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ICS Flashcards

1
Q

What is inflammation?

A

A reaction to an injury or infection involving cells such as neutrophils and macrophages.

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2
Q

How is inflammation classified?

A

Acute and Chronic

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3
Q

What cells are common in acute inflammation?

A

Neutrophils

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4
Q

What cells are common in chronic inflammation?

A

Lymphocytes & macrophages

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5
Q

Features of acute inflammation?

A
  • Sudden onset
  • Short duration
  • Usually resolves
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6
Q

Features of chronic inflammation?

A
  • Slow onset or sequel to acute
  • Long duration
  • May never resolve
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7
Q

What do neutrophil polymorphs do in inflammation?

A
  • Short lived
  • First on scene
  • Cytoplasmic granules containing enzymes
  • Die at scene of inflammation -Releases yellowy puss
  • Releases chemicals that attract other inflammatory cells eg. macrophages
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8
Q

What do macrophages do in inflammation?

A
  • Long life (weeks to months)
  • Phagocytic
  • Carry debris away (eg. to lymph nodes)
  • Present antigens to lymphocytes
  • Don’t always die
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9
Q

What do lymphocytes do in inflammation?

A
  • Memory cells
  • Long life (years)
  • Produce chemicals which attract inflammatory cells
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10
Q

What do endothelial cells do in inflammation?

A
  1. become sticky

2. become porous (precapillary sphincters open = more blood flows through = more inflammatory cells)

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11
Q

Why is there redness and swelling in inflammation?

A

Red = increased blood flow

Swelling = more protein out, less/no liquid in

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12
Q

What cells are involved in chronic inflammation?

A

Lymphocytes, plasma & macrophages

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13
Q

What is a granuloma?

A

Aggregate of epitheliod histiocytes (macrophages) surrounded by lymphocytes.

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14
Q

Systemic effects of inflammation?

A
  • Fever (pyrexia)
  • Weight loss
  • Amyloidosis
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15
Q

How do you treat inflammation?

A

Aspirin
NSAIDs - stop prostaglandin synthase
Betnovate cream

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16
Q

What is betnovate cream?

A

Corticosteroid

Can cause skin to atrophy
Powerful/potent anti inflammatory
Binds to DNA to upregulate inhibitors of inflammation and downregulate chemical mediators of inflammation.

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17
Q

What is prostaglandin synthase?

A

It is a chemical mediator of inflammation.

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18
Q

When is cell damage resolved?

A

When initiating factor is removed.

Tissue is undamaged or able to regenerate.

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19
Q

When is cell damaged repaired?

A

Initiating factor is still present. Tissue damaged and unable to regenerate.

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20
Q

What causes cirrhosis?

A

Architectual damage –> fibrous scarring –> regenerative nodules –> cirrhosis

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21
Q

How do skin abrasions heal?

A

Scab forms over surface, root hair cells and weat glads still there, grows up under the scab.

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22
Q

How do 1st intention (edges together) wounds heal?

A

Fibrin from blood - fibroblasts produce collagen.

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23
Q

How do 2nd intention (edges can’t be pulled together) wounds heal?

A

Fibroblasts grow from the edges of the wound.

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24
Q

What cells regenerate?

A
  • Hepatocytes
  • Pneumocytes
  • All blood cells
  • Gut epithelium
  • Skin epithelium
  • Osteocytes
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25
Q

What cells don’t regenerate?

A
  • Myocardial cells

- Neurones

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26
Q

What is ischaemia?

A

Reduction in blood flow

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27
Q

What is infarction?

A

Death of cells due to ischaemia.

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28
Q

What is a reperfusion injury and why are they caused?

A

When blood is reintroduced after ischaemia cells produce damaging chemicals eg. superoxides.

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29
Q

Features of RCA obstruction?

A
  • Inferior obstruction
  • ECG changes in leads II, III, aVF
  • Can involve post. septum
  • 30% of cases
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30
Q

Features of LAD obstruction?

A
  • Artery of sudden death
  • Anterior infartion
  • ECG changes in anterior chest leads
  • 50% cases
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31
Q

Features of circumflex obstruction?

A
  • Lateral infaction
  • ECG changes in I, aVL and lateral chest leads (V4-6)
  • 20% cases
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32
Q

What is a thrombosis?

A

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

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33
Q

What are the three components that make up thrombosis risk?

A
  • Change in vessel wall
  • Change in blood flow
  • Change in blood constituents
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34
Q

How do you prevent thrombosis?

A
  • Exercise
  • Tight elastic stockings/socks
  • Wiggle toes
  • Aspirin = anti-platelet = stops platelet aggregation
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35
Q

What is an embolus?

A

Mass of material in the vascular system able to become lodged within a vessel and block it.
The most common is a piece of thrombus but can be others eg. gas.

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36
Q

What is hypertrophy?

A

Increase in size of a tissue caused by an increase in size of the constituent cells.

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37
Q

What is hyperplasia?

A

Increase in size of a tissue caused by an increase in number of the consituent cells.

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38
Q

What is atrophy?

A

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

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39
Q

What is metaplasia?

A

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

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40
Q

What is dysplasia?

A

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

(Not yet but could become cancer)

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41
Q

What is apoptosis?

A

Programmed cell death.

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42
Q

What causes cells to apoptose?

A

DNA damage

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43
Q

How do cell apoptose?

A
  • Enzymes released which kills nucleus
  • Nucleus condenses
  • Cells shrink
  • Nucleus fragments
  • Cleaned by macrophages
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44
Q

What is p53?

A

A protein which detects DNA damage and produces chemicals to cause apoptosis.

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45
Q

What is necrosis?

A

Mass death of cells.

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46
Q

What are the two types of necrosis?

A

Coagulative - thick and goey

Liquifactive - goes liquidy

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47
Q

What is caseous necrosis?

A

Has holes in it - common in TB

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48
Q

What are telomeres?

A

Section at the end of chromosomes, each time a cell divides the telomere shortens.

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49
Q

What affects how quickly a cell wears out?

A

-Cross-linking/mutations of DNA
-Loss of Ca2+ influx controls
-Cross-linking of proteins
-Telomere shortening
-Accumulation of toxic by-products of metabolism
-Free radical generation
-Peroxidation of membranes
etc.

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50
Q

What does UVB light cause?

A

Protein cross linking - makes collagen no longer elastic

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51
Q

What is osteoporosis in women?

A

Lack of aestrogen = increased bone resorption and decreased bone formation.

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52
Q

How are cataracts caused?

A

UV-B light causes protein cross linking which makes the proteins opaque.

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53
Q

What causes sarcopaenia (lack of muscle)?

A

Decreased growth hormones, decreased testosterone, increased catabolic cytokines.

Increasing testosterone does decrease sarcopaenia but increased GH doesn’t.

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54
Q

When does atheroschlerosis occur?

A
  • In more deprived area

- Age 50+

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55
Q

Where is there rarely atherosclerosis?

A

Low pressure systems.

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56
Q

What’s in plaque?

A
  • Fibrous tissue
  • Lipids, cholesterol
  • Lymphocytes, chronic inflammation
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57
Q

What are risk factors of atherosclerosis?

A
  • Smoking cigarettes = free radicals, nicotine, carbon monoxide which cause damage to endothelial cells
  • Hypertension = shearing forces
  • Poorly controlled diabetes = superoxide anions, glycosylation products
  • Hyperlipidaemia
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58
Q

Why does atheroslerosis form?

A

Endothelial cell damage.

They are delicate and metabolically active cells.

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59
Q

What is acute inflammation?

A

The initial and often transient series of tissue reactions to injury.

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60
Q

What is chronic inflammation?

A

The subsequent and often prolonged tissue reactions following the initial response.

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61
Q

What is tissue necrosis?

A

Death of tissues from lack of oxygen or nutriients resulting from inadequate blood flow.

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62
Q

Treatment for basal cell carcinoma?

A

Complete local excision

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63
Q

Breast cancer treatment:

It has spread to the axilla.. treatment?

A

Axillary node clearance

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64
Q

Breast cancer treatment:

It has spread to the rest of the body.. treatment?

A

Systemic chemo therapy

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65
Q

Breast cancer treatment: it hasn’t spread to the rest of your body or axilla.. treatment?

A

Surgery with or without axillary lymph node clearance.

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66
Q

What is adjuvant therapy?

A

Treatment given after surgical treatment.

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67
Q

What is carcinogenesis?

A

Transformation of normal cells to neoplasticism cells through permanent genetic alterations or mutations.

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68
Q

What is oncogenesis?

A

Formation of benign and malignant tumours.

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69
Q

What’s the difference between carcinogenic and oncogenic?

A

Carcinogen: agents thought to cause rumours
Oncogen: cancer tumour causing

Both act on DNA

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70
Q

What percentage of cancer risk is environmental?

A

85%

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71
Q

What are the carcinogens for hepatocellular carcinoma?

A

Hep B/C and mycotoxins

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72
Q

What are the carcinogens for Oesophageal carcinoma?

A

Linhsien chickens and very very hot coffee.

Increased incidence in Japan, China , Turkey, Iran

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73
Q

What are the carcinogens for Lung cancer?

A

Smoking

35,000 deaths/year

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74
Q

What are the carcinogens for Bladder cancer?

A

Anyone dye and rubber industries

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75
Q

What are the carcinogens for Scrotal cancer?

A

Higher risk in chimney sweeps. Polycyclic aromatic hydrocarbons.

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76
Q

What is Thorotrast?

A
  • Colliidal suspension of thorium
  • radiographic contrast medium 1930-1950
  • 1947 post-thorotrast angiosarcoma
  • it is radioactive
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77
Q

What are the classes of carcinogens?

A
  • Chemical
  • Viral
  • ionising and non-ionising radiation
  • hormones, parasites and micro toxins
  • misc
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78
Q

What can polycyclic hydrocarbons cause?

A

Lung & skin cancer

Found in cigarettes and mineral oils

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79
Q

What can aromatic amines?

A

Bladder cancer

From rubber/dye workers

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80
Q

What can nitrosamines cause?

A

Gut cancer

In processed/smoked

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81
Q

What can alkylating agents cause?

A

Leukaemia

Used to kill certain cancers
Small risk in humans

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82
Q

What does increased exposure to UV(A & B) light increase the risk of?

A

Basal cell carcinoma, melanoma, squamous cell carcinoma

Much higher risk of xeroderma pigmentosum

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83
Q

Name some biological, hormonal carcinogens?

A

Oestrogen - increases mammary/endometrial cancer

Steroids- hepatocellular carcinoma

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84
Q

Name a biological, mycotoxin carcinogen?

A

Aflatoxin B - hepatocellular carcinoma

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85
Q

Name some biological, parasitic carcinogens?

A

Clonorchis sinensis - cholangiocarcinoma

Shistosoma - bladder cancer

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86
Q

What does asbestos cause?

A

Malignant mesothelioma, lung cancer, asbestosis

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87
Q

What is a neoplasm?

A

A lesion resulting from the AUTONOMOUS or relatively autonomous ABNORMAL growth of cells which PERSISTS after the irritating stimulus has been removed.
A new growth.

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88
Q

What is the epidemiology of neoplasm?

A 
25% of population
All ages
Increased risk with age
Mortality rate high
20% all deaths
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89
Q

What are the two parts of neoplasm?

A

Neoplastic cells and stroma

90
Q

What are features of neoplastic cells?

A
  • Nucleated cells
  • Usually monoclonal
  • Growth pattern mirrors parent cell
  • Synthetic activity same as parent cell
91
Q

What are features of neoplastic stroma?

A
  • Connective tissue framework
  • Mechanical support
  • Provides nutrition
  • Fibroblasts and blood vessels
92
Q

What are the three behavioural classifications of neoplasms?

A
  • Benign
  • Borderline
  • Malignant
93
Q

What are features of benign neoplams?

A
  • Localised, non-invasive
  • Slow growth rate
  • Low mitotic index
  • Close resemblance to normal tissue
  • Circumscribed/encapsulated
  • Nuclear morphometry often normal
  • Necrosis and ulceration rare
  • Growth on mucosal surfaces often exophytic
94
Q

How does benign neoplasm cause morbidity/mortality?

A
  • Pressure on adjacent structures
  • Obstruct flow
  • Produce hormones
  • Transform to malignant
  • Anxiety
95
Q

What are features of malignant neoplasms?

A

MUST BE INVASIVE

  • Metastases
  • Rapid growth rate (compared to benign)
  • Variable resemblance to normal tissue
  • Poorly defined/irregular border
  • Increased mitotic activity (metaphase)
  • Necrosis and ulceration common
  • Endophytic
  • Encroach upon/destroy surrounding tissue
96
Q

What is histogenesis?

A

The specific cell of origin of a tumour

97
Q

What is the suffix for all neoplasms?

98
Q

What is a papilloma?

A

Benign tumour of non-glandular, non-secretory epithelium.

99
Q

What is an adenoma?

A

Benign tumour of glandular/secretory epithelium

100
Q

What is a carcinoma?

A

Malignant tumour of epithelial cells

101
Q

What is an adenocarcinoma?

A

Carcinoma of glandular epithelium

102
Q

What is a lipoma?

A

Benign neoplasm of adipocytes

103
Q

What is a chondroma?

A

Benign neoplasm of cartilage

104
Q

What is an osteoma?

A

Benign neoplasm of bone

105
Q

What is an angioma?

A

Benign neoplasm of vessels

106
Q

What is a rhabdomyoma?

A

Benign neoplasm of striated muscle

107
Q

What is a leioma?

A

Benign neoplasm of smooth muscle

108
Q

What is neuroma?

A

Benign neoplasm of nerves

109
Q

What is a sarcoma?

A

Fleshy, MALIGNANT

110
Q

What is a liposarcoma?

A

Malignant neoplasm of adipose tissue

111
Q

What is anaplastic?

A

Cell-type of origin unknown?

112
Q

Explain the process of invasion?

A

Carcinoma in situ -> BM -> Extracellilar matrix -> lymph/blood vessels -> Travel (avoiding WBCs) -> Land -> Stick to vessel wall -> Into extracellular matrix

113
Q

What do tumours have to do at 1-2mm?

A

Angiogenesis

114
Q

Why do lymphoma and other sarcomas spread to bone?

A

When in blood the first small vessels broken off bits of tumour come across are in the lungs.

115
Q

How does cancer evade immune defence?

A
  • Aggregation with platelets/themselves

- Shed surface antigens

116
Q

What neoplasias commonly met in the liver?

A

Anything colorectal, stomach, pancreas. Through the portal vein.

117
Q

What commonly met in bone?

A
  • Lung
  • Thyroid
  • Breast
  • Prostate
  • Kidney
118
Q

What is innate immunity?

A

Instinctive, non-specific, doesn’t depend on lymphoctyes, present from birth.

119
Q

What is adaptive immunity?

A

Specific ‘aquired/learned’ immunity requires lymphocytes, antibodies.

Made up of cells & soluble factors (humoral)

120
Q

What is the haematocrit?

A

RBC volume, ~45%

121
Q

What is serum?

A

Plasma without fibrinogen and other clotting factors.

122
Q

Where do immune system cells originate from?

A

Multipotent haemopoetic stem cells. Differentiation depends on which cytokines are released.

123
Q

What type of stain do neutrophils stain with?

124
Q

What type of stain do Eosinophils stain with?

125
Q

What type of stain do basoophils stain with?

126
Q

What are the early mononuclear leukocytes and what do they really differentiate into?

A

Monocyte —> Macrophage

T-Cells —> T regulators, T Helpers (CD4) (Th1, Th2), Cytotoxic

B-Cells —> Plasma

127
Q

What are soluble factors?

A

Tell cells to do things.

Compliment
Antibodies
Cytokines, chemokines

128
Q

What are compliments?

A 
Group of ~20 serum proteins secreted by the liver. 
Need to be activated.
Action:
-direct lysis
-attract more leukocytes
-coat invading organisms 
-lysis, chemotaxis, oponisation
129
Q

What are the antibodies and their proportion?

A 
IgG - 70-80%
IgM - ~10%
IgA - 15%
IgD ~1%
IgE ~ 0.05% Allergic reactions/parasites
130
Q

What are interferons?

A

A type of cytokine which induce a state of antiviral resistance in uninfected cells & limit spread of infection?

131
Q

What are interleukins?

A

A type of cytokine
>30 types.
IL1 = pro-inflammatory
IL10 = anti-inflammatory

132
Q

What are colony stimulating factors?

A

A type of cytokine

Cause division and differentiation on basement membrane stem cells.

133
Q

What are tumour necrosis factors?

A

A type of cytokine

Mediate inflammation & cytotoxic reactions

134
Q

What are chemokines?

A

They tell cells where to go
~40 types
Certain chemokines attract certain cells

135
Q

What are innate immunity components?

A
  • Physical & chemical barriers
  • Phagocytic cells (neutrophils and macrophages)
  • Blood proteins (compliment, acute phase)
136
Q

Define inflammation?

A

A series of reactions that brings cells and molecules of the immune system to sites of infection/damage.

137
Q

What is extravasation?

A

Attracting other cells

Lymphoctyes releases TNF alpha –> Causes endothelium to become sticky –> other cells go through endothelium

138
Q

What is involved in oxygen dependant microbial killing?

A
  • Reactive oxygen intermediates (ROI)
  • Super oxides O2- are converted into H2O2 then OH radicals
  • NO = vasodilation (viagra)
139
Q

What is involved in oxygen independant microbial killing?

A
  • Enzymes
  • Proteins
  • pH
140
Q

What cells kill which microbes in the adaptive immune system?

A
  • T cells = intracellular microbes

- B cells = extracellular microbes

141
Q

Primary and secondary lymphoid of T-Cells?

A

Thymus –> Spleen, lymph nodes, MALT

142
Q

Primary and secondary lymphoid of B-Cells?

A

Bone Marrow –> Spleen, lymph nodes, MALT

143
Q

Primary and secondary lymphoid of APC, dendritic Cells, macrophages, B Cells?

A

Bone Marrow –> tissue –> Spleen, lymph nodes, MALT

144
Q

What are features of T Lymphoctyes?

A
  • Don’t respond to soluble antigens, only intracellular ‘presented antigens’
  • T Cells that recognise ‘self’ killed in thymus
  • Receptors detect antigens & associated with major histocompatibility complex (MHC)
145
Q

What are the MHCs?

A

Major histocompatibility complexes
MHC1 - all nucleated cells (8-10aa’s)
MHC2 - only antigen presenting cells (13-24aa’s)

146
Q

What do all T cells stem from?

A

Alpha, beta T

147
Q

What do Alpha-beta T cells develop to?

148
Q

What does CD4 develop into?

A

When IL-12 is high = TH1

When IL-12 is low = TH2

149
Q

What do CD8 T cells do

A

Kill intracellular pathogens directly by producing perforin (apoptosis) and granulysin (punch holes in cells - killing)

150
Q

What do CD4 - TH1 cells do?

A

IFN gamma helps kill intracellular pathogens

151
Q

What do CD4 - TH2 cells do?

A

Antibody production

152
Q

What is the process of immunisation?

A

Exposure/vaccination —> antigen presentation to T Cells —> IgM produced —> highly specific IgG produced –> large amounts of IgGs from plasma cells

153
Q

How does the body handle bacteria/fungi?

A

Phagocytosis & killing

154
Q

How does the body handle viruses?

A

Cellular shut-down, self-sacrifice, cellular resistance.

155
Q

What are the problems with immunity?

A
  • Take long time
  • Highly specific
  • Lots of bacteria/pathogens
156
Q

What patterns on pathogens are detected?

A
  • Gram +ve/-ve
  • double stranded RNA
  • CpG motifs
157
Q

What are TLRs?

A

Toll like receptors. The most common type of recpetor.

Endotoxin is present in gram -ve bacteria.

158
Q

What are secreted/circulating PRRs?

A

Pattern recognition receptors.

  • Antimicrobial peptides secreted in lining fluids, from epithelia and phagocytes.
  • Lectins and collectings are carbohydrate-containing proteins that bind carbohydrates or lipids in microbe walls. Activate complement. improve phagocytosis.
  • Pentracins - proteins like CRP which have some antimicrobial actions. React with C protein of pneumococci, activate compliment.
159
Q

What are cell associated PRRs?

A

Pattern recognition receptors.
Present on cell membrane/cytosol of cells.
!!!TLRs are main family!!!

160
Q

What are NLRs?

A

Nod like receptors.
22 human proteins that detect intracellular microbial pathogens.
Known as NOD1, NOd2 NLRP” etc.

161
Q

What do NOD2 receptors do?

A
  • Recognise muramyl dipeptide (MDP), a breakdown product of peptoglycan.
  • Activates inflammatory signalling pathways
  • Chron’s = non-functioning
162
Q

What are RLRs?

A

Rig like receptors.
Named after first members of the family Rig-I. Rig Like Helicases.
Couple to activate interferon production for antiviral response.

163
Q

What is natural passive immunisation?

A

The transfer of maternal antibodies across the placenta.

164
Q

What is artificial passive immunisation?

A

Treatment with pooled normal human IgG or immunoserum against pathogens or toxins.

165
Q

What vaccines are passive?

A

Botulism, tetanus, diphtheria (anti toxins)
Hepatitis, measles, rabies (prophylactically)
Anti-venins

166
Q

What are the steps of active immunisation?

A

Engage innate immune system

Elicit danger signals eg. PAMPs

Engage TLR receptors

Activate specialised antigen presenting cells eg. Langerhans cells

Engage adaptive immune systems - generate T & B cells. Activate T cell helper.

167
Q

What antibodies are active at different parts after exposure?

A

~ 2 days in = IgM starts
~6 days in = IgG starts
Secondary exposure = lots more IgG, about 900 times more than IgM which is less than the first exposure.

See graph.

168
Q

Why does flu require repeated immunisation?

A

Rapid onset - become infected before immunological memory activated. So high level of antibody must be kept, also requires different types due to annual escape variants.

169
Q

What are the types of antigens for vaccines?

A

a) Whole organism
- -> Live attenuated
- -> Killed, inactivated
b) Subunit
c) Peptides
d) DNA Vaccines
e) Engineered virus

170
Q

What vaccines are live attenuated pathogens?

A

TB- BCG
Polio Sabin

Correct preparation is essential

171
Q

Name some advantages to live attenuated pathogen vaccines?

A
  • Activates natural response machanism
  • Prolonged contact with immune system
  • Memory response
  • Single immunisation required
172
Q

Name some disadvantages to live attenuated pathogen vaccines?

A
  • Can’t be used in immunocompromised patients
  • Complications
  • Occationally can become virulent
173
Q

Name some advantages to the whole inactivated pathogen vaccines?

A
  • No infection risk
  • Storage not critical
  • Wide range of antigens = good immune response
174
Q

Name some disadvantages to live attenuated pathogen vaccines?

A
  • Just activate humoral - lack of T
  • Weak immune response
  • Boosters needed
  • Patient compliance issue
175
Q

Name some advantages to subunit vaccines?

A
  • Safe
  • No risk of infection
  • Easy to store and preserve
176
Q

Name some disadvantages to subunit vaccines?

A
  • Immune response less powerful

- Repeated vaccinations and ajuvants

177
Q

What is a toxoid?

A

Heat/chemically treated toxin modified to eliminate toxicity

178
Q

What vaccines use bacterial exotoxins?

A
  • Diptheria

- Tetanus

179
Q

Name some advantages to DNA vaccines?

A
  • Safe
  • Not complex storage & transportation
  • Drug delivery simple and adaptable to widespread vaccination programmes
180
Q

Name some disadvantages to DNA vaccines?

A
  • Mild response
  • Subsequent boosting
  • No transient infections
  • Limited to proteins, could induce tolerance or anti-DNA antibodies
181
Q

How do recombinant vector vaccines work?

A

Imitate the effect of transient infection with pathogen but using a non-pathogenic organism

182
Q

Name some advantages to recombinant viral vaccines?

A
  • Create ideal stimulus to immune system
  • Produce immunological memory
  • Flexible - different components can be engineered in
  • Safe - relative to live attenuated pathogen
183
Q

Name some disadvantages to recombinant viral vaccines?

A

Require refrigeration for transport
Can cause illness in compromised individuals
Immune response to virus in subjects can negate effectiveness

184
Q

What should the ideal vaccine be?

A

-Safe!
-Should induce a suitable immune response
-Generate T and B cell memory
-Stable and easy to transport
for use in remote areas
-Should not require repeated boosting

185
Q

Define physicochemical properties?

A

The physical and chemical properties of substances..

eg. sticks to paracetamol and is excreted - adsorption

186
Q

Define pharmacodynamics?

A

Effect of drugs on the body

187
Q

Define summation?

A

When drugs have additive effects on the body.
1 + 1 = 2

Pharmacodynamics

188
Q

Define synergistic drug effects

A

When you give two drugs together it amplifies the results of either one.
1 + 1 > 2

Pharmacodynamics

189
Q

Define drug antagonism?

A

When two drugs act against each other
1 + 1 = 0

eg. counteract opioid/drug overdose
Pharmacodynamics

190
Q

Define drug potentiation?

A

When competition means drug A works like normal, drug B changes - may prolong the effect of drug B/

191
Q

Define pharmacokinetics?

A

The effect of the body on the drug?

192
Q

What does ADME stand for?

