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From Flashcardlet > MoD > Flashcards

MoD Flashcards

0
Q

What are moulds ?

A

Fungi that grow in flat mats (mycelia) of tiny filaments (hyphae)

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1
Q

What is a capsid?

A

The protein shell of a virus, made up of units called capsomeres
Capsid encloses genetic material

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2
Q

What type of infections do moulds cause ?

A

Superficial infections e.g. Ringworm, athletes foot

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3
Q

What is the most common fungal infection in humans ?

A

Yeats infection called thrush, caused by Candida albicans

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4
Q

Chronic, persistent diarrhoea caused by cryptosporidia (Protista) is associated with the onset of which disease ?

A

AIDS

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5
Q

Which Protista usually causes vaginal infections (e.g. The cause of foul-smelling discharge)

A

Trichomonas vaginalis

- can be transmitted sexually, men often asymptomatic carriers, but can cause balanitis

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6
Q

What are pili ? (With regards to bacterial cell features)

A

A pilus is a tube which joins two cells together during conjugation - function is to exchange genetic information
- only on gram -ve bacteria

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7
Q

Function of fimbriae on bacterial cells ?

A

Aids adhesion

Gram -ve cells

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8
Q

Function of bacterial cell capsule

A

Protection, prevents bacteria being killed - even within phagocytes

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9
Q

Function of slime produced by bacterial cells ?

A

To help them stick to surfaces e.g. Streptococcus mutans produces slime which enables it to stick to surfaces- helping to form plaques and eventually causes dental caries

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10
Q

Which bacteria cause infection associated with implanted plastic medical devices and why ?

A

Coagulase negative staphylococci

This bacteria live on skin and produce slime which enables them to stick to plastics

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11
Q

Function if bacterial endo spores ?

A

Resist a range of hazardous environments, protecting against: heat, radiation, desiccation

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12
Q

Malaria:
Causative organism
Mode of transmission

A

Caused by plasmodium falciparum (a Protista)

Transmitted by female anopheles Mosquitos

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13
Q

Define fomite

A

Any inanimate object that can transmit infectious agents from one person to another

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14
Q

Name the 6 routes of person-to-person transmission of infection

A
  1. Airbourne e.g. Droplet transmission
  2. Faecal-oral route
  3. Sexually transmitted
  4. Direct inoculation e.g. IV drug use
  5. Animal
  6. Fomites
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15
Q

Describe the cycle of infection

A
  1. Pathogenic microbes encounter and adhere to a host
  2. They multiply within host
  3. Dispersed to encounter other host
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16
Q

What causes rheumatic fever ?

A

Immunological cross reactions between human tissue antigen and antigens on streptococcus pyogenes.
Cause autoimmune disease

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17
Q

What does the prefix Ana- mean ?

A

Lack of/absence

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18
Q

What does the prefix Dys- mean ?

A

Disordered

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19
Q

What does the prefix Hyper- mean ?

A

An excess over normal

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20
Q

What does the prefix Hypo-

A

A deficiency under normal

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21
Q

What does the prefix meta- mean ?

A

Change from one type to another

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22
Q

What does the suffix -it is mean ?

A

Inflammatory process

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23
Q

What does the suffix-Oma mean ?

A

Tumour

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24
Q

What does the suffix -osis mean ?

A

A state or condition, not necessarily pathological

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25
Q

What does the suffix -oid mean ?

A

Bearing a resemblance

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26
Q

What does the suffix -Penia mean ?

A

Lack of

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27
Q

What does the suffix -cytosis mean ?

A

Increased number if cells

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28
Q

What does the suffix -ectasia mean ?

A

Dilation

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29
Q

What does the suffix -plasia mean ?

A

(Disorder of) growth

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30
Q

What does the suffix -opathy mean ?

A

Abnormal state lacking specific characteristics

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31
Q

Define cell injury

A

A set of biochemical and/or morphological changes that occur when the state of homeostasis is perturbed by adverse influences

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32
Q

What is the innate immune system ?

A

The defence mechanisms present before infection that have evolved to specifically recognise microbes & protect multicellular organisms against infection

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33
Q

What is the adaptive immune system ?

A

Mechanisms that are stimulated by microbes and are capable of recognising non-microbial substances (antigens)

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34
Q

Type 1 hypersensitivity:

  1. Underlying mechanism, Ig involved
  2. Examples
A
  1. IgE, rapid response, mast cells and degranulation of basophils mediates inflammatory response
  2. Systemic anaphylaxis and atopic allergy
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35
Q

Type 2 hypersensitivity:

  1. Underlying mechanism, Ig involved
  2. Examples
A
  1. Initiated by IgM or complement binding IgG (IgM more fficient as pentavalent), cytotoxic reaction, antibody mediated
    Response= Ab-Ag binding> activate complement> cell lysis & opsonisation> phagocytosis & destruction
  2. Autoimmune disease e.g. Haemolytic anaemia, organ rejection, graves
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36
Q

Type 3 hypersensitivity:

  1. Underlying mechanism
  2. Examples
A
  1. Mediated by deposition of antigen-antibody complexes> complement activation> accumulation of leukocytes> C5a attracts neutrophils, C3b= opsonisation
  2. Seen in SLE, polyarteritis nodosa
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37
Q

Type 4 hypersensitivity

  1. Underlying mechanism
  2. Example
A
  1. Mediated by specifically sensitised T cells (rather than Ab), sub divided into two types:
    - delayed: initiated by CD4+ cells! causing TH1 CD4+ T cells to secrete cytokines, recruitment of macrophages etc = major effector cell
    - direct cell cytotoxicity- mediated by cd8+ T cells. These assume the effector function - contact dermatitis
  2. Type1 diabetes, MS, response to microbial infection
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38
Q

Ischaemia causes an increase in which intracellular ion ?

A

Ca2+

Due to influx across plasma membrane and release from mitochondria and ER

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39
Q

What does a sustained rise in intracellular calcium levels result in

A

Non-specific increases in membrane permeability > further increases in calcium ?

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40
Q

Increased intracellular calcium levels can activate which enzymes ?

A

ATPases (hastens ATP depletion)
Phospholipases (membrane damage)
Proteases (breakdown of membrane and cytoskeleton)
Endonucleases (DNA and chromatin fragmentation)

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41
Q

Define necrosis

A

Form of cell injury resulting in the premature death of cells and living tissue- caused by external factors

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42
Q

Coagulative necrosis:

  1. Cause
  2. Appearance (macroscopic & microscopic)
  3. Mechanism
A
  1. Usually due to lack of oxygen
  2. Macroscopic = pale segment of tissue
    Microscopic = ‘ghost cells’ no nuclei but very little structural damage
  3. Thought that the injury denatures structural proteins & lysosomal enzymes - so maintains coagulated morphology
    regeneration can occur if enough viable cells
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43
Q

Liquefactive/colliquative necrosis:

  1. Cause
  2. Appearance (macro & micro)
  3. Mechanism
A
  1. Hypoxia cell death in brain
  2. Tissue becomes liquid mass- complete digestion of dead cells
  3. Affected cells digested by hydrolytic enzymes> soft lesion consisting of pus & fluid. After removal of debris fluid filled space is left- associated with abscesses and fungal and focal bacterial infections
    * also occurs in lung*
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44
Q

Caseous necrosis:

  1. Cause
  2. Appearance (macro & micro)
  3. Mechanism
A
  1. TB infections, syphilis & some fungi.
  2. No histology cal architecture preserved- acellular pink areas of necrosis surrounded by granulomatous inflam. Process
    Macro= soft, white, proteinaceous dead cell mass
  3. ?
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45
Q

Gangrenous necrosis:

  1. Cause
  2. Appearance (macro & micro)
  3. Mechanism
A
  1. Dry= distal limb due to Ischaemia, arterial occlusion wet= in naturally moist tissues, bacteria, infections
    2 darkened discolouration
  2. Dry= form of coagulative necrosis
    Wet= blockage of venous flow! affected part saturated with stagnant blood - bacteria thrive. Toxic products from bacteria may be absorbed causing septicaemia
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46
Q

Fat necrosis:

  1. Cause
  2. Appearance (macro & micro)
  3. Mechanism
A
  1. trauma of pancreas/pancreatitis
  2. white chalky deposits within fat
  3. Enzyme lipase (pancreatic enzymes) releases fatty acids from triglycerides, fatty acids complex with calcium forming soaps (fat soponification)
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47
Q

What are the ultra structural changes in reversible cell injury?

A

Swelling of ER, mitochondria, clumping of chromatin

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48
Q

What are the ultra structural changes in irreversible cell injury?

