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is a granuloma

A

An aggregate of epithelioid histiocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Describe the process of repair

A
  1. Capillary endothelial cells proliferate into the area forming a series of loops
  2. Fibroblasts are stimulated and divide and secrete collagen
  3. Fibroblasts acquire muscle filaments to form myofibroblasts
  4. Capillary endothelial cells and the myofibroblasts = granulation tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Describe the process of healing by first intention

A
  1. cut blood vessels either side are occluded by thrombosis and fibrin deposition binds the two sides
  2. Coagulated blood on surface forms a scab to keep wound clean
  3. Capillaries proliferate to bridge gap and fibroblasts secrete collagen
  4. elastic network of dermis fails to reconnect
  5. Basal epidermal cells proliferate over the gap
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

When does healing by second intention occur?

A

When there is tissue loss or the wound margins aren’t apposed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Describe the characteristics of healing by second intention

A
  1. Phagocytosis to remove debris
  2. Granulation tissue to fill in the defects and repair specialised tissue
  3. Epithelial regeneration to cover the surface
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Describe the process of mucosal alteration

A
  1. damaged mucosa replaced from margins
  2. Damaged blood vessels bleed and surface becomes covered with fibrin layer
  3. Macrophages remove dead tissue by phagocytosis
  4. Granulation tissue produced in ulcer base as capillaries and myofibroblasts proliferate
  5. Mucosa regenerates at margins and spreads across ulcer floor
  6. Fibrous scar tissue replaces the muscle and distorts the stomach upon contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Define end artery

A

Tissues that only have one arterial supply and such if this is blocked there is no possibility of collateral supplies taking over

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What two things determine whether ischaemia is reversible or not

A
  1. Duration of the ischaemic period

2. Metabolic demands of the tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Name the 5 macroscopic appearances of chronic inflammation

A
  1. Chronic ulcer - breach of mucosa with a base lined by granulation tissue with fibrous tissue extending through the muscle layers of the wall
  2. Chronic abscess cavity
  3. Thickening of the wall of a hollow viscus by fibrous tissue
  4. Granulomatous inflammation
  5. Fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What do B lymphocytes become?

A

On contact with the antigen they become plasma cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What do T lymphocytes become

A
  1. On contact with antigen they produce cytokines which causes recruitment and activation of other cells
  2. Responsible for cell mediated immunity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is granulation tissue?

A

Important component of healing that comprises small blood vessels in a connective tissue matrix with myofibroblasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the causes of chronic inflammation

A

Primary chronic inflammation
Transplant rejection
Progression/recurrent episode of acute inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Define atherosclerosis

A

Disease characterised by the formation of elevated lesions in the intimal of large and medium sized arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the earliest lesion of an atherosclerotic plaque?

A

Fatty streak

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is a fatty streak?

A

Yellow linear elevation of the intimal lining composed of masses of lipid laden macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Where do fatty streaks occur in the body?

A

In the systemic part of the body which is under higher pressure, not in the pulmonary part because these arteries are under low pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Where do atherosclerotic plaques form in the body?

A

Form at arterial branching points and bifurcations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are the components of an atherosclerotic plaque?

A 
Central lipid cholesterol core
Fibrous tissue 
Collagen connective tissue cap
Bordered by foam cells 
Lymphocytes (Chronic inflammation)
Smooth muscle cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the causes of atherosclerosis

A 
Hypercholesterolaemia 
Smoking (Nicotine free radicals)
Hypertension (Increased shearing forces)
Diabetes (If poorly controlled) (Glucose damages endothelium)
Hyperlipidaemia (Lipid damages endothelial cells)
Low socioeconomic status]
Male gender 
Increasing age
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Describe the formation of an atherosclerotic plaque

A
  1. Endothelial cell damage leading to increase expression of cell adhesion molecules and increased permeability to LDL
  2. Inflammatory cells and lipids enter intimal layer and form plaques
  3. Foam cells phagocytose LDL and die through apoptosis and spill their lipid content in enlarging lipid core
  4. Plaques contains capillaries that can burst forming thrombi and haemorrhage causing plaque to increase in size
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are the complications of atherosclerosis?

A

Cerebral/myocardial infarct
Abdominal aortic aneurysm leading to rupture or dilation
Peripheral vascular disease –> Gangrene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Define apoptosis

A

Programmed cell death - defined sequence of intracellular events that lead to the removal of the cell without the release of products harmful to surrounding cells (enzymatic digestion of nuclear and cytoplasmic contents followed by phagocytosis of breakdown products)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are the external signals that initiate apoptosis?

A

Detachment from extracellular matrix
Withdrawal of growth factors
Specific signals from other cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What are the intracellular signals that initiate apoptosis?

A

DNA damage

Failure to conduct cell division

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are the characteristics of apoptosis?

A
  1. Switch in cell determines time to die
  2. Release internal enzymes that cause nucleus to shrivel, organelles moved to membrane bound vesicles
  3. Macrophages eat this and no scar tissue remains
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What causes DNA damage and triggers apoptosis?

A

cosmic rays and UV light

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Which gene identifies DNA damage, induces cell cycle arrest and triggers the chemicals that switch on apoptosis

A

P53

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What enzymes does p53 cause to be released to trigger apoptosis

A

Caspase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the affect of BCL2 on apoptosis?

A

Inhibiting caspases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What is the affect of Bax proteins on apoptosis?

A

Promote caspases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is the affect of FAS ligand on apoptosis?

A

Stimulates caspases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Why is apoptosis important in development?

A
  1. Interdigital cell death to separate fingers
  2. Cell death to remove redundant tissue following palatine fusion during mouth of the roof development
  3. Cell death to close the dorsal neural tube
  4. Urachus cell death to remove redundant tissue between bladder and umbilicus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Define necrosis

A

Unintended cell death in response to cellular injury - traumatic process which induces inflammation and repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Give 5 examples of necrosis

A 
Toxic spider venom 
Frost bite 
Cerebral infarction
Avascular necrosis of bone (Head of the femur and scaphoid)
Pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Define hypertrophy

A

Increase in the size of the tissue due to increases in the size of constituent cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Define hyperplasia

A

Increase in the size of a tissue due to increases in the numbers of constituent cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Give some examples of hyperplasia

A

Prostate
Endometrial
Endothelial
Neuronal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

When does a mix of hyperplasia and hypertrophy occur

A

In the uterus where the placental cells increase in size but also divide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Define atrophy

A

Decrease in the size of tissue caused by a decrease in the number of the constituent cells or a decrease in their size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Define metaplasia

A

Change in the differentiation of a cell from one fully differentiated type to a different fully differentiated type

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Give two examples of metaplasia

A

Normally the lining of the bronchius is ciliated columnar epithelium but heavy smoking causes this epithelium to change to simple squamous

Barrett’s oesophagus - cells at the Lower end of the oesophagus change from stratified squamous epithelium to columnar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Define dysplasia

A

Imprecise term for morphological changes seen in the cells progression to becoming cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Why does the incidence of disease increase with age?

A
  1. Probability of contact with an environmental cause increases with duration of exposure risk
  2. Disease may depend on the cumulative effects of one or more environmental agent
  3. Impaired immunity with ageing increases susceptibility to some infections
  4. Latent interval between the exposure and appearance of symptoms may take decades
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Define autosomal dominant

A

One copy of the gene is required for an individual to be affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Define autosomal recessive

A

Both copies of the paired gene are required to be abnormal for expression of the disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Define acquired disease

A

Caused by non genetic environmental factors ie. foetal alcohol syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Name 5 mechanisms that cause cellular damage

A

Protein cross linking
DNA cross linking
DNA mutations that functionally alter the genes
Mitochondrial damage
Defects in oxygen and nutrient utilisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What is the importance of telomeric shortening?

A

Telomere is non-coding region at end of chromosome - this sequence is not fully copied prior to mitosis
As the cells divide the telomeres get shorter and shorter to the point the cell can no longer divide further

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Name 6 age related conditions

A
  1. Dermal elastosis - UVB hight causes collagen protein cross linking = wrinkles
  2. Osteoporosis = loss of bone matrix due to lack of oestrogen
    increased resorption and decreased formation
  3. Cataracts = UVB light crosslinks proteins making them opaque
  4. Senile dementia - Brain atrophy
  5. Sarcopenia = lack of muscle due to decreased growth hormone, decreased testosterone and increased catabolic cytokines
  6. Deafness as the cilia in ears aren’t replaced - loss of hair cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What is the name of the main effector cell in acute inflammation

A

Neutrophil polymorph

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What is the name of the cell that produces collagen in fibrous scarring?

A

Fibroblast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q 
Which of the following is an example of acute inflammation 
Glandular fever 
Leprosy 
Appendicitis 
Tuberculosis
A

Appendicitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What are the crystals deposited in joints in gout?

A

Uric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q 
In which of the following does granulatomous inflammation occur?
Crohns disease 
Acute appendicitis 
Infectious mononucleosis 
Lobar pneumonia
A

Crohns disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What Is the specific name of calcification in diseased as opposed to normal tissues?

A

Stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q 
Which of the following is a chronic inflammatory process from its start?
Appendicitis 
Cholecystitis 
Infectious mononucleosis 
Lobar Pneumonia
A

Infectious mononucleosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What is the name given to cells that produce antibodies?

A

Plasma cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What is the main cause of basal cell carcinoma?

A

Ultra violet light damaging the skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What is the treatment for basal cell carcinoma and why is it the most appropriate option

A

Complete local excision because BCC only invades the skin locally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What is leukaemia?

A

Tumour of the WBC’s so WBC circulate round the body and so will any tumours of the white blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What are some of the symptoms of leukaemia?

A 
Weight loss
Fever
Frequent infections 
Muscular weakness 
Pain and tenderness in the joints and bones 
Fatigue 
Loss of appetite 
Swelling of lymph nodes 
Enlarged spleen 
Night sweats 
Easy bleeding and bruising 
Purple patches or spots
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What is the treatment for leukaemia?

A

Chemotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Which cancers most commonly spread to the bone?

A

Breast, prostate, lung, thyroid and kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What is adjuvant therapy?

A

Extra treatment given after surgical resection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Name two ways to confirm a diagnosis of breast cancer?

A

Mammogram

Biopsy using core needle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

How can you determine if breast cancer has spread to the axillary lymph nodes?

A

Ultrasound of the axilla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

How can you check if breast cancer has spread to the rest of the body?

A

Bone and CT scan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What are the adjuvant therapies for breast cancer following lumpectomy?

A

Anti-oestrogen therapy
Radiotherapy
Herceptin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Define carcinogenesis

A

Transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Define carcinogen

A

agents known or suspects to cause tumours by acting on DNA (Mutagenic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What experimental evidence can be used to determine if something is a carcinogen?

A

Incidence of tumours in laboratory animals
Cell/Tissue cultures
Mutagenicity testing in bacterial cultures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What are the 5 classes of carcinogens?

