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From Flashcardlet > MoD Black & White version > Flashcards

MoD Black & White version Flashcards

1
Q

Irreversible cell injury leads to ______ whereas reversible cell injury leads to ______.

A
  1. necrosis

2. adaptation (e.g atrophy, metaplasia or dysplasia)

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2
Q

What type of hypersensitivity reaction is immediate?

A

Type 1
Tissue response that occurs rapidly after the interaction of allergen with IgE antibody previously bound to the surface of mast cells and basophils in a sensitized host.

e.g seasonal rhinitis, asthma, anaphylaxis, atopic allergy

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3
Q

What type of hypersensitivity reaction is antibody mediated? + examples?

A

Type 2
Results in one of three different antibody-dependent mechanisms :
-phagocytosis
-complement activation, inflammation and tissue damage
-antibody mediated cellular dysfunction - Ab binds to receptor to stop release of hormone

examples: transfusion reaction, AI diseases, organ rejection

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4
Q

What type of hypersensitivity reaction is mediated by antigen-antibody complexes?

A

Type 3 - complement activation followed by accumulation of polymorphonucelear leukocytes. Leading to fibrinoid necrosis

e.g systemic lupus erythematosus, polyarteritis nodosa

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5
Q

What type of hypersensitivity reaction is T cell mediated?

A

Type 4
Delayed hypersensitivity reaction (2-3 days). T helper cells secrete cytokines, attracting macrophages. T killer cells are directly cytotoxic.

e.g type 1 diabetes mellitus, multiple sclerosis, rheumatoid arthritis, response to microbial infection

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6
Q

What type of necrosis leaves anuclear cells and preserves architecture?

A

Coagulative necrosis

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7
Q

What type of necrosis occurs in the brain?

A

Colliquative (liquefactive) necrosis - complete digestion of dead cells

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8
Q

What type of necrosis is typical seen in TB?

A

Caseous necrosis - loss of architecture

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9
Q

Fat necrosis results in what product?

A

Soaps.

Pancreatic lipase breaks down fat. Fatty acids combine with calcium to form soap (fat saponification). Liquefaction of cell membranes

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10
Q

What are the four “cardinal “ signs of inflammation?

A

Calor (heat)
Rubor (redness)
Dolor (pain)
Tumor (swelling)

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11
Q

Give one purpose of acute inflammation.

A

Clear away dead tissue.
Protect against infection.
Allow access of immune system components.

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12
Q

Pus can be formed due to acute inflammation. What does it comprise of?

A

Neutrophils, cellular debris, bacteria

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13
Q

The innate immune system recognises conserved structures on pathogens called?

A

Pathogen-associated Molecular Patterns (PAMPs)

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14
Q

Which complement component plays a role in opsonization?

A

C3b

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15
Q

What immunoglobulin isotype can cross the placenta?

A

IgG

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16
Q

Which MHC class (I or II) present larger epitopes?

A

MHC class II

Class I epitopes 7-10 amino acids, class II epitopes 10-15 amino acids.

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17
Q

What cells play a role in the early phase response of type 1 hypersensitivity reactions?

A

Mast cells and T cells

Cross-linking of FceR1 on mast cells by the allergen causes the release of pre-formed mediators (e.g. histamine) and the synthesis of lipid mediators (e.g. leukotrienes).

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18
Q

What cells play a role in the late phase response of type 1 hypersensitivity reactions?

A

Basophils, eosinophils and T cells

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19
Q

What inflammatory cells are present in chronic inflammation?

A

Lymphocytes, plasma cells and macrophages

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20
Q

Which are labile cell populations are more likely to undergo repair or regeneration?

A

Regeneration

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21
Q

Which cell population has the highest proportion of stem cells; labile, stable or architectural?

A

Labile cell populations

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22
Q

What vessels are most commonly effected by atherosclerosis?

A

Coronary and cerebral arteries

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23
Q

What are lines of Zahn and what make up the red and white stripes?

A

Histological appearance of arterial thrombosis. Alternating bands of white platelets and red blood cells.

http://library.med.utah.edu/WebPath/jpeg1/LUNG117.jpg

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24
Q

What is the most common form of emboli?

A

Thrombosis

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25
Q

What is a saddle emboli?

A

A large pulmonary emboli at the bifurcation right and left main pulmonary arteries

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26
Q

What is a paradoxical embolism?

A

An embolism that originates in the venous system and moves into the arterial system through a septal defect

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27
Q

Where do the majority of systemic thromboembolism originate?

A

Intra-cardiac mural thrombi (80%)

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28
Q

Reversible cell injury leads back to a dead or normal cell?

A

Normal :)

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29
Q

Physical Causes of cell injury?

A

trauma, temp, pressure, shock, radiation

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30
Q

Chemical causes of cell injury?

A

alcohol, smoking, drugs, poisons, asbestos, pollutants

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31
Q

Microbial agents that cause cell injury?

A

protozoa, helminths, bacteria, viruses, fungi

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32
Q

Example of exotoxin?

A

Diptheria

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33
Q

Example of endotoxin?

A

Staphylococcus

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34
Q

CD4 T cells = helper or cytotoxic?

A

helper - recruit shit like macrophages

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35
Q

Cytotoxic T cells are what CD4 or CD8?

A

CD8 - kill the fuckers

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36
Q

Lack of essential metabolites can lead to cell death, list 5 things which will lead to cell death?

A

Lack of blood supply leads to 1) lack of glucose 2) lack of oxygen (altitude, anaemia, resp failure). Reduced growth factor, hormone deficiency, liver or renal failure.

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37
Q

List 3 mechanisms of cell injury

A

1) Membrane damage (toxins inc intracellular calcium leads to inc in protease and phospholipase activation)
2) Reactive oxygen species - damage to lipids, proteins & DNA
3) Ischaemia - decreased ox phosphorylation so reduced ATP levels

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38
Q

Name some reactive oxygen species

A

Inflammation, radiation, oxygen toxicity and chemicals lead to reactive oxygen species

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39
Q

Major antioxidant enzyme neutralise free radicals - examples?

A

catalase, glutathione peroxidase, SOD

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40
Q

Two types of gangrene?

A

Wet = tissue death & infection. Dry = no infection

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41
Q

3 components of acute inflammation?

A

vascular, exudation and cellular reaction

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42
Q

What happens in the vascular reaction of acute inflam?

A

Dilatation = rubor then increase in permeability mediated by histamine, bradykinin, NO, Leukotriene B4

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43
Q

What happens in the exudation reaction in acute inflam?

A

Tumor = swelling. acute inflam exudate = protein rich and dilution of noxious agents, transport to lymph nodes to dealt with.

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44
Q

What is suppuration?

A

Pus production

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45
Q

What is involved in cellular reaction in acute inflam?

A

migration of inflam cells out of vessels so accumulation of neutrophils in extracellular space. neutrophils = directional chemotaxis. can lead to suppuration.

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46
Q

Test for acute inflammation?

A

FBC, acute phase proteins (+ve = CRP, haptoglobin, alpha 1 antitrypsin, Ig. -ve = albumin, apoB)

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47
Q

What is fibrinous inflammation?

A

large inc in vascular permeability and allows fibrin through

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48
Q

What is purulent inflammation?

A

infectious pus caused by pyogenic bacteria and consists of neutrophils, dead cells

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49
Q

What is serous inflammation?

A

skin blisters for example

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50
Q

The kinin system, clotting pathway, thrombolytic pathway and complement pathway are plasma derived mediators of what?

A

acute inflammation

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51
Q

What are the cell derived mediators of acute inflammation?

A

Stored = histamine. Synthesised = prostaglandins, leukotriens, cytokines, NO, chemokines

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52
Q

Features of Necrosis vs apoptosis - No of cells involved in necrosis compared to apop?

A

Multiple to single

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53
Q

Cell size of necrosis vs apoptosis cells?

A

Nec = enlarged compared to apop = reduced

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54
Q

Between necrosis and apoptosis, who’s plasma membrane remains intact?

A

apoptosis

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55
Q

Is there adjacent inflammation during apoptosis?

A

No but there is in necrosis

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56
Q

The fate of a cell during necrosis compared to that of a cell during apop?

A

Phagocytosed by neutrophils compared to neighbouring cells in apop

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57
Q

Necrosis is pathological or physiological?

A

Pathological whereas apop is physiological

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58
Q

Name 2 groups of PAMPs?

A

Cell surface receptors (TLRs & mannose receptors) + fluid phase soluble molecules (shizz about C-lectin family - collectins which have a role in recruitment of adaptive response)

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59
Q

Pattern recognition receptors detect various types of structures, name 4!

A

proteoglycans, flagellum, RNA strands, lipopolysaccharide

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60
Q

Humoral and cellular response are part of innate or adaptive immune response?

A

Innate

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61
Q

Activation of what happens in the Humoral component of innate response?

A

Complement - production of Membrane attack complex to perforate membranes of bad buggers. Attract neutrophils to site. produces anaphylatoxins.

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62
Q

Describe the 3 pathways involved in the complement system?

A

Common - activated by antigen:antibody complex. Cleavage of factors from C1 to C5 which then joins complex with C6-C9 to form MAC
Lectin or mannose-binding pathway: activated by pathogens. Mannose binding lectin binds to mannose to activate pathway forming MBL associated serene protease which cleaves C2 & C4 to join common path
Alternative: auto activation of C3 into C3b (occurs at low rate). binds with properdin which activates more C3 and so C5

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63
Q

What type of enzymes are complement factors?

A

Proteolytic enzymes which cleave each other to activate it

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64
Q

Name another proteolytic enzyme other than complement factors?

A

trypsin - not as specific as the complement factors

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65
Q

Name the three complement factors which are anaphylatoxins?

A

C2b, C3a, C4a

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66
Q

Which complement factor is involved in opsonisation?

A

C3b - labels bacteria for phagocytosis and viruses

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67
Q

Name pathogens which have Mannose binding lectin on their surface?

A

Yeast = candida albicans, Viruses = HIV, Influenza A, Bacteria = salmonella and strep. Parasites = Leisghmania

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68
Q

Cellular response in innate immunity involves what cells?

A

Macrophages, neutrophils and Natural killer cells

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69
Q

Precursor to macrophages?

A

Monocytes which are found in blood

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70
Q

3 activation states of macrophages?

A 
resting - expresses little MHC class II. collects debris from tissues
Primed - activated by interferon gamma. takes up larger objects
Hyperactive = activated by interferon gamma and LPS. Produces TNF, Il-1
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71
Q

What ligand is expressed on surface of neutrophils?

A

Selectin ligand - needs the expression of selection on endothelium so that neutrophil and endo can bind

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72
Q

What is f-met?

A

Bacterial proteins start with a different form of methionine and neutrophils can track these F-met peptides secreted by macrophages after pahgocyotsis

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73
Q

How do Natural killer cells destroy infected cells?

A

Perforin protein injects granzyme B into cells and essentially induces apoptosis. Saves host cells by recognising MHC class I molecules.

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74
Q

Which hypersensitivity reaction is characteristic of the weal and flare reaction?

A

type I - IgE mediated

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75
Q

Common antigens of Type I hypersensitivity?

A

pollen, bee venom, animal dander

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76
Q

Which hypersensitivity reaction is Myasthenia Gravis classed as?

A

type III - immune complex

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77
Q

What is lactoferrin?

A

enzyme which breaks down proteins and bugs

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78
Q

Who came up with the idea of adaptive immune response?

A

Edward jenner

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79
Q

What does LAM stand for with regards to adaptive immune response?

A

Learning, adaptability and memory

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80
Q

Why does class switching take place?

A

So antibodies become better adapted to destroy the invader

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81
Q

Where does class switching occur?

A

germinal centres of lymphoid organs

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82
Q

Which region of the Antibody does class switching occur?

A

Constant region = Fc region

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83
Q

What region of an Ab is involved into antigen binding?

A

Fab region = variable region

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84
Q

What is hypermutation?

A

Changing on the Fab region on an antibody

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85
Q

What is affected by the V,D,J regions in DNA?

A

Fab region on Antibodies

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86
Q

5 types of Ig?

A

IgM, IgG, IgA, IgE, IgD

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87
Q

What Ig is most abundant?

A

IgG

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88
Q

What is the first Ig and then second Ig to be produced in an immune response?

A

IgM then IgG

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89
Q

What Ig is involved in allergic reactions?

A

IgE - also effective against parasites

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90
Q

Where is IgA found?

A

mucous membranes, Gi tract, saliva

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91
Q

Old or early infection - higher IgG than IgM?

A

old

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92
Q

Name three APCs?

A

Dendritic cells, macrophages and B cells

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93
Q

What class of MHC presents to T helper cells?

A

Class II

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94
Q

Class I MHC is detected by what T cell?

A

CD8+ cytotoxic T cell

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95
Q

What infection kills Th cells?

A

HIV - attaches to CD4 proteins via the gp120 antigen on its cell surface

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96
Q

2 signals activate T cells, what do they involve?

A

1) APC processes antigen and presents on cell surface with corresponding MHC class
2) stops autoimmune response. recognition of CD28 on the T cell by a CD80 on the APC. Without this the cell fails to be activated and becomes ANERGIC - does not respond to antigen

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97
Q

Th1 involved in tuberculoid leprosy or lepromatous leprosy?

A

Tuberculoid as Th2 is involved with lepromatous leprosy

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98
Q

Two types of tolerance?

A

Central - B & T cells

Peripheral - regulator cell eliminate immune cells directed against self antigens

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99
Q

Examples of organ specific disease that occurs due to self tolerance being broken?

A

type I DM & thyroid disease

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100
Q

Focal collections of inflammatory cells in tissues is a result of what reaction?

A

Granulomatous reaction

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101
Q

Types of granulomatous reactions?

A

Tb, atypical mycobacteria, Leprosy (Th1 = protective where Th2 = non protective)

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102
Q

granulomatous reactions with unknown aetiology ?

A

sarcoidosis, wegeners granulomatosis, crohn’s disease

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103
Q

Difference between atopy and allergy?

A 
Atopy = exaggerated IgE-mediated immune response; all atopic disorders are type I hypersensitivity. All atopic disorders are considered allergic.
Allergy = exaggerated immune response to foreign antigen regardless of mechanism. Many allergic disorders are not atopic (hypersensitivity pneumonitis)
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104
Q

Where do atopic disorders usually affect?

A

Nose, eyes, skin and lungs

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105
Q

Histamine causes what? *(list 5 things)

A

local vasodilation, increased capillary permeability, stimulation of sensory nerves (itching), smooth muscle contraction, increased nasal, salivary and bronchial gland secretions.

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106
Q

Does angiogenesis occur in acute or chronic inflam?

A

Chronic as acute just increases permeability

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107
Q

Definition of chronic inflammation?

A

Inflammation of prolonged duration, constant tissue destruction and repair, mononuclear inflammatory cells

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108
Q

Pathogenesis of chronic inflammation

A

progressed from acute inflam, persistent infection by certain micro-organisms, Autoimmunity, prolonged exposure to toxic agents + unknown causes

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109
Q

Healing by fibrosis is characteristic of what inflammation?

A

Chronic

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110
Q

Types of mononuclear cells

A

macrophages, lymphocytes, plasma cells

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111
Q

What type of infections do eosinophils help fight?

A

Parasitic

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112
Q

Connective tissue cells found in chronic inflammation?

A

Mast cells, fibroblasts (deposit collagen) & macrophages

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113
Q

What is the name of a macrophage in the liver?

A

Kupffer cells

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114
Q

Macrophage in lungs is called?

A

Alveolar macrophage?

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115
Q

What are microglia?

A

Macrophages in the CNS

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116
Q

What are osteoclasts?

A

Macrophages in the bone

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117
Q

What are epithelioid cells and what are they characteristic of?

A

Activated macrophages resembling epithelium cells and are characteristic of granulomas

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118
Q

3 stage process of macrophage accumulation in tissues?

A

Recruitment (of monocytes from blood vessel),
Proliferation (after emigration from blood)
Immobilisation (within site of inflammation)

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119
Q

Name 3 components of the connective tissue matrix?

A

Elastic fibres,
collagen fibres,
proteoglycans

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120
Q

Chronic inflammation of the pelvis of the kidney is called?

A

Chronic pyelonephritis

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121
Q

Prolonged exposure to exogenous toxic agents to the liver results in?

A

Liver cirrhosis

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122
Q

Asbestos exposure will lead to what lung disease?

A

Interstitial fibrosis

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123
Q

Granulation tissue is good or bad?

A

Good as it is part of the healing process in chronic inflammation

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124
Q

Function of granulation tissue?

A

Repair by replacement of injured tissue by fibrous tissue with angiogenesis

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125
Q

Components of an early granuloma? 2 layers

A

Macrophages on the inside and lymphocytes on the outside

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126
Q

Components of a non caseating epithelioid granuloma? 3 layers

A

Macrophages on the inside, lymphocytes next layer then fibroblasts forming the out layer?

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127
Q

Components of a caseating epithelioid granuloma? 4 layers

A

Caseous necrosis in centre, epithelioid macrophages + Langhans cells 2nd layer, lymphocytes 3rd layer and fibroblasts 4th layer

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128
Q

List one cause of granulomatous inflammation form each of these categories bacterial, parasitic, fungal, dust/metals, foreign body, unknown?

A

Tb/leprosy/syphilis/cat-scratch, schistosomiasis, histoplasma/cryptococcus, silicosis/berryliosis, suture/vasculargraft, sarcoidosis/crohn’s

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129
Q

Damaged cells through tissue injury can be replaced by same cells is called?

A

Regeneration

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130
Q

Damaged cells through tissue injury that cannot be replaced by same cells

A

repair - resulting in fibrosis and scarring

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131
Q

Maturation of granulation tissue, 3 things change with time, what are they?

A

Inc in time results in a dec in vascularity and cellularity but and inc in collagen and ECM thus inc wound strength

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132
Q

What do myofibroblasts do?

A

Synthesis collagen and ECM and have myofibrils which have contractile ability to allow for wound contraction

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133
Q

Is there a loss of specialised function during the repair process of damaged tissue?

A

YES

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134
Q

Wound strength reaches 80% strength after what week?

A

4

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135
Q

What forms at the site of a fracture to help organise and gather things together?

A

Haematoma

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136
Q

Osteoblasts lay down woven bone during fracture healing which is called?

A

Callus

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137
Q

Lamellar bone is a result of what?

A

remodelling of a callus during the healing of a fracture

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138
Q

problems associated with the non union of fractures?

A

lack of movement
infection
weakened bone

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139
Q

What is the supporting tissue in the brain? (hint not collagen)

A

glial cells

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140
Q

The word that means scarring in the brain? (think of the supporting cells)

A

Gliosis - leaves a cyst

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141
Q

If You’re Thinkin’ Of Being My Brother It Don’t Matter If You’re…..?

A

Black or White

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142
Q

Which of these contains stagnant blood? Clot or thrombus?

A

Clot

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143
Q

Is familial hypercholesterolaemia a modifiable or non modifiable risk factor for atherosclerosis?

A

non modifiable - cholesterol in the skin leads to xanthomas

144
Q

Modifiable risk factors of atherosclerosis - list 6

A 
smoking
alcohol,
hyperlipidaemia,
obesity
diabetes
hypertension
145
Q

4 sequelae of atherosclerosis?

A

Occlusion, haemorrhage, erosion and aneurysm formation

146
Q

Causes of endothelial injury in atherosclerosis?

A

irradiation, haemodynamic injury, chemicals (aromatic hydrocarbons), immune complex deposition

147
Q

Which layer of the tunica of blood vessels does lipid accumulate?

A

Tunica intima

148
Q

What is a fattaaaaaay streak?

A

when monocytes migrate into the intima - to get to the lipids

149
Q

What are foam cells?

A

Macrophages ingest the lipids and become foam cells - occurs at an early age

150
Q

What is an atheroma?

A

Accumulation of degenerative material in the tunica intima

151
Q

What is the term used to describe a solidification of blood contents formed in the vessel during life?

A

Thrombosis

152
Q

What are the precursors of platelets?

A

Megakaryocytes

153
Q

How do platelets become activated?

A

By binding to sub endothelial collagen

154
Q

Alpha granules (fibrinogen, vWF, PDGF) and dense granules are secreted by what cell in the myeloid lineage?

A

Platelets. PDGF = platelet derived growth factor

Dense granules are chemotactic chemicals

155
Q

Where do thrombi form in veins?

A

At the valves

156
Q

Do you get atheromas in veins?

A

NO

157
Q

Mural thrombi occur where?

A

In da heart

158
Q

Lines of Zahn are associated with what?

A

Arterial thrombosis

159
Q

Sequalae of thrombosis - LIST 5?

A 
occlusion of vessel
resolution
incorporation into vessel wall
re-canalisation
embolisation!!!
160
Q

List 7 types of emboli

A

Fat, Thrombus, foreign material, amniotic, gas, tumour, infective

161
Q

Where does the majority of systemic thromboembolisms come from?

A

intra-cardiac mural thrombi

162
Q

Name given to an emboli originating in the venous system but gets into the arterial system via a VSD

A

Paradoxical emboli

163
Q

Risk of of death due to pulmonary emboli if left untreated?

A

85%

164
Q

Emboli from a DVT passes through which two chambers of the heart before becoming a PE in the lungs?

A

IVC into Right atrium through the tricuspid valve into the Right ventricle then leaves via the pulmonary artery

165
Q

Are in-situ pulmonary artery thrombosis common?

A

No - 95% come from venous thrombosis in the Deep veins

166
Q

Does a saddle embolus give a good prognosis?

A

No - common cause of sudden death, obstruction of 60% of pulmonary flow. If on bifurcation then almost always fatal

167
Q

Symptoms of pulmonary emboli in a medium pulmonary artery?

A

Pleuritic chest pain - felt on inspiration.

Dyspnoea

168
Q

Majority of PE’s affect what pulmonary artery - main,medium or small?

A

Small end arteriolar

169
Q

What is a greenfield filter?

A

IVC filter which is used a prophylactic treatment against PEs to stop emboli entering the heart

170
Q

What is ischaemia?

A

Insufficient blood flow to provide to provide adequate oxidation.

171
Q

Can ischaemia result in tissue hypoxia?

A

Yes - always

172
Q

Can hypoxia occur without ischaemia?

A

yes - if the arterial concentration of oxygen decreases due to anaemia, high altitude.

173
Q

4 factors affecting degree of ischaemic damage?

A

nature of blood supply - if dual then thats good (lung,liver, hand. but only single = bad (kidney, spleen, testis)
rate of occlusion = slower = better
tissue vulnerability to hypoxia = brain can’t go more than 4 mins without oxygen compared to heart = 20 mins
blood oxygen content

174
Q

What are watershed regions?

A

regions which occur at a point of anastomosis between two vascular supplies

175
Q

Is angina, ischaemic or infarction?

A

ischaemia

176
Q

Is a CVA ischaemic or infarction?

A

infarction

177
Q

Where would a thrombosis occur if someone were to get an ischaemic bowel?

A

SMA or IMA

178
Q

Is gangrene ischaemia or infarct?

A

Infarction

179
Q

What type of necrosis is dry gangrene?

A

ischaemic coagulative

180
Q

what does Clostridium perfringens give rise to?

A

Gas gangrene

181
Q

Is infarction more common in arteries or veins?

A

arteries

182
Q

What shape are most infarcts?

A

Wedged shape due to obstruction usually occurring at an upstream position so all downstream is affected

183
Q

Red infarction signifies anaemic or haemorrhagic infarction?

A

Haemorrhagic - seen in places where there is dual blood supply

184
Q

What receptors detect changes in BP?

A

Baroreceptors - in carotid sinus and aortic arch

185
Q

Classification of primary hypertension?

A

> 140/>90

186
Q

why do we need blood pressure?

A

It’s required to deliver oxygen to tissues

187
Q

MAP?

A

Mean arterial pressure = average blood pressure across cardiac cycle

188
Q

Equation for MAP?

A

MAP = diastolic pressure +1/3(pulse pressure)
Pulse pressure = systolic + diastolic
MAP = CO X SVR (systemic vascular resistance)

189
Q

Tissue perfusion is maintained at what minimum level of MAP?

A

60mmHg

190
Q

Decrease in BP will lead to what response and effect?

A

sympathetic response to inc HR (beta receptors) and inc SVR (alpha receptors)

191
Q

Volume overload will lead to what response in bp? How?

A

Decrease in bp via secretion of atrial natriuretic peptide from atria

  • causes kidneys excrete sodium and so water
  • vasodilation of blood vessels
192
Q

Where is angiotensinogen produced?

A

Liver

193
Q

Where is renin produced?

A

Juxtaglomerular apparatus in da kidneys

194
Q

Where is ACE secreted from?

A

Lungs

195
Q

Effect of aldosterone?

A

Kidneys resorb sodium and water to increase blood volume to increase bp

196
Q

Nitric oxide, prostacyclin, kinins, ANP cause dilation or constriction of vessels to increase or decrease resistance?

A

Cause dilation to decrease resistance

197
Q

Nitric oxide, prostacyclin, kinins, ANP cause dilation or constriction of vessels to increase or decrease resistance?

A

Cause dilation to decrease resistance

198
Q

Chemicals that lead to constriction of blood vessels to increase resistance?

A

Catecheloamines, thromboxane

angiotensin II

199
Q

What is essential hypertension?

A

Cause of hypertension is unknown - 95% of cases

200
Q

What syndrome presents from a single gene disorder causing sodium reabsorption?

A

Liddle syndrome

201
Q

What is malignant hypertension classed as?

A

> 200/>130mmHg

202
Q

4 categorical causes of secondary hypertension? + subtypes of the categories

A

Renal disease - glomerulonephritis, Polyarteritis nodosa, renal artery stenosis, chronic kidney disease
Endocrine causes - Cushing’s, Conn, phaeochromocytoma, hyperparathyroidism
Coarctation of aorta
Drugs - contraceptives, corticosteroids

203
Q

What is coarctation of aorta?

A

Narrowing of the aorta near the ligamentum arteriosum

204
Q

What us a phaeochromocytoma?

A

catecholamine producing tumour - found in adrenal medulla

205
Q

4 consequences of malignant hypertension?

A
  • cardiac failure with LV hypertrophy and dilation
  • blurred vision due to papilloedema & retinal haemorrhages
  • haematuria and renal failure due to fibrinoid necrosis of glomeruli
  • severe headache and cerebral haemorrhage
206
Q

LVF, mitral stenosis, emphysema, chronic bronchitis can give rise to what type of hypertension?

A

Pulmonary hypertension

207
Q

When to treat hypertension?

A

> 160/100 or high CVS risk with 140/90

208
Q

Low CVS risk and hypertension <160/100, how should patient be treated?

A

Lifestyle modification - the usual

209
Q

Drugs used in treating hypertension?

A

ACE inhibitors, calcium channel blockers, thiazide diuretics

210
Q

Definition of shock?

A

Circulatory failure resulting in inadequate organ perfusion. systolic <90mmHg

211
Q

Signs of shock

A

pallor, long capillary refill, inc pulse, oliguria

212
Q

Cellular effects of shock? (impaired tissue perfusion)

A

intracellular swelling, anaerobic respiration leads to lactic acid which drops the pH

213
Q

3 main categories of shock?

A

Hypovolaemic
Cardiogenic
Distributive (septic, anaphylactic, neurogenic, toxic shock)

214
Q

Causes of hypovolaemic shock?

A

Haemorrhagic loss - trauma, GI bleeding, haemorrhagic pancreatitis, AA
Non-haemorrhagic loss - diarrhoea, vomiting, heat stroke, burns, acute loss of fluid into third spaces

215
Q

Compensatory mechanism to hypovolaemic shock?

A

Due to decreases venous return there is decreased SV so decreased Cardiac output. therefore there’s a compensatory vasoconstriction to increase systemic vascular resistance

216
Q

Characteristic appearance of a hypovolaemic shock patient? (think of vasoconstriction’s effect)

A

cool, clammy & shut down

217
Q

What is Cardiogenic shock?

A

Cardiac pump failure —> decrease in Cardiac output so compensation is increase in SVR

218
Q

Most common cause of cardiogenic shock?

A

Acute MI

219
Q

4 categories of cardiogenic shock?

A

Myopathic - MI
Arrythmia related - AF or VF
mechanical - VSD, valvular defects
extra-cardiac - tension pneumothorax, PE, pericardial tamponade

220
Q

4 types of distributive shock?

A

Septic
Anaphylactic
Neurogenic
Toxic shock syndrome

221
Q

What happens in distributive shock?

A

Decrease in SVR due to severe vasodilation, compensation by increasing cardiac output

222
Q

Systemic infection leads to what type of shock?

A

Septic shock

223
Q

What type of hypersensitivity reaction is anaphylactic shock?

A

Type I IgE mediated leading to massive mast cell degranulation = VASODILATION

224
Q

Spinal injury leads to what type of shock?

A

Neurogenic shock

225
Q

Prolonged retention of a tampon which become infected by staph would give rise to what type of shock?

A

Toxic shock syndrome

226
Q

Why do cells adapt?

A

Changes in environment or demand

- size, number, metabolic activity, function

227
Q

What type of cells cannot adapt?

A

Terminally differentiated e.g cerebral neurons

permanent cell population

228
Q

What cells don’t need to adapt?

A

Fibroblasts as they are very resistant to damage

229
Q

Define agenesis

A

Failure to produce

230
Q

Define dysgenesis

A

Failure to organise tissue

231
Q

Define Aplasia

A

Failure to differentiate

232
Q

Define Hypoplasia

A

Failure of organ to grow to full size

233
Q

Define metaplasia

A

Transformation of one cell type into another e.g cervix undergoes metaplasia in puberty and menopause. squamocolumnar junction changes

234
Q

2 ways that cell adapts an increase in demand?

A

Hypertrophy - increase in size of existing cells and inc in functional capacity
Hyperplasia - increase in number. Possible in both labile and stable cell populations. Physiological or pathological (excess hormones, growth factors). e.g gynaecomastia - phys in puberty but path in liver cirrhosis

235
Q

Denervation or disuse of an organ or tissue will lead to what type of cellular adaptation?

A

Atrophy

236
Q

What is cachexia?

A

Loss of body mass

237
Q

What is involution?

A

Physiological atrophy by apoptosis

238
Q

What hypertrophy occurs due to aortic stenosis?

A

Left ventricular hypertrophy (also occurs due to systemic hypertension)

239
Q

Thyroid stimulating antibody (graves’ disease) gives rise to what hyperplasia?

A

Follicular epithelial hyperplasia

240
Q

Cortical hyperplasia occurs in what gland?

A

Adrenal cortex - response to inc ACTH production

241
Q

Why does the prostate undergo hyperplasia?

A

Excess of oestrogens stimulates oestrogen sensitive central zone leading to epithelial and connective tissue hyperplasia

242
Q

Difference between congenital and genetic?

A

Congenital = condition present at birth
Genetic conditions = caused by abnormalities in genes and chromosomes but may be modulated by environmental factors as well

243
Q

Metaplastic change due to acid reflux?

A

Oesophageal squamous epithelium to columnar (glandular) epithelium

244
Q

Metaplastic change due to chronic trauma?

A

Fibrocollagenous tissue to bone

245
Q

Metaplastic change due to cigarette smoke? (lungs)

A

Pseudostratified ciliated bronchial epithelium to squamous epithelium

246
Q

Metaplastic change due to bladder calculi, longstanding catheter or schistomosiasis?

A

Transitional epithelium of bladder to squamous epithelium

247
Q

Glandular metaplasia in the oesophagus can result in what neoplasia?

A

adenocarcinoma

248
Q

Squamous metaplasia in bladder increases risk of what carcinoma?

A

squamous cell carcinoma

249
Q

Squamous metaplasia in cervix increases risk of what?

A

Cervical intraepithelial neoplasia and squamous cell carcinoma

250
Q

Squamous metaplasia in bronchus increases risk of what carcinoma?

A

Dysplasia and squamous cell carcinoma

251
Q

What is dysplasia?

A

Earliest manifestation of multistage process of neoplasia. Dysplasia = disordered growth

252
Q

Dystrophy?

A

Abnormal development

253
Q

Criteria for Koch’s postulates?

A
  • Causative organism must be isolate from every person with disease
  • causative organism must be cultivated artificially in pure culture
  • typical symptoms must result from inoculation of causative organism
  • causative organism must be recoverable from individuals who are infected experimentally
254
Q

What are viroids?

A

Virus that infects plants

255
Q

Are fungi eukaryote or prokaryote?

A

eukaryote

256
Q

What are the cell walls made of in fungi?

A

chitin

257
Q

What fungi is unicellular - yeasts or moulds?

A

Yeasts (moulds are multicellular)

258
Q

What type of micro-organism causes toxoplasmosis, leishmanisasis, trichomanas vaginalis?

A

Protista

259
Q

What are fomites?

A

inanimate objects which can transmit infection

260
Q

What colour does gram +ve bacteria stain?

A

bluey purple

261
Q

Term given to loss of differentiation?

A

Anaplasia

262
Q

Term given to new formation of abnormal new growth?

A

neoplasia

263
Q

Why are benign neoplasms not always harmless?

A

Pressure on adjacent tissue
Obstruction of flow
Hormone production
Transform into malignant neoplasms

264
Q

Are low grade neoplasms, well or poorly differentiated?

A

Well differentiated = tissue looks like original tissue

265
Q

Rapid growth rate of neoplasms is characteristic of benign or malignant neoplasms?

A

Malignant - many mitotic figures with necrotic areas due to lack of vessels

266
Q

Do benign neoplasms metastasise?

A

No

267
Q

What type of border to benign neoplasms have?

A

Well circumscribed. Malignant have invasive and irregular borders

268
Q

4 Routes of spread of metastasis?

A

Lymphatic channels - common in carcinomas
Haematogenous - mainly sarcomas
Transcoelomic - pleural/pericardial/peritoneal
Implantation - spillage of tumours during surgery

269
Q

What route of metastasis is more common in carcinomas?

A

Lymphatic channels

270
Q

What is TMN staging?

A

Stages I-IV depending on stage in each T,M,N
Tumour = size and extent of primary tumour. T1 5cm. T4 = involves skin or chest wall
Metastasis = M0 = no distant mets. M1 = distant mets
Nodes = N0 = no nodes, N1 = ipsilateral nodes, N2 > node involvement

271
Q

Using TMN staging, what stage would it be with T(any), N(any), M1?

A

IV

272
Q

What does staging of a cancer mean?

A

How advanced the tumour is - has the cancer spread and if so to what extent

273
Q

What is Dukes staging?

A 
A = invades but not through bowel wall
B = invades through wall but no lymph node mets
C = local lymph nodes
D = distant mets
274
Q

What is grading of a tumour?

A

How aggressive the tumour is - how different it looks from the tissue of origin

275
Q

What is another name for Grade 4 in tumour grading?

A

Anaplastic - undifferentiated

276
Q

Are telomerases activated in carcinogenesis or not?

A

Yes they are activated. They replace the lost telomeres (bit at the end of the chromosome which gets shorter with each cell division). Gives cancer cell replicative immortality.

277
Q

What are TSGs?

A

Tumour suppressor genes - negative regulators of proliferation and cell cycle

278
Q

Gatekeeper and caretakers are what type of gene?

A

TSG

279
Q

What type of TSG maintains genomic integrity by repairing DNA?

A

Caretaker

280
Q

What type of TSG inhibits proliferation?

A

Gatekeepers - promote apoptosis of cells with damaged DNA

281
Q

p53 gene is an important…..?

A

gatekeeper - p53 inactivation is the most common genetic abnormality in tumours >50%

282
Q

Genomic instability is a result of mutation in which TSG?

A

Caretaker

283
Q

What would happen as a result of a mutation of a gatekeeper?

A

increased proliferation and avoidance of apoptosis

284
Q

Inactivation of TSGs can lead to increase of developing what?

A

cancer

285
Q

What is Knudson’s 2 hit hypothesis?

A

Inheriting one germline copy of a damaged gene present in every cell in the body was not sufficient to enable this cancer to develop. A second hit (or loss) to the good copy in the gene pair could occur somatically, though, producing cancer.

286
Q

How does a sarcoma generally metastasise?

A

Haematogenously

287
Q

What was the tumour that was used to demonstrate Knudson’s two hit hypothesis?

A

Retinoblastoma

288
Q

What do proto-oncogenes do in a normal cell?

A

Promote cell proliferation,
angiogenesis
negative regulator of apoptosis
inc survival of cells

289
Q

What is an oncogene?

A

A proto-oncogene is a normal gene that can become an oncogene due to mutations or increased expression producing oncoproteins. essentially a cancer causing gene

290
Q

Classification of oncogenes?

A

Growth factors,
Regulatory GTPases
Transcription factors
Receptor tyrosine kinase

291
Q

What sort of gene is myc?

A

oncogene - transcription factor function

292
Q

Oncogene example which has a function in intracellular signalling?

A

Ras,
abl
erk
src

293
Q

What is the function of the oncoprotein produced by the sis oncogene?

A

Growth factor

294
Q

What does HER2 code for?

A

positive growth factor receptor - over expression seen in 30% of breast tumours

295
Q

Current biomarkers for cancer?

A

Prostate specific antigen
Carcinoembryonic antigen
cancer antigen 125

296
Q

What gene mutation causes Li Fraumeni syndrome?

A

p53 gatekeeper TSG

297
Q

What gene mutation causes Familial adenomatous polyposis?

A

APC gatekeeper TSG

298
Q

Which is seen more in prostate and pancreatic cancer - BRCA1 or BRCA2?

A

BRCA2

299
Q

Mutation in the RB1 TSG would increase risk of what cancer?

A

Familial retinoblastoma

300
Q

6 key hallmarks of cancer?

A 
Self sufficiency for growth signals
Insensitivity to antigrowth signals
Evades apoptosis
Replicative immortality
Sustained Angiogenesis
Tissue Invasion & Metastasis
301
Q

EGFR overexpression is associated with what cancers?

A

Lung cancers - 40-80%
Colorectal
Pancreatic

302
Q

Ras mutation is seen in 90% of cases of what cancer?

A

Pancreatic cancer

303
Q

Are tumour cells able to respond to negative growth factors?

A

No - one of the hallmarks of cancer

304
Q

How do tumour cells evade apoptosis?

A

Inactivates pro-apoptotic factors - Bax
Activation of anti-apoptotic factors - BCL-2
switch of regulators that induce apoptosis - p53

305
Q

How big does the tumour need to be to start needing a new blood supply?

A

1-2mm in diameter

306
Q

Switch in what adhesion molecules allows for tumour cells to invade and metastasise?

A

E-cadherin to N-cadherin = become more motile

307
Q

What enzyme is secreted by tumour cells to digest the basement membrane?

A

Matrix metalloproteinases

308
Q

Benign tumour of surface epithelium?

A

Papilloma e.g squamous cell papilloma in the skin

309
Q

Malignant tumour of surface epithelium?

A

Carcinoma e.g squamous cell carcinoma

310
Q

What is an adenoma?

A

Benign tumour of glandular epithelium

311
Q

What is an adenocarcinoma?

A

Malignant tumour of glandular epithelium

312
Q

What is a follicular adenoma?

A

Benign tumour of the glandular epithelium of thyroid

313
Q

Benign tumour of transitional epithelium of the bladder?

A

Transitional cell papilloma

314
Q

What is a basal cell carcinoma?

A

Malignant tumour of the basal cells of the skin

315
Q

Malignant tumour of the glandular epithelium of the colon?

A

Colonic adenocarcinoma

316
Q

Is a seminoma benign or malignant?

A

Malignant - despite ending with ‘oma.

317
Q

Prefix = Angio = what tissue?

A

Blood vessel

318
Q

Chondro = what tissue?

A

Cartilage

319
Q

Rhabdomyo = what tissue?

A

Skeletal muscle

320
Q

Leiomyo = what tissue?

A

smooth muscle

321
Q

Benign mesenchymal tumour of adipose tissue?

A

Lipoma

322
Q

Benign mesenchymal tumour of fibrous tissue?

A

Fibroma

323
Q

What is a rhabdomyoma?

A

Benign mesenchymal tumour of skeletal muscle

324
Q

Malignant mesenchymal tumour of smooth muscle?

A

LeiomyoSARCOMA

325
Q

What is an osteosarcoma?

A

Malignant mesenchymal tumour of bone

326
Q

Malignant tumour of cartilage?

A

Chondrosarcoma

327
Q

Malignant melanocytes?

A

Melanoma

328
Q

Melanocytic nevus is benign or malignant?

A

Benign tumour of melanocytes

329
Q

List 4 CNS tumours?

A 
Meningioma - meninges
Astrocytoma - astrocytes
Oligodendroglioma - oligodendrocytes
Ependyoma - ventricles 
Medulloblastoma - originates from cerebellum
330
Q

Benign tumour of salivary glands?

A

Pleomorphic salivary adenoma

331
Q

Two types of germ cell tumours?

A

Seminomatous = seminoma

Non-seminatous germ cell tumour = teratoma

332
Q

What is a Wilms tumour?

A

Nephroblastoma

333
Q

Name given to a non neoplastic overgrowth of normal tissue?

A

Hamartoma - uncoordinated growth

334
Q

Name given to excess tissue in an abnormal location?

A

Choristoma - heterotopia

335
Q

Classification of carcinogens?

A

Genotoxic - Initiators = chemically modify or damage DNA

Non-genotoxic - Promoters = induce proliferation and replication

336
Q

What percentage of cancers are due to preventable causes?

A

90%

337
Q

What is carcinogen results in the most cancer deaths? Diet, tobacco, infection?

A

Diet then tobacco then infection

338
Q

What organ does aflatoxin damage?

A

Liver

339
Q

X-rays can damage bone marrow and so increase the risk of what cancer?

A

Leukaemia

340
Q

Carcinogen that causes mesothelioma?

A

Asbestos

341
Q

How many carcinogens are there within tobacco smoke?

A

19! PAH, acrolein, nitrosamines, heavy metals

342
Q

What carcinogen do you find in sausages?

A

Nitrosamines

343
Q

OCP, alcohol consumption, HRT, early menarche, late menopause all increase exposure to what hormone?

A

Oestrogen = stimulate cell division and induce DNA damage

344
Q

Examples of direct acting carcinogens?

A 
All interact directly with DNA;
Oxygen radicals
nitrosamines
UV light
ionising radiation
345
Q

What happens to pro carcinogens?

A

Require enzymatic activation before they react with DNA;
aromatic amines
PAHs

346
Q

Is benzopyrene a direct acting or pro-carcinogen?

A

Pro-carcinogen - initially is not a mutagen when taking in through smoking but gets metabolised and covered to BPDE which can get excreted but is very reactive - ultimate carcinogen

347
Q

Mutation in mismatch repair can lead to to what cancer?

A

Hereditary non polyposis colorectal cancer

348
Q

List 6 common genetic abnormalities?

A 
Point mutation
Deletion
Insertion
Gene amplification
Chromosomal inversion
Aneuploidy
349
Q

What is the principal feature of malignant spread?

A

Spread along lines of least resistance

350
Q

Interstitial collagenase, gelatinases, stomolysins are all types of what?

A

Matrix metalloproteinases

351
Q

What are TIMPs?

A

Tissue inhibitors of metalloproteinases

352
Q

When does a tumour become a systemic disease?

A

When tumour metastasises from its primary site to form a secondary tumour

353
Q

Promoters of angiogenesis?

A

VEGF family

354
Q

Are Bone mets in the lung sclerotic or lytic?

A

Lytic

355
Q

Are Bone mets in the prostate sclerotic or lytic?

A

Sclerotic

356
Q

What type of metastatic spread does ovarian cancer show?

A

Transcoelomic spread

From Flashcardlet (22 decks)

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