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Week 2 - Pathological Mechanisms Flashcards

1
Q

What is pathology?

A

Study of disease

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2
Q

What is a disease?

A
  • Abnormality of cell/tissue structure &/or function

- Loss of homeostasis

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3
Q

What is another name for the mechanisms?

A

Pathogenesis

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4
Q

What are the 7 categories to consider in pathology?

A
  1. Broad patterns- epidemiology
  2. Causes- aetiology
  3. Pathogenesis
  4. Nature of disease
  5. Complications- sequelae
  6. Clinical presentation
  7. Clinical management
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5
Q

What are the 4 levels of magnification in pathology?

A
  1. Gross (naked-eye)
  2. Light microscopy
  3. Electron microscopy
  4. Molecular cell biology
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6
Q

What are the levels of organisation in pathology?

A

Body –> System –> Organ –> Tissue –> Cell –> Molecules

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7
Q

Describe the 3 processing in making protein?

A
  1. DNA polymerase: replication (DNA –> DNA)
  2. RNA polymerase: transcription (DNA –> RNA)
  3. Ribosome: translation (RNA –> Protein)
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8
Q

What are the 3 normal cellular processes?

A
  1. Cell proliferation
  2. Cell growth & differentiation (specialist function)
  3. Cell death
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9
Q

What are the 6 broad tissue types?

A
  1. Epithelial
  2. Connective tissue
  3. Haemato-lymphoid
  4. Neuro-glial
  5. Melanocytic
  6. Germ cell
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10
Q

What are the 3 broad tissue types for epithelia?

A
  1. Squamous
  2. Glandular
  3. Solid organs ie. liver, kidney, thyroid
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11
Q

What are the 6 broad tissue types for connective tissue?

A
  1. Fibrous
  2. Blood vessel
  3. Fat
  4. Muscle
  5. Bone
  6. Cartilage
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12
Q

What is disease a combination of?

A

The causative agent & the body’s response to it

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13
Q

Describe homeostasis in normal cells?

A
  • Achieved through normal cell biological mechanisms

- Usually sense & easily adjust to mild environmental changes

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14
Q

What are some external environmental changes (stresses)?

A
  • Physical factors
  • Chemical factors
  • Infection
  • Nutrition, etc
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15
Q

What are some internal environmental changes (stresses)?

A
  • More/less functional demand
  • Hormones/metabolic
  • Immune response, etc
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16
Q

Define cell Atrophy?

A

Smaller/fewer cells

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17
Q

Define cell hyperplasia?

A

More cells

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18
Q

Define cell hypertrophy?

A

Bigger cells

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19
Q

Define cell metaplasia?

A

Change from 1 mature differentiated cell type to another

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20
Q

Define cell dysplasia?

A

Abnormal genetic changes which may lead to cancer

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21
Q

When does cell adaptation occur?

A

If environmental change (stress) is more than can be dealt with by homeostasis, then affected cell may undergo further adaptation esp. changes in cell growth (more, less, different)

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22
Q

When may the cells undergo injury?

A

If the stress is more intense, longer-lasting or of a specific type, or if the cell is very sensitive

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23
Q

What 2 things can cells undergo if they are directly affected?

A
  1. Sub-lethal cell injury

2. Cell death

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24
Q

How does the body respond to cell injury?

A

Inflammation (acute/chronic)

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25
Q

What can happen to cells affected by injury over many years?

A

Neoplasia

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26
Q

List the cell process from normal to cell death?

A

Normal –> Cell with adaptation –> Cell with reversible injury –> Cell with irreversible injury –> Cell death

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27
Q

What does the mnemonic VITAMIN CDEF stand for in the possible categories of disease?

A

Vascular, Infective/ Inflammatory, Traumatic, Autoimmune, Metabolic, Iatrogenic/ Idiopathic, Neoplastic, Congenital, Degenerative/ Developmental, Endocrine/ Environmental & Functional

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28
Q

Describe the 4 types of physical agents which can cause disease?

A
  1. Mechanical trauma: stricture, adhesions, hernia, criminal
  2. Temperature extremes: heat or cold
  3. Ionising radiation: causes DNA damage
  4. Electric shock
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29
Q

What can chemicals/ drugs do?

A

May damage various cell organelles & processes ie. disruption of cell membranes (osmotic damage), protein production or folding

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30
Q

What are the 4 types of chemicals/drugs that can cause disease?