A
  1. Chemical
  2. Viral
  3. Ionising and non-ionising radiation
  4. Biological agents = Hormones, parasites and mycotoxins
  5. Miscellaneous
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What sort of cancers is exposure to polycyclic aromatic hydrocarbons associated with?

A

Lung cancer

Skin cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What sort of cancer is exposure to aromatic amines associated with

A

Bladder cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What sort of cancer is exposure to nitrosamines associated with

A

Gut cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What sort of cancer is exposure to alkylating agents associated with?

A

Leukaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Increase exposure to UVA and UVB in ultraviolet light increases the risk of what conditions?

A

Basal cell carcinoma
Melanoma
Squamous cell carcinoma
Xeroderma pigmentosum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Name three classes of biological agent that are carcinogens

A

Hormones
Mycotoxins
Parasites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Name 2 types of hormone that are considered carcinogens and the cancers they are associated with

A

Increased oestrogen = increased mammary/endometrial cancer

Anabolic steroids = hepatocellular carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Name a type of mycotoxin that is a carcinogen and what type of cancer it is associated with

A

Aflatoxin B1 –> Hepatocellular carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Name two types of parasites that are considered carcinogens and the cancers they are associated with

A

Chlonorchis sinensis –> Cholangiocarcinoma

Shistosoma –> Bladder cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Name 2 types of miscellaneous carcinogens and the cancers they are associated with?

A

Asbestos = mesothelioma, asbestosis, lung cancer

Metals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Name some host factors that may determine susceptibility to carcinogenesis

A 
Race
Diet 
Constitutional factors = Age, inherited predisposition, gender
Premalignant lesions
Transplacental exposure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Define tumour

A

Any abnormal swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Define Neoplasm

A

A lesion resulting from the autonomous or relatively autonomous abnormal growth of cells which persists after the initiating stimulus has been removed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Which processes initiate the formation of neoplasms

A

Accumulation of genetic alterations such as mutations, translocations, rearrangements, amplifications and epigenetic changes that enable the cell to escape normal growth regulatory mechanisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

What are the two main components of a neoplasm?

A
  1. Neoplastic cells - synthesise and secrete collagen, mucin and keratin that accumulate in the tumour
  2. Stroma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Where are neoplastic cells derived from

A

Monoclonal nucleated cells that have a growth pattern similar to the parent cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Where is the purpose of the stroma component of a neoplasm?

A

mechanical support
Intracellular signalling
Nutrition to neoplastic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

How is the stroma component of a neoplasm formed?

A

Connective tissue fibroblast proliferation by growth factors from the tumour cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Which growth factor induces angiogenesis?

A

Vascular endothelial growth factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

What is the maximum size of a tumour before angiogenesis occurs and why is the case?

A

1-2mm because without blood vessels its supply of nutrients is limited due to the constraints of effective diffusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What are the 6 types of tumour shape?

A 
Sessile 
Polypoid 
Papillary 
Exophytic/fungating 
Ulcerate 
Annular
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Give two reasons why we classify neoplasms?

A

To determine the appropriate treatment

To provide prognostic information

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

What are the two main ways of classifying neoplasms?

A 
Behavioural = benign or malignant 
Histogenetic = cell of origin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

What are the characteristics of a benign neoplasm?

A 
Localised and non-invasive 
Slow growth rate 
Low mitotic activity 
Close resemblance to the normal tissue 
Encapsulated by thin layer of connective tissue 
Nuclear morphometry normal 
Necrosis rare 
Ulceration rare 
Growth of mucosal surfaces often exophytic (Upwards an outwards from surface)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Why should we worry about benign neoplasms?

A
  1. Pressure on adjacent structures - lead to necrosis
  2. Obstruct flow
  3. Production of hormones (benign thyroid tumour causing thyrotoxicosis)
  4. Transformation to malignant neoplasm
  5. Anxiety to patient
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

What are the characteristics of a malignant tumour?

A 
Invasive 
Metastases 
Rapid growth compared to benign 
Do not resemble the parent tissue as much as benign neoplasms do 
Poorly defined or irregular border 
Hyperchromatic nuclei 
Pleomorphic nuclei
Increased mitotic activity 
necrosis common 
Ulceration common 
Growth on mucosal surfaces is endophytic (Inwards and downwards from surface)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

Why should we worry about malignant neoplasms?

A

Destruction of adjacent tissues
Metastases leading to formation of secondary tumours
Blood loss from ulcerated surfaces
Obstruction of blood flow
Hormone production (ACTH and ADH)
Paraneoplastic effects - symptoms not just due to cancer at that site (Weight loss)
Anxiety and pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

Why do malignant tumours show central necrosis?

A

Inadequate perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Define histogenesis?

A

Specific cell of origin of a tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

What neoplasm arises from epithelial cells

A

Carcinomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

What neoplasm arises from connective tissues?

A

Sarcomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

What neoplasm arises from lymphoid/haemopoietic organs

A

Lymphomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

What is a papilloma?

A

A benign tumour of non-glandular, non-secretory epithelium such as squamous cell papilloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

What is an adenoma?

A

A benign tumour of glandular or secretory epithelium such as colonic adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

What is a carcinoma?

A

A malignant epithelial neoplasm of non-glandular epithelial cells ie. transitional cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

What is an adenocarcinoma?

A

A malignant epithelial neoplasm of glandular epithelium such as adenocarcinoma of the breast or prostate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

Name 7 types of benign connective tissue neoplasm?

A
  1. Lipoma = adipocytes
  2. Chondroma = cartilage
  3. Osteoma = bone
  4. Angioma = vascular
  5. Rabdomyoma = striated muscle
  6. Leiomyoma = Smooth muscle
  7. Neuroma = benign neoplasm of nerves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

Name 6 types of malignant connective tissue neoplasm

A
  1. Liposarcoma = adipocytes
  2. Rhabdomyosarcoma = striated muscle
  3. Leiomyosarcoma = smooth muscle
  4. Chondrosarcoma = cartilage
  5. Osteosarcoma = bone
  6. Angiosarcoma = blood vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

What is a melanoma?

A

Malignant neoplasm of melanocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

What is a mesothelioma?

A

Malignant tumour of mesothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

What is a lymphoma?

A

Malignant neoplasm of lymphoid cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

What is Burkitts lymphoma

A

B-cell lymphoma associated with Epstein Barr virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

What is Ewings sarcoma?

A

Malignant tumour of the bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

What is Grawitz tumour?

A

Renal cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

What is Kaposi sarcoma?

A

Malignant neoplasm derived from vascular endothelium commonly associated with AIDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

What are the three ways of grading a malignancy?

A

Low grade = looks like parent tissue
High grade= doesn’t look like parent tissue
Anaplastic = unknown origin cell type

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

What is carcinoma in situ?

A

When the cancer divides quicker than the normal cells and doesn’t apoptosis but is yet to invade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

What enzymes are required for cancers to invade through the basement membrane

A

Matrix metalloproteinases
Collagenases
Cathepsin D
Urokinase-type plasminogen activator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

What is metastasis?

A

Metastasis is the process by which a malignant tumour spreads from its primary site of origin to produce secondary tumours at distant sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

What are the three factors influencing tumour invasion?

A
  1. decreased cellular adhesion
  2. Secretion of proteolytic enzymes
  3. Abnormal or increased cellular motility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

Describe the process of cancer cell metastasis

A
  1. Detachment of tumour cells from their neighbours
  2. Invasion of the surrounding connective tissue to reach conduits for metastasis (blood and lymphatic vessels)
  3. Intravasation into the lumen of vessels
  4. Evasion of host defence mechanism such as natural killers cells In the blood
  5. Adherence to the endothelium at remote location
  6. Extravasation of cells from the vessel lumen into the surrounding tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

Name three ways in which cancer cells avoid the host immune defence

A
  • Aggregate with platelets so body cant detect it
  • Shedding surface antigens so not recognised
  • Adhesion to other tumour cells – ‘safety in numbers’
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

Name two factors that promote angiogenesis

A

Vascular endothelial growth factor

Basic fibroblast growth factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

Name three factors that inhibit angiogenesis

A

Angiostatin
Endostatin
Vasculostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

What are the three possible routes for metastasis?

A

Hamatogenous - bloodstream
Lymphatic
Transcoelomic - pleural, pericardial and peritoneal cavities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

Where do sarcomas commonly metastasise to?

A

Lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

Where does colorectal cancer normaly end up

A

Liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

Where to tumours of the colon, stomach, pancreas, and intestine normally end up?

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

Where do tumours of the prostate, breast, thyroid, lung and kidney normally metastasise to?

A

bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

Define inflammation

A

A local physiological response to tissue injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

Give a benefit of inflammation

A

Inflammation can destroy invading micro-organisms and can prevent the spread of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

Give a disadvantage of inflammation

A

Inflammation can produce disease and can lead to distorted tissues with permanently altered function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

Define exudate

A

A protein rich fluid that leaks out of vessel walls du to increased vascular permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

What does viral infection result in?

A

Cell death due to intracellular multiplication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

What does bacterial infection result in?

A

Release of exotoxins involved in initiation of inflammation or endotoxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

How can acute inflammation be diagnosed histologically?

A

By looking for the presence of neutrophil polymorphs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

Give three endogenous chemical mediators of acute inflammation?

A
  1. Bradykinin
  2. Histamine
  3. Nitric oxide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

What are the 4 systemic effects of acute inflammation?

A
  1. Fever
  2. Feeling unwell
  3. Weight loss
  4. Reactive hyperplasia of reticuloendothelial system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

What cells are involved in chronic inflammation

A

Macrophages and plasma cells (B and T lymphocytes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

What are 4 macroscopic features of chronic inflammation

A
  1. chronic ulcer
  2. Chronic abscess cavity
  3. Granulomatous inflammation
  4. Fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

What is the difference between resolution and repair

A

Resolution is when the initiating factor is removed and the tissue is able to regenerate. In repair the initiating factor is still present and the tissue is unable to regenerate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

Give 2 reasons why thrombosis formation is uncommon?

A
  1. Laminar flow

2. Non-sticky endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

Why are tissues with an end arterial supply more susceptible to infarction

A

Because they have a single arterial supply and if this becomes interrupted then infarction is likely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

Give three examples of organs with a dual arterial supply

A
  1. Lungs (Bronchial and pulmonary veins
  2. Liver hepatic arteries and portal veins
  3. Some areas of the brain around the circle of Willis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

What are the consequences of a venous embolus

A

Embolus in the venous system goes to vena can and through the pulmonary arteries becoming lodged in the lungs and causing a pulmonary embolism which decreases perfusion to the lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

Give an example of a disease where there is a lack of apoptosis

A

Cancer, mutations In p53 mean cell damage isn’t detected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

Give an example of a disease where there is too much apoptosis

A

HIV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

Give three differences between apoptosis and necrosis

A
  1. Apoptosis is programmed cell death whereas necrosis is unprogrammed
  2. Apoptosis tends to effect a single cell whereas necrosis affects a number of cells
  3. Apoptosis is a response to DA damage whereas necrosis is triggered by an adverse event
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

Give three examples of events that can lead to necrosis

A
  1. Frost bite
  2. Avascular necrosis
  3. Infarction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

Why is adjuvant therapy often used in the treatment of carcinomas

A

Micrometastes are possible even if the tumour is excised so adjuvant therapy is given to suppress the secondary tumour formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
194
Q

Give an advantage and disadvantage of conventional chemotherapy

A

Advantage = Works well for treatment against fast dividing tumours

Disadvantage = non selective for tumour cells resulting in effects such as diarrhoea and hair losss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
195
Q

What type of carcinomas would be targeted chemotherapy be most effective against

A

Slower dividing tumours ie. lung, colon and breast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
196
Q

What is the theory behind targeted chemotherapy

A

It exploits the differences between cancer cells and normal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
197
Q

What kind of drugs can be used in targeted chemotherapy?

A

Monoclonal antibodies (MAB) and small molecular inhibitors (SMI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
198
Q

What Is required for a tumour to invade through the basement membrane

A
  1. Proteases

2. Cell motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
199
Q

What is required for a tumour to enter the blood stream (Intravasation)

A
  1. Collagenases

2. Cell motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
200
Q

What is required for a tumour to exit the blood steam (extravasation)

A
  1. Adhesion receptors
  2. Collagenases
  3. Cell motility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
201
Q

What causes the pain associated with acute inflammation

A
  1. Stretching and distortion of tissues due to oedema and pus under high pressure in an abscess cavity
  2. Chemical mediators such as bradykinin and prostaglandins which induce pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
202
Q

Define carcinogenesis

A

A multistep process in which normal cells become neoplastic cells due to mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
203
Q

What percentage of cancer risk is due to environmental factors?

A

85%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
204
Q

Give an example of a situation when transplacental exposure leads to an increase in cancer risk

A

Daughters of mothers who had taken diethylstilbestrol for morning sickness had an increased risk of vaginal cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
205
Q

Define carcinoma

A

Malignant epithelial neoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
206
Q

Define sarcoma

A

Malignant connective tissue neoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
207
Q

What are the 4 characteristics of innate immunity?

A 
Instinctive 
Non-specific 
Does not depend on lymphocytes 
Present from birth
Immediate, rapid response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
208
Q

What are the 3 characteristics of adaptive immunity?

A

Specific/Acquired immunity
Requires lymphocytes and antibodies
Slower response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
209
Q

What are the three observable layers when blood is centrifuged?

A
  1. Upper plasma layer containing 90% water, electrolytes, proteins, lipids and sugars
  2. Middle white fluffy layer containing lymphocytes
  3. Lower layer (45%) containing erythrocytes and platelets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
210
Q

What is serum?

A

Plasma without fibrinogen and other clotting factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
211
Q

Which cell is the cell of origin of immune cells

A

Multipotent Haemopoietic stem cell (Haemocytoblast)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
212
Q

Draw a diagram to show the origin of immune cells

A

Find diagram on internet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
213
Q

What chemical stimulates stem cells to differentiate into blood cells?

A

Cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
214
Q

What are the three types of polymorphonuclear leukocytes

A

Neutrophil
Eosinophil
Basophil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
215
Q

What are the three types of mononuclear leukocytes and what do they become

A

Monocyte –> becomes macrophage when moves from blood to tissue

T cell becomes T-Reg, T-Helper (CD4) or cytotoxic (CD8)

B-cell becomes plasma cells when activated which become antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
216
Q

What is complement

A

Group of 20 serum proteins secreted by the liver that need to be activated to be functional as part of the immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
217
Q

What are the three modes of action of the complement system?

A
  1. Direct lysis (Membrane attack complex that makes a hole in pathogen)
  2. Attract more leukocytes to the site of infection (Chemotaxis)
  3. Coat invading organisms to make it more easy for them to be engulfed by phagocytic cells (Opsonisation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
218
Q

what do antibodies bind to?

A

Antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
219
Q

What are the 5 classes of antibody?

A 
IgG
IgA
IgM
IgD
IgE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
220
Q

Describe the properties of IgG

A

Most predominant in human
70-75% of antibodies
Can get anywhere in the body
Only Ig that can cross the placenta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
221
Q

Describe the properties IgA

A

Monomer
Accounts for 15% in serum
Predominant Ig in mucous secretions including milk, saliva, bronchiolar and genitourinary secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
222
Q

Describe the properties of IgM

A

Pentagon molecule
Mainly resides in the blood serum because its so large
Primary immune response
Accounts for 10% of Ig in serum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
223
Q

Describe the properties of IgD

A

1% of serum

Expressed on naive B cells and acts as B-cell antigen receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
224
Q

Describe the properties of IgE

A

0.05% in serum
Basophils and mast cells express IgE receptor so have high affinity for IgE
IgE associated with hypersensitivity allergic reactions and defence against parasites
binding antigen triggers release of histamine by basophils and mast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
225
Q

What are cytokines

A

Proteins secreted by immune and non-immune cells that acts as stimulatory or inhibitory signals between the cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
226
Q

Give 4 examples of cytokines

A

Interferons
Interleukins
Colony stimulating factors
Tumour necrosis factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
227
Q

Describe the function of interferons and give two examples

A

Induce a state of antiviral resistance in unaffected cells and limit the spread of infection
IFNa and IFNb
IFNy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
228
Q

What cells produced IFNa and IFNb

A

Virus infected cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
229
Q

What cells produce IFNy

A

Activated Th1 cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
230
Q

What is the function of Interleukins?

A

Can produce a pro inflammatory (IL1) or anti-inflammatory (IL-10) response the can cause cells to divide, differentiate and secrete factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
231
Q

What is the function of colony stimulating factor?

A

Involved in directing the division and differentiation on bone marrow stem cells - precursors to leukocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
232
Q

What is the function of tumour necrosis factor and give 2 examples

A

Mediate inflammation and cytoxic reactions

TNFa and TNFb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
233
Q

What are chemokines

A

Group of 40 proteins that direct the movement of leukocytes from the bloodstream into tissues or lymph by binding to specific receptors on cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
234
Q

What are the 8 characteristics of the innate defence mechanism?

A
  1. Non specific
  2. 1st line of defence
  3. Provides barrier to antigen
  4. Instinctive
  5. Present from birth
  6. Slow response
  7. No memory
  8. Does not depend on immune recognition by lymphocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
235
Q

What are the 5 characteristics of the adaptive defence mechanism?

A
  1. Specific
  2. Response to a specific antigen
  3. Learnt behaviour
  4. Memory to specific antigen
  5. Quicker response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
236
Q

What is the innate immunity composed of?

A 
Physical and chemical barriers 
Phagocytic cells (Neutrophils and macrophages)
Blood proteins (Complementt)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
237
Q

What are the physical barriers to infection?

A
  1. Lysozymes in tears
  2. Skin
  3. Skin sebum secretions
  4. Acidic pH in vagina
  5. Acidic pH in gut
  6. Removal of particles by passing air over turbinates bones
  7. Mucus and cilia in bronchi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
238
Q

What are the 7 stages of the response to inflammation?

A
  1. Stop bleeding
  2. Acute inflammation (Leukocyte recruitment)
  3. Kill pathogen, neutralise toxins and limit pathogen spread
  4. Clear pathogens and dead cells (Phagocytosis)
  5. Proliferation of cells to repair the damage
  6. Remove blood clot and remodel the extracellular matrix
  7. Re-establish normal structure and function of tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
239
Q

Define inflammation

A

Series of reactions that brings cells and molecules of the immune system to sites of infection or damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
240
Q

What are three signs of inflammation

A
  1. Increased blood supply
  2. Increased vascular permeability
  3. Increased leukocyte transendothelial migration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
241
Q

Define acute inflammation?

A

Complete elimination of a pathogen followed by resolution of damage, disappearance of leukocytes and full tissue regeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
242
Q

Define chronic inflammation?

A

Persistent unresolved inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
243
Q

What senses microbes in the blood?

A

Monocytes and neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
244
Q

What senses microbes in the tissues?

A

macrophages and dendritic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
245
Q

Where are pattern recognition receptors found

A

On immune cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
246
Q

Where are pathogen associated molecular patterns found

A

On the microbe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
247
Q

Describe the process of extravasation?

A
  1. Microbe in tissue with macrophage bound
  2. Macrophage secretes pro-inflmmatory TNFa
  3. TNF interacts with endothelium making it sticky
  4. Neutrophil sticks to endothelium and rolls along its surface
  5. TNFa causes secretion of chemokines that stick to molecules on endothelial surface and cause neutrophil to stop rolling
  6. Neutrophil is held on the endothelial surface by adhesion molecules and then squeezes through endothelium and moves up concentration gradient of cytokines to the site of infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
248
Q

Describe the process of phagocytosis

A
  1. Bacteria binds to the macrophage
  2. Engluflment
  3. Phagosome formation
  4. Phagolysosome
  5. Membrane disruption
  6. Secretion of H2O2, NO and TNFa
  7. MHC class II antigen presentation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
249
Q

What are the two pathways present in neutrophils and macrophages for microbial killing?

A
  1. Oxygen dependent

2. Oxygen independent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
250
Q

Describe 3 methods of O2 dependent method of microbial killing

A
  1. Killing using reactive oxygen intermediates
  2. Superoxides are converted to H2O2 then OH free radical
  3. Nitric oxide which causes vasodilation increasing extravasation so more neutrophils in the tissue to kill pathogens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
251
Q

Describe the O2 independent method of microbial killing

A

Enzymes (Lysozyme)
Proteins (Defensins inserted into membrane)
pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
252
Q

Name three characteristics that adaptive immunity has?

A

Antigen specificity and diversity
Immunological memory
Specific self and non-self recognition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
253
Q

What must the immune system do in order to be effective

A

Discriminate between self and non self

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
254
Q

What is the function of lysozyme?

A

Destroys bacterial cell walls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
255
Q

In which primary lymphoid tissue do T cells mature?

A

Thymus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
256
Q

IN which primary lymphoid tissue do B cells mature?

A

Bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
257
Q

How do T cells recognise antigens?

A

For T cell recognition, antigens must be displayed by an antigen presenting cell bound to MHC1/2 - T cells cant recognise soluble antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
258
Q

What is the function of T-helper 1 (CD4)?

