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Phase2 > Introduction to Clinical Sciences > Flashcards

Introduction to Clinical Sciences Flashcards

1
Q

Define inflammation.

A

A local physiological response to tissue injury

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2
Q

Give a benefit of inflammation.

A

It can destroy invading microorganisms thus preventing the spread of infection

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3
Q

Give a disadvantage of inflammation.

A

It can produce disease

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4
Q

What are the two types of inflammation?

A

Acute and chronic

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5
Q

What is acute inflammation?

A
  • Initial response of tissue to injury
  • Early onset
  • Short duration
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6
Q

Which cells are involved with acute inflammation? What are their roles?

A
  • Neutrophils and monocytes
  • Neutrophils phagocytise pathogens, monocytes migrate to tissue and become macrophages which secrete chemical mediators for chemotaxis
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7
Q

What are the 6 causes of acute inflammation?

A
  • Microbial infections (bacteria, viruses)
  • Hypersensitivity reactions
  • Physical agents (trauma, heat, cold)
  • Chemicals (corrosives, acids)
  • Bacterial toxins
  • Tissue necrosis
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8
Q

What are the steps for acute inflammation?

A
  • Vascular component: dilation of vessels
  • Exudative component: vascular leakage of protein-rich fluid
  • Neutrophil polymorph (the cell type recruited to the tissue)
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9
Q

What is exudate?

A

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

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10
Q

What is transudate?

A

Transudate is fluid buildup caused by systemic conditions that alter the pressure in blood vessels, causing fluid to leave the vascular system

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11
Q

Explain the 4 steps for neutrophil polymorph emigration.

A
  1. Migration of neutrophils: due to increased plasma viscosity and slowing of flow due to injury, neutrophils migrate to plasmatic zone
  2. Adhesion of neutrophils: adhesion to the vascular endothelium occurs in venules (‘pavementing’)
  3. Neutrophil emigration: neutrophils pass through endothelial cells, onto the basal lamina and then the vessel wall
  4. Diapedesis: RBCs may also escape from vessels, this is a passive process and indicates severe vascular injury
    Neutrophils digest the bacteria.
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12
Q

What are the 4 outcomes of acute inflammation?

A
  • Resolution = complete restoration of tissues to normal
  • Supparation = formation of pus. This becomes surrounded by a pyogenic membrane, which is the start of healing, leads to scarring
  • Organisation = replacement by granulation tissue. New capillaries grow into the inflammatory exudate, macrophages migrate and fibrosis occurs
  • Progression = causative agent not removed, so progression to chronic inflammation
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13
Q

Give 5 cardinal signs of acute inflammation.

A
  • Rubor - redness; due to dilation of small vessels
  • Calor - heat; due to increased blood flow, resulting in vascular dilation + delivery of warm blood
  • Tumor - swelling; results from oedema (accumulation of fluid in extravascular space as part of the fluid exudate). Also from physical mass of inflammatory cells migrating to area
  • Dolor - pain; results from stretching and distortion of tissues due to inflammatory oedema
  • Loss of function
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14
Q

How can acute inflammation be diagnosed histologically?

A

By looking for the presence of neutrophil polymorphs.

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15
Q

Give 3 endogenous chemical mediators of acute inflammation.

A
  1. Bradykinin
  2. Histamine
  3. Nitric oxide
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16
Q

What are 4 systemic effects of acute inflammation?

A
  1. Fever
  2. Feeling unwell
  3. Weight loss
  4. Reactive hyperplasia of the reticuloendothelial system
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17
Q

What causes the pain associated with acute inflammation?

A
  1. Stretching and distortion of tissue due to oedema and pus under high pressure in an abcess cavity
  2. Chemical mediators, e.g. bradykinin and prostaglandins, are also known to induce pain
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18
Q

Describe the process of neutrophil polymorph migration into tissues as seen in acute inflammation.

A
  1. Margination of neutrophils
  2. Pavementing of neutrophils
  3. Neutrophils pass between endothelial cells
  4. Neutrophils pass through basal lamina and migrate into adventitia
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19
Q

What is the role of tissue macrophages in acute inflammation?

A

They secrete chemical mediators that attract neutrophil polymorphs

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20
Q

What is the role of the lymphatic system in acute inflammation?

A

Lymphatic channels dilate and drain away oedematous fluid therefore reducing swelling. Antigens are also carried lymph nodes for recognition by lymphocytes

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21
Q

What is the major role of neutrophil polymorphs in acute inflammation?

A

Phagocytosis

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22
Q

What does viral infection result in?

A

Cell death due to intracellular multiplication

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23
Q

What does bacterial infection result in?

A

The release of exotoxins (involved in the initiation of inflammation) or endotoxins

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24
Q

What is chronic inflammation?

A
  • Slow onset or sequel to acute
  • Long duration
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25
Q

What cells are involved with chronic inflammation?

A

Macrophages, lymphocytes and plasma cells

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26
Q

What cell can form when several macrophages try to ingest the same particle?

A

Multinucleate giant cell

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27
Q

Give 4 causes of chronic inflammation.

A
  1. Primary chronic inflammation:
    - Resistance of infective agent, e.g. TB
    - Endogenous materials, e.g. necrotic tissue
    - Exogenous materials, e.g. asbestos
    - Autoimmune conditions, e.g. Hashimoto’s
    - Primary granulomatous diseases, e.g. Crohn’s
  2. Transplant rejection
  3. Recurrent acute inflammation
  4. Progression from acute inflammation
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28
Q

In which type of inflammation would you see neutrophil polymorphs?

A

Acute inflammation

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29
Q

What are some macroscopic appearances of chronic inflammation?

A
  • Chronic ulcer
  • Chronic abscess cavity
  • Granulomatous inflammation
  • Fibrosis
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30
Q

What are some microscopic appearances of chronic inflammation?

A
  • Macrophages, lymphocytes and plasma cells
  • Exudation not a common feature
  • Evidence of continuing destruction
  • Possible tissue necrosis
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31
Q

What are the roles of B lymphocytes, T lymphocytes and macrophages in chronic inflammation?

A
  • B lymphocytes = transform into plasma cells + produce antibodies
  • T lymphocytes = responsible for cell-mediated immunity
  • Macrophages = respond to chemotactic stimuli, produce cytokines: interferon alpha and beta, IL1, 6, 8, TNF-alpha
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32
Q

What is granulation tissue?

A

Granulation tissue is composed of small blood vessels in a connective tissue matrix with myofibroblasts = important for healing

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33
Q

What is a granuloma?

A

An aggregate of epithelioid histiocytes

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34
Q

Give examples of granulomatous diseases. What do they cause?

A

TB, leprosy, Crohn’s and sarcoidosis. They cause granulomas to develop

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35
Q

What do granulomas and eosinophil presence indicate?

A

A parasite

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36
Q

The activity of what enzyme in the blood can act as a marker for granulomatous disease?

A

Angiotensin converting enzyme

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37
Q

Compare acute inflammation vs. chronic inflammation - onset and duration, cells involved, what these cells do and the macroscopic features.

A
  • Acute inflammation:
  • Fast onset, short duration
  • Neutrophils and monocytes
  • Neutrophil extravasation
  • Rubor, calor, tumor, dolor
  • Chronic inflammation:
  • Slower onset, long duration
  • Macrophages, lymphocytes, plasma cells
  • Cellular infiltrate of lymphocytes, macrophages and plasma cells. Possible granulomas
  • Fibrosis, scar tissue
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38
Q

What is the difference between resolution and repair?

A
  • Resolution is where the initiating factor is removed and the tissue is able to regenerate
  • Repair is where the initiating factor is still present and the tissue is unable to regenerate. Replacement of damaged tissue by fibrous tissue, collagen produced by fibroblasts
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39
Q

Name 5 types of cells that are capable of regeneration.

A
  1. Hepatocytes
  2. Osteocytes
  3. Pneumocytes
  4. Blood cells
  5. Gut and skin epithelial cells
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40
Q

Name 2 types of cells that are incapable of regeneration.

A
  1. Myocardial cells
  2. Neurones
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41
Q

In skin wounds, what is healing by 1st intention?

A

When the edges of the wound are brought together, e.g. sutures

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42
Q

In skin wounds, what is healing by 2nd intention?

A

Wound left open and to heal by itself

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43
Q

What is an abcess?

A

Acute inflammation with a fibrotic wall

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44
Q

Define thrombosis.

A

The formation of a solid mass from blood constituents in an intact vessel in the living

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45
Q

Give 2 reasons why thrombosis formation is uncommon.

A
  1. Laminar flow
  2. Endothelial cells not ‘sticky’
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46
Q

What is the first stage of thrombosis formation? Why is this hard to stop?

A
  • Platelet aggregation, which starts the clotting cascade of proteins in the blood
  • These both have positive feedback loops, so are hard to stop
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47
Q

Which two granules do platelets contain? What are these involved in? Why would platelets release these?

A
  • Platelets have alpha and dense granules
  • Alpha granules are involved in platelet adhesion, e.g. fibrinogen
  • Dense granules cause platelets to aggregate, e.g. ADP
  • Platelets are activated, releasing their granules when they come into contact with collagen. If this happens within an intact vessel, a thrombus is formed
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48
Q

What are the three major factors that cause thrombosis? What is this called? How many are typically needed to form a thrombus?

A
  1. Change in vessel wall
  2. Change in blood constituents
  3. Change in blood flow

This is called Virchow’s triad. Thrombosis typically formed by 2 of these factors

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49
Q

Detail the steps of arterial thrombosis.

A
  • An atheromatous plaque will result in a change in the vessel wall
    1. Atheromatous plaque may have a fatty streak
    2. Plaque grows + protrudes into lumen causing degree of turbulence in blood flow
    3. Turbulence results in loss of intima cells
    4. Fibrin deposited and platelet clumping occurs
    5. This process is self-perpetuating, leading to the formation of the platelet layer (first layer of thrombus)
    6. This layer allows for the precipitation of a fibrin mesh work in which RBCs get trapped
    7. This structure protrudes further into lumen causing more turbulence + more platelet deposition
    8. Thrombi grow in the direction of blood flow -> propagation
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50
Q

Detail the steps of venous thrombosis.

A
  1. There is lower BP in veins and atheroma does not occur
  2. Thrombi begin at valves
  3. Valves produce a degree of turbulence + can be damaged, e.g. trauma, stasis
  4. When blood pressure falls, flow through begins to slows, allowing for a thrombus to form
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51
Q

What are the 3 clinical features of arterial thrombi?

A
  1. Loss of pulse distal to thrombus
  2. Area becomes cold, pale + painful
  3. Possible gangrene
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52
Q

What are the 2 clinical features of venous thrombi?

A
  1. Tender
  2. Area becomes reddened + swollen
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53
Q

What are the 4 outcomes of thrombi?

A
  1. Resolve
  2. Organised - becomes a scar, results in slight narrowing of vessel lumen
  3. Recanalisation - intimal cells may proliferate, capillaries may grow into the thrombus and fuse to form larger vessels
  4. Embolus - fragments of the thrombus break off into the circulation
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54
Q

Compare arterial thrombus vs. venous thrombus - what is it caused by, blood pressure, what the thrombus is made of, what can it lead to, and its treatment

A
  • Arterial thrombus:
  • Commonly caused by atheroma
  • High pressure
  • Mainly made of platelets
  • Can lead to MI/stroke
  • Anti-platelets, e.g. aspirin
  • Venous thrombus:
  • Commonly caused by stasis
  • Low pressure
  • Mainly made of RBCs
  • Can lead to DVT/PE
  • Anti-coagulants
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55
Q

What drug can be used to prevent thrombosis?

A

Aspirin

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56
Q

Define embolus.

A

A mass of material (often a thrombus) in the vascular system able to lodge in a vessel and block its lumen

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57
Q

What are the consequences of an arterial embolus?

A

An arterial embolus can go anywhere. The consequences could be stroke, MI, gangrene etc.

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58
Q

What are the consequences of a venous embolus?

A

An embolus in the venous system will go onto the vena cava and then through the pulmonary arteries and become lodged in the lungs, causing a pulmonary embolism. This means there is a decreased perfusion to the lungs

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59
Q

Define ischaemia.

A

Reduction in blood flow

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60
Q

Define infarction.

A

Decreased blood flow with subsequent cell death (this is because the surrounding cells don’t get enough oxygen)

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61
Q

Can the effects of ischaemia be reversible? Is the duration of an ischaemic attack short or long? Which cells are the most vulnerable to an ischaemic attack?

A
  • Effects can be reversible
  • Duration of an ischaemic attack is brief
  • Cardiomyocytes and cerebral neurons are most vulnerable
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62
Q

What can happen if ischaemia is rectified?

A

Re-perfusion injury can occur due to the release of waste products

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63
Q

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

A

They only have a single arterial supply and so if this vessel is interrupted, infarction is likely

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64
Q

Give 3 examples of organs with a dual arterial supply. Are these organs more or less susceptible to an infarction?

A
  1. Lungs (bronchial arteries + pulmonary veins)
  2. Liver (hepatic arteries + portal veins)
  3. Some areas of the brain around the Circle of Willis
    - Organs with a dual blood supply are less susceptible to infarction
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65
Q

Is infarction a microscopic or macroscopic event? What is it usually caused by?

A

Infarction is a macroscopic event usually caused by thrombosis.

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66
Q

Through which blood system would an embolus have travelled if it resulted in a pulmonary embolism?

A

Venous system

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67
Q

Define atherosclerosis.

A

Inflammatory process characterised by hardened plaques in the intima of a vessel wall

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68
Q

What are the 3 main constituents of an atheromatous plaque?

A
  1. Lipids (cholesterol)
  2. Fibrous tissue
  3. Lymphocytes
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69
Q

Give 6 risk factors for atherosclerosis.

A
  • Hyperlipidaemia = most important risk factor
  • Smoking
  • Hypertension
  • Uncontrolled diabetes mellitus
  • Increasing age
  • Male sex
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70
Q

Why can cigarette smoking lead to atherosclerosis?

A

Cigarette smoking releases free radicals, nicotine and CO into the body. These all damage endothelial cells

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71
Q

Why can hypertension lead to atherosclerosis?

A

A higher blood pressure means there is a greater force exerted onto the endothelial cells and this can lead to damage

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72
Q

Why can hyperlipidaemia lead to atherosclerosis?

A

Direct damage to endothelial cells

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73
Q

Is atherosclerosis more common in the systemic or pulmonary circulation?

A

It is more common in the systemic circulation because there is a higher pressure system

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74
Q

What can be done to prevent atherosclerosis?

A

Reduce risk factors and taking low dose aspirin regularly

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75
Q

What is the primary cause of atherosclerosis?

A

Endothelial cell damage

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76
Q

Describe the process of atherosclerosis.

A
  1. High levels of LDL in the blood. Some deposits in the tunica initima and becoome oxidised - this activates endothelial cells to attract leukocytes (ENDOTHELIAL CELL DYSFUNCTION)
  2. Monocytes etc. are attracted to the site of damage (endothelium) - move to tunica intima (become macrophages)
  3. Macrophages take up oxidised lipid to form foam cells (inflammatory response). These foam cells encourage plaque progression by serving as a source of pro inflammatory cytokines. They also promote the migration of smooth muscle cells from the tunica media to the tunica intima and smooth muscle cell proliferation - this causes heightened synthesis of collagen
  4. Foam cells die - release lipid contents
  5. Fibrous cap maintaining the plaque has to be maintained by resorption and redeposition. However, if the balance is shifted, e.g. in favour of inflammatory conditions we get a plaque rupture. This causes blood coagulation = thrombus = impedes blood flow (occludes vessel)
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77
Q

What are the conditions that atherosclerosis can cause?

A
  • Cerebral infarction
  • Carotid atheroma, leading to TIAs
  • MI
  • Aortic aneurysm (can cause sudden death)
  • Peripheral vascular disease
  • Gangrene
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78
Q

Define apoptosis.

A

Programmed cell death of a single cell

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79
Q

What is the role of p53 protein?

A

The p53 protein looks for DNA damage. If DNA damage is present, p53 switches on apoptosis to prevent damaged DNA from replicating

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80
Q

What protein can switch on apoptosis if DNA damage is present?

A

p53 protein

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81
Q

In the regulation of apoptosis, what are the 3 inhibitors and 3 inducers?

A
  • Inhibitors:
  • Growth factors
  • Extracellular cell matrix
  • Sex steroids
  • Inducers:
  • Glucocorticoids
  • Free radicals
  • Ionising radiation
  • DNA damage
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82
Q

Activation of which family of protease enzymes can turn on apoptosis?

A

Caspases

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83
Q

Activation of what receptor can activate caspase and therefore apoptosis?

A

FAS receptor

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84
Q

Describe the intrinsic pathway for apoptosis.

A
  • Uses pro- and anti-apoptotic members of the Blc-2 family
  • Bax forms Bax-Bax diners which enhance apoptotic stimuli
  • The Bcl-2:Bax ratio determines the cell’s susceptibility to apoptotic stimuli
  • Responds to growth factors and biochemical stress
  • p53 gene induces cell cycle arrest and initiates DNA damage repair - if damage is difficult to repair, p53 can induce apoptosis
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85
Q

Describe the extrinsic pathway for apoptosis.

A
  • Ligand-binding at death receptors on the cell surface
  • Receptors include TNFR1 and CD95
  • Ligand-binding results in clustering of receptor molecules on the cell surface and the initiation of signal transduction cascade
  • Caspases are activated, triggering apoptosis
  • This pathway is used by the immune system to eliminate lymphocytes
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86
Q

What is an example of a disease where there is a lack of apoptosis.

A

Cancer; mutations in p53 mean cell isn’t damaged

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87
Q

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

A

HIV

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88
Q

Define necrosis.

A

Unprogrammed death of a large number of cells due to an adverse event

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89
Q

What are the different types of necrosis?

A
  • Coagulation necrosis = most common type, can occur in most organs, caused by ischaemia
  • Liquefactive necrosis = occurs in the brain due to its lack of substantial supporting stroma
  • Causeous necrosis = causes a ‘cheese’ pattern, TB is characterised by this form of necrosis
  • Gangrene = necrosis with rotting of the tissue, affected tissue appears black due to deposition of iron sulphide (from degraded haemoglobin)
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90
Q

Give 3 examples of events that can lead to necrosis.

A
  1. Frost bite
  2. Avascular necrosis
  3. Infarction
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91
Q

Give 3 differences between apoptosis and necrosis.

A
  1. Apoptosis is programmed cell death whereas necrosis is unprogammed
  2. Apoptosis tends to affect only a single cell whereas necrosis affects a large number of cells
  3. Apoptosis is often in response to DNA damage, necrosis is triggered by an adverse event, e.g. frost bite
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92
Q

What does congenital mean?

A

Present at birth

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93
Q

What does inherited mean? What does acquired mean?

A
  • Inherited = caused by an inherited genetic abnormality
  • Acquired = caused by non-genetic environmental factors
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94
Q

Define hypertrophy. Give an example.

A
  • Increase in the size of a tissue due to an increase in the size of constituent cells
  • Muscle hypertrophy can be seen in athletes due to increased muscle mass
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95
Q

Define hyperplasia. What can this only happen in? Give an example.

A
  • Increase in the size of a tissue due to an increase in the number of constituent cells
  • This can only happen in cells that divide -> cannot happen in myocardial cells or nerve cells
  • Hyperplasia of bone marrow cells can be seen in those living at high altitudes
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96
Q

Define atrophy. Give an example.

A
  • Decrease in the size of a tissue due to a decrease in the size of the constituent cells OR due to a decrease in the number of constituent cells
  • Occurs in disease, e.g. muscle atrophy
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97
Q

Define metaplasia. Why does it occur? Give an example.

A
  • A change in the differentiation of a cell from one fully differentiated cell type to another fully differentiated cells type
  • Occurs in response to alterations in the cellular environment
  • Barrett’s oesophagus = squamous epithelium of the oesophagus can become columnar epithelium in response to stomach acid
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98
Q

Define dysplasia.

A

Morphological changes seen in cells in progression to becoming cancer. The cells become more ‘jumbled up’

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99
Q

What limits cell growth?

A

Telomeres - found on end of chromosomes + get shorter with every cell division

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100
Q

What happens to a cell when the telomere gets too short?

A

It can no longer divide

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101
Q

Why do we get dermal elastosis as we age?

A

UV-B light leads to inadequate synthesis of proteins required for the correct assembly of elastic fibres

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102
Q

Why do we get osteoporosis? Who is therefore more likely to get osteoporosis?

A
  • Increased bone resorption caused by a LACK of OESTROGEN
  • Decreased bone formation caused by a LACK of OESTROGEN
  • Post-menopausal women most likely, so put on hormone replacement therapy
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103
Q

Why do we get cataracts as we age?

A
  • UV-B light
  • Protein cross-linking
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104
Q

Why do we get deafness as we age?

A

Damage to hairs or nerve cells on the cochlea that send sound signals to the brain. When these hairs or nerve cells are damaged or missing, electrical signals aren’t transmitted as efficiently, and hearing loss occurs

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105
Q

Give an example of:

a) a dividing tissue
b) a non-dividing tissue

A

a) gut or skin tissue can divide
b) brain tissue is non-dividing

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106
Q

Which cancer of the skin never metastasises?

A

Basal cell carcinoma of the skin

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107
Q

Why can excision only be used as a cure for basal cell carcinoma?

A

Because it never metastasises

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108
Q

Where do white blood cells circulate? What does this mean for tumours of white blood cells?

A

White blood cells circulate around the body and so will any tumour of the white blood cells

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109
Q

Suggest a treatment that could be used for leukaemia?

A

Chemotherapy. Leukaemia is systemic, it circulates all around the body, therefore excision can’t be used

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110
Q

Define carcinoma.

A

Malignant tumour of epithelial cells

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111
Q

Where do carcinomas spread to?

A

Carcinomas spread to lymph nodes that drain the site of the carcinoma, e.g. breast carcinoma to axillary lymph nodes

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112
Q

Where can carcinomas spread from the blood to?

A

Carcinomas can spread through the blood to bone

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113
Q

Give 5 carcinomas that can spread to the bone.

A

PB KTL (lead kettle):

  1. Prostate
  2. Breast
  3. Kidney
  4. Thyroid
  5. Lung
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114
Q

Give an example of a carcinoma that can spread to the axillary lymph nodes.

A

Breast carcinomas

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115
Q

What can still be present even if a tumour is completely excised?

A

Micro metastases

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116
Q

Why is adjuvant therapy often used in the treatment of carcinomas?

A

Micrometastases are possible even if a tumour is excised and so adjuvant therapy is given to suppress secondary tumour formation

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117
Q

Give an advantage and disadvantage of conventional chemotherapy.

A
  • Advantage: works well for treatment against fast dividing tumours, e.g. lymphomas
  • Disadvantage: it is non-selective for tumour cells, so normal cells are hit too; this results in side effects such as diarrhoea and hair loss
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118
Q

What kind of carcinomas would targeted chemotherapy be most effective against?

A

Slower dividing tumours, e.g. lung, colon and breast

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119
Q

What is the theory behind targeted chemotherapy?

A

It exploits the differences between cancer cells and normal cells; this means it is more effective and has less side effects

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120
Q

What kind of drugs can be used in targeted chemotherapy?

A

Monoclonal antibodies (MAB) and small molecule inhibitors (SMIs)

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121
Q

Give an example of a malignant tumour that often spreads to the lungs.

A

Sarcoma (via venae cavae -> heart -> pulmonary arteries)

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122
Q

Give an example of carcinomas that can spread to the liver.

A

Colon, stomach and pancreatic carcinomas can spread to the liver via the portal vein

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123
Q

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

A

Neutrophil polymorph

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124
Q

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

A

Fibroblasts

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125
Q

Which of the following is an example of acute inflammation?

A. Glandular fever

B. Leprosy

C. Appendicitis

D. Tuberculosis

A

C. Appendicitis

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126
Q

Which one of the following is a chronic inflammatory process form its start?

A. Appendicitis

B. Cholecystitis

C. Infectious mononucleosis

D. Lobar pneumonia

A

C. Infectious mononucleosis (glandular fever)

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127
Q

In which of the following does granulomatous inflammation occur?

A. Crohn’s disease

B. Acute appendicitis

C. Infectious mononucleosis

D. Lobar pneumonia

A

A. Crohn’s disease

Granulomatous inflammation is a collection of epithelioid macrophages

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128
Q

Which of the following is an example of hyperplasia?

A. Bodybuilder’s biceps

B. Enlarged left ventricle

C. Benign prostate enlargement

D. Wasting of quadriceps after immobilisation

A

C. Benign prostate enlargement

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129
Q

Which one of the following is not an example of apoptosis?

A. Loss of cells from tips of duodenal villi

B. Loss of cells during embryogenesis

C. Renal infarction

D. Graft versus host disease

A

C. Renal infarction

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130
Q

Which one of the following is an example of atrophy?

A. Biceps of a bodybuilder

B. Uterus in pregnancy

C. Brain in dementia

D. Prostate in older age

A

C. Brain in dementia

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131
Q

What is the pattern of differentiation of meta plastic cells lining the bronchi of cigarette smokers?

A

Ciliated pseudostratified columnar (respiratory) epithelium to squamous epithelial cells (skin-like)

This is more resistant to smoke but doesn’t protect the airways

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132
Q

Which one of the following is an example of necrosis?

A. Loss of cells from duodenal tips

B. Loss of individual cells during development

C. Loss of individual cells during development

D. Renal infarction

A

D. Renal infarction

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133
Q

What process 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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134
Q

Name a drug that inhibits platelet aggregation.

A

Aspirin

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135
Q

What are the crystals in gout formed from?

A

Uric acid

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136
Q

What is calcification in diseased tissues called?

A

Dystrophic calcification

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137
Q

Which cells produce antibodies?

A

Plasma cells

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138
Q

Define carcinogenesis.

A

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

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139
Q

What is the difference between carcinogenesis and oncogenesis? By this logic, what do carcinogenic and oncogenic mean?

A
  • Carcinogenesis applies to malignant neoplasms, whereas oncogenesis applies to benign and malignant tumours
  • Carcinogenic = cancer causing, oncogenic = tumour causing
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140
Q

What percentage of cancer risk is due to environmental factors?

A

85% environmental, 15% genetic

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141
Q

Give 5 factors that can affect cancer risk.

A
  1. Race
  2. Diet
  3. Constitutional factors (gender, age)
  4. Premalignant conditions
  5. Transplacental exposure
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142
Q

Give an example of a situation when transplancental exposure lead to an increase in cancer risk.

A

The daughters of mothers who had taken diethylstiboestrol for morning sickness had an increased risk of vaginal cancer

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143
Q

Name 5 different categories of carcinogens.

A
  1. Viral
  2. Chemical
  3. Ionising and non-ionising radiation
  4. Hormones, parasites and mycotoxins
  5. Miscellaneous
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144
Q

What causes skin cancer?

A

Exposure to UV light

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145
Q

Chemical carcinogens: what types of cancer do polycyclic aromatic hydrocarbons cause?

A

Lung cancer and skin cancer

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146
Q

Chemical carcinogens: what can expose people to polycyclic aromatic hydrocarbons?

A

Smoking cigarettes and mineral oils

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147
Q

Chemical carcinogens: what types of cancer do aromatic amines cause?

A

Bladder cancer

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148
Q

Chemical carcinogens: what types of people are more susceptible to bladder cancer caused by aromatic amine exposure?

A

People who work in the rubber/dye industry

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149
Q

Chemical carcinogens: what types of cancer do nitrosamines cause?

A

Gut cancer

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150
Q

Chemical carcinogens: what types of cancer do alkylating agents cause?

A

Leukaemia; the risk is small in humans

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151
Q

Give 3 reasons why alcohol causes cancer.

A
  1. Ethanol makes it easier for cells in the oropharynx to absorb other carcinogens
  2. Ethanol increases oestrogen (carcinogen) levels
  3. Alcohol’s metabolite, acetaldehyde, is a mutagen
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152
Q

Give 4 examples of viral DNA carcinogens.

A
  1. Epstein-Barr virus
  2. Human Papillomavirus
  3. Hepatitis B Virus
  4. Human Herpes Virus 8
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153
Q

Give 2 examples of viral RNA carcinogens.

A
  1. Human T lymphotrophic Virus-1
  2. Hepatitis C virus
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154
Q

What can B-naphthylamine cause? What is EBV linked to? What is HPV linked to? What are aflatoxins linked to? What is asbestos linked to?

A
  • B-naphthylamine (dyes and rubber industry) can cause bladder cancer
  • EBV is linked to Burkitt’s lymphoma
  • HPV is linked to cervical cancer
  • Aflatoxins (mycotoxin) linked to hepatocellular carcinoma
  • Asbestos has been linked to mesothelioma
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155
Q

What is a tumour?

A

Any abnormal swelling. Encompasses: neoplasms, inflammation, hypertrophy, hyperplasia

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156
Q

Define neoplasm.

A

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

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157
Q

What is a neoplasm composed of?

A
  1. Neoplastic cells
  2. Stroma
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158
Q

Describe neoplastic cells.

A

Derived from nucleated cells. They’re usually monoclonal and their growth is related to the parent cell

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159
Q

Can erythrocytes become neoplastic cells?

A

No. This is because they are unnucelated

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160
Q

Describe the stroma of a neoplasm.

A

Connective tissue composed of fibroblasts and collagen; it is very dense. There is a lot of mechanical support and blood vessels provide nutrition for the neoplastic cells

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161
Q

What is essential for neoplasm growth?

A

Angiogenesis

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162
Q

What does a neoplasm release in order to initiate angiogenesis?

A

Vascular endothelial growth factors

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163
Q

Why does necrosis often occur in the centre of a neoplasm?

A

The neoplasm grows quickly and outgrows its vascular supply

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164
Q

What are the advantages of classifying neoplasms?

A

It helps to determine the appropriate treatment and diagnosis

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165
Q

What are the two ways in which neoplasms can be classified?

A
  1. Behavioural classification (benign, malignant or borderline. Borderline tumours, e.g. ovarian lesions defy classification)
  2. Histogenetic classification (cell of origin. If the origin is unknown the tumour is ANAPLASTIC)
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166
Q

What are the 7 main features of benign neoplasms?

A
  1. Localised
  2. Non-invasive
  3. Slow growth, low mitotic activity
  4. Close resemblance to normal tissue
  5. Normal nuclei
  6. Necrosis and ulceration are rare due to slow growth
  7. Exophytic growth (grows outwards)
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167
Q

What are the consequences of benign neoplasms?

A
  1. Pressure on adjacent structures
  2. Obstruction to flow
  3. Transformation into malignant neoplasms
  4. Production of hormones
  5. Anxiety
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168
Q

What are the 7 main features of malignant neoplasms?

A
  1. INVASIVE!
  2. Metastasise
  3. Rapid growth, high mitotic activity
  4. Resemblance to normal tissue
  5. Poorly defined border due to invasive nature
  6. Necrosis and ulceration are common
  7. Endophytic growth (grows inwards)
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169
Q

What are the consequences of malignant neoplasms?

A

Destroy surrounding tissue, blood loss due to ulceration, pain, anxiety

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170
Q

How do we classify tumours?

A
  • Based on the specific cell or origin of the tumour:
  • Epithelial cells form carcinomas
  • Connective tissues form sarcomas
  • Lymphoid forms lymphomas or leukaemia
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171
Q

How do we grade tumours?

A
  • Grade is based on the extent to which the tumour resembles its original histology:
  • Grade 1 = well differentiated (most closely resembles parent tissue)
  • Grade 2 = moderately differentiated
  • Grade 3 = poorly differentiated
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172
Q

What are the benign and malignant epithelial neoplasms?

A
  • Benign = papilloma and adenoma
  • Malignant = carcinoma and adenocarcinoma
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173
Q

What is a:

a) papilloma
b) adenoma

A

a) papilloma = benign tumour of non-glandular epithelium
b) adenoma = benign tumour of glandular or secretory epithelium

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174
Q

Define carcinoma.

A

MALIGNANT EPITHELIAL NEOPLASM (malignant tumour of epithelial cells)!

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175
Q

Define adenocarcinoma.

A

Malignant tumour of glandular epithelium

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176
Q

What are the benign connective tissue tumours?

A
  • Lipoma = benign tumour of adipocytes
  • Rhabdomyoma = benign tumour of striated muscle
  • Leiomyoma = benign tumour of smooth muscle cells
  • Chondroma = benign tumour of cartilage
  • Osteoma = benign tumour of bone
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177
Q

Define sarcoma.

A

Malignant connective tissue neoplasm

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178
Q

What are the malignant connective tissue neoplasms?

A
  • Liposarcoma = malignant tumour of adipocytes
  • Rhabdomyosarcoma = malignant tumour of striated muscle
  • Leiomyosarcoma = malignant tumour of smooth muscle cells
  • Chondrosarcoma = malignant tumour of cartilage
  • Osteosarcoma = malignant tumour of bone
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179
Q

What is a melanoma?

A

A malignant neoplasm of melanocytes (EXCEPTION)

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180
Q

What is a neuroma?

A

A benign neoplasm of nerves

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181
Q

What is a lymphoma?

A

A malignant neoplasm of lymphoid cells (EXCEPTION)

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182
Q

What is a mesothelioma?

A

A malignant neoplasm of mesothelial cells (EXCEPTION)

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183
Q

Carcinomas and sarcomas are further classified according to the degree of differentiation. Is a carcinoma/sarcoma with a close resemblance to normal tissue classified as well differentiated or poorly differentiated?

A

A carcinoma/sarcoma with a close resemblance to normal tissue is classified as well differentiated. These types of neoplasms are low grade and have a better prognosis

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184
Q

Define metastasis.

A

The process whereby malignant tumours spread from their site of origin to form other tumours at distant sites

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185
Q

Which neoplasm never metastasises?

A

Basal cell carcinoma never metastasises

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186
Q

What is it called when cancer cells have not yet made it through the basement membrane?

A

Carcinoma in situ

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187
Q

What is required for a tumour to invade through a basement membrane?

A
  1. Proteases
  2. Cell motility
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188
Q

What is it called when the tumour invades through a basement membrane?

A

Invasive carcinoma

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189
Q

What is required for a tumour to enter the bloodstream (intravasation)?

A
  1. Collegenases
  2. Cell motility
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190
Q

What is required for the tumour to exit the bloodstream (extravasation)?

A
  1. Adhesion receptors
  2. Collegenases
  3. Cell motility
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191
Q

Give 2 promotors of tumour angiogenesis.

A
  1. Vascular endothelial growth factors
  2. Fibroblast growth factors
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192
Q

Give 3 inhibitors of tumour angiogenesis.

A
  1. Angiostatin
  2. Endostatin
  3. Vasculostatin
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193
Q

Which 3 mechanisms do tumour cells use to evade host immune defence in the blood?

A
  1. Platelet aggregation
  2. Adhesion to other tumour cells
  3. They shed surface antigens to ‘distract’ lymphocytes
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194
Q

Describe the process of metastasis.

A
  1. Detachment of tumour cells from their neighbours
  2. Invasion of the surrounding connective tissue
  3. Intravasation into the lumen of vessels
  4. Evasion of host defence mechanisms, such as NK cells
  5. Adherence to endothelium at a remote location
  6. Extravasation of the cells from the vessel lumen into the surrounding tissue
  7. Tumour cells proliferate in the new environment (angiogenesis etc.)
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195
Q

Which tumours more commonly metastasise to the liver?

A

Colon, stomach, pancreas, carcinoid tumours of intestine

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196
Q

Which tumours more commonly metastasise to the bone?

A

Prostate, breast, thyroid, lung, kidney

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197
Q

Which spread do carcinomas prefer? Which spread do sarcomas prefer?

A
  • Carcinomas prefer lymphatic spread
  • Sarcomas prefer heamatogenous spread
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198
Q

Is lymphatic metastasis common?

A

Yes

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199
Q

What is tumour staging?

A

Staging is the extent of a tumour’s spread. Determined by histopathological examination and clinical examination

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200
Q

What is TNM staging?

A

T - refers to the primary tumour

N - refers to lymph node status

M - refers to metastatic status

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201
Q

Which 2 cell types are involved in the response to acute inflammation?

A. Neutrophils and basophils

B. Eosinophils and basophils

C. Neutrophils and monocytes

D. Neutrophils and lymphocytes

E. Lymphocytes and monocytes

A

C. Neutrophils (6-24hrs) and monocytes (24-48hrs) are the cells involved in acute inflammation. Neutrophils phagocytise pathogens while monocytes migrate to tissue and become macrophages which secrete chemical mediators for chemotaxis

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202
Q

Which of these is not an outcome of acute inflammation?

A. Pus formation

B. Destruction

C. Organisation

D. Resolution

E. Progression

A

B. Pus formation (also known as supparation) occurs when there is excessive exudate production during acute inflammation, organisation occurs when a tissue is replaced with granulation tissue as part of healing process, resolution is complete restoration of tissues to normal and progression to chronic inflammation

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203
Q

Hypertrophy is best described as:

a) Increased size of organ/tissue due to increased number of cells
b) Increased size of organ/tissue due to decreased number of cells
c) Increased cell growth and decreased differentiation
d) Increased size of organ/tissue due to increased size of cells
e) Replacement of one differentiated tissue by another

A

D. Hypertrophy is an increase in size of organ/tissue due to an increase in the size of cells (this ins due to an increase in protein synthesis and an increase in the size of intracellular organelles). Option a= hyperplasia, e.g. uterine enlargement, option b = doesn’t make sense, option c = dysplasia, e.g. pre-cancer state, option e = metaplasia, e.g. Barrett’s oesophagus

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204
Q

In which pathological process would you expect:

  • Organelles to be damaged
  • Cell lysis
  • Inflammation
  • Altered chromatin
    a) Metaplasia
    b) Apoptosis
    c) Dysplasia
    d) Hypertrophy
    e) Necrosis
A

E. This is a description of cell death therefore the only answers can be B or E - apoptosis, however, is programmed cell death

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205
Q

What is a malignant neoplasm of smooth muscle called?

A) Adenocarcinoma

B) Leiomyoma

C) Rhabdomyoma

D) Leiomyosarcoma

E) Adenoma

A

D. An adenocarcinoma is a malignant neoplasm of glandular origin, a leiomyoma is a benign neoplasm of smooth muscle, a rhabdomyoma is a benign neoplasm of striated muscle and an adenoma is a benign neoplasm of glandular origin

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206
Q

Which one of the following tumours never metastasises?
A. Malignant melanoma

B. Small cell carcinoma of the lung

C. Basal cell carcinoma of the skin

D. Breast cancer

A

C. Basal cell carcinoma of the skin

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207
Q

What is the name of a malignant tumour of striated muscle?

A

Rhabdomyosarcoma. Rhabdo-myo = striated-muscle. Sarcoma = malignant + connective tissue

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208
Q

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

A. Breast cancer

B. Lung cancer

C. Prostate cancer

D. Liposarcoma

A

D. Liposarcoma. Bone metastases:

  • Breast cancer
  • Lung cancer
  • Prostate cancer
  • Renal cell cancer
  • Thyroid cancer
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209
Q

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

A

Carcinoma in situ (still bounded by BM)

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210
Q

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

A

Adenoma. Adeno = glandular epithelium, oma = benign tumour

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211
Q

Which one of these tumours does not have a screening programme in the UK?

A. Breast cancer

B. Colorectal cancer

C. Cervical cancer

D. Lung cancer

A

D. Lung cancer

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212
Q

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

A. Hepatitis C virus

B. Ionising radiation

C. Aromatic amines

D. Aspergillus niger

A

D. Aspergillus niger (fungus)

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213
Q

What is the name of a benign tumor of fat cells?

A

Lipoma

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214
Q

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

A

Adenocarcinoma. Adeno = glandular epithelium, carcinoma = malignant tumour

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215
Q

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

A. Vascular invasion

B. Metastasis

C. Increased cell division

D. Growth related to overall body growth

A

D. Growth related to overall body growth

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216
Q

A transitional cell carcinoma of the bladder is a malignant tumour?

A. True

B. False

A

A. True

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217
Q

A leiomyoma is a benign tumour of smooth muscle?

A. True

B. False

A

A. True. Leio = smooth muscle, muons = benign (sarcoma would have been malignant). Most common smooth muscle tumours are in the uterus - called fibroids - uterine myomas

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218
Q

Radon gas is a cause of lung cancer?
A. True

B. False

A

A. True

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219
Q

Asbestos is a human carcinogen?
A. True

B. False

A

A. True

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220
Q

Which lifestyle factor is most likely to cause cancer?
A. Drinking half a bottle of wine a day

B. Being obese

C. Running for 20 mins twice a week

D. Smoking 20 cigarettes a day

A

D. Smoking 20 cigarettes a day

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221
Q

Which tumours has the shortest median survival?
A. Basal cell carcinoma of the skin

B. Malignant melanoma of the skin

C. Breast cancer

D. Anaplastic carcinoma of the thyroid

A

D. Anaplastic carcinoma of the thyroid (2 months survival time!)

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222
Q

Ovarian cancer commonly spreads in the peritoneum.

A. True

B. False

A

A. True

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223
Q

What is the main source of histamine?

A

Mast cells; the histamine is stored in the granules in their cytoplasm

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224
Q

What enzymatic cascade systems does plasma contain?

A
  1. The complement system
  2. The kinin system
  3. The coagulation system
  4. The fibrinolytic system
225
Q

Describe innate immunity.

A

Non-specific, instinctive, present from birth, first line of defence. Focused around physical and chemical barriers + phagocytosis. No lymphocyte involvement

226
Q

Give examples of physical and chemical barriers used in innate immunity.

A

Physical: skin, hair, cilia, mucous membranes, digestive enzymes in mouth

Chemical: stomach acid, antimicrobial molecules

227
Q

What is the function of a lysozyme?

A

It destroys bacterial cell walls

228
Q

Describe adaptive immunity.

A

Specific ‘acquired’ immunity, requires lymphocytes. Memory and quicker response

229
Q

Compare innate vs adaptive immunity. Include receptors, kinetics, regulation, amplification, self-discrimination, duration and memory.

A
  • Innate = primitive and broad, fast, not much regulation, no amplification, no self-discrimination, short and no memory
  • Adaptive = highly specific (B and T cell receptors), slow, regulated, amplification, self-discrimination, long and memory
230
Q

Where do all immune cells originate? Where do B and T cells accumulate? Where are RBCs removed?

A
  • All immune cells originate in the bone marrow (including B and T cells). T cells then mature in the thymus
  • Lymph nodes are where B and T cells can accumulate - lymphomas can cause enlarged, rubbery lymph nodes
  • The spleen is where RBCs are removed - leukaemias can cause splenomegaly
231
Q

Which cell do all cells originate from? Descendants of which cell can be considered the innate branch of the immune system? Descendants of which cell can be considered cells of the adaptive immune response?

A
  • All stem from multipotential haematopoeitic stem cells (haemocytoblast)
  • Common myeloid progenitor descendants = innate branch
  • Common lymphoid progenitor descendants = adaptive branch
232
Q

Give examples of 3 polymorphonuclear leukocytes.

A
  1. Neutrophils
  2. Basophils
  3. Eosinophils
233
Q

Give 3 examples of mononuclear leukocytes.

A
  1. Monocytes
  2. B lymphocytes
  3. T lymphocytes
234
Q

What is the most abundant white blood cell? Is this innate or adaptive? Is it mononuclear or polymorphonuclear? How long does it live?

A
  • Neutrophil
  • Adaptive
  • Polymorphonuclear
  • Short lived
235
Q

How are macrophages formed? What are their functions?

A
  • When monocytes migrate from blood to tissue they become macrophages
  • Phagocytosis, antigen presenting, cytokine secretion (TNF-alpha, IL-1, IL-2)
236
Q

What are basophils involved in, what are they the circulating form of and what do they release? What are eosinophils involved in? Are these cells innate or adaptive?

A
  • Basophils are involved in allergic reactions, eczema, hay fever. Circulating mast cells that release histamine upon IgE crosslinking Fce receptors
  • Eosinophils deal with parasitic infections and release ROS, eicosanoids, leukotrienes etc.
  • These are both innate cells
237
Q

What are mast cells involved in? What happens when IgE binds to allergens? Innate or adaptive?

A
  • Important in parasitic infection and allergic reactions
  • IgE binds to allergen, which binds to mast cells, causing them to release histamine, causing the response, e.g. bronchoconstriction
  • Innate
238
Q

What is the function of Natural Killer cells? Innate or adaptive?

A
  • Release lytic granules that kill virus infected cells
  • Innate
239
Q

What are the functions of antigen presenting cells? What are the professional antigen presenting cells?

A
  • APCs process and present antigens from pathogens for recognition by cells, e.g. T cells
  • The main APCs are dendritic cells (egress to secondary organs to aid immune response), however macrophages and B cells are also APCs. They all present exogenous antigens in the context of MHC-II
240
Q

What is central tolerance?

A

In the human immune system, central tolerance is the process of eliminating any developing T or B lymphocytes that are reactive to self

241
Q

What is peripheral tolerance?

A

Peripheral tolerance is the second branch of immunological tolerance, after central tolerance. It takes place in the immune periphery (after T and B cells egress from primary lymphoid organs). Its main purpose is to ensure that self-reactive T and B cells which escaped central tolerance do not cause autoimmune disease

242
Q

What is anergy? When are lymphocytes said to be anergic?

A
  • Anergy is a term that describes a lack of reaction by the body’s defense mechanisms to foreign substances. It is one of three processes that induce tolerance
  • Lymphocytes are said to be anergic when they fail to respond to their specific antigen
243
Q

How do T cells recognise antigens?

A

For T cells to recognise antigens they must be displayed by an antigen presenting cell bound to MHC I/II. T cells can’t recognise soluble antigens

244
Q

What is the common T cell marker?

A

CD3

245
Q

What can T helper cells express? What do they help activate?

A
  • Can express CD4
  • Help activate B cells and cytotoxic T cells
246
Q

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

A

It helps the immune response against intracellular pathogens. Secretes cytokines. Cell-mediated immunity

247
Q

What is the function of T helper 2 (CD4)?

A

It helps produce antibodies against extracellular pathogens. Secretes cytokines. Humoral immunity

248
Q

What is the function of Cytotoxic T cell (CD8)?

A

Release perforins and granzymes to kill the antigens

249
Q

What is the function of Treg? What is their key cytokine?

A

Regulate the immune response. IL-10 is their key cytokine that has a mass anti-inflammatory action

250
Q

What is the function of Th17? What is their principle cytokine?

A
  • Important cells at mucosal membranes
  • Principal cytokine is IL-17 (affects innate immune cells to produce IL-8)
251
Q

Which cells express MHC I?

A

All nucleated cells express MHC I

252
Q

Which cells express MHC II?

A

Antigen presenting cells ONLY

253
Q

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

A

MHC I

254
Q

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

A

MHC II

255
Q

What type of T cell binds to MHC I?

A

Cytotoxic T cells (CD8)

256
Q

What type of T cells bind to MHC II?

A

Helper T cells (CD4)

257
Q

What do B cells differentiate into?

A

Plasma cells. The plasma cells then produce antibodies

258
Q

What does a helper T cell bind to?

A

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

259
Q

Which interleukin is secreted when a helper T cell is bound to a T cell receptor?

A

IL-2. This then binds to an IL-2 receptor on the T cell and produces a positive feedback mechanism leading to division and differentiation

260
Q

What is the mature B cell marker?

A

CD20. Monoclonal antibodies (e.g. Rituximab) target CD20

261
Q

How many antibodies can each B cell make?

A

Each B cell can only make 1 antibody. This 1 antibody can only bind to 1 epitope

262
Q

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

A

A B cell antibody binds to an antigen-> phagocytosis-> epitope is displayed on the surface of the B-cell bound to an MHC II-> TH2 binds to B-cells-> cytokine secretion induces B-cell clonal expansion-> differentiation into plasma cells and memory B cells

263
Q

What are the 3 roles of phagocytes?

A
  1. Neutralise toxins
  2. Opsonisation of pathogens
  3. Destroy pathogens
264
Q

Which region of an antibody binds to antigens?

A

Fab region

265
Q

Which region of an antibody binds with Fc receptors and some proteins of the complement system?

A

Fc region

266
Q

What are the 5 antibodies?

A

IgG, IgA, IgM, IgE, IgD

267
Q

What are the functions and features of IgA?

A

The mucosal antibody as a dimer. Present in colostrum and coats neonate gut

268
Q

What are the functions and features of IgM?

A

Pentameric and not entirely specific to antigen. Highest capacity to activate complement (system of plasma proteins that can be activated directly by pathogens or indirectly by pathogen-bound antibody, leading to a cascade of reactions)

269
Q

What are the functions and features of IgG?

A

Most abundant in the blood. Highly specific. Important during secondary responses. 4 subclasses. Can cross the placenta

270
Q

What are the functions and features of IgE?

A

Bound to mast cells and basophils by Fcer. Important in allergy and helminth infection. Least abundant in the blood

271
Q

What are the functions and features of IgD?

A

Not that important. Function debated in literature

272
Q

Which immunoglobulin is found in breast milk and other secretions?

A

IgA

273
Q

What are the two most common immunoglobulins?

A

IgG and IgM

274
Q

In the second exposure to an antigen, which antibody is secreted more: IgG or IgM?

A

IgG

275
Q

What are the primary lymphoid organs?

A
  • Bone marrow; all immune cell origin. B cell maturation site
  • Thymus; T cell maturation site
276
Q

What are the secondary lymphoid organs?

A
  • Lymph nodes; site of B and T cell interactions
  • Spleen; site of removal of RBCs and antibody-coated bacteria
277
Q

Name 4 types of cytokines.

A
  1. Interferons
  2. Interleukins
  3. Colony stimulating factors
  4. Tumour necrosis factors
278
Q

What is the function of interferons?

A

Interferons produce antiviral proteins

279
Q

What is the function of interleukins?

A

Interleukins cause cell differentiation and division

280
Q

What is the function of colony stimulating factor (CSF)?

A

Causes differentiation of bone marrow and stem cells

281
Q

What is the function of tumour necrosis factor (TNF)?

A

TNF mediates inflammation and cytotoxic reactions

282
Q

What is the function of chemokines?

A

Chemokines attract leukocytes and sites of infection

283
Q

Describe the process of phagocytosis.

A
  1. Pathogen binds to neutrophil/macrophage
  2. Engulfment of pathogen
  3. Phagosome formation
  4. Lysosome fusion - phagolysosome
  5. Pathogen is destroyed
284
Q

Where are complement system plasma proteins derived from?

A

Liver

285
Q

What are the 3 main outcomes of complement system activation?

A
  1. Pathogen lysis
  2. Increased phagocytosis
  3. Activation of leukocytes
286
Q

What is the complement system?

A

The complement system is a part of the immune system that enhances (complements) the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promote inflammation, and attack the pathogen’s cell membrane

287
Q

What are the 3 complement system pathways?

A
  1. Classical
  2. Lectin
  3. Alternative
288
Q

What activates the classical compliment pathway?

A

Antigen:antibody complex

289
Q

What activates the lectin pathway?

A

Mannose binding protein

290
Q

What activates the alternative pathway?

A

Bacterial cell walls and endotoxins

291
Q

What kind of immunity are PRR’s and PAMP’s associated with?

A

Innate immunity

292
Q

What are PRR’s a receptor for?

A

PAMP’s

293
Q

Name 3 receptors that make up the PRR family.

A
  1. Toll-like receptors
  2. Nod-like receptors
  3. Rig-like receptors
294
Q

What is the main function of TLR’s?

A

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

295
Q

What is the main function of NLR’s?

A

NLR’s detect intracellular microbial pathogens. They release cytokines and can cause apoptosis if the cell is infected

296
Q

What is the main function of RLR’s?

A

RLR’s detect intracellular double stranded RNA. This triggers interferon production and so an antiviral response

297
Q

TLR’s are adapted to recognise damaged molecules. What characteristic do these damaged molecules often have in common?

A

They are often hydrophobic

298
Q

What kind of TLR’s can be used in vaccine adjuvants?

A

TLR 4 agonists

299
Q

What happens when a PAMP binds to a PRR?

A

The innate immune response and inflammatory response is triggered

300
Q

What is extravasation?

A

Leukocyte migration across the endothelium

301
Q

What do macrophages at the tissues secrete to initiate extravasation?

A

TNF alpha

302
Q

Describe the process of extravasation.

A
  1. Macrophages at tissues release TNF alpha
  2. The endothelium is stimulated to express adhesion molecules and stimulate chemokines
  3. Neutrophils bind to adhesion molecules; they roll, slow down and become stuck to endothelium
  4. Neutrophils are activated by chemokines
  5. Neutrophils pass through the endothelium to the tissue to help fight infection
303
Q

What type of cancers result from transformations in the germ line?

A

Inheritable cancers (<10%)

304
Q

What type of cancers result from transformations in somatic cells?

A

Non-inheritable cancers (>90%)

305
Q

What are the 7 hallmarks for cancer?

A
  1. Evade apoptosis
  2. Ignore anti-proliferative signals
  3. Growth and self-sufficiency
  4. Limitless replication potential
  5. Sustained angiogenesis
  6. Invade surrounding tissues
  7. Escape immune-surveillance
306
Q

What are the two types of tumour antigens and where are they found?

A
  1. Tumour specific antigens = only found on tumour cells
  2. Tumour associated antigens = found on normal cells
307
Q

Why is hypoxia a prominent feature of a lot of malignant tumours?

A

Malignant tumours grow rapidly and so outgrow their blood supply

308
Q

What is active immunity?

A

Produced by host immune system, induced by infections or vaccines, durable effective protection, effective after initial lag period, immunological memory is present, boosted effect on subsequent dose, negative phase

309
Q

What is passive immunity?

A

Passive with no host participation, usually pooled antibodies transferred into host, transient and less effective, no lag period + effective immediately, no memory present, subsequent doses do not boost immunity due to elimination, no negative phase

310
Q

Give 2 advantages of passive immunity.

A
  1. Immediate effect
  2. Useful treatment for acute dangers, e.g. snake venom
311
Q

Give 3 disadvantages of passive immunity.

A
  1. Short term
  2. No immunological memory produced
  3. Reaction is possible
312
Q

Describe the first immune response to initial exposure.

A
  1. Innate immune response
  2. IgM predominates
  3. Low affinity
313
Q

Give 3 disadvantages of inactivated vaccines.

A
  1. Inactivated vaccines tend to only activate the humoral response; there is a lack of T cell involvement
  2. The response is often weak
  3. Boosters are needed so patient compliance may be poor
314
Q

Describe the second immune response following exposure to a pathogen encountered before.

A
  1. Rapid and larger than the first
  2. High affinity IgG
  3. Adaptive immunity, T cell help
315
Q

Give 3 advantages of live vaccines.

A
  1. Very effective, prolonged and comprehensive
  2. Immunological memory produced
  3. Often only 1 vaccine is needed
316
Q

Give 2 disadvantages of live vaccines.

A
  1. Immunocompromised patients may become ill
  2. Vaccines often need to be refrigerated which can be a problem in remote areas
317
Q

Give 2 advantages of inactivated vaccines.

A
  1. There is no risk of infection
  2. Storage is less critical
318
Q

What is the role of an adjuvant?

A

An adjuvant is a substance added to a vaccination to stimulate an immune response. They convince your immune system that you’re infected

319
Q

What can be used as an adjuvant?

A

Toxoids, proteins, chemicals (aluminium salts) etc.

320
Q

What are the 5 features of an ideal vaccine?

A
  1. Safe
  2. Induces a suitable immune response
  3. Shouldn’t require repeated boosters
  4. Generates immunological memory
  5. Stable and easy to transport
321
Q

Give 3 advantages of active immunity.

A
  1. Produced immunological memory
  2. Produces high affinity antibodies
  3. It produces a persistent protective response against pathogens
322
Q

Give 3 advantages of transplantation.

A
  1. Improved quality of life
  2. Improved survival rates
  3. Cost effective
323
Q

Why are immunosuppressive agents needed to prevent rejection?

A

Transplanted organs are recognised as non-self and therefore are seen as a threat

324
Q

What are the consequences of transplant rejection?

A

Fibrosis and scarring

325
Q

What are the two types of immune response in humans?

A) Immunological tolerance

B) Immune surveillance

C) Innate and acquired

D) Intrinsic and extrinsic

E) Overt and covert

A

C) Innate and acquired

326
Q

What cell type is described below?

These are the most abundant white blood cell in humans and are characterised by the multi-lobed shape of their nucleus.

A) Macrophage

B) Neutrophil

C) Eosinophil

D) Mast cell

E) Fibroblast

A

B) Neutrophil

327
Q

Which antigen presenting cell is considered a professional at activating lymphocytes?

A) Neutrophils

B) Mast cells

C) Macrophages

D) Dendritic cells

E) Monocyte

A

D) Dendritic cells

328
Q

Which of the following is not a component of innate immune mechanisms?

A) Mucosa

B) Inflammatory mechanisms

C) Antibody production

D) Skin

E) Antimicrobial peptides

A

C) Antibody production

329
Q

Antigen presenting cells process and present antigens for recognition by:

A) Neutrophils

B) Red blood cells

C) Eosinophils

D) T cells

A

D) T cells

330
Q

Which of the following are features of the adaptive immune response

A) Does not require prior contact with the pathogen

B) It works with B and T lymphocytes

C) Lacks specificity

D) Distinguishes “self” from “non-self”

E) Enhanced by complement

A

B) It works with B and T lymphocytes

331
Q

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

A) Opsonisation

B) Production of interferons

C) Target cell lysis

D) Chemoattraction of leukocytes

E) Phagocytosis

A

B) Production of interferons

332
Q

Which of the following are administered as a live attenuated vaccine in the UK?

A) Hepatitis A

B) Tetanus

C) MMR

D) Flu

E) BCG (TB)

A

C) MMR and E) BCG (TB)

333
Q

Polysaccharide vaccines are composed of long chains of sugar molecules that make up the surface capsule of certain bacteria. These vaccines are available for the treatment of which of the following diseases?

A) Pneumococcal disease

B) Influenza type b

C) Rabies

D) Salmonella Typhi

E) Meningococcal disease

A

A) Pneumococcal disease

D) Salmonella Typhi

E) Meningococcal disease

334
Q

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

A) Asthmatics

B) 16 years old

C) Diabetics

D) The obese of any age

E) 6 months of age and over

A

E) 6 months of age and over

335
Q

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

A) Type 1 diabetes mellitus

B) Graves disease

C) Ulcerative colitis

D) Hashimoto’s thyroiditis

E) Sjogren’s syndrome

A

C) Ulcerative colitis

336
Q

Which of the following are classical PAMPs?

A) Flagellin, a protein found in bacterial flagella

B) Lipopolysaccharide (LPS) from the outer membrane of gram-negative bacteria

C) Peptidoglycan, found in bacterial cell walls

D) Lipoarabinomannan of mycobacteria

E) Interleukin 12

A

A) Flagellin, a protein found in bacterial flagella

B) Lipopolysaccharide (LPS) from the outer membrane of gram-negative bacteria

C) Peptidoglycan, found in bacterial cell walls

D) Lipoarabinomannan of mycobacteria

337
Q

What is the role of the Major Histocompatibility Complex (MHC)?

A

To present antigen showing self or non-self on the cell surface

338
Q

What compound prevents excessive activation of the classical complement pathway?

A

C1 inhibitor. C1 inhibitor leads to a negative feedback loop

339
Q

Which complement plasma proteins have opsonisec properties when bound to a pathogen?

A

C3b and C4b

340
Q

What is the function of MAC in a pathogens’ membrane?

A

MAC is a leaky pore channel. Ions and water pass through the channel and disrupt the intracellular microbe environment -> microbe lysis

341
Q

Which complement plasma proteins are pro-inflammatory and cause chemotaxis and activation of neutrophils and monocytes?

A

C3a and C5a

342
Q

Define allorecognition.

A

The ability of an organism to distinguish its own tissues from those of another. Recognition of non-self antigens

343
Q

What are the consequences of transplant rejection?

A

Fibrosis and scarring

344
Q

Define xenotransplantation.

A

Transplantation of tissues from one species to another

345
Q

Define pharmacokinetics.

A

The action of the body on the drug (how it’s broken down)

346
Q

What are the 4 stages of pharmacokinetics?

A

ADME:

  • Absorption
  • Distribution
  • Metabolism
  • Excretion
347
Q

Define pharmacodynamics.

A

The action of the drug on the body

348
Q

What are the main routes of administration?

A
  • Oral → first pass metabolism
  • IV → directly into systemic circulation
  • Subcut → has to diffuse through the subcut fat, so absorbed more slowly
  • IM → muscle tissue is vascular so rapidly absorbed
  • Topical → directly onto the skin/mucosa. Avoids first pass metabolism, slowly absorbs into circulation
  • Rectal → can be used when patient is unable to tolerate oral route. Highly vascular tissue so absorbs quickly
  • Intrathecal → into the spinal column so it will reach the CSF
  • Sublingual/buccal → avoids first pass metabolism and rapidly enters circulation. Drugs like GTN
  • Inhalation → passes through the trachea into the lungs. Good if this is the target site of the drug
349
Q

In the absorption phase of pharmacokinetics, how do drugs pass through membranes?

A
  • Unless given straight into the blood stream, drugs cross membranes by:
  • Passive diffusion
  • Facilitated diffusion
  • Active transport
  • Endocytosis
350
Q

In the absorption phase of pharmacokinetics, do all of the drugs make it into the circulation? Why? What is this called?

A
  • Not all
  • This is because the gut and liver metabolise drugs given orally before reaching the circulation
  • This is called first pass metabolism
351
Q

What is bioavailability? What is the bioavailability of IV drugs assumed to be?

A
  • The amount of drug taken up into systemic circulation in proportion to the amount administered
  • The bioavailability of IV drugs is assumed to be 100%
352
Q

Define the distribution phase of pharmacokinetics.

A

The journey of the drug through the bloodstream into the target tissue

353
Q

What does the distribution of drugs depend on?

A
  • BLOOD FLOW to area
  • MOLECULAR WEIGHT/SIZE
  • LIPOPHILICITY - lipophilic drugs can penetrate the cell membrane easily
  • Permeability of capillaries (some capillaries have slit junctions that allow drugs through, e.g. in liver) - BLOOD-BRAIN BARRIER/BLOOD TESTICLE BARRIER
  • Binding to proteins. If they are bound to albumin in the blood, distribution will be SLOWED because drugs must be FREE FROM ALBUMIN to cross membranes
354
Q

In the distribution phase of pharmacokinetics, what do drugs target?

A
  • Cellular receptors
  • Enzymes (ramipril is an ACE inhibitor which blocks angiotensin converting enzyme)
  • Membrane ion channels (e.g. lidocaine blocks sodium ion channels)
  • Membrane transporters (proton pump inhibitors like omeprazole inhibit membrane transporters)
355
Q

Define the metabolism phase of pharmacokinetics.

A

Drugs are broken down so that they can be eliminated

356
Q

What is the main route of drug elimination? What can it not eliminate?

A
  • Kidney is the main route of elimination
  • It can’t eliminate lipid soluble drugs
357
Q

What is the role of the liver in drug metabolism?

A

The liver converts lipid soluble drugs into water soluble drugs so they can be excreted by the kidney. This happens in two stages

358
Q

What are the two stages of drug metabolism in the liver?

A
  • Phase 1 = make drug hydrophilic (Cytochrome P450 catalysed)
  • Phase 2 = if it is still to lipophilic, make the drug polar, e.g. acetylation
359
Q

Can drugs change or inhibit the action of cytochrome p450? Is there more than one Cytochrome P450 enzyme?

A
  • Yes. Drugs can alter the activity of Cytochrome P450 enzymes, so can alter the metabolism of other drugs
  • There are many Cytochrome P450 enzymes
360
Q

What is an inducer? Give an example.

A

An inducer will increase Cytochrome P450 activity, and speed up the metabolism of other drugs - may result in sub therapeutic dose. Example = phenytoin

361
Q

What is an inhibitor? Give an example. What are the two types?

A
  • An inhibitor will decrease Cytochrome P450 activity and reduce the metabolism of other drugs - may result in toxicity. Example = amiodarone
  • The competitive inhibitor binds to the active site and prevents the substrate from binding there. The noncompetitive inhibitor binds to a different site on the enzyme (allosteric site); it doesn’t block substrate binding, but it causes other changes in the enzyme so that it can no longer catalyse the reaction efficiently
362
Q

Give examples of inducers.

A
  • Anti-epileptics: phenytoin, carbamazepine
  • Rifampicin
  • St John’s Wort
  • Chronic alcohol intake
  • Smokers (CYP1A2)
363
Q

Give examples of inhibitors.

A
  • Ciproflaxacin, erythromycin
  • Isoniazid
  • Amiodarone
  • Allopurinol
  • Anti-fungal: ketoconazole, fluconazole
  • SSRI: fluoxetine, setraline
  • Sodium valproate
  • Acute alcohol
364
Q

In the rate of elimination of drugs, what do first order and zero order mean?

A
  • First order = catalysed by enzymes, rate of metabolism directly proportional to drug concentration
  • Zero order = enzymes saturated by high drug doses, rate of metabolism constant, e.g. ethanol, phenytoin
365
Q

In the excretion phase of pharmacokinetics, how are most drugs excreted? How about the rest?

A
  • Most drugs are excreted by the kidneys in urine
  • Some are also excreted by the liver in the bile and then faeces
366
Q

What happens to the doses/drugs if a patient has renal failure?

A

They may need to be altered

367
Q

What is pKa?

A
  • A number that shows how strong or weak an acid is, lower value = stronger acid
  • The pH at which a drug is 50% protonated and 50% non-protonated (ratio 1:1)
  • Example: if aspirin has a pKa of 3.8 and the pH of the GI tract is 4.8, there is a 1:10 ratio. This means that 10% of the drug will be lipid soluble at this pH
368
Q

What is the effect of an increase in pH on a weak acid?

A

The weak acid will become more ionised

369
Q

What is the effect of an increase in pH on a weak base?

A

The weak base will become less ionised

370
Q

What is the effect of a decrease in pH on a weak acid?

A

The weak acid will become less ionised

371
Q

What is the effect of a decrease in pH on a weak base?

A

The weak base will become more ionised

372
Q

Explain what would happen to the bioavailability of aspirin if gastric pH increased.

A

The bioavailability would decrease. Aspirin would be more ionised and so wouldn’t diffuse across the gut into the plasma as rapidly this would mean aspirin uptake would decrease

373
Q

Write an equation for the volume of distribution (Vd).

A

Vd = amount of drug administered/concentration of drug in plasma

374
Q

If a drug had a high Vd what would that tell us about the drug?

A

This would indicate that the drug was highly lipid soluble and that most of the drug had moved into the intracellular space, less was in the plasma

375
Q

What is the relationship between plasma concentration and Vd?

A

Plasma concentration is inversely proportional to Vd

376
Q

Give the two definitions for clearance.

A
  1. The volume of plasma from which a drug is completely removed per unit time
  2. The rate at which plasma drug is eliminated per unit plasma concentration
377
Q

Write an equation for renal clearance.

A

Renal clearance = Rate of appearance in urine / plasma concentration

378
Q

What are the two ways by which drugs can be eliminated in the kidneys?

A
  1. Glomerular filtration
  2. Active secretion
379
Q

What are the possible dangers of kidney damage with regards to renal clearance?

A

Kidney damage results in decreased renal clearance and so there is danger of accumulation, over dosage and toxicity

380
Q

What compound do many lipid soluble drugs combine with to increase their hydrophilicity?

A

Glucuronic acid

381
Q

Define hepatic extraction ratio (HER).

A

The proportion of a drug removed by one passage through the liver

382
Q

What is the limiting factor when a drug has a high HER?

A

Hepatic blood flow, perfusion limited

383
Q

What is the limiting factor when a drug has a low HER?

A

Diffusion limited. A low HER is slow and not efficient

384
Q

What happens to high and low HER drugs when enzyme induction is increased?

A

The clearance of low HER drugs increases. There is minimal effect on high HER drugs

385
Q

Give 4 properties of the ‘ideal drug’.