A

A - Absorption
D - Distribution
M - Metabolism - changes them so they can be excreted in the kidney. Turns pro-drugs into drugs that work.
E - Excretion

pharmacokinetics

193
Q

How does the type of drug affect absorption?

A

IV = acts instantly for a short time but very high concentration
Orally = takes a bit of time to be absorbed but longer to excrete
Oral needs a higher dose

pharmacokinetics

194
Q

What is bioavailability?

A

Comparing drugs using area under the time-concentration graph

pharmacokinetics

195
Q

How is motility important in drugs?

A

Any drugs that affect motility will affect absorption

pharmacokinetics

196
Q

How does acidity affect absorption?

A
  • Drugs are in ionised and unionised portions
  • The portion that crosses the membrane is unionised
  • More alkali = more unionised
  • Maintains concentration gradients to get drug into nerve cell

Abscess means local anaesthetic - ruins concentration gradients

pharmacokinetics

197
Q

Explain the effect of distribution on drugs?

A
  • Drugs will attach to proteins, other tissues and the effect sites
  • Big volume of distribution = going everywhere - less to where you’re aiming for/in blood
  • If you give two protein bound drugs - more will float around in blood and can make it toxic

pharmacokinetics

198
Q

Explain the effect of metabolism on drugs?

A
  • Liver
  • Morphine –> CYP450 –> morphine-6-glucuronide (6 x more potent) in a normal patient excreted quickly so no affect
  • Phenytoin (anti epileptic drug) causes CYP450 to be increased so way more M-6-G
  • Alcohol induces CYP450 – careful giving morphine to chronic alcoholics = increased M-6-G
  • Metronidazole slows down/inhibits CYP450 so morphine sticks around a lot longer

Pharmacokinetics

199
Q

Explain how excretion affects drugs?

A
  • Most drugs renally excreted
  • Aspirin (acidic) – give bicarb of soda = alkalinise urine

pharmacokinetics

200
Q

What is an important drug interaction of warfarin?

A

Warfarin inhibits vit. K factors with coagulation cascade

Highly protein bond - add another protein drug = increased effect.

Enzyme inhibition/induction highly affect it.

201
Q

What drugs is AKI caused by?

A

NSAIDs, Gentamicin, ACE inhibitors, Furosemide

202
Q

What juice interacts with lots of drugs including warfarin?

A

Grapefruit juice

203
Q

What is druggability?

A

The ability of a protein target to bind small molecules with high affinity. 10-15% human genome may be druggable.

204
Q

What is a receptor?

A

• A component of a cell that interacts with a specific ligand and initiates a change of biochemical events leading to the ligands observed effects.

205
Q

What is an exogenous ligand?

206
Q

What is an endogenous ligand?

A

Hormone/neurotransmitter

207
Q

What are the main features of G protein coupled receptors?

A
  • Largest & most diverse group
  • Targeted by >30% drugs
  • When G proteins bound to GDP = on, when G proteins bound to GTP = off
  • Most GPCRs interact with PLC or adenylyl cyclase
208
Q

What are kinase-linked receptors?

A
  • Transmembrane

- Activated by extracellular ligang –> causes enzymatic activity on the intracellular side

209
Q

How do nuclear receptors work?

A

Modifying gene transcription

210
Q

What is efficacy?

A

(Emax) = maximum response achievable from a dose

211
Q

What is intrinsic activity (IA)

A

ability of a drug-receptor complex to produce a maximum functional response

212
Q

What are the two types of cholinergic receptor?

A

Muscarine mAChR

Nicotine nAChR

213
Q

What is the antagonist to mAChR?

214
Q

What is the antagonist to nAChR?

215
Q

What sort of reaction is caused by histamine 1 receptors?

216
Q

What sort of reaction is caused by histamine 2 receptors?

A

Gatsric acid secretion

217
Q

What sort of reaction is caused by histamine 3 receptors?

A

CNS disorders

218
Q

What sort of reaction is caused by histamine 4 receptors?

A

Immune system/inflammation

219
Q

What is ligand affinity?

A

How well a ligand binds to a receptor (agonist and antagonist)

220
Q

What is ligand efficacy?

A

how well a ligand activates the receptor (only agonists)

221
Q

What is a receptor reserve?

A

Agonists only need to activate a small fraction of receptors to produce maximal system response (spare receptors)

222
Q

What is receptor tolerance?

A

Reduction in agonist effect over time due to continuous, high concentrations

Phase 2a Lauren (15 decks)

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