A
  1. Drugs e.g. chemotherapy (cytotoxic by
    definition) , paracetamol
  2. Poisons (cyanide)
  3. Environmental (insecticides)
  4. Occupational hazards (asbestos)
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31
Q

What are the 2 possible causes of hypoxia?

A
  1. Anaemia

2. Respiratory failure

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32
Q

What does hypoxia cause?

A

Disrupts oxidative respiratory processes (in mitochondria) in cell & decreases ATP

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33
Q

Define ischaemia?

A

Reduction in blood supply to tissue

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34
Q

What is ischaemia caused by?

A

Blockage of arterial supply or venous drainage e.g. atherosclerosis

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35
Q

What is ischaemia a depletion of what two things?

A

Oxygen & Nutrients (glucose)

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36
Q

Describe the immunological reaction anaphylaxis?

A

Type 1 hypersensitivity: IgE mediated

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37
Q

Describe the immunological reaction auto-immune reactions?

A
  • Type 2: antibodies directed towards antigens on cells

- Type 3: antigen-antibody complexes and their deposition

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38
Q

Describe how genetic defects can cause disease?

A
  • Abnormalities of gene structure or number (too many or too few)
  • Leads to abnormal protein or to too much or not enough protein
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39
Q

Give 2 examples of genetic defects leading to disease?

A
  1. Sickle cell anaemia: abnormal haemoglobin chain

2. Inborn error of metabolism (lack of enzyme causes build up of enzyme substrate)

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40
Q

What are the 5 questions to ask when describing pathology specimens (gross or microscopic)?

A
  1. What is the magnification (low vs. high power image)?
  2. What is the organ/tissue?
  3. And/or how & what is sampled?
  4. Normal/abnormal?
  5. If abnormal, describe (including whether it is focal or diffuse)?
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41
Q

What are the 4 questions to ask when describing pathology specimens (gross)?

A
  1. Size?
  2. Shape?
  3. Colour?
  4. Texture?
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42
Q

How you would describe microscopic pathology specimens?

A
  • If not sure, consider which tissues are present, where, & whether normal or abnormal
  • Abnormalities quantitative or qualitative
  • Go through systematically first if no obvious abnormality, to ensure nothing missed
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43
Q

Why should you establish disease diagnosis & severity?

A

Predict outcome (prognosis) & guide treatment

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44
Q

Describe inflammation?

A
  • Universal response to tissue damage

- Can be acute or chronic, continuum

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45
Q

What 3 things can inflammatory damage be caused by?

A
  1. Infection
  2. Necrosis
  3. Trauma
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46
Q

What is the purpose of inflammation?

A

Destroy or control the harmful stimulus, initiate repair & restore function

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47
Q

What 4 things does the inflammatory process also have a role in?

A
  1. Autoimmune disease
  2. Atheroma
  3. Cancer progression
  4. Treatment
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48
Q

Describe how vascular dilatation occurs?

A
  • Arterioles dilate increasing blood flow
  • Stasis of blood flow
  • Fluid passes into tissues causing swelling
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49
Q

What 3 chemical mediators are involved in vascular dilatation?

A
  1. Histamine (mast cells)
  2. Prostaglandins
  3. NO
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50
Q

What 3 chemical mediators are involved in neutrophil activation?

A
  1. C5a
  2. Leukotriene B4
  3. Bacterial products
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51
Q

Describe how neutrophil activation occurs?

A
  • Activation of neutrophils
  • Rolling, adhesion, pass between endothelial cells
  • Chemotaxis
  • Phagocytosis & bactericidal
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52
Q

What 6 chemical mediators are involved in endothelial activation?

A
  1. 5-HT
  2. Histamine
  3. C3a
  4. C5a
  5. Bradykinin
  6. Leukotriene
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53
Q

Describe how endothelial activation occurs?

A
  • Activates vascular endothelium
  • Increased cell adhesion molecules –> leakiness of endothelium
  • Plasma proteins travel into tissues including Immumoglobulins, Complement, Fibrinogen
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54
Q

What are the 3 vascular & cell changes that occur in acute inflammation?

A
  1. Vascular dilatation
  2. Neutrophil activation
  3. Endothelial activation
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55
Q

What are the 5 clinical signs of acute inflammation?

A
  1. Redness: caused by hyperaemia
  2. Swelling: caused by fluid exudate & hyperaemia
  3. Heat: caused by hyperaemia
  4. Pain: caused by release of bradykinin & PGE2
  5. Loss of function
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56
Q

What are the 3 different exudates that you get with inflammation?