A
  1. Small Vd
  2. Drug broken down effectively by enzymes
  3. Predictable dose:response relationship
  4. Low risk of toxicity
386
Q

What is GFR?

A

GFR stands for glomerular filtration rate. GFR is a measure of how well your kidneys filter blood

387
Q

What is creatinine clearance? How is it measured?

A
  • Volume of blood plasma cleared of creatinine per unit of time. Used to estimate GFR, since glomeruli freely filter creatinine
  • Done by comparing serum creatinine with urine creatinine
388
Q

What is the gate-control theory of pain?

A

The gate control theory of pain asserts that non-painful input closes the nerve “gates” to painful input, which prevents pain sensation from traveling to the central nervous system

389
Q

Pharmacodynamics is what the drug does to the body. It is the effect on cellular receptors via signal transduction. What is signal transduction, what are some receptors, and what does it lead to?

A
  • Binding of a drug to extracellular or intracellular receptors
  • Via a variety of receptors: ligand-gated ion channels, G protein-coupled receptors etc.
  • Either leads to amplification or down-regulation of signals
390
Q

Give an example of a ligand gated ion channel.

A

Nicotinic ACh receptor

391
Q

Give an example of a G protein-coupled receptor.

A

Muscarinic and beta-2 adrenoreceptor

392
Q

Give an example of a kinase linked receptor.

A

Receptors for growth factors

393
Q

Give an example of a cytosolic/nuclear receptor.

A

Steroid receptors

394
Q

What is the shape of a log dose-response curve?

A

Sigmoidal

395
Q

What is EC50? What does it tell us about a drug? Would a drug with a lower EC50 have a lower or greater potency?

A
  • EC50 is the concentration of a drug that gives half the maximal response
  • It tells us its potency
  • Greater potency
396
Q

What does Emax tell us about a drug?

A

Its efficacy

397
Q

Which is more efficacious, a full against or partial agonist?

A

A full agonist is more efficacious because it can give an 100% response

398
Q

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

A

The antagonist would shift the dose-response curve to the RHS. The drug therefore becomes less potent

399
Q

How do we calculate Intrinsic Activity (IA)?

A

Intrinsic Activity = Emax of partial agonist / Emax of full agonist

400
Q

What is receptor reserve?

A

Some agonists need to activate only a small fraction of the existing receptors to produce the maximal system response

401
Q

What is an agonist? Give an example.

A
  • Agonists bind to a receptor and activate it
  • Mimics endogenous substance
  • Can be FULL (causes same response as endogenous substance) or PARTIAL
  • Example: salbutamol is a beta 2 agonist
402
Q

What is an antagonist? Give an example.

A
  • Antagonists bind to receptor and prevents its activation
  • Can be reversible or irreversible (if covalent bind forms)
  • Antagonist can also bind at another site to the main active site (allosteric site)
  • Example: propranolol (hypertension) is a beta blocker
403
Q

What does the term affinity mean?

A

Affinity is how avidly a drug binds its receptor

404
Q

Define efficacy.

A

The maximum effect a drug can have in the body

405
Q

Define potency.

A

How much of a drug is needed to elicit a response in the body

406
Q

Define specificity.

A

Specificity is the measure of a receptors ability to respond to a single ligand

407
Q

Define selectivity.

A

Selectivity refers to a drug’s ability to preferentially produce a particular effect

408
Q

Define bioavailability.

A

The fraction of the drug that reaches the systemic circulation unaltered

409
Q

Define first pass metabolism.

A

Metabolism of the drug by the gut and liver before it reaches the bloodstream

410
Q

What does a narrow therapeutic index mean? Give examples of drugs with a low therapeutic index.

A
  • A narrow therapeutic index/range means there is an increased chance of toxicity + a decreased chance of an affective dose
  • Examples: digoxin, theophylline, lithium, phenytoin, gentamicin + vancomycin
411
Q

How is paracetamol metabolised?

A
  • Paracetamol is mostly converted to non-toxic metabolites via Phase II metabolism. Here, it conjugated with sulfate and glucuronide, with a small portion being oxidised via the Cytochrome P450 enzyme
  • Cytochromes P450 2E1 and 3A4 convert approximately 5% of paracetamol to a highly reactive intermediate metabolite, N-acetyl-p-benzoquinone imine (NAPQI). Under normal conditions, NAPQI is detoxified by conjugation with glutathione to form cytsteine and mercapturic acid conjugates
412
Q

What happens to paracetamol metabolism in the case of a paracetamol overdose?

A
  • Phase II metabolic pathways become saturated + more paracetamol is shunted to the Cytochrome P450 system to produce NAPQI. As a result, hepatocellular supplies of glutathione become depleted, as the demand for glutathione is higher than its regeneration
  • NAPQI remains in its toxic form in the liver and reacts with cellular membrane molecules, resulting in widespread hepatocytes damage and death, leading to acute liver necrosis
413
Q

How do we manage a paracetamol overdose?

A
  • Activated charcoal should be considered if patient pares to within 1 hour of ingestion of >150mg/kg paracetamol
  • Ingestion in last 8 hours, wait 4 hours from ingestion then measure plasma level and send for analysis. Paracetamol plasma <4 hours after ingestion can’t be interpreted. If the results suggest acute liver injury = IV N-acetylcysteine
  • If the overdose was staggered (>1 hour), treatment nomogram is unreliable + based on paracetamol levels and further blood tests
  • Liver transplant may be required. Need often based on low blood pH, high blood lactate, poor blood clotting, or significant encephalopathy
414
Q

Give an example of a proton pump inhibitor.

A

Omeprazole

415
Q

Give an example of a statin.

A

Simvastatin

416
Q

Give an example of an ACE inhibitor.

A

Enalapril

417
Q

Give an example of a COX inhibitor.

A

Aspirin and paracetamol

418
Q

Give an example of a beta-2 adrenoceptor agonist.

A

Salbutamol

419
Q

Give an example of a beta-1 adrenoceptor blocker.

A

Atenolol

420
Q

Give an example of a Ca2+ channel blocker.

A

Amlodipine

421
Q

Give an example of a broad spectrum antibiotic.

A

Amoxicillin

422
Q

Give an example of an opiate analgesic.

A

Tramadol

423
Q

What do most drugs target?

A

Proteins, e.g. ligand gated ion channels, GPCR, kinase linked, cytosolic/nuclear

424
Q

What is the effect of fewer receptors on drug potency?

A

Fewer receptors will shift the dose-response curve to the RHS, this means drug potency will be reduced

425
Q

What is the effect of fewer receptors on receptor response?

A

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

426
Q

Approximately 60% of the body is comprised of water. In an average 70kg male this constitutes 42L of water. Approximately how many litres of water would you expect to find in the following compartments of this patient: intracellular, extracellular, plasma?

A
  • Intracellular = 28L
  • Extracellular = 14L
  • Plasma = 3L
427
Q

Name 3 drug targets.

A

Receptors, enzymes, transporters

428
Q

What do they terms afferent and efferent mean?

A
  • Afferent = carries signals towards the brain or spinal cord
  • Efferent = carries signals away from the brain or spinal cord
429
Q

What do the terms adrenergic and cholinergic mean?

A
  • Adrenergic = relating to adrenaline or noradrenaline and their receptors
  • Cholinergic = relating to acetylcholine and its receptor
430
Q

How is the nervous system divided?

A
  • Central nervous system (brain and spinal cord) + peripheral nervous system (connects CNS to muscles and organs)
  • PNS into efferent and afferent
  • Efferent into autonomic nervous system (controls internal organs) and somatic nervous system (controls skeletal muscles)
  • Autonomic nervous system into sympathetic and parasympathetic (+ enteric)
431
Q

Which neurotransmitter do cholinergic receptors bind to?

A

Acetylcholine

432
Q

What are the two types of cholinergic receptors?

A
  • Muscarinic receptor
  • Nicotinic receptor
433
Q

What do preganglionic neurons release? Which nervous system(s) is this in? What does this neurotransmitter bind to?

A
  • Preganglionic neurons in both the sympathetic and parasympathetic nervous system release acetylcholine (ACh)
  • Binds to nicotinic receptors
434
Q

What do most postganglionic neurons release? What are these known as? What do these bind to? Which nervous system is this in?

A
  • Most postganglionic neurons release adrenaline (epinephrine) and noradrenaline (norepinephrine)
  • These are collectively called catecholamines
  • These bind to adrenergic receptors
  • This is in the sympathetic nervous system
435
Q

What are the 5 effects of the sympathetic nervous system?

A
  • IMPORTANT:
  • Increased HR, increased CO, vasoconstriction
  • Bronchodilation
  • Reduced GI motility + secretions
  • Reduced bladder detrusor activity
  • Increased sweating and reduced salivation
436
Q

In the parasympathetic nervous system, what do postganglionic neurons release? What does this neurotransmitter bind to?

A
  • Postganglionic neurons in the parasympathetic nervous system release acetylcholine
  • Acetylcholine binds to muscarinic receptors on the target organ cells
437
Q

What are the 5 effects of the parasympathetic nervous system?

A
  • Decreased HR, decreased CO, vasodilation
  • Bronchoconstriction
  • Increased digestion
  • Increased bladder detrusor activity
  • Reduced sweating
438
Q

How are cholinergic drugs divided?

A
  • Cholinergic agonists = either mimic or enhance the action of ACh at the neuromuscular junction
  • Cholinergic antagonists = inhibit the action of ACh (enhances SNS activity)
439
Q

What can cholinergic agonists be divided into?

A
  • Direct-acting agents
  • Indirect-acting agents split into competitive (reversible) and non-competitive (irreversible)
440
Q

Direct-acting agents are synonymous with what term?

A

Cholinomimetics

441
Q

How are cholinergic antagonists divided?

A

Competitive antagonists and non competitive antagonists

442
Q

Cholinergic antagonists are synonymous with which terms?

A

Cholinergic antagonists are synonymous with the terms anticholinergics, parampatholytic, antimuscarinics or antinicotinics

443
Q

How do cholinergic agonists work? Give examples.

A
  • Cholinergic agonists mimic ACh and bind to ACh receptors
  • Examples: carbachol (constricts pupil), bethanechol (increases smooth muscle tone in GI and GU tract) + pilocarpine (stimulate saliva secretion)
444
Q

How do indirect-acting cholinergic agonists work? Give examples.

A
  • Indirect-acting cholinergic agonists inhibit acetylcholinesterase (AChE), increasing the concentration of ACh available at the synapse
  • Examples: neostigmine, pyridostigmine (myasthenia gravis, reverse anaesthesia), donepezil, rivastigmine, galantamine (boost cholinergic activity in Alzheimer’s)
445
Q

How do nicotinic antagonists work? Give examples.

A
  • Nicotinic antagonists compete with ACh for binding to the nicotinic receptor
  • Examples: curare, pancuronium (relax skeletal muscles during surgery)
446
Q

How do muscarinic antagonists work? Give examples.

A
  • Compete with ACh for binding to the muscarinic receptor
  • Examples: atropine, scopolamine, belladonna alkaloids (treat bradycardia, diarrhoea, bladder spasms, dilate bronchi, reduce secretions, dilate pupils)
447
Q

What do catecholamines help trigger?

A

Catecholamines released from postganglionic neurons in the SNS, so help to trigger the fight or flight response

448
Q

Where are adrenergic receptors located?

A

Adrenergic receptors are located in the plasma membrane of the cells of the target organs

449
Q

What type of receptors are adrenergic receptors? Why?

A
  • Adrenergic receptors are one type of GPCR as they work directly with intracellular G proteins
  • They bind to a GDP molecule when they’re inactive + to GTP when they’re active
450
Q

What are the different types of adrenergic receptors?

A

Alpha-1, alpha-2, beta-1 + beta-2

451
Q

What are the functions of alpha-1 adrenoreceptor?

A

Smooth muscle contraction (ONE):

  • O = blood vessels
  • N = neck of bladder, prosate and stomach
  • E = eyes
452
Q

What are the functions of alpha-2 adrenoreceptor?

A
  • Inhibition of presynaptic nerve terminals - TWO (terminal weaning off):
  • Inhibition of noradrenaline release, inhibition of acetylcholine release + inhibitor of insulin release
453
Q

What are the functions of beta-1 adrenoreceptor?

A
  • Beta 1 = 1 heart - heart and kidneys:
  • Tachycardia, increased lipolysis, increased myocardial contractility + increased release of renin
454
Q

What are the functions of beta-2 adrenoreceptors?

A
  • Beta-2 - 2 lungs. Smooth muscle relaxation in the lungs, blood vessels, GI tract, bladder, uterus, and liver:
  • Vasodilation, decreased peripheral resistance, bronchodilation, increased muscle and liver glycogenolysis, increased release of glucagon + relaxed uterine smooth muscle
455
Q

What is the mechanism of action for alpha agonists?

A

Alpha-adrenoceptor agonists (α-agonists) bind to α-receptors on vascular smooth muscle and induce smooth contraction and vasoconstriction, thus mimicking the effects of sympathetic adrenergic nerve activation to the blood vessels

456
Q

What is the mechanism of action for beta agonists?

A

Beta-2 agonists act directly on beta-2 receptors, causing smooth muscle relaxation and dilatation of the airways

457
Q

What are agonists for:

a) alpha-1
b) alpha-2
c) beta-1
d) beta-2
e) indirect

A

a) decongestants (phenylephrine)
b) centrally-acting vasodilator, e.g. clinicians, alpha-methyldopa
c) inotropes (epinephrine, dopamine, dobutamine)
d) SABA/LABA
e) cocaine, amphetamine

458
Q

What are antagonists for:

a) alpha-1
b) alpha-2
c) beta-1
d) beta-2

A

a) tamsulosin, doxazosin
b) yohimbine
c) selective/non-selective beta-blockers
d) non-selective beta-blockers

459
Q

Where does Tamsulosin exert its greatest effect?

A

Tamsulosin is a selective alpha-1-adrenoreceptor antagonist that exerts its greatest effect in the prostate and bladder, where these receptors are most common

460
Q

Based on the fact that alpha-1-adrenoreceptors are most common in the prostate and bladder, name a condition that Tamsulosin could be used to treat.

A

Tamsulosin is indicated for the treatment of benign prostate hypertrophy. Antagonism of these receptors leads to relaxation of smooth muscle in the prostate and detrusor muscles in the bladder, allowing for better urinary flow

461
Q

Define tolerance.

A

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

462
Q

What is the mechanism of a Type 1 hypersensitivity reaction? Give an example.

A
  • Type 1 = antigen reacts with IgE bound to mass cells
  • Example = anaphylaxis
463
Q

What is the mechanism of Type 2 hypersensitivity? Give examples.

A
  • Type 2 = IgG or IgM binds or antigen on cell surface
  • Examples: haemolytic anaemia, Goodpasture’s syndrome, pernicious anaemia, rheumatic fever
464
Q

What is the mechanism of Type 3 hypersensitivity?

A
  • Free antigen and antibody (IgG, IgA) combine
  • Examples: systemic lupus erythematosus, post-streptococcal glomerulonephritis
465
Q

What is the mechanism for Type IV hypersensitivity? Give examples.

A
  • T-cell mediated
  • Examples: tuberculosis/tuberculin skin reaction, graft versus host disease, multiple sclerosis, Guillain-Barré syndrome
466
Q

What are the signs and symptoms of anaphylaxis?

A
  • CVS = vasodilation, increased vascular permeability, lowered BP
  • Respiratory = dyspnoea due to bronchoconstriction, mucus production
  • Skin = rash, swelling
  • GI = pain, vomiting
467
Q

What is the mechanism of anaphylaxis? How can we treat anaphylaxis?

A
  • IgE binds antigen which then cross-links FceRI (high affinity IgE receptor) on mast cells and basophils leading to massive degranulation and histamine release
  • The resuscitation council’s algorithm for anaphylaxis says:
    1. ABCDE
    2. Check for obvious potential diagnosis
    3. Call for help
    4. Adrenaline
    5. Establish airway / high flow O2 / IV fluid challenge / chlorphenamine / hydrocortisone
  • IM ADRENALINE (1st line) - opens airway and blood vessels helping to reverse the effects of anaphylaxis. 500 MICROGRAMS (0.5 mL) OF 1:1000 IM
  • IV FLUIDS - fluid loss from increased vascular permeability. Signs of shock, vasodilation and a low BP
  • CHLORPHENAMINE is an antihistamine which takes 15-20 mins to work. Histamine release is the cause of anaphylaxis so this helps reverse the effects
  • HYDROCORTISONE is a corticosteroid, its benefit in anaphylaxis is still unproven but aims to stop a biphasic reaction, reduce the symptom recurrence, and wheezing
468
Q

How does autoimmunity develop?

A
  • Thymic education
  • Tregs
  • CD4 activation against autoantigen
469
Q

What is the difference between primary immunodeficiency and secondary immunodeficiency?

A
  • Primary immunodeficiency = those born with intrinsic defects in their immune system, rare and mostly genetic disorders
  • Secondary immunodeficiency = these are acquired and referred to generally as immunosuppression. Drug induced, cancers of the bone marrow and blood cells, AIDS
470
Q

A 34-year-old male comes into the GP complaining of haemoptysis. He notes that he wakes up at night due to waking up in a pool of sweat and mentions he recently returned from a holiday in Pakistan. The GP suspects tuberculosis. Which of the following cytokines is primarily responsible for activating macrophages?

a) IL-2
b) IL-4
c) TNFα
d) IL-1β
e) IFN-γ

A

E. INF gamma is the main activator of macrophages. IL-2 is secreted by macrophages. IL-4 is involved in B-cell differentiation. IL-1β is a pyrogen

471
Q

A 5-year-old girl is brought to the GP after repeated episodes of allergic rhinitis and eczema. Which cytokine is involved in atopy and, amongst other things, causes class switching of immunoglobulins to IgE?

a) IL-4
b) IL-17
c) IL-5
d) IL-1β
e) IFN-γ

A

A) IL-4 is the key cytokine for allergic inflammation and has multiple roles in allergy and asthma including; IgE class switching, Th2 polerisation, Increases VCAM-1 expression, promotes eosinophils to enter tissues, and mucous secretions.

472
Q

An infant presents to hospital with a fever, shortness of breath and a cough producing yellow sputum. She has had many previous admissions due to similar infections and has been diagnosed with a deficiency in mannose binding lectin (MBL). Which substance is failing to trigger a complement cascade reaction in this patient?

a) IgE
b) IgM
c) C3 Convertase
d) Pathogen surface carbohydrates
e) Membrane attack complex

A

D. Mannose is a carbohydrate found on bacterial cell walls but not human cells. The lectin pathway of the complement system is triggered when MBL binds to mannose on bacteria. a and b are incorrect as antibodies activate the classical complement pathway. C3 convertase and the membrane attack complex are downstream components of the complement system and therefore do not trigger the cascade

473
Q

A 13-year-old boy has been brought to the GP by his dad after having a sore throat and a cough for the last week. After an examination, the GP concludes that he likely has a viral infection that will resolve without other treatment. Which immune cells are responsible for directly combating this type of infection through apoptosis?

a) Basophils
b) Plasma Cells
c) T helper cells (CD4)
d) Neutrophils
e) Cytotoxic T-cells (CD8)

A

E) CD8 T cells are responsible for inducing apoptosis in virally infected cells. Cytotoxic T cells are responsible for inducing apoptosis. T helper cells produce cytokines for promoting the immune response. Basophils are a sign of chronic inflammation and produce histamine. Neutrophils (macrophages) kill extracellular microbes through phagocytosis and not apoptosis. T helper cells release cytokines to alter the immune response.

474
Q

A 10-year-old boy presents with an itchy rash on his elbows. The rash is red and there are excoriation marks. He has a past history of hay fever and has generally dry skin. The GP diagnoses him with eczema and he is prescribed hydrocortisone. Which antibody is responsible for mediating type 1 hypersensitivity?

a) IgG
b) IgA
c) IgM
d) IgE
e) IgD

A

D) IgE is the antibody responsible for type I hypersensitivity

475
Q

A 38-year-old male attends the human immunodeficiency virus (HIV) clinic for routine blood tests for monitoring of his condition. The number of which of the following cells is used to measure the progression of disease in HIV positive patients?

a) Neutrophils
b) B Cells
c) NK cells
d) CD4 T cells
e) CD8 T cells

A

D) CD4+ T cells are the specific cell tropism for HIV are is correlated to disease progression. HIV uses CD4 to enter CD4+ cells. Other immunological changes are seen but are not correlated clinically with progression. The following immunological changes are seen in progressive HIV:

●Reduction in CD4 count

●Increase B2-macroglobulin

●Decreased IL-2 production

●Polyclonal B-cell activation

●Decrease NK cell function

●Reduced delayed hypersensitivity responses

476
Q

A 34-year-old man is referred to the gastroenterologist due to persistent epigastric pain and nausea. He returned travelling from south-east Asia ten weeks ago. Blood tests reveal iron deficiency anaemia, and faecal microscopy reveals the presence of hookworm eggs. Which immune cell is responsible for the defense against helminths?

a) Basophils
b) Eosinophils
c) Neutrophils
d) Macrophages
e) Dendritic Cells

A

B) Eosinophils are the innate response to helminth infection. Basophils could be thought of as circulating mast cells that secrete histamine. Neutrophils are the principle cell in acute inflammation and are particularly good at combating pyogenic (pus forming) bacteria. Macrophages serve a similar role to neutrophils but also antigen present and are present in chronic inflammation. Dendritic cells are antigen presenting cells that serve as a joining of the adaptive and innate immunity.

477
Q

A 14-year-old boy complains of a 3-day history of fatigue, aches and pains, and fever. Upon examination his temperature is 38ºC and his tonsils are inflamed. He is suspected to have a bacterial infection which will be fought by his adaptive immune system. Which of the following cell-surface proteins are found on cytotoxic T-cells?

a) CD4
b) CRP
c) MHC I
d) CD 8
e) MHC II

A

D) CD8 is the identifying surface marker for cytotoxic T cells. CD4 is the marker for T helper cells. CRP is an acute phase protein raised during infection and inflammatory responses. MHC I and MHC I are antigen presenting molecules.

478
Q

A 24-year-old lady collapses after being stung by a wasp. You run to her aid and find marked facial oedema and a loud wheeze. You suspect anaphylaxis. Which type of immunoglobulin (Ig) is associated with this kind of reaction?

a) IgG
b) IgA
c) IgM
d) IgE
e) IgD

A

D) IgE is the principle antibody involved in type 1 hypersensitivity.

479
Q

Which of the following is not a component of the innate immune system?

A.Complement system

B.Toll-like receptors

C.Macrophages

D.T helper cells

E.C-reactive protein

A

D. T helper cells

480
Q

Which of the following statements about the adaptive immune system is false?

  • MHC class I is found on all nucleated cells
  • MHC is coded for on Chromosome 6
  • Treg cells are involved in regulating autoimmunity
  • B cells undergo monoclonal expansion in the thymus
  • Active immunisation involves harnessing the adaptive immune system
A

B cells undergo monoclonal expansion in the thymus

481
Q

Which of the following is a Type III hypersensitivity reaction?

  • Tuberculosis
  • Goodpasture’s Disease
  • Systemic Lupus Erythematosus
  • Contact Dermatitis
  • Anaphylaxis
A

Systemic Lupus Erythematosus

482
Q

Which of the following antibodies is implicated in asthma?

  • IgG
  • IgA
  • IgM
  • IgE
  • IgD
A

IgE

483
Q

Which of the following antibodies is implicated in the secondary response to infection?

  • IgG
  • IgA
  • IgM
  • IgE
  • IgD
A

IgG

484
Q

You are an F1 at A/E. A young boy has come in with signs of anaphylaxis after eating food containing peanuts. He has a peanut allergy.

  • Give 2 signs/symptoms on general inspection you might see
  • The boy has a known peanut allergy. What drug might he be carrying around?
  • Give 2 drugs that can be used to treat Anaphylaxis. What is the route of administration?
A
  • Rash (urticaria), swollen lips (angioedema)
  • Noradrenaline (Epipen)
  • IV Hydrocortisone, IV Chlorphenamine
485
Q

Which complement plasma proteins are pro-inflammatory and cause chemotaxis and activation of neutrophils and monocytes etc?

A

C3a and C5a

486
Q

Define allorecognition.

A

The ability of an organism to distinguish its own tissues from those of another. Recognition of non-self antigens

487
Q

Describe the immune responses to detection of graft antigens.

A
  1. Innate immune response is activated
  2. T cell mediated cytotoxicity
  3. Ab mediated cytotoxicity
  4. Hypersensitivity
  5. Tolerance
488
Q

Give 6 ways of preventing transplant rejection.

A
  1. Manage risk factors
  2. Tissue typing
  3. Cross match
  4. Immunosuppressive agents
  5. Sensitisation and desensitisation
  6. Tolerance
489
Q

Why is it important to get the balance right when using immunosuppressive agents?

A

Too much = infection

Too little = rejection

490
Q

What is involved in tissue typing?

A
  1. Blood group matching
  2. HLA typing
491
Q

What is atopy?

A

The tendency to develop allergies

492
Q

What happens to IgE receptors when a ‘threat’ is identified?

A

The receptors cross-link

493
Q

Which compound causes blood vessel dilation and vascular leakage in an allergic response?

A

Histamine

494
Q

Which complement proteins:

a) are involved in the formation of MAC
b) increase chemotaxis
c) are involved in opsonisation?

A

a) C3b, C5b-C9
b) C3a, C5a
c) C3b

495
Q

What are the exogenous ligands for:

a) TLR1/2
b) TLR3
c) TLR4
d) TLR5
e) TLR9

A

a) gram positive lipopeptides
b) double-stranded RNA
c) LPS
d) flagellin
e) CpG DNA

496
Q

What is VDJ recombination?

A

The process by which T + B cells randomly assemble different gene segments (VDJ) in order to generate unique receptors

497
Q

What is an adverse drug reaction? How is it different from a side effect?

A
  • An adverse drug reaction is an unwanted or harmful reaction following administration of a drug
  • A side effect is different because side effects can be beneficial
498
Q

Give 4 risk factors for ADRs.

A
  1. Female
  2. Genetic factors
  3. Allergies
  4. Polypharmacy
499
Q

Why are drug interactions such a big problem today?

A
  1. Ageing population
  2. Polypharmacy
  3. Increased use of over the counter drugs
500
Q

Give 2 drug related risk factors for drug interactions.

A
  1. Narrow therapeutic index
  2. Steep dose-response curve
501
Q

What are the types of adverse drug reactions according to the Rawlins Thompson classification?

A
  • Type A (augmented) = very common, predictable, often dose related
  • Type B (bizarre) = unpredictable, not dose dependent
  • Type C (chronic) = occurs after long term therapy
  • Type D (delayed) = occurs many years after treatment
  • Type E (end of use) = withdrawal reaction after long-term use
  • Type F (failure of therapy)
502
Q

When there is suspected anaphylaxis, what is the first thing we do?

A
  • ABCDE = airways, breathing, circulation, disability, exposure
  • Then raise legs if breathing not impaired
  • IM adrenaline
  • Stop infusion of drugs if they have been given any (could be causing the anaphylaxis)
503
Q

What are the two types of NSAIDs? What do they both do?

A
  • Non-selective NSAIDs = competitive reversible inhibitors of COX1 and 2, e.g. ibuprofen, naproxen
  • COX2-selective NSAIDs = selectively inhibit COX2, e.g. celecoxib
504
Q

What is the role of COX?

A
  • COX is required to convert arachidonic acid into thromboxanes, prostaglandins, and prostacyclins - thromboxanes play a role in platelet adhesion, prostaglandins cause vasodilation
  • COX1 plays a role in maintaining GI mucosa lining, kidney function + platelet aggregation
  • COX2 inducibly expresses during an inflammatory response (therefore COX-2 selective NSAIDs should provide anti-inflammatory relief without compromise the gastric mucosa)
505
Q

What is the action of NSAIDs?

A

Cyclooxygenase (COX) inhibitors → prevents production of prostaglandins. COX-2 inhibition is useful, COX-1 inhibition causes the adverse effects

506
Q

What are the anti-platelet effects of aspirin?

A

Aspirin irreversibly inhibits COX1/2 = decreased thromboxane A2 = decreased platelet aggregation = increased bleeding time

507
Q

What are the anti-platelet effects of clopidogrel and ticlodipine?

A

They are metabolised in the liver to active compounds which covalently bind to the ADP receptor on platelets and dramatically reduce platelet activation

508
Q

What are the anti-platelet effects of dipyridamole?

A

Dipyridamole inhibits phosphodiesterase, which inactivates cyclic AMP. It also stimulates prostacyclin release and inhibits thromboxane A2 formation. This leads to decreased platelet aggregation and vasodilation

509
Q

What is the purpose of anti-coagulants?

A

Anti-coagulants act at different points within the coagulation cascade to prolong clotting time

510
Q

Where do the intrinsic and extrinsic coagulation cascade pathways converge? What does this lead to?

A

Factor Xa. This leads to fibrin activation

511
Q

What are some direct inhibitors of Factor Xa? What could be a side effect?

A
  • Apixaban, Betrixaban, Edoxaban, Rivaroxaban
  • Side effect = bleeding
512
Q

What does heparin activate?

A

Heparin activates antithrombin (decreased thrombin and Factor Xa)

513
Q

What is the purpose of warfarin?

A
  • Anti-vitamin K = decreased FII (prothrombin)/VII/IX/X and Protein C/S
  • Increased time for the blood to clot
514
Q

Give examples of thrombolytics. What do they do? What are they used for? Give a side effect.

A
  • Activate Plasminogen, which forms the cleaved product Plasmin. Plasmin is a proteolytic enzyme that is capable of breaking cross-links between fibrin molecules, which provide the structural integrity of blood clots. Increased PT
  • Examples: Alteplase/Tenecteplase (tPA), Streptokinase
  • SE: Bleeding
515
Q

How do loop diuretics work? What are they used for? Give examples.

A
  • Loop diuretics act at the ascending limb of the loop of Henle and reversibly INHIBIT THE NA+/K+/CL- COTRANSPORTER, inhibiting the reabsorption of sodium and chloride ions. This reduces the hypertonicity of the renal medulla, thus inhibiting water reabsorption by the collecting ducts
  • Loop diuretics are indicated for the treatment of hypertension and oedema often caused by ischaemia heart disease or chronic kidney disease
  • SEs = hypokalaemia (as less K+ absorbed)
  • Loop diuretic examples: FUROSEMIDE, BUMETANIDE
516
Q

How do thiazide diuretics work? What are they used for? Give examples. Give side effects.

A
  • Thiazide diuretics - INHIBIT NA+/CL- CONTRANSPORTER IN THE DCT. Less Na+ reabsorbed = less water follows
  • Thiazide diuretics are indicated for hypertension and heart failure, as well as nephrogenic DI
  • Examples: BENDROFLUMETHIAZIDE, INDAPAMIDE
  • SE: hypokalaemia (more Na+ in the DCT where it can be exchanged for K+ so more K+ lost in the urine), alkalosis hypochloraemic, diarrhoea, hyperglycaemia, hyperuricaemia
517
Q

What is the mechanism of action for K+ sparing diuretics?

A

Inhibit reabsorption of Na+ and water in ENaC channels in DCTs leading to Na+ and water excretion and K+ retention = hyperakalaemia

518
Q

What is the action of spironolactone? What is it used to treat? Give side effects.

A
  • Spironolactone = ALDOSTERONE ANTAGONIST
  • Binds competitively to the aldosterone receptor at the aldosterone-dependent sodium-potassium exchange site. This promotes sodium and potassium retention
  • Spironolactone is indicated to treat a number of condition including heart failure, hypoaldosteronism, hypertension, and nephrotic syndrome
  • SE: HYPERKALAEMIA, drowsiness, dizziness, nausea, vomiting
519
Q

What is the dosage of oral morphine:IM morphine?

A

Oral is double, 10:5mg. This is because oral drugs have a lower bioavailability and have to undergo first pass metabolism

520
Q

What is the mechanism of action for antidiabetic drugs?

A

These agents work by closing potassium channels on the surface of beta cells, which causes an influx of calcium ions into the cells and a consequent outflow of insulin from cellular storage vesicles

521
Q

What is the mechanism of action for adrenaline?

A
  • Epinephrine acts on alpha and beta receptors and is the strongest alpha receptor activator.
  • Through its action on alpha-adrenergic receptors, epinephrine minimises the vasodilation and increased the vascular permeability that occurs during anaphylaxis, which can cause the loss of intravascular fluid volume as well as hypotension. Epinephrine relaxes the smooth muscle of the bronchi and iris and is a histamine antagonist, rendering it useful in treating the manifestations of allergic reactions and associated conditions
  • Through its action on beta-adrenergic receptors, epinephrine leads to bronchial smooth muscle relaxation that helps to relieve bronchospasm, wheezing, and dyspnea that may occur during anaphylaxis
522
Q

What is the mechanism of action for ACE inhibitors?

A

Block the action of ACE and prevent angiotensin I being converted to angiotensin II, so no aldosterone secreted and no vasodilation etc.

523
Q

What is the mechanism of action for PPIs?

A

Proton pump inhibitors (PPIs) irreversibly inhibit H+/K+-ATPase pump in gastric parietal cells to reduce H+ (acid) secretion

524
Q

What is the mechanism of action for anaesthetics?

A

In general the anaesthetics inhibit or block excitatory ligand-gated ion channels and enhance the sensitivity of inhibitory ion channels such as γ-aminobutyric acid A (GABAa) receptor that function as inhibitory CNS receptors

525
Q

What is the mechanism of action for opioids?

A

Activation of mu receptors in the CNS

526
Q

What is the action of antihistamines?

A

H1 receptor antagonist. Prevents release of histamine from storage granules in mast cells which cause allergic reaction symptoms

527
Q

What are the side effects of these drugs:

a) NSAIDS
b) Anti-histamines
c) Beta-2 agonists
d) ACE-INHIBITORS
e) PPIs
f) OPIOIDS
g) Diuretics?

A

a) NSAIDs → GI upset, GI bleeding, renal impairment
b) Anti-histamines → older ones can cross BBB and cause sedation. Many H1 receptors in vomiting centre, so can act as anti-emetics too!
c) Beta-2 agonists → can agonise B2 receptors in other tissue → fight or flight response (sweating, tachycardia etc.)
d) ACE-i → DRY COUGH DUE To BRADYKININ!!! Dilates afferent glomerular arteriole, so worsens kidney function
e) PPI → prolonged use in elderly can increase risk of fracture
f) Opioids → RESPIRATORY DEPRESSION → GIVE NALOXONE!! N&V, constipation, tolerance and withdrawal.
g) Diuretics → spironolactone can cause hyperkalemia (remember it’s potassium sparing), they can all cause increased frequency and dehydration

528
Q

What is diamorphine? How does it work? Which class of drug does it fall under?

A
  • Diamorphine is a painkiller
  • It behaves as an agonist at a complex group of receptors (the μ, κ and δ subtypes) that are normally acted upon by endorphins
  • It is an opioid
529
Q

What are the side effects, indications, contra-indications and interactions of diamorphine?

A
  • Side effects: biliary spasm, circulatory depression, intracranial pressure increased, mood altered, postural hypotension (frequency not known). For opioids (common): arrhythmias, confusion, constipation, dizziness, drowsiness, dry mouth, euphoric mood
  • Indications: acute pain, chronic pain not currently treated with a strong opioid analgesic, acute pulmonary oedema, myocardial infarction
  • Contra-indications: delayed gastric emptying, phaeochromocytoma. Opioids: acute respiratory depression, comatose patients, head injury, raised intercranial pressure
  • Interactions: alcohol, buprenorphine, isocarboxazid, naltrexone
530
Q

What are the side effects, indications, contra-indications and interactions of paracetamol?

A
  • Side effects: thromobocytopenia (rare). With rectal use: anorectal erythema (common)
  • Indications: mild to moderate pain, pyrexia, acute migraine
  • Contra-indications: before administering, check when paracetamol last administered and cumulative paracetamol dose over previous 24 hours, body-weight under 50 kg, chronic alcohol consumption, chronic dehydration, chronic malnutrition, long-term use
  • Interactions: alcohol, dapsone, flucloxacillin, imatinib, phenindione, prilocaine
531
Q

What is ramipril?

A

Ramipril is an ACE inhibitor used to treat high blood pressure, heart failure, and diabetic kidney disease

532
Q

What are the side effects, indications, contra-indications and interactions of ramipril?

A
  • Side effects: gastrointestinal disorders, increased risk of infection, muscle spasms
  • Indications: hypertension, symptomatic heart failure, prophylaxis after myocardial infarction in patients with clinical evidence of heart failure (started at least 48 hours after infarction), nephropathy
  • Contra-indications (these are CAUTIONS): concomitant diuretics, diabetes, patients of Black African or African-Caribbean descent, aortic or mitral valve stenosis
  • Interactions: aliskiren, allopurinol, azathioprine, everolimus, lithium,
533
Q

What is salmeterol?

A

Salmeterol is a long-acting β2 adrenergic receptor agonist (LABA) used in the maintenance and prevention of asthma symptoms and maintenance of chronic obstructive pulmonary disease (COPD) symptoms

534
Q

What are the side effects, indications, contra-indications and interactions of salmeterol?

A
  • Side effects: muscle cramps (common), nervousness, skin reactions (uncommon)
  • Indications: reversible airways obstruction in patients requiring long-term regular bronchodilator therapy, asthma, COPD
  • Contra-indications (these are cautions for beta-2 agonists): arrhythmias, cardiovascular disease, diabetes, hypertension, hyperthyroidism, hypokalaemia, susceptibility to QT-interval prolongation
  • Interactions: amifampridine, amiodarone, amisulpride, apomorphine, clarithromycin, erythromycin, lithium
535
Q

What is suxamethonium chloride? How does it work?

A
  • Suxamethonium chloride is a medication used to cause short-term paralysis as part of general anaesthesia
  • Suxamethonium acts by mimicking acetylcholine at the neuromuscular junction but hydrolysis is much slower than for acetylcholine; depolarisation is therefore prolonged, resulting in neuromuscular blockade
536
Q

What are the side effects, indications, contra-indications and interactions of suxamethonium chloride?

A
  • Side effects: arrhythmias, bradycardia, flushing, involuntary muscle contractions, myoglobinuria, post-procedural muscle pain, rash
  • Indications: neuromuscular blockade (short duration) during surgery and intubation
  • Contra-indications: hyperkalaemia, low plasma-cholinesterase activity, major trauma, neurological disease, personal or family history of congenital myotonic disease or malignant hyperthermia, prolonged immobilisation, severe burns, skeletal muscle myopathies
  • Interactions: betamethasone, hydrocortisone, prednisolone
537
Q

What is tramadol?

A

Tramadol is an opioid pain medication used to treat moderate to moderately severe pain

538
Q

What are the side effects, indications, contra-indications and interactions?

A
  • Side effects: fatigue (common), postural hypotension (uncommon)
  • Indications: moderate to severe pain, postoperative pain
  • Contra-indications: acute intoxication with alcohol/analgesics/hypnotics/opioids, compromised respiratory function, uncontrolled epilepsy
  • Interactions: buprenorphine, carbamazepine, fluoxetine
539
Q
A

C. One or more alternative genes coding for the same trait found at the same locus on homologous chromosomes

540
Q
A

C. 50%

541
Q
A

C. 50%

542
Q
A

C. 50%

543
Q
A

C. Trisomy 21

544
Q
A

C. Convulsions

545
Q
A

B. Calf atrophy

546
Q
A

C. Commonly affects the Alpha chain in haemoglobin

547
Q
A

C. Trachea

548
Q
A

C. It consists of chondrocytes and fibroblasts surrounded by type I collagen

549
Q
A

D. Internal elastic lamina

550
Q
A

A. Tunica intima

551
Q
A

B. Merkel

552
Q
A

C. Neutrophil

553
Q
A

E. Podocytes

554
Q
A

E. Transmit electrical impulses

555
Q
A

B. Are multinucleated

556
Q
A

B. Kupffer cells

557
Q

What are the antibodies for:

a) rheumatoid arthritis
b) SLE
c) Sjorgen syndrome, SLE
d) Antiphospholipid syndrome, SLE
e) primary biliary cirrhosis
f) Hashimoto thyroiditis
g) Goodpasture syndrome
h) Coeliac disease
i) Microscopic polyangiitis, Churg-Strauss syndrome
j) Granulomatosis with polyangiitis
k) Type 1 diabetes mellitus

A

a) Rheumatoid factor (anti-IgG), anti-CCP
b) ANA, anti-dsDNA, Anti-Sm
c) anti-SSA (Ro) and SSB (La)
d) anti-phospholipid
e) anti-mitochondrial
f) anti-thyroid peroxidase, anti-thyroglobulin
g) anti-basement membrane
h) anti-gliadin IgA, anti-endomysial IgA, anti-transglutinase IgA
i) P-ANCA
j) C-ANCA
k) anti-glutamic acid decarboxylase

558
Q

What are the different toll-like receptors, their ligand, and their origin?

A

Phase2 (19 decks)

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