A

Swelling of ER and mitochondria (with amorphous densities), Loss of ribosomes, lysosomes rupture, membrane blebs, nuclear condensation,

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49
Q

Name the two causes of acute inflammation:

A
  1. Tissue death

2. Infection (usually pyogenic bacteria)

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50
Q

Functions of acute inflammation

A
  1. Clear away dead tissues
  2. locally protect from infection
  3. Allow access of immune components
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51
Q

Name the 4 cardinal signs of inflammation

A
  1. Calor (heat)
  2. Dolor (pain)
  3. Rubor (redness)
  4. Tumour (swelling)
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52
Q

Which morphological pattern of inflammation is often seen in serous cavities ?

A

Fibrinous

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53
Q

The name for loathe localised collections of pus enclosed by surrounding tissue and the causative type of inflammation

A
  1. Abscess

2. Purulent inflammation

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54
Q

What type of inflammation is a skin blister an example of ?

A

Serous inflammation:

Characterised by copious effusion of non-viscous serous fluid (often produced by mesothelial cells)

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55
Q

What is ulcerative inflammation ?

A

Inflammation occurring near epithelium - resulting in necrotic loss of tuissue on surface therefore exposing lower layers- forming an ulcer

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56
Q

Examples of granulomatous inflammation

A

TB, leprosy, sarcoidosis, syphilis

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57
Q

How is the increase in permeability of blood vessels mediated in an acute inflammatory response ?

A

Histamine, bradykinin, NO

Or direct damage to endothelium by toxins

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58
Q

Composition of pus ?

A

Neutrophils, cellular debris, fluid

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59
Q

Function of acute phase proteins

A

Cause the systemic effects of inflammation:

Pyrexia, inc. BP, dec. sweating, malaise, loss of appetite, somnolence

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60
Q

What problem can acute phase proteins contribute to during chronic inflammation ?

A

Amyloidosis

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61
Q

Where in the body are acute phase proteins produced ?

A

Liver

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62
Q

Erythrocyte sedimentation rate (ESR) is used for a differential diagnosis of which disease ?

A

Kawasakis disease

A necrotising vasculitis affecting medium sized vessels of body, usually seen in children under 5

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63
Q

How is neutrophil adhesion mediated in acute inflammation ?

A

Up regulation of adhesion mols:

IL-8, IL-1, C5a,PAF, TNF

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64
Q

Define resolution (e.g. Following inflammation)

A

The complete restoration of inflamed tissue back to normal status.
Vasodilation to cease and damage parenchymal cells regenerate.
Usually the outcome from acute inflammation

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65
Q

What is tissue fibrosis ?

A

Large amounts of tissue destruction, tissues unable to regenerate.
Fibrous scarring occurs- scars won’t contain any specialised structures such as parenchymal cells, hence functional impairment may occur

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66
Q

Main characteristic of chronic inflammation (histologically)

A

Dominating presence of macrophages in the injured tissue,

the toxins they release injure own tissues (as well as invading organisms) > tissue destruction

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67
Q

What is the alternative complement pathway ?

What do the products promote ?

A

The cleavage of C3>C3a + C3b. Occurs at very low levels at all times
Production of C3a promotes inflammation (ANAPHYLAXIS).
c3b promotes cell lysis and coats bacteria so that they become visible to macrophages and neutrophils > removed from circulation (OPSONIZATION)

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68
Q

Estimated Range of antigenic variability of adaptive immune system ?

A

10^9

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69
Q

How does the adaptive immune system generate repertoire of specificities needed ?

A

Germaine DNA insufficient - somatic hyper mutation - changes the variable region, diversifying B cell receptors (used to recognise antigens)

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70
Q

Which immunoglobulin can cross the placenta ?

A

IgG

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71
Q

Which two immunoglobulin isotypes involve complement fixation?

A

IgG and IgM

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72
Q

Which immunoglobulin isotype is involved in mucosal immunity ?

A

IgA

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73
Q

Low or absent IgA suggest what clinically ?

A

Significant immunodeficiency

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74
Q

Which immunoglobulin isotype is involved in parasitic immunity ?

A

IgE

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75
Q

Atopic individuals have higher levels of which immunoglobulin class that non-atopic individuals ?

A

IgE

Used Diagnosis of allergies

76
Q

Which Ig seen early in primary infections and which are seen in secondary immune response ?

A 
Primary = IgM
Secondary = IgG (demonstrates serological immunity)
77
Q

What is a granuloma ? (Granulomatous reaction)

not to be confused with granulation tissue

A

An inflammation - collection of macrophages.

Form when the immune system attempts to ‘wall off’ substances which are foreign but unable to eliminate

78
Q

What is granulation tissue ?

not to be confused with granuloma

A

New connective tissue and tiny blood vessels that for, on the surface of a wound during the healing process

79
Q

Examples of granulomatous disease of unknown aetiology

A
  • Sarcoidosis
  • wegeners granulomatosis
  • Crohn’s disease
80
Q

Examples of infectious granulomatous disease

A

TB
leprosy
(Both mycobacterial)

81
Q

What are the defining characteristics of chronic inflammation ?

A

Prolonged duration of inflammation
Tissue destruction and repair
Mononuclear inflammatory cells

82
Q

Outline the Morphological features of chronic inflammation ?

A

Infiltration with mononuclear cells ( macrophages, lymphocytes, plasma cells)
Tissue destruction and healing by fibrosis

83
Q

Describe where macrophages originate from and how their development progresses

A

Pluripotent stem cell> myeloid stem cell in bone marrow> monocytes in blood> macrophage in tissues -activated macrophage- giant or epithelioid cells

84
Q

What is a giant cell (macrophage) ?

A

A cell formed from the union of several cells in response to infection, multinucleate.
Different types e.g. Langerhans (granulomatous)

85
Q

What is an epithelioid cell (macrophage) ?

A

An activated macrophage resembling epithelial cells
Elongated, finely granular, pale, eosinophilic
Characteristic of granulomas

86
Q

What at e the roles of activated macrophages ?

A

Phagocytosis
Antigen processing
Secretions of proteins and lipid-derived mediators (complement, coagulation, cytokines, NO)

87
Q

What is healing by regeneration ?

A

Damaged cells replaced by LIKE

Tissues return to normal

88
Q

What is healing by repair ?

A

Damaged cells cannot be replaced by like

Fibrosis and scarring

89
Q

What is a labile cell population ?

Example

A

A population which the highest capacity for regeneration
High normal turnover
E.g. Epithelium
Adapt easily

90
Q

What is a stable (quiescent) population ?

Example

A

Population of cells l’s with low physiological turnover
Turnover can increase if needed
Good regenerative capacity
E.g. Liver, renal tubules

91
Q

What is a permanent cell population ?

A 
Population of cells l's with NO physiological turnover
Long lie cells
No regenerative capacity
E.g. Neurons, muscle cells
Can't adapt
92
Q

How is regeneration controlled ?

A

Contact inhibition - just covers defect then stops

Complex control by growth factors, cell-cell and cell-matrix interactions

93
Q

Examples of local factors which could inhibit healing ?

A

Infection, haematoma, dec. blood supply, foreign bodies, mechanical stress

94
Q

Examples of systemic factors inhibiting healing?

A

Age, drugs, anaemia, diabetes, malnutrition, vit C or trace metal deficit

95
Q

Explain healing by first intention

A

The healing of a clean, uninfected, surgical wound
Good homeostasis
Edges apposed e.g. Sutures/staples

96
Q

Describe healing by second intention

A

The healing of a wound where edges not apposed:
Extensive tissue loss
Apposition not physically possible
Large haematoma or foreign body
Foreign body
Results in florid granulation tissue and extensive scarring

97
Q

Define atherosclerosis

A

Degeneration of arterial walls characterised by fibrosis, lipid deposition and inflammation which limits blood circulation and predisposes to thrombosis

98
Q

Describe the formation of atherosclerotic plaques

A

Endothelial injury due to chemical etc
Lipid accumulates in intima of vessel
Adherence of circulating monocytes, which migrate to intima and ingest lipids becoming FOAM CELLS - fatty streak stage
Smooth cells proliferate and secrete connective tissue
Mixture of fat and Extra cellular material, leukocytes and smooth muscles forms the atherosclerotic plaque

99
Q

Define embolus

A

Mass of material (any) in the vascular system able to lodge in a vessel and block it

100
Q

What is the most common type of embolus ?

A

Thrombosis : a solidification of blood contents formed in the vessel during life

101
Q

What is the difference between a blood clot and and a thrombus ?

A

Thrombus must for I n the body during life, whereas a blood clot forms in stagnant blood, can be outside the body or in death.
Blood clots due to enzymatic process, coagulation cascade, fairly elastic.
Thrombus depends on platelets, more firm than clot

102
Q

What are platelets ?

A

Fragments of megakaryocytes in bone marrow which circulate in blood stream

103
Q

How are platelets activated ?

A

By binding to collagen exposed by endothelial damage

104
Q

What do platelets secrete ?

A

Aplha granules: fibrinogen, fibronectin, PDGF

Dense granules: chemotactic

105
Q

What is described by virchows triad?

A

Three broad categories thought to cause thrombosis:

  1. Endothelial injury
  2. Hyper-coagulability
  3. Abnormal flow
106
Q

What are lines of Zahn ?

A

Characteristic appearance of thrombi that was formed at site of fast blood flow (heart,aorta)
Visible and microscopic alternating layers of platelets mixed with fibrin, which appear as lighter, darker layers = red blood cells

107
Q

What are thrombi in the heart known as ?

A

Mural thrombi

108
Q

What are the clinical effects of pulmonary embolism ?

A

Small: asymptomatic- pul. Hypertension
Med: acute resp. And cardiac failure (V/Q mismatch, RV strain)
Large: DEATH: ‘saddle emboli’

109
Q

Where does a PE most comply originate from?

A

DVT in leg or pelvis

110
Q

Where do infective embolisms usually originate from ?

A

Vegetations on infective heart valves

111
Q

How do amniotic fluid embolisms arise ?

A

Increased uterine pressure during labour may force AF into maternal uterine veins

112
Q

Where do embolisms impacting the brain usually arise from ?

A

The arterial system - 80% from intra cardiac mural thrombi

113
Q

What is a paradoxical emboli ?

A

Passes from one circulation to the other, usually via VSD

114
Q

Why may re-perfusion of non-infarcted Ischaemia tissues not always be good?

A

Generation of reactive oxygen species by inflammatory cells cause further cell damage (reperfusion injury)

115
Q

Define infarction

A

Ischaemic necrosis cause by an occlusion of the arterial supply or venous drainage

116
Q

Which type of necrosis does infarction usually result In ?

A

Coagulative necrosis (colliquative in the brain)

117
Q

Which organs are vulnerable to infarction and why ?

A

Kidneys, testis, spleen etc as only have single blood supply

118
Q

What percentage of total cardiac output does the brain require ?

A

15%

119
Q

How is the mean arterial pressure (MAP) calculated ?

A

MAP= diastolic + 1/3(pulse pressure)
MAP= COxSVR
Pulse pressure= systolic pressure - diastolic pressure
CO= strike vol. x HR

120
Q

What is the minimum mean arterial pressure required to maintain perfusion ?

A

MAP must be > 60mmHg

121
Q

What is the sympathetic effect on regulating BP ?

A 
Decrease BP
increase HR (beta receptors)
Inc. systemic vascular resistance (SVR) by vasoconstriction (alpha receptors)
122
Q

Outline how the renin-angiotensin system (RAS) regulates blood volume

A

Low blood vol= juxtaglomerular cells activate prorenin & secrete renin
Renin converts angiotensinogen > angiotensin 1
Angiotensin 1> antiotensin 2 via ACE
Angiotensin 2 causes vasoconstriction which increases BP

123
Q

Describe the Histological appearance of hyperplastic arteriosclerosis

A

Narrowed lumen, onion skin appearance, thickened concentric smooth muscle cell layers and thickened duplicate basement membrane

124
Q

At what point are drugs used to treat hypertension?

A

BP>160/100mmHg

Or BP >140/90mmHg and high CVS risk

125
Q

What types of drugs are used to treat hypertension ?

A

Ace inhibitors
Ca channel blockers
Thiazide diuretics

126
Q

Define shock

A

A physiological state characterised by a significant reduction of systemic tissue perfusion (severe hypotension) resulting in decreased oxygen delivery to the tissue

127
Q

What are the cellular effects of shock?

A

Membrane ion pump dysfunction
Intracellular swelling
Leakage of intracellular contents
Inadequate pH regulation

128
Q

What are the systemic effects of shock ?

A

Alteration in serum pH (acidaemia)
Endothelial dysfunction/vascular leakage
Stimulation of inflam. And anti-inflam. Cascades
End organ damage (Ischaemia)

129
Q

What is hypovolaemic shock and what causes it ?

A

Decreased venous return to heart, decreasing cardiac output
Haemorrhagic causes: trauma ,GI bleed, ruptured aorta etc
Non-haemorrhagic: diarrhoea, vomiting, heat stroke, burns, third spacing

130
Q

Define third spacing

A

Fluid shift from vessels to cavities which do not normally contain large amounts of fluid e.g. Peritoneal cavity

131
Q

What are the different types of cardiogenic shock?

A

Myopathic (heart muscle failure)
Arrhythmia-related (abn. Electrical activity)
Mechanical (valvular defects etc)
Extra-cardiac (obstruction to blood outflow)

132
Q

What is distributive shock ?

A

Decreased systemic vascular resistance due to severe vasodilation, this is compensated for by increased cardiac output - patient appears flushed/bounding heart

133
Q

Name the 4 subtypes of distributive shock

A
  1. Septic (vasodilation due to inc. cytokines from infection)
  2. Anaphylactic (type1 hypersensitivity reaction, mast cell degranulation> vasodilation)
  3. Neurogenic (loss of sym. Vascular tone>vasodilation)
  4. Toxic shock syndrome (s. Aureus, exotoxins, cytokines> dec. SVR)
134
Q

Define cellular adaption

A

Reversible adaption in cellular: size, number, phenotype, metabolic activity and function due to changes in environment or demand

135
Q

Define hypertrophy

A

Increase in size of existing cells and functional capacity

136
Q

Define hyperplasia

A

Increase in number of cells caused by cell division

137
Q

What type of cell population is hypertrophy usually seen in ?

A

Permanent cell populations e.g. Skeletal muscle

138
Q

Which types of cell populations is hyperplasia possible in?

A

Labile and stable

139
Q

Define atrophy

A

Reduction in size of organ or tissue by decrease in cell size and number

140
Q

Define dysplasia

A

Earliest morphological manifestation of multistage process of neoplasia
Irreversible

141
Q

Define involution

A

The shrinkage of an organ in old age or when inactive e.g. Womb after childbirth

142
Q

Define agenesis

A

Imperfect development or non development of a part

143
Q

Define carcinoma-in-situ

A

Av early form of cancer with the absence of invasion into surrounding tissues
I.e. ‘Dysplastic cells proliferate in their normal habitat’
Precursor to invasive malignant
High grade dysplasia

144
Q

Squamous metaplasia in cervix is a precursor to which type of carcinoma ?

A

CIN and squamous cell carcinoma

145
Q

Endometrial hyperplasia due to increased oestrogen is a precursor to which type of carcinoma ?

A

Adenocarcinoma

146
Q

Parathyroid hyperplasia due to chronic renal failure is a precursor to which malignancy ?

A

Adenoma

147
Q

Squamous metaplasia in bronchus is a precursor to which what ?

A

Dysplasia and squamous cell carcinoma

148
Q

Squamous metaplasia in the bladder can lead to which type of carcinoma ?

A

Squamous cell carcinoma

149
Q

Glandular metaplasia of oesophagus is a precursor to which type of carcinoma ?

A

Adenocarcinoma

150
Q

What are the main components of normal skin flora ?

A 
Coagulase neg. staphylococcus (staph. Epidermis)
Staphylococcus aureus (esp. In nasal carriers)
Proprionibacterium species (esp. Proprionibacterium acnes)
151
Q

Common components are normal mouth flora?

A

Viridans/streptococci (alpha-haemolytic group)

Anaerobes

152
Q

Normal flora of the nostrils consists of ?

A

Mainly s. Aureus

Skin flora

153
Q

Normal flora of the pharynx consists of ?

A 
Streptococcus pyogenes (group a)
H. Influenzae
Strep. Pneumoniae
Neisseria meningitidis
S. Aureus
154
Q

What does the normal vaginal flora consist of post puberty ?

A

Lactobacillus spp & acidophilus
Skin flora
C albicans

155
Q

How does H. Pylori survive well in the stomach ?

A

Produces urease to convert urea into ammonia and CO2

156
Q

What is normal flora of large intestines made of ?

A

Mainly anaerobes:
Bacterioides spp, clostridium spp, bifidobacteria spp
Aerobic:
Enteric gram neg. bacteria:
E. Coli, klebsiella spp, enterbacter spp, proteus spp, citrobacter spp.

157
Q

Define histogenesis:

A

Formation of different tissues from undifferentiated cells (embryogenesis: from germ layers to specific tissues)

158
Q

Define anaplasia:

A

Loss of differentiation

159
Q

What tissue do Adenomas originate from ?

A

Glandular structures in the epithelial tissue

160
Q

What tissue do carcinomas originate from ?

A

Epithelial tissue, linings of internal organs

161
Q

Sarcomas originate from which tissues ?

A

Connective tissue

162
Q

Lymphomas and leukaemias originate from where ?

A

Lymphoid or haemopoietic organs

163
Q

Which malignancies form from germ cells ?

A

Seminoma
Choriocarcinoma
Yolk-sac carcinoma
Teratoma

164
Q

What are the characteristics of a malignant neoplasm ?

A

Rapid proliferation
Many mitotic figures
Necrotic areas due to lack of vessels
Invasive, irregular borders

165
Q

Most common way carcinomas metastasise ?

A

Via lymphatic channels

166
Q

Most common way sarcomas metastasise ?

A

Haematogenously

167
Q

Define transcoelomic metastasis

A

Spread across peritoneal cavity

168
Q

What isa papilloma ?

A

Benign tumour of surface epithelium

169
Q

What is the most common acne most aggressive malignant primary brain tumour ?

A

Glioblastoma multiforme

170
Q

What is a harmatoma ?

A

Tumour-like lesion exhibiting uncoordinated growth.

Benign, non-neoplastic, indigenous to organ of origin

171
Q

What is a choristoma?

A

Nodules of organ parenchyma in another organ

E.g. Nodules of normal pancreatic tissue in the stomach

172
Q

Aflatoxin is associated with cancer in which organ ?

A

Liver

173
Q

Name 5 ways alcohol increases risk of cancer:

A
  1. Converted into acetaldehyde- can cause DNA damage
  2. Increases levels of oestrogen and testosterone
  3. Increases uptake of carcinogenic chemicals into cells within upper GI
  4. Reduces levels of folate needed for accurate DNA replication
  5. Kills surface epithelium= unscheduled proliferation
174
Q

The parasite schistosoma haematobium is associated with cancer of which organ ?

A

Bladder

175
Q

EBV virus is associated with which malignancies ?

A 
Burkitts lymphoma (endemic/African variant)
Nasopharyngeal
176
Q

Kaposi’s sarcoma is associated with which virus ?

A

Herpes virus (8)

177
Q

Which protein is the key regulator of the cell cycle by preventing progression from G1 to S phase

A 
Rb protein (encoded by Rb gene)
-ve growth factors inhibit progression of cell cycle by activating Rb protein
178
Q

How do cancer cells achieve replication immortality?

A

Activating telomerase

179
Q

Name the 6 hallmarks of cancer:

A
  1. Self-sufficiency of growth signals
  2. Insensitivity to anti growth signals
  3. Tissue invasion and metastasis
  4. Sustained angiogenesis
  5. Evading apoptosis
180
Q

How to cancer cells increase motility for metastasis ?

A

Epithelial-mesenchymal transition:
Switch adhesion molecules: E-cadherin to N-cadherin
Secretion of pro teases to digest basement membrane

181
Q

What are the key cells linked with inflammation and cancer ?

A

Tumour-associated macrophages

182
Q

Where do carcinomas typically metastasise to first ?

A

Lymph nodes

183
Q

What route do sarcomas typically spread by?

A

Haematogenous spread

184
Q

What are bone metastases characteristic if ?

A

Breast, lung, prostate, kidney and thyroid cancers

185
Q

What type of spread is characteristic of ovarian cancer ?

A

Transcoelomic

186
Q

Two common metastases do lung cancer ?

A

Brain and adrenal

187
Q

What is the difference between stage and grade of a tumour ?

A 
Stage = how advanced I.e. As it spread, extent of spread
Grade= how aggressive I.e. Ow different does it look from tissue of origin
188
Q

In TMN staging system, what does each letter stand for, and what does it look for ?

A 
T= tumour size +/- extent of primary tumour
M= metastases - presence and extent 
N= nodes - presence and number of lymph node metastases

From Flashcardlet (22 decks)

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