A
  1. Neutrophilic (suppurative/purulent)
  2. Fibrinous
  3. Serous
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57
Q

What are 4 factors which lead to a spread of infection?

A
  1. Natural barriers
  2. Air borne
  3. Blood borne
  4. Immune factors (IgA)
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58
Q

What 3 things can result from acute inflammation?

A
  1. Resolution
  2. Healing by repair
  3. Chronic inflammation
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59
Q

What clinical sign can form in acute inflammation?

A

Abscess

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60
Q

What results in chronic inflammation?

A

Persisting tissue damage & ongoing acute inflammation or de novo

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61
Q

What are 3 cell infiltrates present in chronic inflammation?

A
  1. Lymphocytes
  2. Macrophages
  3. Plasma cells
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62
Q

What 2 things does chronic inflammation usually lead to?

A
  1. Fibrosis

2. Scarring

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63
Q

What is a subtype of chronic inflammation?

A

Granulomatous inflammation (specific histological appearance)

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64
Q

What is Granulomatous inflammation?

A

Presence of granulomas, collections of epithelioid macrophages & multinucleate giant cells

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65
Q

What are the 3 subtypes of Granulomatous inflammation?

A
  1. Necrotising
  2. Non-necrotising
  3. Foreign body granulomas
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66
Q

What are the 2 types of wound healing?

A
  1. Primary intention (simple incision, easy healing & less obvious scarring)
  2. Secondary intention (dirty, infected, gaping wound with more obvious scarring)
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67
Q

Describe granulation tissue in healing?

A

Early blood vessels which grow in the inflammed wound

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68
Q

Does a primary or secondary intention wound have more granulation tissue during healing?

A

Secondary intention has more

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69
Q

What is involved in wound healing leading to fibrous scarring?

A

Inflammatory cells & Fibrin –> Fibrous scar

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70
Q

Describe how bone heals?

A

Regeneration rather than repair, callus (has osteoblasts & osteoclasts) formation

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71
Q

Give 4 reasons why we should perform a post mortem in the 21st century?

A
  1. Confirming diagnosis/ its extent (audit of medical care)
  2. Revealing diagnosis or explaining unexplainable findings (diagnostic tool)
  3. Investigating possible failings in surgery or other medical care (monitor medical care)
  4. Medico-legal reasons (crime, violence, suicide etc)
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72
Q

Describe a Medico-legal post mortem?

A
  • At the instruction of the Procurator Fiscal (Scotland) or Coroner (England and Wales)
  • Does not require consent of the family
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73
Q

What are forensic pathologists & what do they perform?

A

Sub-speciality within pathology who perform post mortem’s required in certain circumstances e.g. homicide

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74
Q

What are the 2 types of background information needed from medical notes for post mortem examinations?

A
  1. Past medical history

2. Summary of clinical events & treatment

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75
Q

What are the 2 types of autopsy information needed for post mortem examinations?

A
  1. External examination
    - general appearances, external disease, medical treatment
  2. Internal examination
    - body cavities & systems, organs examined in turn
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76
Q

What are the 2 further investigations for post mortem examinations?

A
  1. Histology, neuropathology

2. Bacteriology, biochemistry etc.

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77
Q

Describe the external examination done during post mortem’s?

A
  • Identification of deceased by pathologist
  • Height/weight/BMI
  • Skin/hair/eye colour
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78
Q

What 3 things should you look for in an external examination during post mortem’s?

A
  1. Iatrogenic: Scars, drains, IV lines
  2. Evidence of trauma
  3. Jaundice, cyanosis, finger clubbing, oedema, lymphadenopathy
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79
Q

Describe Evisceration in post mortem’s (internal examination)?

A
  • Single incision from sternal notch to symphysis pubis to remove thoracic, abdominal & pelvic organs
  • 2nd incision around post skull to reflect the scalp, skull is opened & brain removed
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80
Q

Who usually performs a Evisceration?

A

Anatomical pathology technicians

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81
Q

What happens at the end of the post mortem examination?

A
  • Organs returned to body (minus tissue taken for microscopic assessment)
  • If no death certificate has been issued, pathologist will write a death certificate
  • Report sent to the PF, or for ‘consented/’Hospital’’ cases, to the patient’s GP & clinician
  • Body reconstructed to permit viewing
  • Body released for burial/cremation
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82
Q

Describe the layout of the medical certificate of cause of death (MCCD)?

A

1a. Disease or condition directly leading to death
1b. