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Phase 2a - Jemima > Introduction to Clinical Sciences > Flashcards

Introduction to Clinical Sciences Flashcards

1
Q

What is inflammation

A

cellular reaction to injury involving neutrophils and polymorphs

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2
Q

what are neutrophil polymorphs

A

they are white blood cells made in the bone marrow. They have a short lifespan (2-3 days), and are called polymorphs cause they have a polylobed nucleus

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3
Q

what do neutrophils contain to remove pathogens

A

contain lysosomes of enzymes which can kill phagocytosed bacteria

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4
Q

what types of immune cells are the first to arrive at the site of acute inflammation

A

neutrophils

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5
Q

what is the lifespan of macrophages

A

months to years

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6
Q

what are features of macrophages

A

they have a circular nucleus, and acts as antigen presenting cells. They have different names dependent on what tissue they reside

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7
Q

Define exudate

A

Exudate is fluid that leaks out of blood vessels into nearby tissues. The fluid is made of cells, proteins, and solid materials.

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8
Q

what are lymphocytes

A

they are T or B cells which are long lives cells which produce chemicals involved in controlling inflammation and production of antibodies. Lymphocytes are the immunological memory of the body

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9
Q

what are plasma cells

A

they are specialised B cells which are antibody producing

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10
Q

what are fibroblasts

A

they are cells which produce collagenous connective tissue- spindle shaped cells

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11
Q

what are the features of acute inflammation

A

injury or infection
early onset - seconds to minutes
short duration - hours to days
cells involved - neutrophils and then macrophages

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12
Q

what are examples of acute inflammation

A

microbial infections - bacteria and viruses
hypersensitivity reactions - parasites
physical agents - trauma, heat, cold
chemicals - corrosives and acids
bacterial toxins
tissue necrosis – ischemic

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13
Q

what is the sequence of events of chronic inflammation

A

either progression from acute inflammation or starts as chronic inflammation
there are no or few neutrophils in this case
macrophages and lymphocytes and then fibroblasts involved
can resolve if there is no tissue damage but this often ends up with repair and formation of scar tissue

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14
Q

what is an example of primary chronic inflammation

A

infection mononucleosis

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15
Q

what is a granuloma

A

it is a particular type of chronic inflammation with collections of macrophages/histiocytes surrounded by lymphocytes

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16
Q

what are the reasons for granuloma formation

A

seen in mycobacterial infection such as TB or leprosy, also seen in crohns disease and sarcoidosis

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17
Q

what are the features of endothelial cells

A

the line blood vessels and produce nitric oxide to prevent platelets sticking to them.

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18
Q

why might an inflamed area be red and swollen

A

because of the larger blood flow to the area - increased capillary action

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19
Q

what are the outcomes of acute inflammation

A

resolution
supporation - pus formation
organisation - granulation tissue and fibrosis
progression - excessive inflammaiton - becomes chronic

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20
Q

what is resolution

A

where the problem causing inflammation is resolved, inflammation is solved and there is no tissue damage

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21
Q

what is first intension healing

A

it is when the edges of the wound can be joint back together, making it much easier for the body to repair the wound.
initial weak fibrin joint and then collagen joint after

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22
Q

what is second intension healing

A

when the edges of the wound cant be joint back together which can be either due to trauma or with certain surgeries.. cells have to grow into the wound, with initilal capillary cells, then fibroblasts and then epithelial cells

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23
Q

what is granulation tissue

A

where capillary loops are growing into wound (looks a bit like granular tissue)

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24
Q

what is tissue repair

A

when there is replacement of damaged tissue that cant regenerate, collagen is therefore produced by fibroblasts, leaving a scar
- original tissue lost

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25
Q

what cells regenerate within the body

A

hepatocytes, blood cells, pneumocytes, gut epithelium, skin epithelium and osteocytes

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26
Q

what cells dont regenerate

A

myocardial cells and neurons

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27
Q

what is the steps of acute inflammation

A

vascular component = dilation of vessels
exudative component = vascular leakage of protein rich fluid
neutrophil polymorph = cells type recruited to tissue

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28
Q

what is the appearance of acute inflammation

A

red in colour, heat, swelling, pain and loss of function

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29
Q

what happens during acute inflammation

A
  1. migration of neutrophils; increased plasma viscosity and slowing of flow during injury meaning neutrophils migrate to plasmatic zone
  2. Adhesion of neutrophils to the endothelium
  3. neutrophil emigration as they pass through the endothelial cells onto the basal lamina
  4. diapedesis; RBC may also escape from vessels
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30
Q

what are the four outcomes of acute inflammation

A
  1. resolution - complete restoration of tissue to normal w/minimal cell death
  2. suppuration - formation of pus, leads to scarring
  3. organisation - replacement by granular tissue, new capillaries grow into inflammatory exudate, macrophages migrate and fibrosis occurs
  4. progression - causative agents is not removes so there is progression to chronic inflammation
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31
Q

what is chronic inflammation

A

subsequent and prolonged response to tissue injury

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32
Q

what are the cells involved in chronic inflammation

A

lymphocytes, macrophages, plasma cells

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33
Q

what are causes of chronic inflammation

A

primary chronic inflammation, transplant rejection, autoimmune conditions, endogenous and exogenous conditions

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34
Q

what is the macroscopic appearance of chronic inflammation

A

chronic ulcer
crohns abscess cavity
granulomatous inflammation
fibrosis

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35
Q

what is the microscopic appearance of chronic inflammation

A

lymphocytes, plasma cell, macrophages, continuing destruction and possible necrosis

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36
Q

what is laminar flow

A

cells travel in the centre of arterial vessels and dont touch the sides

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37
Q

what is a thrombosis

A

it is the formation of a solid mass from blood constituents in an intact vessel in a living person

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38
Q

what is the first stage of thrombosis formation

A

platelet aggregation - platelets release chemicals when they aggregate which causes other platelets to migrate and stick - starts of a positive feedback cascade

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39
Q

what are the three things that can cause thrombosis formation

A
  1. change in the vessel wall
  2. change in the blood flow
  3. change in the blood constituents
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40
Q

what is an embolism

A

the process of a solid mass in the blood being carried through the circulation to a place where it gets stuck and blocks a vessel

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41
Q

what is the most common cause of embolism

A

a thrombus

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42
Q

what are some less common causes of embolism

A

air, cholesterol crystals, tumours, amniotic fluid, fat

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43
Q

what happens if an embolus enters the venous system

A

will travel to vena cava, through the right side of the heart and lodge in the pulmonary arteries, causing pulmonary oedema

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44
Q

what is ischemia

A

a reduction in blood flow to a tissue

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45
Q

what is infarction

A

a reduction in blood flow to a tissue that results in cell death

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46
Q

what is end arterial supply

A

when an organ/tissue only has a single artery supplying it

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47
Q

what are the few organs with a duel arterial supply

A

the lungs, liver and parts of the brain

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48
Q

what are the granules that platelets contain

A

alpha and dense

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49
Q

what is the function of alpha granules

A

platelet adhesion - fibrinogen

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50
Q

what is the function of dense granules

A

platelet aggregation - ADP

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51
Q

How does a thrombus form

A

a change in the vessel wall will cause a plaque to form there, which will protrude into the lumen and cause some turbulence. this results in the loss of intimal cells. Clumping will occur and fibrin is deposited. this structure will continue to protrude into the lumen

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52
Q

do thrombi form in veins

A

not likely as there is lower pressure in veins - can occurs around valve sites

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53
Q

what are the clinical features of arterial thrombi

A

loss of pulse distal to thrombus, area becomes cold and pale and painful. there could be gangrene

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54
Q

what is the fate of thrombi

A
  1. resolution
  2. organised - becomes a scar with slight narrowing
  3. recanalisation - intimal cells proliferate and capillaries may grow into the thrombus
  4. embolus - fragments break off into circulation
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55
Q

what could a venous thrombus lead to

A

DVT

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56
Q

what is an atherosclerosis

A

accumulation of fibrolipid plaques systemic arteries

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57
Q

what is the time course of atherosclerosis

A

birth - none
late teen/early 20s - fatty streaks in aorta, may not progress to established atherosclerosis
30s/40s/50s - development of established atherosclerotic plaques
40s -80s - complications of atherosclerotic plaques

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58
Q

what are rick factors of atherosclerosis

A

hypertension
hyperlipidemia
cigarette smoking
poorly controlled diabetes

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59
Q

what is the pathogenesis of atherosclerosis

A

endothelial damage theory - endothelial cells are delicate and can become damaged by cigarette smoke, shearing forces, hyperlipidemia, glycosylation products

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60
Q

what can cumulative damage of the endothelial barrier lead to

A

it leads to endothelial ulceration, microthrombi and eventual development of established atherosclerotic plaques

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61
Q

what are the complications of atherosclerosis

A

blocked vessels - infarct
embolism leading to cerebral infarction, carotid atheroma, myocardial infarction, aortic aneurysm, peripheral vascular disease and gangrene

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62
Q

how does atherosclerosis form

A
  1. endothelial cell dysfunction (lots of cholesterol damages wall)
  2. High levels of LDLs will begin to accumulate
  3. macrophages are attracted to the site of damage at take up lipid to form foam cells
  4. platelet aggregation and the plaque starts to protrude into the artery lumen disrupting flow. thinning of media occurs
  5. fibrin mesh and red blood cell trapping occurs
  6. fibrous cap forms over smooth muscle cap forming a stable atheroma
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63
Q

what are preventative measures for atherosclerosis

A

smoking cessation
blood pressure control
weight reduction
low dose aspirin
statins - cholesterol reducing

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64
Q

what is apoptosis

A

it is programmed cell death - orderly event without the release of products harmful to surrounding cells

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65
Q

what is the purpose of apoptosis

A

it is a process in normal cell turnover which prevents cells with accumulated genetic damage from dividing and producing cells which might eventually develop into cancer

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66
Q

what protein detects DNA damage

A

p53

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67
Q

what is the function of p53

A

it is a protein in cells which detects the level of DNA damage which will trigger apoptosis if DNA damage is high

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68
Q

how does a cell apoptose

A

the cell triggers a series of proteins which leads to the release of enzymes called caspases which auto digests the cell

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69
Q

when does apoptosis occur in health

A

development - removal of cells during development such as interdigital webs
cell turnover - removal of cells during normal turnover, such as the intestinal villi

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70
Q

when does apoptosis occur in disease

A

cancer - cells in tumours often dont apoptose due to accumulation of genetic mutations, including those in the p53 gene
HIV - HIV can induce apoptosis in CD4 T helper cells to produce an immunodeficient state

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71
Q

what is necrosis

A

it is the traumatic loss of cells - uncontrolled

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72
Q

what are clinical examples of necrosis

A

infarction due to loss of blood supply
frostbite
pancreatitis

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73
Q

what are the inhibitors of apoptosis

A

growth factors, extracellular cell matrix, sex steroids

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74
Q

what are the inducers of apoptosis

A

glucocorticoids, free radicals, ionising radiation, DNA damage

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75
Q

what is the intrinsic pathway of apoptosis

A

this uses pro and anti apoptotic members of the Bcl-2 family. Bax forms Bax-Bax dimers which enhance apoptotic stimuli. the Bcl-2:Bax ratio determines the cells susceptibility to apoptotic stimuli.
it responds to growth factors and biochemical stress.
the p53 gene induces cell cycle arrest and DNA damage repair, and if it cant be fixed it induces apoptosis

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76
Q

what is the extrinsic apoptotic pathway

A

this involves ligand binding to death receptors on the cell surface. this includes the TNFR1, CD95 and the main one the Fas-FasL
the ligand binding causes the clustering of receptor molecules on the cell surface and the initiation of signal transduction cascades
caspases are activated and triggers apoptosis

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77
Q

what is coagulative necrosis

A

most common type - ischemia

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78
Q

what is liquefactive necrosis

A

occurs in brain due to lack of supportive stroma

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79
Q

what is caseous necrosis

A

causes ‘cheese’ pattern - TB characterised by this

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80
Q

what is gangrene

A

necrosis with rotting tissue - affected tissue is black due to deposition of iron sulphate

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81
Q

What is the definition of hypertrophy

A

It is the increase in cell size without cell division.

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82
Q

what is the definition of hyperplasia

A

Increase in cell number by mitosis - this can only happen in cells that can divide `

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83
Q

what cells cant undergo hyperplasia

A

Myocardial cells or nerve cells

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84
Q

what is the definition of atrophy

A

The decrease in the size of an organ or cell which can be reduction in cell size or number

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85
Q

when is there natural atrophy in the body

A

Occurs during the development of the GU tract

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86
Q

what is the definition of metaplasia

A

the change in differentiation of a cell from one fully differentiated cell type to another

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87
Q

what are examples of metaplasia

A

Barretts oesophagus - squamous epithelium to columnar epithelium

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88
Q

what is the definition of dysplasia

A

morphological changes seen in cells in the progression to becoming cancer
not cancer but could become cancer

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89
Q

what is a genetic disease

A

a disease that occurs primarily from a genetic abnormality

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90
Q

what is a single gene disorder

A

abnormality of a single gene causes a disease - can be recessive or dominant

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91
Q

what are the two further classifications of single gene disorder

A

autosomal or sex linked

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92
Q

what is polygenic gene disorder

A

a genetic disease which is the result of the interaction of several different genes (usually on different chromosomes)

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93
Q

what is a congenital disease

A

a disease which someone is born with - but can also be acquired. This will often be a disease which is due to environmental factors but it may be a strong genetic background

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94
Q

what is a homeobox gene

A

genes which code for particular region of the body and control migration of cells

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95
Q

what is benign prostatic hyperplasia

A

smooth muscle in the prostate divides and causes the prostate to crow and constricts the urethra

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96
Q

when do you have combined hypertrophy and hyperplasia

A

in the uterus during pregnancy

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97
Q

what is a classic example of atrophy in aging

A

dementia

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98
Q

What is the limit of aging

A

number of times a cell can divide

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99
Q

what are the limiting factors of cell division

A

telomerase length - telomeres get shorter after each cell division which then limits the amount of divisions that can occur

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100
Q

what things can induce apoptosis in cells

A

crosslinking or mutation of DNA
accumulation of toxic by products of metabolism
telomere shortening
time dependent activation of aging and death genes
free radical generation
crosslinking of proteins
damage to mitochondrial DNA
loss of DNA repair mechanism

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101
Q

what is dermal elastosis

A

the accumulation of abnormal elastic in the dermis of the skin, which is the result of prolonged or excessive sun exposure. This is because UVB light causes protein cross linking

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102
Q

what is osteoporosis

A

caused by the loss of coupling in the bone remodeling process with increased bone resorption and reduced bone formation. the bone matrix is mineralised as normal but the trabeculae are thinned

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103
Q

what is cataracts and its cause

A

it is the formation of opaque proteins within the lens which usually results in the loss of lens elasticity. It is caused by UVB light causing protein cross linking

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104
Q

what causes dementia

A

plaques and neurofibrillary tangles in the brain

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105
Q

what is sarcopenia

A

it is decreased growth hormone, decreased testosterones and increased catabolic cytokines. This causes involuntary loss of skeletal muscle mass and strength

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106
Q

what is the cause of deafness in age

A

the hair cells cant divide or regenerate in the ear which means once damage occurs it cant be undone

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107
Q

What cancer only invades locally

A

basal cell carcinoma - doesnt metastasize

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108
Q

what is the cure for basal cell carcinoma

A

complete local excision of the cancer

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109
Q

what type of cancer is leukemia

A

it is the cancer of white blood cells

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110
Q

what has to happen before cancer removal surgery

A

they generally do an ultrasound of the area to ensure that there is no growth into surrounding lymph nodes. Can also send a lymph node sample to the lab

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111
Q

what cancers commonly spread to the bone

A

breast, prostate, thyroid, lung and kidney cancers commonly spread to the bone

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112
Q

what biopsy can be done to check if cancer is present

A

a needle core biopsy

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113
Q

what is adjuvant therapy

A

it is extra treatment given after the surgery to help prevent the regrowth of cancer

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114
Q

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

A

Neutrophil polymorphs

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115
Q

What is the name of the cells that produce collagen in fibrous scarring

A

fibroblasts

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116
Q

what is a common example of acute inflammation

A

acute appendicitis

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117
Q

what is the pattern of differentiation of neoplastic cells lining the bronchi of cigarette smokers

A

respiratory epithelium to stratified squamous

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118
Q

what process is is defined by the formation of a solid mass of blood constituents within an intact vascular system during life

A

thrombosis

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119
Q

what is the definition of carcinogenesis

A

normal cells to neoplastic cells via permanent genetic mutation or alteration

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120
Q

where in the cell do all carcinogens act

A

the level of the DNA

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121
Q

what are the different classes of carcinogen

A

chemical, viral, radiation, hormones, parasites, mycotoxins and miscellaneous
they all act on DNA

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122
Q

what type of neoplasms do carcinogens produce

A

malignant
cancer causing

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123
Q

what is oncogenesis

A

the formation of benign and malignant tumours
- tumour causing

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124
Q

what are carcinogens

A

agents which are known or suspected to cause tumours

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125
Q

what are occupational or behavioral risks for cancer

A

lung cancer - strong association with smoking
bladder cancer - increased incidence in aniline dye and rubber industries
scrotal cancer - increased incidence in chimney sweeps

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126
Q

what are chemical carcinogens

A

they show no common structural features, where some act directly. Most require metabolic conversation from pro-carcinogens to ultimate carcinogens. Enzymes are required for this which may be ubiquitous or confined to certain organs (meaning you can only get cancer in those organs)

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127
Q

what is a tumour

A

it is any abnormal swelling

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128
Q

what are examples of chemical carcinogens

A

polycyclic aromatic hydrocarbons - found in soot, cigarette smoke and pollution
nitrosamines - processed meats
alkylating agents - used as chemotherapeutic agents to treat other cancers

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129
Q

what are examples of viral carcinogens

A

HepB - liver cancer
HHV8 - Kaposi sarcoma
EBV - Birkett lymphoma, nasopharyngeal carcinoma
HPV - cervix, penis, anus, head and neck
MCV - merkel cell carcinoma
HTLV-1 - leukemia
HCV - hepatocellular carcinoma

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130
Q

what type of radiation can cause cancer

A

UV light - increases all kinds of skin cancer
ionising radiation - can cause cancer over long term exposure

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131
Q

what biological agents can cause cancer

A

oestrogen - breast and endometrial
anabolic steriods - hepatocellular carcinoma

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132
Q

what are miscellaneous carcinogens

A

arsenic, asbestos and metals

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133
Q

what host factors can affect cancer risk

A

ethnicity - more melanin decreases melanoma incidence
diet and lifestyle - alcohol excess increases risk of cancers of the mouth, liver and colon
obesity - breast, oesophagus, colon (exercise reduces this risk)
inherited predisposition - retinoblastoma and FPC
age - increased age increases the risk
biological sex will impact on certain cancer risk

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134
Q

what is pre-malignant condition

A

a localised abnormality which increases the risk of developing cancer such as polyps, ulcerative colitis and undescended testicles

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135
Q

what is an example of placental transmission

A

diethylstilbestrol - was sued for morning sickness which increased the risk of vaginal cancer in the foetus

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136
Q

what percentage of all cancer risks are inherited

A

15%

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137
Q

what does in situ mean, in terms of cancer

A

where the cancer hasnt invaded surrounding tissue, and is still within the area it started. No access to blood or lymphatic vessels
In situ only applies to epithelial neoplasms and the BM is intact

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138
Q

how do you treat an in situ cancer

A

you can excise it

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139
Q

what is an invasive carcinoma

A

where the cancer has invaded the surrounding tissues - has access to blood or lymphatic vessels

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140
Q

what is a micro-invasive cancer

A

one that has invaded surrounding tissues, but not very far

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141
Q

what enzymes will cancers need to produce to move through the basement membrane

A

metalloproteinases - collagenase, cathepsin D

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142
Q

what are the stages of metastasis

A

tumour grows and invades the basement membrane and the extracellular matrix. It will then travel in either the lymphatic or blood vessel, and will then move back into a tissue elsewhere and invade another extracellular matrix to grow there

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143
Q

how large must a tumour be for it to need its own blood supply

A

larger than 1mm

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144
Q

what can tumours do to remain undetected by immune cells in the blood

A
  • tumours can aggregate with platelets
  • they can shed surface antigens which can be taken up by lymphocytes rather than the tumour cell itself
  • they can adhere to other tumour cells to increase size
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145
Q

what can tumour cells produce to promote angiogenesis

A

VEGF and BFGF

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146
Q

what cancers commonly spread to the lungs

A

sarcomas

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147
Q

what cancers often invade the liver

A

colon, stomach, pancreas, carcinoid tumours of the intestine

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148
Q

what cancers commonly metasasise to the bone

A

prostate, breast, thyroid, lung and kidney

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149
Q

what are the two types of bone metastasis

A

sclerotic metastasis (gain of bone)
lytic metastasis (loss of bone)

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150
Q

what is a neoplasm

A

a lesion resulting from the autonomous, or relatively autonomous abnormal growth of cells which persists after the initiating stimulus has been removed (a new growth)

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151
Q

what do solid neoplasms contain

A

neoplastic cells and stroma (supporting network) - except leukemia

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152
Q

what are the behavioral classification of neoplasms

A

malignant, borderline or benign

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153
Q

what are the features of benign neoplasms

A

Localised, non invasive, slow growth rate. They have a low mitotic rate. They have a close resemblance of normal tissue. They are well circumscribes of encapsulated.

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154
Q

what is an example of malignant neoplasms

A

squamous cell carcinoma and prostate cancer

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155
Q

what are features of malignant neoplasms

A

INVASIVE. they can metastases. They have a rapid growth rate and have some varying resemblance to normal tissue. They have a poorly defined boarder.

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156
Q

where can neoplasms arise from

A

epithelial cells, connective tissues, lymphoid or haemopoietic organs

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157
Q

what is an adenoma

A

a benign tumour of glandular or secretory epithelium
- add prefix to add what type it is

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158
Q

what is a papilloma

A

a benign tumour of non glandular non secretory epithelium
-can add a prefix to add what type it is

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159
Q

what is a carcinoma

A

a malignant epithelial neoplasm
- this is a common exam question

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160
Q

what is a lipoma

A

adipocyte neoplasm (benign)

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161
Q

what is a chondroma

A

cartilage neoplasm (Benign)

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162
Q

what is an osteoma

A

a bone neoplasm (benign)

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163
Q

what is an angioma

A

vascular neoplasm (benign)

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164
Q

what suffix do benign connective tissue neoplasm have

A
  • oma
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165
Q

what suffix do malignant connective tissue neoplasms have

A
  • sarcoma
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166
Q

what is a liposarcoma

A

an adipose tissue neoplasm

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167
Q

what is a rhabdomyosarcoma

A

a striated muscle neoplasm

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168
Q

what is a leiomyosarcoma

A

smooth muscle neoplasm

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169
Q

what is a carcinoma in situ

A

a malignant epithelial neoplasm that has not yet invaded through the original basement membrane

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170
Q

How can a metastasis occur

A

via blood vessels, lymphocytes, across body cavities, along nerves or as a direct implantation of neoplastic cells during surgery

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171
Q

what must a tumour have to undergo extravasation

A

adhesion receptors, collagenases and cell motiity

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172
Q

what are examples of angiogenesis inhibitors

A

angiostatin ,endostatin and casculostatin

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173
Q

what are the consequences of a malignant neoplasm

A

they can cause destruction of adjacent tissue, metastasis, blood loss from ulcers, obstruction of flow, hormone productions, paraneoplastic affects, anxiety

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174
Q

what are the consequences of benign neoplasm

A

They can cause morbidity and mortality cause they can cause obstruction, cause pressure on adjacent structures, produce hormones and can transform. Can cause anxiety

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175
Q

what is an anaplastic neoplasm

A

where the cell - type of origin is unknown

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176
Q

what is serum

A

plasma without fibrinogen and other clotting factors

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177
Q

what is the most common white blood cell

A

neutrophils

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178
Q

what white blood cell has a kidney shaped nucleus

A

monocytes

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179
Q

what are the primary lymphoid organs

A

Bone marrow: origin for all and the B cell maturation site
Thymus: T-cell maturation site

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180
Q

what are the secondary lymphoid organs

A

the lymph nodes: site of DC, B and T cell interactions
Spleen: site of removal or RBC and bacteria

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181
Q

what are tertiary lymphoid organs

A

transient formation of germinal centers which are usually pathology related

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182
Q

what is the definition of hematopoiesis

A

production of all cellular components of blood and blood plasma

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183
Q

what stem cell produces all types of white blood cells

A

hematopoietic stem cells

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184
Q

what progenitor cell descendants can be considered as the innate branch of the immune system

A

the common myeloid progenitor cells

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185
Q

what progenitor cell descendants can be considered cells of the adaptive immune response

A

the common lymphoid progenitor cells

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186
Q

what causes ALL

A

lymphoid progenitors causing increased amounts of immature lymphocytes

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187
Q

what causes CLL

A

increased naive mature B cells

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188
Q

what is lymphoma

A

cancer involving expansion of mature naive T cells and B cells in germinal centres

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189
Q

what is multiple myeloma

A

cancer of the plasma cells

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190
Q

what are 7 key points about the innate immune system

A
  1. it is primitive and broad
  2. it is fast
  3. there is little regulation
  4. there is no amplification
  5. there is no self discrimination
  6. it is short (days)
  7. it has no memory
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191
Q

what are the 7 key points about the adaptive immune system

A
  1. it is highly specific
  2. it is slow
  3. it has lots of regulation
  4. there is amplification
  5. it shows high self discrimination
  6. it is long
  7. it can produce memory
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192
Q

what cells are polymorphonuclear leukocytes

A

neutrophils, eosinophils, basophils

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193
Q

what are mononuclear leukocytes

A

monocytes, T cells and B cells

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194
Q

what immune cell has a kidney shaped nuclei

A

monocytes

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195
Q

what is the role of monocytes in immunity

A

they play a role in both innate and adaptive immunity as they phagocytose and present antigens.

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196
Q

what is the main function of neutrophils in immunity

A

innate immunity - they have two main intracellular granules. Primary lysosomes kill microbes but secreting toxic substances and secondary granules.

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197
Q

what is the main function of macrophages in immunity

A

they are involved in innate and adaptive immunity. they reside in tissues and have a long lifespan. their main role is removal of foreign and self material as well as antigen presentation to T cells

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198
Q

what is the main function of eosinophils

A

mainly associated with parasitic infections and allergic reactions. they can activate neutrophils, inducing histamine release from mast cells

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199
Q

what is the main function of basophils

A

mainly involved in immunity to parasitic infections and allergic reactions. they bind to IgE and cause de-granulation releasing histamine

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200
Q

what is the function of mast cells

A

they are only found in tissues and induce release of histamine via IgE

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201
Q

what are the four main types of T cell

A

T helper 1 - CD4
T helper 2 - CD4
cytotoxic T cell - CD8
Treg

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202
Q

what is the function of natural killer cells

A

they recognise and kill by apoptosis - tumour cells and viral infected ones

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203
Q

what percentage of lymphocytes are natural killer cells

A

about 15%

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204
Q

what are the types of soluble factors in immunity

A

complement, antibodies and cytokines and chemokines

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205
Q

what is compliment function in immunity

A

direct lysis of pathogen
attraction of leukocytes to sites of infection
opsinisation - coat organisms and aid in phagocytosis

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206
Q

what are the five distinct classes of antibodies

A
  1. IgG
  2. IgA
  3. IgD
  4. IgE
  5. IgM
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207
Q

what is the most predominant antibody

A

IgG

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208
Q

what antibody can cross the placenta

A

IgG

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209
Q

where is IgA antibody found

A

it is the predominant antibody found in secretions such as saliva, milk, vaginal and bronchiolar secretions

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210
Q

where is IgM predominantly found

A

found in the blood - makes up a pentamer so cant cross endothelium and it is the primary response

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211
Q

what are the features of IgE

A

Basophils and mast cells express an IgE-specific receptor that has high affinity for IgE – binding triggers release of histamine
Associated with allergic response and defence against parasitic infections

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212
Q

what is an epitope

A

it is the part of the antigen that binds to the antibody/receptor binding site

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213
Q

what are cytokines

A

they are proteins secreted by the immune and non-immune cells. they influence the behaviour of cells

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214
Q

what do interferons do

A

they are important in antiviral immunity

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215
Q

what do interleukins do

A

over 30 types - they can stimulate cells to divide, differentiate and secrete factors

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216
Q

what is colony stimulating factors

A

it is involved in directing the division and differentiation on the bone marrow stem cells - precursors of leukocytes

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217
Q

what is tissue necrosis factors

A

it mediates inflammation and cytotoxic reactions

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218
Q

what are chemokines

A

40 proteins that direct movement of leukocytes and attract leukocytes to sites of infection or inflammation

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219
Q

what three factors are in the innate immune system

A
  1. physical and chemical barriers
  2. phagocytic cells
  3. serum proteins
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220
Q

what are anatomical barriers to infection

A
  1. skin
  2. sebum
  3. intact skin
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221
Q

What physical barriers are there to infection (mucous membranes)

A

Saliva, tears, low pH, commensals of vagina, mucous secretions, mucous, cilia, commensal colonies

222
Q

what are physiological barriers to infection

A

temperature
fever response
pH
Gastric acidity

223
Q

what is inflammation

A

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

224
Q

what is the response to a barrier being breached - tissue damage or infection

A
  1. stop bleeding
  2. acute inflammation
  3. kill pathogens, neutralise toxins and limit spread
  4. clear pathogens or dead cells
  5. proliferation of cells to repair damage
  6. removal of blood cot
  7. re-establish normal structure
225
Q

what are the hallmarks of inflammation

A

increased blood supply, increased vascular permeability and increased leukocyte trans-endothelial migration extravasion

226
Q

what complement factor is required for opsonisation

A

C3b

227
Q

what are the stages of phagocytosis

A
  1. binding
  2. engulfment
  3. phagosome formation
  4. lysosome fusion
  5. membrane disruption
  6. antigen presentation/secretion
228
Q

What are MHCs

A

major histocompatibility complex - displays peptide from self or non self proteins on the cell surface - invasion alert

229
Q

where is MHCI found

A

found on all nucleated cells

230
Q

where is MHCII found

A

only on antigen presenting cells

231
Q

what do MHCI do

A

Intrinsic (intracellular) - this interacts with CD8 cells which then kils the infected cells with intracellular pathogens

232
Q

what do MHCII do

A

extrinsic - interacts with CD4 T helper cells, which helps to make B cells to make antibodies

233
Q

what interactions need to occur for cell mediated immunity

A

interaction between antigen presenting cells and T cells. it requires MHC, intrinsic/extrinsic antigens and the recognition of self or non self

234
Q

what is a summary of B cell activation

A

B cells become activated upon binding with an antigen. These then go to the lymph nodes where clonal expansion takes place with the cells differentiating into plasma cells. These secrete Ab (usually IgM) which later turn into IgG. B cells divide – clonal expansion and differentiate into plasma cells and memory B cells. Re-stimulation of memory B cells lead to secondary response.

235
Q

what are the two types of PRR family

A
  1. secreted and circulating PRRs
  2. Cell-associated PRRs (traditional)
236
Q

what are secreted and circulated PRRs

A
  1. antimicrobial peptides secreted in lining fluids from epithelia
  2. lectins and collectins (carbohydrate-containing proteins that bind carbohydrates or lipids in microbe walls)
237
Q

what is the function of secreted and circulating PRRs

A

they activate compliment and improve phagocytosis

238
Q

what are cell associated PRRs

A

these are receptors that are present on the cell membrane or in the cytosol of the cells. They recognise a broad range of molecular patterns.

239
Q

what are the main cell associated PRRs

A

TLRs are the main ones

240
Q

other than PAMPs what else can PRRs detect

A

damage recognition - cellular damage which activates immunity to issue tissue repair (and enhance local antimicrobial signalling)

241
Q

how are PRRs involved in autoimmunity

A

they can recognise host molecules as foreign

242
Q

what are the 5 cardinal signs

A
  1. Rubor - redness
  2. Dolor - pain
  3. Calor - Heat
  4. Tumor - swelling
  5. loss of function
243
Q

what is neutrophil action in acute inflammation

A
  • margination (migration to edge of BV)
  • adhesion (selectins bind neutrophils, and cause rolling)
  • emigration and diapedesis (movement out of the BV)
  • chemotaxis
244
Q

what molecule do granulomas secrete

A

ACE - blood marker

245
Q

what are the features of an arterial ulcer

A

punched out holes with little exudate - pale cool skin with low distal pulse

246
Q

what are the features of a venous ulcer

A

less demarcated with lots of exudate. warm erythematosus skin
- DVT

247
Q

how does a venous thrombosis form

A

though venous stasis

248
Q

what is found within a plaque

A

lipid, smooth muscle, macrophages, foam cells, platelets and fibroblasts

249
Q

how are tumours graded

A

based on the similarity to the parent cell it came from
1. well differentiated - 75% cells like parent
2. 10-75%
3. poorly differentiated - less than 10% resemble parent

250
Q

in staging tumours what does TNM stand for

A

tumour - node - metastases

251
Q

what cancers are screened for in the UK

A

cervical, breast and colorectal

252
Q

what is the common mutation associated with colorectal cancer

A

familial adenomatosis polyposis - a mutated APC gene causing overexpression of c-MYC and KRAS mutation

253
Q

what is transcolemic spread of cancer

A

when there is spread through the pleural, pericardial and peritoneal effusions (via exudative fluid accumulation)

254
Q

what are the three pathways in the complement system

A
  1. classical
  2. lectin
  3. alternative
255
Q

what in the compliment system causes direct lysis of cells

A

the membrane attack complex formation

256
Q

what factors in the compliment system are important for inflammation

A

C3a and C5a

257
Q

what factor in the compliment system is required for opsonisation

A

C3b

258
Q

what TLRs are intracellular

A

3, 7, 8 and 9

259
Q

what does TLR2 detect

A

gram positive bacteria and TB

260
Q

what does TLR3 detect

A

intracellular pathogens

261
Q

what does TLR4 detect

A

LPS - gram negative

262
Q

what does TLR 5 detect

A

flagellin

263
Q

what does TLR7 detect

A

single stranded RNA - intracellular

264
Q

what does TLR9 detect

A

non methylated DNA

265
Q

what type of toxin in LPS

A

its an endotoxin

266
Q

what 3 things have to occur during immune synapse to activate the T cell

A
  1. receptor binding
  2. co-stimulation (another molecule after primary binding)
  3. cytokine release
267
Q

what are the best antigen presenting cell

A

dendritic cells

268
Q

what is thymic tolerance

A

where T cell in the thymus are checked for self reactivity/to see if they are active to anything

269
Q

what is positive thymic selection

A

where the T cells are tested to see if they recognise MHC 1 and 2. If they do they are selected for

270
Q

what is negative thymic selection

A

if the T cells produce to much of a response to self then they are selected against

271
Q

what cytokine is associated with Th1 cells

A

IFN gamma - activates NK cells and macrophages

272
Q

what cytokine is associated with Th2 cells

A

IL4 - activates B cells to differentiate into plasma cells

273
Q

what two factors do Th2 cells release to activate B cells

A
  1. IL4 which induces B cell proliferation
  2. IL5 which induces B cell differentiation into plasma cells
274
Q

what Ig does IL4 promote class switching to

A

IgA

275
Q

what Ig does IL5 promote class switching to

A

IgE

276
Q

what are the four types of hypersensitivity

A
  1. anaphylaxis
  2. antigen-antibody complex
  3. immune complex deposition
  4. T cell mediated
277
Q

describe type 1 hypersensitivity

A

IgE mediated - IgE binds to basophils and mast cells and causes degranulation and release of histamine which causes vasodilation and increased permeability and bronchoconstriction

278
Q

describe type 2 hypersensitivity

A

where IgG/M binds to antigens and activates MAC compliment at the site of antigen antibody binding.
- goodpastures

279
Q

describe type 3 hypersensitivity

A

IgG/A binds to antigen and activates compliment
SLE

280
Q

describe type 4 hypersensitivity

A

Th1 mediated which are activated by APCs leading to a slow response

281
Q

when treating anaphylaxis what are the steps to take

A
  1. Airway - can they breathe
  2. breathing - is it rapid/wheezy
  3. circulation - are they pale/cold/clammy
  4. disability - are they confused and can they move
  5. exposure
282
Q

what is the immediate treatment for anaphylaxis

A

500mcg of IM adrenaline

283
Q

what else can you give in the case of anaphylaxis

A

antihistamine or cortisol

284
Q

where is central immune tolerance performed

A

in the thymus

285
Q

where is peripheral immune tolerance performed

A

in the secondary lymphoid organs

286
Q

what is autoimmunity

A

a pathological response to self

287
Q

what are examples of organ specific autoimmunity

A

type 1 diabetes - endocrine pancreas - beta cells
multiple sclerosis - oligodendrocytes
pernicious anaemia - parietal cells of the stomach

288
Q

what are examples of non organ specific autoimmunity

A

SLE - affects DNA
Rheumatoid arthritis

289
Q

what are the two ways someone can get immunodeficiency

A
  1. inherited - defect in T cells - SCID
  2. acquired - HIV
290
Q

what are patterns of immunodeficiency

A
  1. decreased CD4 in HIV - increases susceptibility of the disease
  2. B cells may be deficient
  3. Neutrophil and macrophage deficiency
  4. complement deficiency (SLE)
  5. hyposplenism - lack of function of spleen
291
Q

what are the different types of vaccine

A
  1. live attenuated - MMR
  2. antigens
  3. toxins - Tetanus
  4. constituents - HepB
292
Q

what is natural active immunity

A

when the body encounters a pathogen and produces memory cells after infection

293
Q

what is active artificial immunity

A

vaccine mimics encountering pathogen and stimulates immunoglobulin production

294
Q

what is passive natural immunity

A

maternal Igs pass onto the baby in breast milk or colostrum

295
Q

what is passive artificial immunity

A

antivenom - infection of Ig from another organism

296
Q

what are the two routes of drug administration

A
  1. Enteral - GIT involved - oral or rectal
  2. Parenteral - non GIT - IM, IV, SC, Injections
297
Q

what are the 4 drug targets

A
  1. Receptors
  2. Enzymes
  3. Transporters
  4. Ion channels
298
Q

what are the two types of receptor targeting drugs

A
  1. agonists
  2. antagonists
299
Q

what is the most common receptor type

A

G protein coupled receptor

300
Q

what is the potency of a drug

A

how much drug is needed to elicit a response in the body - how well the drug works

301
Q

what is drug synergy

A

when the interaction of drugs is such that the total effect is greater than the sum of the two individual effects

302
Q

what is antagonism

A

when a substance that acts against and block an action (2 drugs apposing each other)

303
Q

what is summation

A

this is an additive reaction - where two drugs have the same affect , where the total effect is the sub or the two drugs together

304
Q

what is potentiation

A

the enhancement of one drug by another - 1+1=1+1.5

305
Q

Define pharmacodynamics

A

the effect a drug has on the body

306
Q

define pharmacokinetics

A

what the body does to the drug - deposition of a compound within an organism

307
Q

what must you consider when discussing drug pharmacokinetics

A
  1. Administration/absorption
  2. distribution
  3. metabolism
  4. excretion
308
Q

what is a drugs efficacy

A

the maximal response a drug can get - how well it activates the receptor

309
Q

what are the properties of an agonist

A

they have full affinity and full efficacy

310
Q

what are the propertied of an antagonist

A

they have full affinity but zero efficacy

311
Q

what is an allosteric modulator

A

a drug which binds to a separate site other than the active site, and increases or decreases normal ligand binding

312
Q

what is an example of an allosteric modulator

A

benzodiazepine

313
Q

what is a selective drug

A

a drug that only binds to a specific receptor type in a family - only binding B1

314
Q

what is an example of a non selective drug

A

propranolol - non selective beta blocker

315
Q

what is a non selective drug

A

a drug that binds to all receptors within a family

316
Q

what is an example of a selective drug

A

verapamil - selective beta blocker (only B1)

317
Q

what is an example of an enzyme targeting drug

A

Cox-1 - NSAIDs
ACE-i - Inhibits conversion of angiotensin 1 to 2

318
Q

What is an example of transporter targeting drugs

A

Proton pump inhibitors
Diuretics - loop - Furosemide inhibits NKCC2 and Thiazides inhibits NaCl cotransporter

319
Q

What is an example of an ion channel targeting drug

A

calcium channel blockers - amlodipine, diltiazem
Local anesthetics - lidocaine

320
Q

what is a specific drug

A

when a drug acts on a certain target

321
Q

what is a selective drug

A

when a drug acts on a subtype of a target

322
Q

what is bioavailability of a drug

A

how fast and to what extent a drug reaches systemic circulation

323
Q

what type of drug administration gives 100% bioavailability

A

intravenous drugs

324
Q

what are the mechanisms of drug administration

A

the route taken and the entry into the body

325
Q

what are the mechanisms of drug distribution

A

drugs can be distributed in the plasma according to chemical properties and size, they may be taken up by organs and tissues.
- protein binding will affect how much drug is available and the strength it will act at

326
Q

what are the mechanisms of drug metabolism

A

drugs are metabolised in the kidneys or liver (CYP450)
- kidneys metabolise mostly small water soluble drugs
- liver hydrophobic molecules: phase 1 and phase 2 reactions

327
Q

what are the mechanisms of drug excretion

A

through urine (mostly) or feces
- renal will be pH dependent

328
Q

what are some drug interactions to be aware of

A

Warfarin - lots of interactions causing enzyme induction (increased activity so warfarin has bigger effect quicker)
Acute kidney injury - NSAIDs and ACEi

329
Q

what drugs work at the neuromuscular junction

A

Botulinum toxin - Ach release inhibited
Curare - nAch receptor antagonist
Ach-ase inhibitors - decreases Ach degradation

330
Q

what happens when there is overstimulation of Ach at the neuromuscular junction

A

you go into cholinergic crisis

331
Q

what are the symptoms of cholinergic crisis

A

Salivation
Lacrimation
Urination
Defecation
GI distress
Emesis

332
Q

where are M1, M2 and M3 receptors found in the body

A

M1 = Brain
M2 = Heart
M3 = Lungs

333
Q

what is the definition of a drug

A

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

334
Q

what are different types of receptors found in the body

A

ligand gated ion channels e.g nicotinic Ach receptor
G - protein couples receptors
Kinase - linked receptors e.g growth factors
Cytosolic/nuclear receptors e.g steroid receptors

335
Q

what is tolerance to a drug

A

where there is reduction in the drug effect over time. This comes from continuous repeated use at high concentrations

336
Q

what is drug desensitisation

A

this is rapid and comes when either the receptor is uncouples, internalised or degraded

337
Q

what does afferent mean

A

takes signals toward the brain/spinal cord

338
Q

what does efferent mean

A

takes signals away from the brain/spinal cord

339
Q

what does adrenergic mean

A

relating to adrenaline or noradrenaline and either receptors

340
Q

what does cholinergic mean

A

relating to acetylcholine and its receptor

341
Q

what is the somatic nervous system

A
  1. there are single neurons between the CNS and skeletal muscle 2. innervates skeletal muscle
  2. leads to muscle excitation
342
Q

what is the autonomic nervous system

A
  1. a two neuron chain
  2. smooth muscle, cardiac muscle, glands and GI
  3. leads to excitation or inhibition
343
Q

what separates the two peripheral neurons of the ANS

A

an autonomic ganglion

344
Q

which branch of the autonomic nervous system (Para or sym) has a longer presynaptic neuron - before ganglion

A

parasympathetic

345
Q

which branch of the autonomic nervous system (para or symp) has a longer post synaptic neuron - after ganglion

A

sympathetic

346
Q

what are the two main neurotransmitters of the ANS

A

acetylcholine and noradrenaline

347
Q

what types of preganglionic receptors does acetylcholine act on

A

nicotinic receptors

348
Q

what type of postganglionic receptors does acetylcholine act on

A

muscarinic (PS)

349
Q

what type of postganglionic receptors does noradrenaline act on

A

alpha and beta receptors (s)

350
Q

in what part of the body is acetylcholine released at sympathetic postganglionic termini

A

sweat glands

351
Q

in blood vessels what can be released from parasympathetic postganglionic termini

A

nitric oxide

352
Q

where are the five types of muscarinic receptor found

A

M1: Brain
M2: Heart
M3: all organs with ps function - most notably the Lungs
M4: Mainly CNS
M5: Mainly CNS

353
Q

what type of receptor are Muscarinic receptors

A

G coupled protein receptors

354
Q

what does activation of M2 receptors in SAN cause

A

decrease in heart rate

355
Q

what does activation of M2 receptors in AVN cause

A
  1. decrease in conduction velocity
  2. Induces an AV node block (increases PR)
356
Q

What does M3 receptors stimulation in the respiratory system cause

A
  1. mucus production
  2. smooth muscle contraction (bronchoconstriction)
357
Q

what does M3 receptor stimulation in the GIT cause

A
  1. increased saliva production
  2. increased gut production
  3. stimulates biliary secretion
358
Q

what does M3 receptor stimulation in the skin cause

A

sweating

359
Q

where is the only place in the body where the sympathetic system releases Ach

A

the skin

360
Q

what does M3 receptor activation of the urinary system cause

A
  1. Contraction of the detrusor muscle
  2. relaxation of the internal urethral sphincter (in males)
361
Q

what does muscarinic receptor activation in the eyes cause

A
  1. increases myosis
  2. increases drainage of aqueous humour
  3. secretion of tears
362
Q

what are pilocarpine eye drops

A

they are M3 agonists - induce tear secretion and increases drainage of aqueous humour

363
Q

what is atropine used for

A

used intravenously to increase heart rate, treat bradyarrythmias and AV node block

364
Q

what type of drug is Hyoscine

A

it is a predominant M3 antagonist

365
Q

what is hyoscine action

A

it is used in palliative care to treat respiratory secretions and symptoms of bowel obstruction

366
Q

what are examples of inhales antimuscarinics

A

tiotropium, glycopyrronium, umeclidinium, aclidinium

367
Q

why would you inhale an antimuscarinic

A

can cause bronchodilation

368
Q

what are side effects of inhaled antimuscarinics

A

they can cause dry mouth, urinary retention, can worsen existing glaucoma

369
Q

what is solifenacin

A

a treatment for an overactive bladder

370
Q

how does solifancacin work

A

blocks M3 receptors in the bladder and inhibits smooth muscle contraction

371
Q

what is mebeverine

A

a treatment for irritable bowel syndrome

372
Q

how does mebeverine work

A

it blocks M3 receptors in the gut to slow contractility

373
Q

why might anticholinergics (antimuscarinics) cause memory problems

A

because Ach is used in CNS as well and implicated in memory

374
Q

what can be used to prevent Ach release in the somatic nervous system

A

Botulinum toxin

375
Q

what are examples of muscle relaxants given during surgery

A

Rocuronium, suxamethonium, pancuronium

376
Q

what is the mode of action for rocuronium, suxamethonium and pancuronium

A

they block nicotinic (N1) receptors to inhibit Ach activity in the somatic nervous system

377
Q

what happens during myaesthenia gravis

A

there is Ach receptor antibodies which prevents Ach binding to post synaptic neurons. This leads to skeletal muscle weakness with the most notable weakness being on repeated attempts at a movement

378
Q

what is a treatment for myaesthenia gravis

A

the treatment includes anti-cholinesterase to increase Ach availability at the neuromuscular junction

379
Q

what is the precursor of noradrenaline

A

dopamine

380
Q

what are the features of alpha 1 receptors

A
  1. Agonist is noradrenaline over adrenaline
  2. mechanism of action is increasing intracellular calcium via Gq signalling
  3. its activation causes contraction of smooth muscle - mainly in the skin and abdomen
381
Q

what are the features of alpha 2 receptors

A
  1. Agonists are both noradrenaline and adrenaline
  2. Mechanism of action is acting through Gi singalling to inhibit cAMP generation
  3. causes mixed effects on smooth muscle
382
Q

what are the features of beta 1 receptors

A
  1. agonists are both noradrenaline and adrenaline
  2. acts through Gs to raise cAMP
  3. causes chronotropic and inotropic effects on the heart
383
Q

what are the features of beta 2 receptors

A
  1. agonist is adrenaline over noradrenaline
  2. acts through Gs to raise cAMP
  3. relaxes smooth muscles
384
Q

What are the features of beta 3 receptors

A
  1. agonist is noradrenaline over adrenaline
  2. acts through Gs to raise cAMP
  3. enhances lipolysis and relaxes the bladder detrusor muscle
385
Q

what is given in ITU for shock

A

IV noradrenaline

386
Q

what is xylometazoline used for

A

a nasal decongestant - topical alpha activation

387
Q

what is clonidine and what is it used for

A

it is an alpha 2 agonist and it is used in ADHD to help concentration

388
Q

what is the action of alpha 2 stimulation in blood vessels

A

it reduces vascular tone and blood pressure

389
Q

what are some examples of alpha 1 blockers

A
  1. doxazosin used to lower blood pressure
    2 phenoxybenzamine used in treating a catecholamine secreting tumour
  2. tamsulosin used to block alpha 1 receptors in the the prostate during benign prostatic hypertrophy
390
Q

where are beta 1 receptors mainly found

A

in the heart, kidney and fat cells

391
Q

what does an activation of B1 receptors lead to

A
  1. tachycardia
  2. increased stroke volume
  3. renin release
  4. lipolysis and hyperglycaemia
392
Q

what do beta 1 blockers cause

A

reduced heart rate, reduced stroke volume, reduced myocardial oxygen demand

393
Q

what are some examples of beta blockers

A

carvedilol, bisoprolol, atenolol

394
Q

what does beta 2 receptor activation in the bronchi cause

A

bronchodilation

395
Q

what does beta 2 receptor activation in the bladder wall cause

A

inhibition of micturition

396
Q

what does beta 2 receptor activation in the uterus cause

A

inhibition of labour

397
Q

what does beta 2 receptor activation in skeletal muscle cause

A

increased contraction speed (induces a tremor)

398
Q

what does beta 2 receptor activation in the pancreas cause

A

insulin and glucagon secretion

399
Q

what are beta 2 receptor agonist drugs used for

A

asthma i.e salbutamol, and chronic obstructive pulmonary disease

400
Q

what are the steps Ach goes through at the neuromuscular junction

A
  1. synthesis
  2. vesicle storage
  3. release
  4. breakdown
  5. reuptake
401
Q

what effects does Ach stimulation have in the parasympathetic nervous system

A
  1. rest and digest
  2. pupil constriction
  3. decreased HR
  4. bronchoconstriction
  5. increased gut motility and secretion
  6. bladder contraction - detrusor muscles
  7. penis erect
402
Q

what effects does noradrenaline stimulation have in the sympathetic nervous system

A
  1. fight or flight
  2. pupil dilation
  3. increased heart rate
  4. bronchodilation
  5. decreased gut motility
  6. detrusor muscle relaxation
  7. ejaculation
403
Q

what is the noradrenergic synthesis pathway

A

tyrosine - DOPA - dopamine - Noradrenaline - Adrenaline

404
Q

what drug is given in cardiogenic shock

A

B1 agonist dobutamine

405
Q

what are the two types of Nad receptors

A

alpha and beta receptors

406
Q

what are dopamine agonists used for

A

prolactinoma (pituitary tumour), acromegaly, and early in Parkinson’s

407
Q

give an example of a dopamine agonist

A

bromocriptine

408
Q

what are dopamine antagonists used for

A

they are often used in psychiatric disorders and for nausea and vomiting

409
Q

what are some examples of dopamine antagonists

A
  1. metoclopramide: antiemetic
  2. halopemide
410
Q

what are GABA agonists used for

A

anxiety, sleep disorders, alcohol withdrawal and states epilepticus

411
Q

what is an example of a GABA agonist

A

benzodiazepines (lorazepam and diazepam)

412
Q

what are histamine H1 antagonists used for

A

for allergy (T1 IgE anaphylaxis)

413
Q

what is an example of H1 histamine antagonist

A

loratadine

414
Q

what are H2 histamine antagonists used for

A

these are second line treatments for GORD or an increased gastric acid after proton pump inhibitors

415
Q

what are examples of a histamine H2 receptor antagonist

A

ranitidine (main)
Cimetidine

416
Q

what is an irreversible inhibitor

A

they react with an enzyme and change it chemically (via covalent bond formation)

417
Q

what is a reversible inhibitor

A

they bind non-covalently and different types of inhibition a produced dependent on whether the inhibitors binds to the enzyme, the enzyme substrate complex or both

418
Q

what are the 4 types of ion channels

A
  1. epithelial - sodium
  2. voltage gated - calcium and sodium
  3. metabolic - potassium
  4. receptor activated - chloride
419
Q

what is the oral bioavailability of opioids

A

at most about 50%

420
Q

why is oral bioavailability of opioids quite low

A

due to first pass metabolism in the liver

421
Q

what class of drugs are opioids

A

class A drugs

422
Q

what are the practical issues with prescribing opioids in hospital

A

they are stored in locked containers and you must have two people sign them out

423
Q

what is the action of codeine in the body

A

it is converted into morphine and then acts on the body

424
Q

why must you not proscribe codeine to new mothers or infants

A

because 5-10% of people have an overactive enzyme which converts codeine to morphine - can lead to respiratory arrect in children (through breast milk)

425
Q

what is the most common form of morphine found in hospitals

A

oromorph - taken orally

426
Q

what does parenteral drug administration mean

A

IV administration

427
Q

what does enteral drug administration mean

A

non-IV

428
Q

how longs does it take an IV drugs, a sub-cutaneous drug and a drug taken orally to go through the body (roughly)

A
  1. IV - minutes
  2. Sub-cutaneous - about half an hour
  3. Orally - about 1-2 hours
429
Q

what is the difference between morphine and diamorphine

A

diamorphine is more potent and faster acting

430
Q

how do opioids work

A

they attach to the opioids receptors in the brain/spinal cord and dampen pain reception.

431
Q

what type of receptor is the opioid receptor

A

a G protein coupled receptor

432
Q

how do naturally occurring opioids work (ones the body makes)

A

they inhibit pain transmission at the spinal cord/midbrain and they change the emotional perception of pain. They are part of the bodies fight or flight response and they have short term activity

433
Q

how quicky does opioid tolerance occur

A

after a couple of days of medication
- receptors lost

434
Q

what are the types of opioid receptor

A

MOP, KOP, DOP. NOP

435
Q

what is tolerance

A

the down regulation of the receptors with a prolonged use. You need a higher dose to achieve the same effect

436
Q

what is dependence

A

the psychological effect - craving, euphoria

437
Q

what is opioid withdrawal

A

when you stop someones opioid medication - there will be withdrawal within 24 hours and it lasts about 72 hours
need to be careful with this as severe withdrawal symptoms can lead to death

438
Q

why do you get opioid side effects

A

because you have opioid receptor outside the pain system - in the digestive tract, respiratory control centre etc

439
Q

what are the side effects of opioid use

A
  1. respiratory depression
  2. sedation
  3. nausea and vomiting
  4. constipation
  5. itching
  6. immune suppression
  7. endocrine effects
440
Q

how are opioids metabolised in the body

A

morphine is metabolised to morphine 6 glucuronide which is more potent than morphine and is renally excreted. With normal renal function this is cleared quickly

441
Q

what is the antidote for morphine

A

naloxone

442
Q

what are the relative potencies of diamorphine, morphine and pethidine (in an average human)

A
  1. diamorphine - 5mg
  2. morphine - 10mg
  3. Pethidine - 100mg
443
Q

how do you treat opioid induced respiratory depression

A
  1. ABC; airway, breathing, circulation
  2. Give them IV naloxone (slowly - titrate)
444
Q

what is the advice on prescribing opioids in chronic, non-cancer pain

A
  1. before prescribing discuss the risks and features of opioid tolerance, dependence and addiction
  2. agree a treatment strategy and when it will end
  3. at the end, taper off the medication to help with withdrawal
445
Q

what is the common antibiotic given for community acquired pneumonia

A
  1. Amoxicillin
  2. clarithromycin
446
Q

what is the common antibiotic given for COPD

A
  1. Amoxicillin
  2. clarithromycin
447
Q

what is the common antibiotic given for TB

A

RIPE
1. Rifampicin
2. Isoniazid
3. Pyrazinamide
4. Ethambutol

448
Q

what is the common antibiotic given for hospital acquired pneumonia

A
  1. co-amoxiclav 3X daily 500mg or 125mg for 5days
449
Q

what are the side effects of rifampicin

A

red pee/tears

450
Q

what are the side effects of isoniazid

A

peripheral neuropathy

451
Q

what are the side effects of Pyrazinamide

A

can cause hepatitis

452
Q

what are the side effects of ethambutol

A

can cause optic neuropathy

453
Q

what is the common antibiotic given for cellulitis

A

flucloxacillin
- if MRSA give vancomycin

454
Q

what is the common antibiotic given for a UTI

A

Trimethoprim or nitrofurantoin (Give nitrofurantoin)
(if pregnant give folate as well as can be teratogenic - nitrofurantoin preferred)

455
Q

what is the common antibiotic given for pyelonephritis

A

cefalexin or co-amoxiclav

456
Q

what is the common antibiotic given for chlamydia trachomatis

A

azithromycin or doxycycline

457
Q

what is the common antibiotic given for Neisseria gonorrhoea

A

IM ceftriaxone and azithromycin (one off)

458
Q

what is the common antibiotic given for syphilis

A

benzathine penicillin or benzylpenicillin

459
Q

what is the common antibiotic given for H.Pylori

A

CAP for 7 days
1. clarithromycin
2. Amoxicillin
3. PPI

460
Q

what is the common antibiotic given for gastroenteritis

A

campylobacter = clarithromycin
salmonella and shigella = ciprofloxacin

461
Q

what is the common antibiotic given for infective endocarditis

A

s.aureus = vancomycin and rifampicin
s.vindans = benzylpenicillin and gentamycin

462
Q

what is the common antibiotic given for bacterial meningitis

A

ceftriaxone in hospital, amoxicillin of listeria suspected and steroids
in the community = benzylpenicillin if meningococcal suspected

463
Q

what is the common antibiotic for C.Difficile

A

vancomycin - 125mg for 4 times a day for 10 days

464
Q

what neurotransmitter does the parasympathetic system release (commonly)

A

Ach which acts on muscarinic receptors

465
Q

what neurotransmitter does the sympathetic nervous system release (commonly)

A

noradrenaline which activates adrenergic receptors (alpha/beta receptors)

466
Q

what do both sympathetic and parasympathetic fibers release pre-ganglionically

A

Ach which acts on nicotinic receptors

467
Q

what are side effects of anti-cholinergics

A

worsening or memory and cause confusion. Constipation, drying of the mouth, blurring of vision and worsening of glaucoma

468
Q

what are the different routes of drug administration

A
  1. oral
  2. intravenous
  3. intra-arterial
  4. intramuscular
  5. subcutaneous
  6. inhalational
  7. topical
  8. sublingual
  9. rectal
  10. intrathecal
469
Q

what are the four major metabolic barriers oral drugs must pass through

A
  1. intestinal lumen
  2. intestinal wall
  3. liver
  4. lungs
470
Q

what are the features of intradermal and subcutaneous absorption

A
  1. it avoids the barrier of the striatum corneum
  2. it is mainly limited by blood flow
  3. only small volume can be given
  4. this is used for local effect or to limit the rate of absorption
471
Q

what are the different types of pain

A

Acute, Cancer, Neuropathic, Chronic non cancer

472
Q

What is the cause of acute pain

A

nociceptor signaling (Ab, Ad and C fibres) to the thalamus

473
Q

what is the gate control theory

A

Pain modulated by:
heat - rubbing the site of pain - decreased pain impulses via the ascending tract
medication acting on the same pathway - NSAIDs, Opioids, anesthesia

474
Q

What are the features of adverse drug reactions

A

ABCDEs
Augmented - is it predictable
Bizarre - is it because of allergy
Chronic - has the drug been used for a long time
Delayed - has the drug been used in the past
End of use - is it because there is withdrawal of drug

475
Q

what are patient factors which must be considered with drug interactions

A
  1. Age
  2. Polypharmacy
  3. Genetics
  4. Hepatitis/renal disease
476
Q

what are the pharmacokinetic influences in drug absorption

A

acidity, motility and solubility

477
Q

what are the pharmacokinetic influences in drug distribution

A

influenced by protein binding

478
Q

what are the pharmacokinetic influences in drug metabolism

A

CYP450 induction and inhibition

479
Q

what are the pharmacokinetic influences of drug excretion

A

affected by urine pH
- acids cleared faster if urine is weakly basic
- bases cleared faster if urine is weakly acidic

480
Q

what are the antiplatelet drug used in practice

A

aspirin - COX inhibition
Clopidogrel - P2Y12 inhibition

481
Q

what are the anticoagulant drugs used in practice

A

Heparin - activates antithrombin 3 and inhibits factor 10
Warfarin - anti vitamin K
DOACs - anti factor Xa
Thrombolytics

482
Q

what is the action of NSAIDs

A

inhibit COX1 and 2 and prevent prostaglandin production
- needs to be given with PPI now (aspirin)

483
Q

what is the common side effect of NSAIDs

A

Peptic Ulcer disease

484
Q

What is the common side effect of ACE inhibitors

A

increased bradykinin accumulation and causes a dry cough
reduces GFR and can cause acute kidney injury

485
Q

what are common side effects of PPIs

A

prolonged use can increase fracture risk

486
Q

what are common side effects of opioids

A

respiratory diseases
tolerance and dependence
nausea and vomiting

487
Q

what are common side effects of loop diuretics and thiazides

A

hypokalemia and dehydration

488
Q

what are common side effects of spironolactone

A

hyperkalemia

489
Q

what is the common loop diuretic and its action

A

Furosemide
inhibits the NKCC2 channels in the ascending loop of henle
it increases Cl-, K+ and Na+ and water excretion

490
Q

what is is the common thiazide used and what is its action

A

Bendroflumethiazide
they inhibit NaCl- channels in the distal convoluted tubule and therefore increase Cl- Na+ and water excretion

491
Q

what is spironolactone and what is its action

A

it is a diuretic and it inhibits ENaC channels (aldosterone antagonist as well) and therefore increases sodium potassium and water excretion

492
Q

what are the common steroid side effects

A

Cataracts Increased infection risk
Ulcers Necrosis of bone
Striae Growth restriction
Osteoporosis Increased ICP
DMT2 Myopathy
Adipose hypertrophy Pancreatitis

493
Q

what does intramuscular absorption depend on

A

blood flow and water solubility with an increase in either enhancing removal of drug from injection site.

494
Q

what are the features of inhalational absorption

A

there is a larger surface area and blood flow but it is limited by the risks of toxicity to the alveoli
it is largely limited to volatiles such as anesthetics and locally acting drugs

495
Q

what is the most common protein drugs bind to in blood

A

albumin (reversibly)

496
Q

what happens during phase 1 metabolism of drugs

A

transforming the drugs to more polar metabolites
- unmasking or adding functional groups
- oxidation reactions catalyzed by CYP450

497
Q

what happens during phase 2 drug metabolism

A

formation of covalent bonds between the drug and endogenous substrates
- glucuronidation

498
Q

what is first order kinetics
- pharmacokinetics

A

when an IV drug is given and rapidly distributed into the tissues, the decline in plasma concentration will be exponential
(constant fraction of the drug is eliminated per unit of time)

499
Q

what is zero order kinetics
- pharmacokinetics

A

if an enzyme that removes a drug is saturated, the rate of removal of the drug is constant and unaffected by any increase in the concentration

500
Q

what are the most common drugs to have allergy to

A

Antibiotics and NSAIDs

501
Q

what percentage of adverse drug reactions are allergy

A

5-10%

502
Q

what is the definition of 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 and non immunologic mechanisms

503
Q

what are examples of delayed drug hypersensitivity

A

rashes, hepatitis and cytopenia’s

504
Q

what is a urticarial rash

A

a fast forming, intensely itchy rash

505
Q

what are the features of anaphylaxis

A

it occurs within minutes and causes vasodilation, increased vascular permeability, bronchoconstriction, urticaria and angio-oedema, swelling of the lips, face, wheeze.

506
Q

what is the most common cause of anaphylaxis

A

insect venom, followed by medications

507
Q

what is a biphasic anaphylactic shock

A

where you have the initial reaction, you are treated for it, and you get the response again (without another stimulus) soon after treatment

508
Q

what percentage of anaphylaxis is biphasic

A

1-20% of responses

509
Q

what drugs are commonly implicated in hypersensitivity reactions

A

Aspirin, Penicillin, sulfonamides, antituberculosis drugs, nitrofurans, anticonvulsants, anesthetics, antiarrhythmia agents, antisera and vaccines, heavy metals, antibiotics, phenolphthalein

510
Q

what is non immune anaphylaxis

A

this is where you need no prior exposure to the allergen, but you still get mast cell degranulation. looks exactly the same as immune mediated anaphylaxis

511
Q

what is the management of anaphylaxis

A

Common basic life support: ABC
Adrenaline IM 500 micrograms and high flow oxygen
IV fluids and antihistamines

512
Q

what are the actions of adrenaline in anaphylaxis

A

causes vasoconstriction increasing PVR and BP via alpha 1 receptors
stimulation of Beta 1 receptors causes positive ionotropic and chronotropic effects on the heart
bronchodilation via beta 2 receptors
stops further mast cell and basophil degranulation via cAMP increase

513
Q

what are risk factors of hypersensitivity

A

medicine factors: protein or polysaccharide based molecules
Host factors: Female, having EBV or HIV, Being in the extremes of life, uncontrolled asthma, previous drug reactions
Genetic factors: certain HLA groups, acetylator status

514
Q

what are the clinical criteria for allergy to drug

A
  1. dont correlate with pharmacological properties of the drug
  2. no linear reaction with dose
  3. reaction similar to those with 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 the drug
515
Q

what are the impacts of adverse drug reactions in healthcare

A
  1. adversely affects patients quality of life
  2. increases the cost of care
  3. precludes the use of a drug in most patients
  4. may mimic disease
  5. very common cause of death
516
Q

what is an adverse drug reaction

A

it is unwanted or harmful reaction following the administration of a drug or combination of drugs under normal conditions of use and suspected to be related to the drug
- has to be noxious and unintended

517
Q

are adverse drug reactions the same as side effects

A

they can be however not all the time as side affects can be beneficial, but adverse drug reactions are never beneficial

518
Q

what is a toxic affect - adverse drug reaction

A

when the drug concentration is beyond the therapeutic range

519
Q

what is a collateral effect - adverse drug reactions

A

when the drug concentration is within the therapeutic range

520
Q

what is a hyper-sensitivity effect - adverse drug reactions

A

when the drug concentration is below the therapeutic range

521
Q

what are examples of toxic drug effects when the drug concentration is too high

A

Gentamicin: causes nephropathy or ototoxicity at high concentrations

522
Q

why can toxic drug affects occur

A

when you have too high drug concentration, you cant excrete the drug correctly, or there are interactions with other drugs

523
Q

what is an example of collateral adverse drug reaction effects

A

beta blockers causing bronchoconstriction
antibiotics causing clostridium difficile

524
Q

what is an example of hypersensitivity adverse drug reaction

A

anaphylaxis and penicillin

525
Q

what can the severity of adverse drug reactions be

A

can range from mild (nausea or drowsiness) to severe (respiratory depression, hemorrhage, anaphylaxis)

526
Q

what are risk factors of adverse drug reactions

A

Patient risk: female, elderly, neonates, polypharmacy, genetics, hypersensitivity or allergies, hepatic or renal impairment
Drug risk: steep dose response curve, low therapeutic index, commonly causes ADRs
Prescriber risk: human error

527
Q

what are causes for ADRs

A
  1. pharmaceutical variation
  2. receptor abnormality
  3. abnormal biological system unmasked by drugs
  4. abnormal drug metabolism
  5. immunological
  6. drug-drug interactions
  7. multifactorial
528
Q

what is an augmented ADR

A

it is an extension of the primary effect or the drug (such as propranolol and bradycardia) and has a high morbidity with a low mortality (excludes overdose)

529
Q

what is a bizarre ADR

A

It is non predictable or related to the pharmacology of the drug and is not dose dependent. It is less common but more serious with low morbidity and high mortality

530
Q

what is idiosyncrasy

A

where there is an inherent abnormal response to a drug
- enzyme abnormality, deficiency or abnormal receptor activity

531
Q

what are continuous ADRs

A

it is related to cumulative dose on dose responses to a drug and it occurs over time. It is uncommon
- steroids and osteopetrosis

532
Q

what are delayed ADRs

A

where the ADR shows itself after the use of the drug. They are uncommon and normally dose related
- Carcinogens

533
Q

what are ending of drug use ADRs

A

where the ADR occurs once a drug has been withdrawn. they are uncommon
- example is opioid withdrawal

534
Q

what is a failure ADR

A

This is often caused by drug interactions causing failure of the drug, it is common and dose related
- failure of oral contraceptive and enzyme inducers

535
Q

when do you suspect ADR

A
  1. symptoms occur soon after new drug starts
  2. Symptoms appear after increased dose
  3. symptoms disappear when drug is stopped
  4. symptoms appear when drug is restarted
536
Q

when do you suspect ADR

A
  1. symptoms occur soon after new drug starts
  2. Symptoms appear after increased dose
  3. symptoms disappear when drug is stopped
  4. symptoms appear when drug is restarted
537
Q

what do you do if there is an ADR

A
  1. assess if urgent action is required
  2. take history
  3. review medication history
  4. review adverse effect profile of suspected drug
  5. modify dose, stop or swap
  6. report
538
Q

what drugs commonly have ADRs

A

antibiotics, NSAIDs, Cardiovascular drugs, hypoglycemics, CNS drugs

539
Q

what are common ADRs

A

confusion, Nausea, balance problems, diarrhea, constipation, hypotension

540
Q

how do you gather information on ADRs

A

pre-clinical trials, post marketing surveillance and yellow card reporting

541
Q

what are the MHRA responsible for

A

approving medicines for use and watching over them and take actions to protect the public if there is an issue

542
Q

what is the yellow card scheme

A

it is a ADR reporting scheme which collects spontaneous reports as well as suspected adverse drug reactions - voluntary

543
Q

why would you report an ADR

A
  1. patient safety
  2. identify ADRs not seen in clinical trial
  3. identify new ADRs quickly
  4. compare drugs within the same class
  5. identify ADRs in at risk groups
544
Q

what is a black triangle drug

A

one that is undergoing additional monitoring

545
Q

what are pharmacokinetic issues with immunotherapy

A
  1. immunoglobulins cant be filtered by the kidney: too big
  2. FcRn receptor - systemic receptors which absorb IgG into cells protecting them from metabolism dont recognise mouse antibodies resulting in a shorter half life
546
Q

how is insulin currently made

A

Recombinant Human Insulin
- insulin gene inserted into a plasmid which is transfected into bacteria. The bacteria will then produce insulin during fermentation which can then be purified and used

547
Q

what are examples of recombinant proteins in clinical use

A
  1. insulin
  2. EPO
  3. growth hormone
  4. interleukin 2
  5. gamma interferon
548
Q

what are the clinical uses of glucocorticoids (steroids)

A

asthma, allergic reaction, hives, eczema, COPD, lupus, IBD, MS

549
Q

what is rational drug design

A

the process of finding new medications based on the knowledge of a biological target
- complementary

550
Q

what is drug re-purposing

A

a technique where existing drugs are used to treat emerging and challenging diseases

551
Q

what is the monoclonal antibody against TNF alpha

A

Infliximab

Phase 2a - Jemima (11 decks)

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