A

Helps the immune response against intracellular pathogens and secretes cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
259
Q

What is the function of T-Helper 2 (CD4)

A

Helps to produce antibodies against extracellular pathogens and secretes cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
260
Q

What is the function of cytotoxic T cell CD8

A

Kills cell directly by binding to antigens, inducing apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
261
Q

Which cells express MHC class I and why is it required

A

All nucleated cells ie a virus infected cell or cancer cell except erythrocytes

CD8 Cytotoxic T cells required antigen to be associate with MHC I before they kill cell containing intracellular pathogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
262
Q

Which cells express MHC class II and why is it required

A

Antigen presenting cells ONLY ie. macrophages, B cells and dendritic cells

Helper T cells (CD4) requires MHC II before they help B cells to make antibodies to the extracellular pathogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
263
Q

Which MHC would an intracellular antigen (Endogenous) lead to expression of?

A

MHC1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
264
Q

Which MHC would an extracellular antigen (Exogenous) lead to expression of?

A

MHC2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
265
Q

What type of T cell binds to MHC1

A

Cytotoxic T cells (CD8)

266
Q

What type of T cells bind to MHC2

A

Helper T cells (CD4)

267
Q

What does a helper T cell bind to?

A

A T cell receptor which is bound to an antigen epitope which bound to MHC2 on an APC

268
Q

What happens to B cells that recognise ‘self’?

A

They are killed in the bone marrow

269
Q

Describe the process of a T helper cell binding to a B cell

A
  1. A B cell binds an antigen
  2. Phagocytosis
  3. Epitope is displayed on the surface of the B-cell bound to an MHC2
  4. TH2 binds the B cell
  5. Cytokines secretion induces B cell clonal expansion
  6. Differentiation into plasma cells and memory B cells
270
Q

Which region of an antibody binds to antigens?

A

FAB region

271
Q

Which region of an antibody binds to B cells

A

Fc region

272
Q

Give examples of secondary lymphoid tissue

A

Spleen
Lymph nodes
Mucosa associated lymphoid tissue (MALT)

273
Q

Where are complement system plasma protein derived from?

A

The liver

274
Q

What activates the classical complement pathway?

A

Antibodies

275
Q

What compound prevents excessive activation of the classical complement pathway

A

C1 inhibitor

276
Q

What activates the lectin path of the complement pathway

A

mannose binding protein

277
Q

What activates the alternate pathway of the complement pathway

A

Bacterial cell walls and endotoxin

278
Q

What are PRR’s a receptor for?

A

PAMPs

279
Q

Name the three receptors that make up the PRR family

A
  1. Toll like receptors
  2. Nod-like receptors
  3. Rig-like receptors
280
Q

What is extravasation

A

Leukocyte migration across the endothelium

281
Q

What do macrophages at the tissue secrete to initiate extravasation

A

TNFalpha

282
Q

Define humoral immunity

A

Humoral immunity is immunity from serum antibodies produced by plasma cells that kills extracellular microbes

283
Q

Define Cell mediated immunity

A

cell-mediated immunity can be acquired through T cells from someone who is immune to the target disease or infection. “Cell-mediated” refers to the fact that the response is carried out by cytotoxic cells - kills intracellular microbes

284
Q

What are the two types of adaptive immunity?

A

Cell mediated

Humoral

285
Q

What happens to T cells that recognise self?

A

They are killed in the foetal thymus

286
Q

Intrinsic antigens are associated with which MHC class

A

Class I

287
Q

Extrinsic antigens are associated with which MHC class

A

Class II

288
Q

If the concentration of IL-12 is high, what does CD4 T cell become?

A

TH1

289
Q

If the concentration of IL-12 is low, what does the CD4 T cell become?

A

TH2

290
Q

Which of the following malignant tumours never metastasises?

  1. malignant melanoma
  2. Small cell carcinoma of the lung
  3. Basal cell carcinoma of the skin
  4. Breast cancer
A

Basal cell carcinoma of the skin

291
Q

What is the name given to a malignant tumour of the striated muscle

A

Rhabdomyosarcoma

292
Q

Which of the following tumours does not commonly metastasise to bone?

  1. Bone cancer
  2. Lung cancer
  3. Prostate cancer
  4. Liposarcoma
A

Liposarcoma

293
Q

What term describes cancer that has not invaded through the basement membrane?

A

Carcinoma in situ

294
Q

What is the name given to a benign tumour of glandular epithelium?

A

Adenoma

295
Q 
Which of the following cancers does not have a screening programme in the UK?
1. Breast
2. Colorectal  
3. Cervical 
4, Lung
A

Lung cancer

296
Q

Which of the following is not a known carcinogen to humans?

a. Hepatitis C (Will cause hepatocellular carcinoma)
b. Ionising radiation
c. Aromatic amines
d. Aspergillus niger

A

Aspergillus Niger

297
Q

What is the name of benign tumour of fat cells?

A

Lipoma

298
Q

What is the name given to a malignant tumour of the glandular epithelium?

A

Adenocarcinoma

299
Q

Which of the following is not a feature of malignant tumours?

a. Vascular invasion
b. Metastasis
c. Increased cell divisions
d. Growth related to overall body growth

A

Growth related to overall body growth

300
Q

Can radon gas causes lung cancer?

A

YEs

301
Q

Is a transitional carcinoma of the bladder a malignant tumour?

A

YEs

302
Q

What is the name of a benign tumour of the smooth muscle

A

Leiomyoma

303
Q

Which lifestyle factor is most likely to cause cancer?

a. Drinking half. Bottle of wine a day
b. Being obese
c. Running for 20 mins twice a week
d. Smoking 20 a day

A

Smoking 20 a day

304
Q

Which tumour has the shortest median survival

a. Basal cell carcinoma of the skin
b. Malignant melanoma of the skin
c. Breast cancer
d. Anaplastic carcinoma of the thyroid

A

Anaplastic carcinoma of the thyroid

305
Q

Does ovarian cancer commonly spread to the peritoneum?

A

Yes

306
Q

Activation of naive T cells is best achieved by which antigen presenting cell?

  1. Neutrophil
  2. Mast cells
  3. Macrophages
  4. Dendritic cells
A

Dendritic cells

307
Q

Which of the following cell types is located exclusively in tissues, has an important role in both the innate and adaptive immune system, are antigen presenting cells and have phagocytic properties

  1. Macrophage
  2. Neutrophil
  3. Eosinophil
  4. Mast cell
  5. Fibroblast
A

Macrophage

308
Q

Which of the following is not a barrier in the innate immune mechanism?

  1. Anatomic barriers
  2. Phagocytic
  3. Inflammatory mechanisms
  4. Antibody production
  5. Skin
A

Antibody production

309
Q

T cells recognise antigens

  1. In solution in plasma
  2. When presented on RBC’s
  3. Following presentation on antigen presenting cells
  4. In a 3-dimensional form
  5. Following presentation on pattern recognition receptors
A

Following presentation on antigen presenting cells

310
Q

Influenza vaccine is targeted towards at risk groups in the Uk. Which of the following are classified as at risk?

  1. Over 65
  2. 16 years
  3. Obese of any age
  4. Teenagers
  5. Under 2 years old
A

Over 65

Under 2 years old

311
Q

Which of the following is administered as a live attenuated vaccine in the uk?

  1. Hep A
  2. Measles, Mumps, Rubella
  3. Tetanus
  4. Flu
  5. Polio
A

Measles, mumps and rubella

312
Q

Complements are the proteins that are involved in the clearance of antigen/bacteria. Which of the following is not part of the elimination phase of complement activation

  1. Opsonisation
  2. Target cell lysis
  3. Chemoattraction of leukocytes
  4. Production of interferons
  5. Phagocytosis
A

Production of interferons

313
Q

Which of the following is a polyssacharide vaccine

  1. Anthrax
  2. Hib vaccine (Haemophilus influenza type b)
  3. Rabies vaccine
  4. Hepatitis A
A

Hib vaccine

314
Q

Which of the following are features of the adaptive immune response?

  1. Does not require prior contact with the pathogen
  2. It works with B and T lymphocytes
  3. Lacks Specificity
  4. Distinguishes self from non-self
  5. Enhanced by complement
A

It works with B and T lymphocytes

315
Q

What are the two types of immune response in humans?

A

Innate and Acquired

316
Q

Which of the following is not an organ specific auto-immune disease?

  1. Ulcerative collitis
  2. Type 1 diabetes mellitus
  3. Graves disease
  4. Hashimoto’s Thyroiditis
  5. Sjorgens syndrome
A

Ulcerative colitis

317
Q

Which of the following is not a classical PAMP?

  1. Peptidoglycan found in bacterial cell walls
  2. Flagellin, a protein in bacterial flagella
  3. Lipopolysaccharide from the outer membrane of gram negative bacteria
  4. Interleukin 12
  5. Nucleic acids such as viral DNA or RNA
A

Interleukin 12

318
Q

How do antibodies protect against infection?

A 
Neutralise toxins 
Immobilise motile microbes 
Prevent binding to and infection of host cells 
Form complexes 
Activate complement (IgG, IgM)
Bind Fc receptors
319
Q

Binding of Fc receptors to phagocytes causes what?

A

Enhanced phagocytosis

320
Q

Binding of FC receptors to mast cells causes what?

A

Release of inflammatory mediators

321
Q

Binding of FC receptors to NK cells causes what?

A

Enhanced killing of infected cells

322
Q

What is the role of T helper cells (CD4+ve)

A

Help B cells make antibody
Activate macrophages and NK cells
help the development of cytotoxic T cells

323
Q

What is the role of T cytotoxic cells (CD8+ve)

A

Recognise and kill infected host cells

324
Q

What is the role of T regulatory cells

A

Suppress immune responses

325
Q

What sort of antigens do B cells recognise?

A

Soluble, free and native antigens

326
Q

What sort of antigens do T cells recognise?

A

Cell-associated processed antigen

327
Q

Which gene codes for major histocompatibility proteins?

A

Major histocompatibility complex on chromosome 6 otherwise known as human leucocyte antigen (HLA)

328
Q

What are the two subsets of Cd4 cells?

A

TH1 and Th2 cells

329
Q

What Is the role of TH1 cells

A
  1. Produce IL-2, y-interferon and TNFb
  2. Activate macrophages leading inflammation
  3. promote production of cytotoxic T cells
  4. Induce B cells to make IgG antibodies
330
Q

What is the role of TH2 cells

A
  1. Produce IL-4,5,6,10 and 13
  2. Activate eosinophils and mast cells
    Induce B cells to make iGE - promotes the release of inflammatory mediators ie. histamine from mast cells
331
Q

How does the body handle bacteria and fungi?

A

Phagocytosis

332
Q

How does the body handle viruses?

A

Cellular shut down
Self-sacrifice
Cellular resistance

333
Q

What are the patterns that enable our immunity to determine between self and non-self?

A
  1. Limited characteristics
  2. Gram +ve bacteria have thick wall with no outer envelope
  3. Gram -ve bacteria have thinner wall with outer envelope
  4. DsRNa (Way of detecting viral infection
  5. CpG motifs
334
Q

What are the two types of pattern recognition receptors

A

Secreted and circulating

Cell associated

335
Q

Name three receptors that’s make up the PRR family

A
  1. Toll like receptors
  2. Nod like receptors
  3. Rig like receptors
336
Q

What is the main function of TLRs

A

TLRs send signals to the nucleus to secrete cytokines and interferons. These signals initiate tissue repair
Enhanced TLR signalling I= improved immune response

337
Q

What is the main function of NLRs

A

NLRs detect intracellular microbial pathogens

They release cytokines and can cause apoptosis if the cell is infected

338
Q

What disease is caused by a non-functioning mutation in NOD2?

A

Crohns disease

339
Q

What is the main function of RLR’s?

A

RLR’s detect intracellular double stranded RNA

This triggers interferon production and an antiviral response

340
Q

TLRs are adapted to recognise damaged molecules. What characteristics do these damaged molecules often have in common

A

They are hydrophobic

341
Q

What kind of TLRs can be used in vaccine adjutants?

A

TLR4 agonists

342
Q

Give 3 examples of diseases that can be caused by PRRs failing to recognise pathogens

A
  1. Atherosclerosis
  2. COPD
  3. Arthritis
343
Q

Give examples of 3 extracellular PRR?

A
  1. Mannose receptors
  2. Scavenger receptors
  3. TLRs
344
Q

What is the function of mannose and scavenger extracellular receptors?

A

Induce pathogen engulfment

345
Q

Give an example of an intracellular PRR

A

NLR

346
Q

Where are circulating PRRs secreted from?

A

Epithelia, phagocytes and the liver where they can activate the complement cascade and induce phagocytosis

347
Q

Give 2 examples of secreted and circulating PRRs

A

Antimicrobial peptides ie. Defensins and Cathelicidin

Lectins and collectins ie. mannose binding lectin

348
Q

What are cell associated PRRs and what is the main family?

A

Receptors that are present on the cell membrane on in the cytosol of cells
TLRs

349
Q

What is the ligand for TLR1/2

A

Gram positive lipopeptides

350
Q

What is the exogenous ligand for TLR3

A

Double stranded RNA

351
Q

What is the endogenous ligand for TLR3

A

mRNA

352
Q

What is the exogenous ligand for TLR4

A

LPS
Pneumolysin
Viral Proteins

353
Q

What are the endogenous ligands for TLR4

A

Heat shock proteins
HMGB1
Hyaluronan
Fibrinogen

354
Q

What is the exogenous ligand for TLR5

A

Flagellin

355
Q

What is the exogenous ligand for TLR2/6

A

Gram positive lipopeptides

356
Q

What are the exogenous ligands for TLR7

A

Single stranded RNA

357
Q

What are the exogenous ligands for TLR8

A

Single stranded RNA

358
Q

What are the exogenous ligands for TLR9

A

CpG DNA

359
Q

What are the three types of membrane bound PRR

A

Mannose receptor on macrophages
Lectin 1
Scavenger receptors on macrophages

360
Q

What do NLRs detect?

A

Peptidoglycan and muramyl dipeptide

361
Q

What disease does a hyper functioning mutation in NOD2 lead to?

A

Blau Syndrome

362
Q

What is the role of RLRs and give two examples

A

detect intracellular double stranded viral DNA and RNA

RIG-I and MDA5

363
Q

Name three extracellular damage molecules

A

Fibrinogen
Hyaluronic acid
Tenascin C

364
Q

Name 5 intracellular damage molecules

A 
HMGB1
mRNA 
Heat shock proteins 
Uric acid and uric acid crystals 
Stathmin
365
Q

Define passive immunisation

A

Give antibodies

366
Q

Define active immunisation

A

Given dead/attenuated pathogens

367
Q

What are the advantages of passive immunisation?

A

Immediate protection

Effective in immunocompromised patients

368
Q

what are the advantages of active immunisation?

A

Dead- no risk of infection

Attenuated - immune response close to real thing

369
Q

Disadvantages of passive immunisation

A

Short lived
Serum sickness
Does not activate immunological memory

370
Q

What are the disadvantages of active immunisation?

A

Dead - just the humour response activated

Attenuated - possible reversion to virulence

Cant be given to an immunocompromised patient

371
Q

Give some examples of passive immmunisation

A

Cross placement transfer of antibodies from mother to child (Natural)

Treated with immunoserum or pooled human IgG (Artificial)

  • Human hepatitis B Ig
  • Varicella Zoster Ig
372
Q

Give 2 examples of active immunisation

A

Non-living = Pertussis, infleunza, diphtheria and tetanus

Attenuated = BCG, MMR, poliomyelitis

373
Q

What are 5 patient risk factors when administering drugs?

A
  1. polypharmacy
  2. Old age
  3. Genetics
  4. Hepatic disease
  5. Renal disease
374
Q

What are 3 drug risk factors

A
  1. Narrow therapeutic index
  2. Steep dose/response curve
  3. Saturable metabolism
375
Q

What are the three types of adsorption?

A

Precipitation
Chelation
Neutralisation

376
Q

What are the 4 types of drug interaction

A
  1. Synergy
  2. Antagonism
  3. Summation
  4. Potentiation
377
Q

What is bioavailability

A

How much of the oral drug is in the system compared to how much of the IV drug

378
Q

Does the ionised or unionised portion of a drug cross the bilayer?

A

Unionised

379
Q

Where are most drugs metabolised?

A

Liver

380
Q

Describe the metabolism of morphine?

A

Morphine metabolised by CYP450 pathway to morphine 6 glucuronide which enables excretion by the kidney

381
Q

What is the effect of phenytoin on morphine metabolism

A

Phenytoin induces CYP450 enzymes leading to increased metabolism of morphine to active morphone 6 glucuronide = ENZYME INDUCTION

382
Q

What is the effect of metronidazole on morphine metabolism?

A

Metronidazole slows CYP450 and reduces production of morphine 6 glucuronide so its less potent = ENZYME INHIBITION

383
Q

Are weak basic drugs cleared faster if the urine is acidic or alkaline?

A

Acidic

384
Q

Are weak acids drugs cleared faster if the urine is acidic or alkaline?

A

Alkaline

385
Q

What drugs can induce acute kidney injury?

A

NSAIDs
Gentamicin
Furosemide
ACEi

386
Q

What is the affect of grapefruit juice in patients taking warfarin?

A

Affects CYP450 and warfarin ability to bind to proteins

387
Q

Define a drug

A

A medicine or other substance which has a physiological effect when ingested or otherwise introduced into the body

388
Q

Define pharmacology

A

Branch of medicine concerned with the use, effects and modes of action of drugs

389
Q

Define pharmacodynamics

A

How the drug affects the body

390
Q

Define pharmacokinetics

A

How the disposition of a compound within an organism - how the body affects a drug (ADME)

391
Q

What is the main target for drugs

A

Proteins

392
Q

Name 4 types of drug targets

A

receptors
enzymes
transporters
Ion channels

393
Q

Define receptor

A

Cell component that interacts with a specific ligand that initiates a change of biochemical events leading to observed effects

394
Q

Give an example of a ligand gated ion channel

A

Nicotinic ACh receptor

395
Q

Give an example of a GPCR

A

Muscarinic and β2 adrenoceptor.

396
Q

Give an example of kinase-linked receptors

A

Receptors for growth factors

397
Q

Give an example of cytosolic/nuclear receptors

A

Steroid receptors - modify gene transcription

398
Q

Describe how GPCRs work

A

Activity regulated by factors that control the ability to bind and hydrolyse GTP to GDP

399
Q

Give 2 examples of GPCRs

A

Muscarinic 3-receptor (Gq)

B2-AR (Gs)

400
Q

What are kinase linked receptors?

A

Transmem receptor that are activated when the binding of extracellular ligand causes enzymatic activity on the intracellular side
(Leads to protein phosphorylation)

401
Q

Define agonist

A

A compound that binds to a receptor and activates it

402
Q

Define antagonist

A

Antagonist decreases the effect of an agonist - shows no response at the receptor

403
Q

Define potency

A

Measure of how well a drug works - EC50 = Concentration that gives half the maximal response

404
Q

Define efficacy (Emax)

A

Maximum response achievable for a dose (Partial agonist will never achieve a full response)

405
Q

Define intrinsic activity (Efficacy)

A

Ability of a drug receptor complex to produce a maximum functional response
(Emax of partial agonist/ Emax of full agonist)

406
Q

Would an antagonist shift the dose response curve to the left or to the right?

A

Shift to the right so a higher concentration of the agonist is required to achieve a full response - agonist becomes less potent

407
Q

Define affinity

A

How well a ligand binds to a receptor

408
Q

Define non-competitive antagonism

A

When the antagonist binds to an allosteric site on the receptor that disrupts its activation

409
Q

What is the H1 histamine receptor associated with?

A

Allergic conditions

410
Q

What is the H2 histamine receptor associated with?

A

Gastric acid secretion

411
Q

What is the H3 histamine receptor associated with?

A

CNS disorders

412
Q

What is the H4 histamine receptor associated with

A

Immune system and inflammatory conditions

413
Q

What is the effect of fewer receptors on receptor response

A

Receptor response is still 100% due to receptor reserve (Partial agonists don’t have a receptor reserve)

414
Q

What is the affect of less signal amplification on drug response

A

Less signal amplification gives a reduced drug response

415
Q

Define inverse agonism

A

When a drug binds to the same receptor as an agonist but induces a pharmacological response that is opposite to that of the agonist

416
Q

Does an antagonist demonstrate efficacy

A

No, antagonist can have affinity but show zero efficacy. Agonist shows affinity and efficacy

417
Q

Define tolerance

A

A reduction in the effect of a drug overtime due to continuous use of repeatedly high concentrations

418
Q

Name 3 ways in which a receptor can be desensitised

A
  1. Uncoupled
  2. Internalised
  3. Degraded
419
Q

Define an enzyme inhibitor

A

a molecule that binds to an enzyme and decreases its normal activity

420
Q

What are the two types of enzyme inhibitor

A
  1. Irreversible - react with enzyme and change it chemically (Via covalent bond formation)
  2. Reversible - Bind non-covalently
421
Q

What do statins do?

A

Class of lipid lowering drugs that reduce the level of bad cholesterol by blocking’ the rate limiting step in the cholesterol pathway

422
Q

What is the effect of inhibiting ACE on blood pressue

A

inhibiting ACE prevents the conversion of Ang 1 to Ang 2 therefore causing a reduction in blood pressure

423
Q

Name 2 ACE inhibitors

A

Captopril

Enalapril

424
Q

What is the precursor molecule for L-DOPA

A

L-tyrosine

425
Q

Which enzyme converts L-DOPA to dopamine>

A

DOPA decarboxylase

426
Q

How does carbidopa works

A

Blocks DOPA decarboxylase in the periphery in the periphery which generates more L-DOPA for the CNS pathway

427
Q

How do peripheral Catechol-O-methyl transferases (COMT) work?
(Tolecapone)
(Entacapone)

A

Peripheral COMT prevent L-DOPA breakdown therefore generating more for CNS pathway

428
Q

How to central COMT inhibitors work? (Tolecapone)

A

Prevent the breakdown of dopamine in the central CNS

429
Q

How do mono amine oxidase inhibitors such as selegiline and rasagiline work?

A

Prevent the breakdown of dopamine into DOPAC in the central CNS

430
Q

How do uniporters work?

A

Use energy from ATP to pull molecules in

431
Q

How do symporters work?

A

Use the movement in of one molecule to pull in another molecule against its concentration gradient

432
Q

How do anti porters work?

A

One substance moves against its gradient using energy from a second substance that is moving down its gradient

433
Q

Give an example of a symporter

A

NKCC2

434
Q

How does furosemide work and what its it used for?

A

Used for oedema and hypertension
Acts by inhibiting luminal NKCC2 in thick ascending limb
Causes sodium, chloride and potassium loss in the urine

435
Q

How does amiloride work?

A

Blocks epithelial sodium channels in the collecting ducts thus preventing sodium reabsorption - used as an antihypertensive

436
Q

Where are voltage gated calcium channels found?

A

in membranes of excitable cells including muscle, glial cells and neurons

437
Q

What does amlodipine do?

A

Calcium channel blocker that inhibits the movement of calcium into the vascular smooth muscle cells and cardiac muscle that inhibits contraction. This causes vasodilation, reduces peripheral vascular resistance and lowers blood pressure

438
Q

What are the three conformational states a voltage gated sodium channel can be in

A

Closed
Open
Inactivated

439
Q

How does lidocaine work?

A

Blocks the transmission of action potential and blocks signalling in the heart, reducing arrhythmia

440
Q

Receptor mediated chloride channels respond to what ligands

A

Neurotransmitters such as GABA which opens the Cl- channel and causes membrane hyper polarisation

441
Q

What compounds increase the permeability of chloride channels

A

Barbituates

442
Q

How does the Na+/K+ ATPase work

A

Pumps 3Na+ out the cell for every 2K+ it returns to the cell

443
Q

How does digoxin work?

A

Inhibits Na+/K+ in the myocardium which increase intracellular Na+ resulting in decreased activity of the Na+/Ca2+ exchanger which increases intracellular Ca2+, lengthening the cardiac action potential leading to a decrease in heart rate

444
Q

What is the role of the K+/H+ ATPase?

A

Responsible for the acidification of the stomach and the activation of the digestive enzyme pepsin

445
Q

How does omeprazole work?

A

Inhibits irreversibly H+/K+ ATPase

446
Q

Organophosphates such as insecticides and nerve gas are irreversible inhibitors of what?

A

Cholinesterases

447
Q

Aspirin is an irreversible inhibitor of what?

A

COX

448
Q

What is a xenobiotic?

A

A compound foreign to an organisms normal biochemistry such as a drug or a poison

449
Q

What are the two divisions of the autonomic nervous system

A

Sympathetic and parasympathetic

450
Q

What are the 6 regulatory roles of the autonomic nervous system?

A
  1. Vascular
  2. Airway
  3. Visceral smooth muscle
  4. Exocrine secretions
  5. Control of heart rate
  6. Energy metabolism in the liver
451
Q

Where are parasympathetic ganglia located?

A

Near their targets with short post ganglionic fibres and long pre-ganglionic fibres

452
Q

Where are sympathetic ganglia located?

A

Near the spinal cord with short pre-ganglionic fibres and longer post-ganglionic fibres

453
Q

Which cranial nerves are parasympathetic

A

Oculomotor (CNIII)
Facial (VII)
IX
X

454
Q

Which hormone Is released on the pre-ganglionic parasympathetic fibres to act on nicotinic receptors

A

ACh

455
Q

Which hormone is release on the post-ganglionic parasympathetic fibres to act on muscarinic receptors

A

ACh

456
Q

Which hormone is released on the pre-ganglionic sympathetic fibres to act on nicotinic receptors

A

ACh

457
Q

Which hormone is released on post-ganglionic sympathetic fibres to act on alpha and beta adrenergic receptors?

A

Noradrenaline

458
Q

Which parts of the body are under sympathetic control only?

A

Sweat glands

Blood vessels

459
Q

Which part of the body is under parasympathetic control only?

A

Bronchial smooth muscle

460
Q

Which parts of the body are under dual sympathetic and parasympathetic control

A

Gut, bladder, heart

461
Q

Name 4 non-adrenergic and non cholinergic autonomic transmitters used by the enteric, sympa and parasympathetic NS

A

Nitric oxide
Vasoactive intestinal peptide
ATP
Neuropeptide Y

462
Q

Which enzymes is responsible for the breakdown of acetylcholine in the synaptic cleft

A

Acetylcholinesterase

463
Q

What type of receptor is muscarinic receptors and how many classes are there?

A

GPCR

M1-M4

464
Q

Where are M1 muscarinic found in the body?

A

Brain

465
Q

Where are M2 muscarinic receptors found in the body and what does their activation cause

A

Found in the heart, activation slows the heart (Bradycardias)
- can be blocked with atropine

466
Q

Where are M3 muscarinic receptors found in the body and what does their activation cause

A

Found in the glandular and smooth muscle

- cause bronchoconstriction, sweating and saliva secretion

467
Q

Where are M4 muscarinic receptors found in the body

A

In the CNS

468
Q

What does pilocarpine do and when might it be useful

A

Stimulates salivation - may be useful after radiotherapy of head and neck or sjorgens syndrome

469
Q

Name a muscarinic antagonist and what condition may it be used to treat

A

Atropine

Used to prevent bradycardia, prevent BP drop and dry up secretions perioperatively

470
Q

Name two different types of anti-muscarinics used in the treatment of bronchoconstriction

A

Short acting - Ipratropium bromide

Long acting - LAMAs including tiotropium and glycopyrrhonium

471
Q

What is solifenacin and what is it used for?

A

Anticholinergic

Used to treat overactive bladder

472
Q

What are suxamethonium and pancuronium and what are they used for?

A

Inhibit muscle activity and induce relaxation in surgery by inhibiting nicotinic blockers

473
Q

What are the side effects of anti-cholinergics?

A 
COnstipation 
Dry mouth 
blurring of vision 
Worsening of glaucoma 
Worsen memory and cause confusion
474
Q

What is the precursor molecule for adrenaline and noradrenaline

A

Dopamine

475
Q

What is the primary agonist of alpha 1 receptors

A

Noradrenaline > Adrenaline

476
Q

What is the mechanism of action act alpha 1 adrenergic receptors and what are the consequences

A

Activation increases intracellular calcium (Gq signalling)
Leads to smooth muscle contraction (pupil, blood vessels) = vasoconstriction
bladder contraction

477
Q

What is the primary agonist of alpha 2 receptors

A

Noradrenaline and adrenaline activate equally

478
Q

What is the mechanism of action at alpha 2 adrenergic receptors and what are the consequences

A

Gi signalling - Inhibition of cAMP generation

Mixed effects on smooth muscle

479
Q

What is the primary agonist of beta 1 receptors

A

Noradrenaline and adrenaline are equal

480
Q

What is the mechanism of action at beta 1 adrenergic receptors and what are the consequences

A

Gs - raises levels of cAMP
Increases the chronotropic and inotropic effects on heart
Increased renin release from kidney which increases blood pressure

481
Q

What is the primary agonist of beta 2 adrenergic receptors

A

Adrenaline > Noradrenaline

482
Q

What is the mechanism of action at beta 2 adrenergic receptors and wha are the consequences

A 
Gs - Raises cAMP
Relaxes smooth muscle in premature labour and asthma
Bronchodilation
vasodilation 
Reduced GI motility
483
Q

What is the primary agonist at beta 3 adrenergic receptors

A

Noradrenaline > Adrenaline

484
Q

What is the mechanism of action at beta 3 adrenergic receptors and what is the consequence

A

Gs - raises cAMP

Enhances lipolysis and relaxes the bladder detrusor muscle

485
Q

When might an Alpha 1 agonist be used?

A

In the treatment of septic shock to cause vasoconstriction and prevent a drop in blood pressure

486
Q

What is Doxazosin and when is it used?

A

Alpha 1 antagonist that blocks alpha 1 receptors to lower blood pressure

487
Q

What is tamsulosin and when is it used

A

Alpha 1a antagonist used in the prostate to prevent prostatic hypertrophy

488
Q

What does beta 1 adrenergic receptor activation do?

A

Increase HR and chronotropic effects

Increases the risk of arrhythmias

489
Q

What does propranolol block and what are the consequences

A 
Beta 1 (Heart) and beta 2 (lungs)
Slows the HR, reduces tremor and may cause wheeze
490
Q

What does atenolol block and what are the consequences

A 
Beta 1 (heart) selective 
Lowers the blood pressure by reducing cardiac output and gradual reduction in sympathetic outflow
491
Q

What are the uses of beta blockers?

A 
Angina 
MI prevention 
High blood pressure 
Anxiety 
Arrhythmias 
Heart failures
492
Q

What are the side effects of beta blockers

A 
Tiredness 
Cold extremities 
Bronchoconstriction 
Bradycardia 
Hypoglycaemia 
Cardiac depression
493
Q

Define hypersensitivity

A

Excessive response that can be mediated immediately, acutely or gradually

494
Q

How many different types of hypersensitivity reaction are there according to Gell and Coombs

A

4

495
Q

What is a type 1 hypersensitivity reaction and name some examples

A

Immunological memory to something causing an allergic reaction - IgE
Anaphylaxis, Asthma and hay fever

496
Q

What are the two potential routes of exposure in a type 1 hypersensitivity reaction

A

Local Exposure
- Hayfever from pollens, animals, occupational exposure
Systemic exposure
- Drugs, foods, treatments

497
Q

What are the effects of histamine release

A

Vasodilation and capillary leakage

498
Q

What do mast cell granules contain

A 
Histamine 
PGD2
Proteases 
Cytokines 
IL-4
IL-13
TNFa
499
Q

Define atopy

A

Inherited tendency to an exaggerated IgE response to an antigen

500
Q

What are 4 treatments for hay fever?

A

Prevent exposure
Anti-histamines
Reduction in local inflammation (Steroids)
Desensitisation

501
Q

What are the treatments for anaphylaxis

A 
Avoid/cease exposure 
Stop acute symptoms (anti-histamines)
Acute resuscitation (Adrenaline, fluids, bronchodilators)
Decrease inflammation (Steroids)
Intramuscular adrenaline to maintain circulation
502
Q

Describe a phase 2 hypersensitivity reaction

A

Immunoglobulins (IgG) bound to surface antigens which causes the immune system to attack the basement membrane of the kidney and lungs

503
Q

Give 4 examples type 2 hypersensitivity reaction

A

Goodpastures syndrome
Mycoplasma Pneumonia
Graves Disease
Myaesenthia Gravis

504
Q

Describe a type 3 hypersensitivity reaction

A

Antibodies and target circulate. Little lumps of antibody and target get deposited in the skin, lung and kidneys and activate immunity so phagocytes go and destroy it resulting in capillary damage in lungs and kidneys

505
Q

Give an example of a type 3 hypersensitivity reaction

A

Extrinsic Allergic Alveolitis

Formation of precipitating antibodies to organic dusts

506
Q

What are the 4 types of extrinsic allergic alveolitis

A

Farmers lung
Malt workers lung
Mushroom workers lung
Pigeon Fanciers Lung

507
Q

Describe type 4 hypersensitivity reactions

A

Formation of granulomas dependent on the activation of T cells

508
Q

Give an example of a type 4 hypersensitivity reaction

A

TB

Sarcoidosis

509
Q

Name two opioids that are naturally occurring

A

Codeine

Morphine

510
Q

Name three opioids formed from simple chemical modifications

A

Diamorphine
Oxycodone
Dihydrocodeine

511
Q

Name 4 synthetic opioids

A

Penthidine
Fentanyl
Alfentanil
Remifentanil

512
Q

Name a synthetic partial opioid agonist

A

Buprenorphine

513
Q

Name an opioid antagonist

A

Naloxone

514
Q

What is the most common route of administration of opioids and what is the normal dose via this method

A

Oral - 10mg

half the dose for s/c, IM or IV

515
Q

What is diamorphine otherwise known as?

A

Heroin

516
Q

How do opioids work

A

Use the existing pain modulation system

Inhibit the release of pain transmitters at spinal cord and midbrain and modulate pain perception in higher centres

517
Q

What are the receptors that opioids bind to?

A

Mu, delta, kappa

518
Q

Define tolerance

A

Downregulation of receptors due to prolonged use - results in a need for higher dose to achieve the same effect

519
Q

Define dependence

A

Psychological - craving, euphoria and physical

520
Q

How long does opioid withdrawal last

A

72 hours

521
Q

What are the side effects of opioid administration

A
  1. respiratory depression
  2. Sedation
  3. Nausea and vomiting
  4. Constipation
  5. Itching
  6. Immune system suppression
  7. Endocrine effects
522
Q

What is the treatment for opioid induced respiratory depression

A
  1. Call for help
  2. ABC
  3. Naloxone - 400ug/ml
    - titrate to effect ie. dilute 1ml in 10ml saline
  4. IV fastest route
523
Q

Give an example of a prodrug

A

Codeine

Tramadol

524
Q

Which enzyme is required to metabolise codeine to its active form

A

CYP2D6

525
Q

What is morphine metabolised to by CYP2D6

A

Morphine 6 glucuronide

526
Q

What enzyme is required to metabolic tramadol into its active form?

A

CYP2D6

527
Q

What is tramadol metabolised to by CYP2D6?

A

O-desmethyl tramadol

528
Q

Define an adverse drug reaction

A

Unwanted or harmful reaction following administration of a drug or combination of drugs under normal conditions of use and is suspected to be drug related - needs to be noxious and unintended

529
Q

Define side effects

A

Unintended effect of a drug relate to its pharmacological properties and can include expected benefits of treatment

530
Q

What are the 3 types of adverse drug reaction

A
  1. Toxic effects - drug applied beyond therapeutic range
  2. Collateral effects - Use drug within its therapeutic range
  3. Hypersusceptibility effects - drug used below its therapeutic range
531
Q

What are the causes of a toxic ADR?

A

Administration of a too high dose
Drug excretion reduced by renal or hepatic functional impairment
Interactions with other drugs

532
Q

What are 4 symptoms of a mild adverse drug reaction?

A

Nausea
Drowsiness
Itching
Rash

533
Q

What are 4 symptoms of a severe adverse drug reaction?

A

Respiratory depression
Neutropenia
Catastrophic haemorrhage
Anaphylaxis

534
Q

Define a time independent adverse drug reaction

A

One that can occur at any time during treatment

535
Q

What are the 6 types of time dependent adverse drug reaction?

A
  1. Rapid reaction
  2. First dose reaction
  3. Early reaction
  4. Intermediate Reaction
  5. Late reaction
  6. Delayed reaction
536
Q

What is the Rawlins Thompson adverse drug reaction classification

A
  1. Type A = Augmented pharmacological (Predictable and dose dependent - extension of the primary effect)
  2. Type B = Bizarre or idiosyncratic (Not predictable or dose dependent)
  3. Type C = Chronic
  4. Type D = delayed
  5. Type E = End of treatment
  6. Type F = Failure of therapy
537
Q

What is the DoTS classification of an adverse drug reaction?

A

Dose relatedness (Toxic, collateral or hypersusceptibility)
Timing
Patient susceptibility

538
Q

What are the patient risk factors for an adverse drug reaction?

A 
Gender (F>M)
Elderly 
Neonates 
Polypharmacy 
Genetic disposition 
Hypersensitivity/allergies 
Hepatic/renal impairment 
Adherence problems
539
Q

What are the drug risk factors for an adverse drug reaction?

A

Steep dose response curve
Low therapeutic index
Commonly causes ADRs

540
Q

What are the prescriber risk factors for an adverse drug reaction?

A

Prescriber may be busy or tired leading them to not realise that two drugs interacting may cause an ADR

541
Q

What are the 7 causes of an ADR?

A
  1. Pharmacological variation
  2. Receptor abnormality
  3. Abnormal biological system unmasked by the drug
  4. Abnormalities in drug metabolism
  5. Immunological
  6. Drug-drug interactions
  7. Multifactorial
542
Q

Give an example of a type A augmented ADR

A

Administration of insulin causing hypoglycaemia

Administration of propranolol causing bradycardia

543
Q

Give an example of a type C continuous ADR

A

Prolonged use of steroids causes thinning of the bones leading to osteoporosis

544
Q

Give an example of a type D delayed ADR

A

teratogenesis - drugs taken in the first trimester ie. thalidomide

545
Q

Give an example of a type E end of treatment ADR

A

Get withdrawal seizures when anti-convulsants are stopped

546
Q

When should we suspect an ADR?

A
  1. Symptoms soon after a drug is started
  2. Symptoms after a dosage increase
  3. Symptoms disappear when the drug is stopped
  4. Symptoms when the drug is restarted
547
Q

What are the most commonly administered drugs that cause ADRs

A 
Antibiotics 
Anti-neoplastics 
Cardiovascular drugs 
Hypoglycaemics 
NSAIDs
CNS drugs
548
Q

What are the most common systems to be affected by ADRs

A 
GI
Renal 
Haemorrhagic 
Metabolic 
Endocrine 
Dermatologic
549
Q

What is the role of the medicines and healthcare products regulatory agency

A

Responsible for ensuring medicines and medical devices work and are acceptably safe

550
Q

What are the strengths of the yellow card scheme

A
  • Early warning for previously unrecognised reactions
  • Provides information about factors which predispose patients to ADRs
  • Allows ADR comparison between products of same therapeutic class
  • Continual safe monitoring of product throughout life span
551
Q

What are the weaknesses of the yellow card scheme

A
  • Cannot provide estimate of risk as true number of cases is underestimated and total number of exposed patients is unknown
  • Relies on ADR being recognised
  • Not all ADRs reported
  • May be stimulated by promotion or publicity
  • Reporting high for newly marketed drugs and then falls off over time
552
Q

Why are yellow card reporting rates low

A 
Ignorance 
Diffidence 
Fear 
Lethargy 
Guilt 
Ambition 
Complacency
553
Q

Why should we report ADRs?

A 
Patient safety 
Identify ADRs not indentified in clinical trials 
Identify new ADRs ASAP
Compare drugs in same therapeutic class 
Identify ADRs in at risk groups
554
Q

What should be reported on a yellow card?

A

Suspected reactions for herbal medicines and black triangle drugs
All serious suspected reactions for drugs, vaccines, contrast media

555
Q

What defines a serious adverse drug reaction

A 
is fatal 
is life threatening 
Is disabling 
results in hospitalisation 
prolongs hospitalisation
556
Q

Define hypersensitivity

A

Objectively reproducible symptoms or signs initiated by exposure to a defined stimulus at a dose tolerated by normal subjects and may be caused by immunologic (allergic) or non immunologic mechanisms

557
Q

Describe what happens in a type 1 hypersensitivity reaction

A
  1. Prior exposure to antigen/drug
  2. IgE antibodies formed after exposure
  3. IgE becomes attached to mast cell and expressed as cell surface receptor
  4. Re-exposure causes mast cell degranulation and release of pharmacologically active substances such as histamine
558
Q

Give an example of a type 1 hypersensitivity reaction

A

Anaphylaxis

559
Q

What occurs during an anaphylactic reaction

A 
Vasodilation which causes increased vascular permeability leading to swelling and oedema 
Bronchoconstriction 
urticaria 
Angio-oedema 
hypotension 
Wheeze
560
Q

Describe what happens in a type 2 hypersensitivity reaction

A

Antibody dependent cytotoxicity -

  • Drug combines with protein
  • Body treats it as foreign proteins and forms antibodies
  • Antibodies combine with antigen and complement activation damages the cells
561
Q

Describe what happens during a type 3 hypersensitivity reaction

A

Immune complex mediated

  • Antigen and IgG antibody form large complexes and activate complement
  • small blood vessels are damaged or blocked
  • Leucocytes are attracted to site and release proinflammtory molecules
562
Q

Give an example of a type 3 hypersensitivity reaction

A

Glomerularnephritis

563
Q

Describe what happens in a type 4 hypersensitivity reaction

A

Antigen specific receptors develop on T-lymphocytes and subsequent administration leads to local tissue allergic reaction

564
Q

Give an example of a type 4 hypersensitivity reaction

A

Contact dermatitis

TB

565
Q

Describe a non-immune anaphylaxis

A

Direct degranulation of mast cells caused directly by the drug with no previous exposure
- Clinically identical to immune anaphylaxis

566
Q

Describe the management of anaphylaxis

A 
Begin life support (ABC) 
Stop the exposure ie. IV fluid
Give Adrenaline (500um) 
High Flow oxygen 
IV fluids to maintain blood pressure 
Anti-histamines (Chlorphenamine)
Steroids (Hydrocortisone)
567
Q

What are the effects of adrenaline administration to an individual having anaphylaxis

A
  1. Vasoconstriction - increase peripheral vascular resistance to increase bp via A1 adrenoceptors
  2. Stimulate B1 adrenoceptors to increase chronotropic and inotropic effects on heart
  3. Reduce oedema and bronco dilate via beta2 adrenoceptors
  4. Attenuate further release of mediators from mast cells and basophils by increasing intracellular c-AMP which reduces inflammatory mediators
568
Q

What are the risk factors for hypersensitivity

A 
Protein or polysaccharides based drugs 
Female > males 
HIV patients 
Previous drug reactions 
Uncontrollled asthma 
Certain HLA groups 
Acetylator status
569
Q

What is the clinical criteria for an allergy to a drug

A
  1. Does not correlate with pharmacological properties of drug
  2. No linear relation with dose
  3. Reaction similar to those produced by other allergens
  4. Induction period of primary exposure
  5. Disappearance on cessation
  6. Re-appears on re-exposure
  7. Occurs in minority of patients on drug
570
Q

What are the two different apoptosis pathways?

A 
intrinsic = Bcl-2 and Bax 
Extrinsic = Fas ligand
571
Q

Give some examples of disease causes by inherited genetic abnormalities

A

CF
Sickle cell
huntingtons

572
Q

Give some examples of diseases caused by spontaneous mutations

A 
Downs = trisomy 21
Edwards = trisomy 18 
Pataus = trisomy 13
573
Q

Give an example of an environmental disease

A

Foetal alcohol syndrome

574
Q

Give some examples of mutlifactorial disease

A

Spina bifida
Anencephaly
Hydrocephaly

575
Q

Define atrophy

A

Decrease in the size of cell tissue due to reduction in cell size and number often due to apoptosis

576
Q

How are malignant tumours classified?

A

Grade 1 = well differentiated
Grade 2 = moderately differentiated
Grade 3 = Poorly differentiated (Most aggressive)

577
Q

What is a teratoma

A

Neoplasm of germ cell origin that forms cells affecting all three germ cell layers

578
Q

Which cancers are screened for in the UK

A

Cervical
Breast
Colorectal

579
Q

What is the function of the immune system?

A

Discriminate between self and non-self

580
Q

What is the role of the complement system

A

Remove or destroy antigens either by direct lysis or opsonisation

581
Q

Describe the process of complement activation

A

2 phase

  1. Activation of C3
  2. Activation of the lytic pathway
582
Q

Which enzyme is responsible for cleaving C3 to activate the complement system

A

C3 convertase

583
Q

When C3 is cleaved, what are the products

A

C3b = mediates opsonisation and lysis

C3a = Enhances inflammation by stimulating mast cells to secrete histamines

584
Q

What are the three pathways that C3 can be cleaved

A

Classical
Alternative
Lectin

585
Q

What is an antibody

A

A protein produced in response to an antigen that can only bind with the antigen that induced its formation

586
Q

What is an epitope

A

Part of an antigen that binds to the antibody binding site

587
Q

Describe the basic structure of an antibody

A

Four chains, two light and two heavy
Constant and variable region
FAB region binds to antigens
FC region binds complement and Fc receptors on phagocytes and NK cells

588
Q

What are the functions of antibodies

A
  1. Neutralise toxins (IgG and A)
  2. Immobilise microbe (IgM)
  3. Increase opsonisation
  4. Activate complement (IgG and IgM
  5. Bind Fc receptors on phagocytes, mast cells and NK cells
589
Q

What are PAMPs, why are they important and give one example

A

Pathogen associated molecular patterns

Allows the innate immune system to recognise pathogens

LPS

590
Q

What are the PRRs and what are the two different types

A

Pattern recognition receptors

  1. Secreted and circulating
  2. Cell associated
591
Q

Name the three different types of secreted and circulating PRRs

A

Antimicrobials = defensins and cathelicidins
Lectin and collectins
Pentraxin

592
Q

Name the cell associated PRRs

A

Toll like receptors
Nod like receptors
Rig like receptors

593
Q

NLR detect what?

A

Muramyl dipeptide and peptidoglycan

594
Q

RLR detect what?

A

Intracellular double stranded RNA and DNA

595
Q

Why do we need an adaptive immunity?

A

Microbes evade the innate
Intracellular viruses and bacteria hide
Need memory to specific antigen

596
Q

What is the function of MHC

A

Present antigenic material to T cells

597
Q

Define Atopy

A

Inherited tendancy to overproduce IgE in response to common environmental antigens

598
Q

What is natural passive immunity

A

Transfer of maternal antibodies across the placenta to foetus

599
Q

Natural passive immunity provides protection from what diseases

A 
Diptheria 
Tetanus 
Streptococcus 
Rubella 
Mumps 
Polio
600
Q

What are the two types of whole organism vaccine

A

Live attenuated

Killed inactivated

601
Q

What diseases does a live attenuated vaccine protect against

A

Tuberculosis
Pollo sabin
Typhoid
Mumps

602
Q

What diseases does a killed inactivated vaccine protect against

A

Anthrax
Cholera
Hep A

603
Q

What is an adjuvant

A

Any substance added to a vaccine to stimulate the immune system

604
Q

What are the two divisions of the peripheral nervous system

A

Autonomic

Somatic

605
Q

What are the adverse effects of muscarinic agonists (DUMBELS)

A 
Diarrhoea
Urination 
Miosis (Excessive pupil constriction)
Bradycardia 
Emesis 
Lacrimation 
Salivation/sweating
606
Q

What GPCR is A1 adrenoceptor

A

Gq + PLC

607
Q

What GPCR is A2 adrenoceptor

A

Gi

608
Q

What GPCR are Beta adrenoceptors

A

Gs

609
Q

Name an alpha 2 adrenoceptor antagonist

A

Yohimbine

610
Q

Define pain

A

Unpleasant sensory + emotional experience associated with actual and potential tissue damage

611
Q

Define absorption

A

Process of transfer from the site of administration into the general or systemic circulation

612
Q

What are the routes of drug administration

A 
Oral 
IV
Intra-arterial 
IM
SC
Inhalation 
Topical 
Sublingual 
Rectal 
Intrathecal (Into spinal canal)
613
Q

How do drugs get across membranes

A
  1. Passive diffusion through lipid layer
  2. Diffusion through pores or ion channels
  3. Carrier mediated processes
  4. Pinocytosis
614
Q

Rate of diffusion is proportional to what?

A

Area of the membrane

Permeability of the membrane

615
Q

Rate of diffusion is inversely proportional to what?

A

Membrane thickness

616
Q

Carrier mediated transport requires what?

A

ATP - moves molecules against a concentration gradient

617
Q

Facilitated diffusion occurs using which gradients

A

Concentration gradient

Electrochemical gradient

618
Q

Define pinocytosis

A

Form of carrier mediated entry into the cytoplasm

619
Q

Name a drug that is transported by pinocytosis

A

Amphotericin

620
Q

What forms are a drug normaly in

A

Weak acid

Weak base

621
Q

What does the extent of ionisation depend on

A

Strength of the ionisable group

pH of the solution

622
Q

Is the ionised form water or lipid soluble

A

Water soluble

623
Q

Is unionised form water or lipid soluble

A

Lipid soluble

624
Q

What is the pKa of a drug

A

pH at which half of the substance is ionised and half is unionised

625
Q

Where are weak acids best absorbed

A

In the stomach

626
Q

Where are weak bases best absorbed

A

in the intestine

627
Q

Why is the oral route most commonly preferred

A

because large surface area with a high blood flow

628
Q

For a drug to cross the phospholipid bilayer it needs to be what?

A

Lipid soluble

629
Q

What factors slow gastric emptying and hence drug absorption?

A

Food
Drugs
Trauma

630
Q

What factors increase gastric emptying and hence drug absorption

A

Gastric surgery
(Gastrectomy)
(Plyloroplasty)

631
Q

Why can some drugs not be given orally

A

Because they are unstable at low pH or in the presence of digestive enzymes

632
Q

What 4 barriers do drugs taken orally have to pass to reach the circulation

A
  1. Intestinal lumen
  2. Intestinal wall
  3. Liver
  4. Lungs
633
Q

What is broken down by enzymes of the intestinal lumen

A

Peptide drugs broken down by proteases

634
Q

luminal membrane of enterocytes contain what which can limit the absorption of a drug

A

P-glycoproteins

635
Q

1st pass metabolism occurs mainly where?

A

in liver

636
Q

How can you avoid first pass metabolism

A

Give drug to region of the gut not drained by splanchnic ie. mouth or the rectum

637
Q

Name a drug given transcutaneously

A

Fentanyl patch in chronic pain (Non potent- non irritant drugs
Delivered slowly

638
Q

Name a drug given intradermally or subcutaneously

A

Local anaesthetic
Insulin (Sc)
Can deliberately limit the rate of absorption

639
Q

What is the issue with IM injections

A

Dependent of blood Flow and water solubility - increase in either will enhance the removal of the drug from the injection site

640
Q

Name a benefit of intranasal administration

A

Large surface area

641
Q

Name an advantage and one disadvantage of inhalation administration

A

Large surface area but limited by risk of toxicity to the alveoli

642
Q

Define distribution

A

Process by which the drug is transferred from the general circulation to the tissues as the blood concentration increases and then returns from the tissues to the blood when the concentration falls

643
Q

Describe how IV drugs become distribute

A

Initial high plasma concentration and drug rapidly enters well perfused tissues but drug will continue to enter less well perfused tissues lowering plasma concentration so concentration in highly perfused tissues then begins to decrease

644
Q

what are the components of the blood brain barrier

A

Tight junctions
Small numbers and sizes of pores in the endothelium
Astrocytes

645
Q

What is the role of efflux transporters in the BBB

A

Protect the brain by returning drug molecules to the circulation

646
Q

How are drugs removed from the BBB

A

Diffusion into the plasma
Active transport in the choroid plexus
Elimination in CSF

647
Q

Do lipid soluble drugs cross the placenta

A

Yes

648
Q

Define elimination

A

Removal of a drugs activity from the body

649
Q

Define metabolism

A

Transformation of a drug molecule into a different molecule

650
Q

Define excretion

A

Molecule expelled in liquid, solid or gaseous waste

651
Q

Describe a phase I reaction

A

Reaction that involves the transformation of a drug to a more polar metabolite
Addition of functional group

652
Q

What is the most common phase I reaction

A

Oxidation - catalysed by cytochrome P450

653
Q

Where are the CYP450 enzymes located

A

In the smooth endoplasmic reticulum in the liver

654
Q

What can induce P450 enzymes

A

Smoking
Alcohol
Drugs
Food

655
Q

What is a phase 2 reaction

A

Conjugation - formation of a covalent bond between the drug or its phase 1 metabolite and an endogenous substrate - resulting products are usually less active and readily excreted by the kidneys

656
Q

What are phase 1 metabolites usually conjugated with?

A

Glucuronic acid

Acetyl methyl groups

657
Q

How are molecular weight polar compounds excreted

A 
In fluids 
Urine 
Bile 
sweat
tears 
Breast milk
658
Q

High molecular weight compounds are excreted by

A

Solid

Faecal

659
Q

Volatile drugs are excreted by

A

Gas

660
Q

Write an equation for total excretion

A

Glomerular filtration + tubular secretion - reabsortption

661
Q

Describe enterohepatic circulation

A

HMW molecules taken into hepatocytes and eliminated in the bile
Bile passes down the gut and some drug may be reabsorbed and enters hepatic portal vein via enterohepatic circulation

Phase 2 (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions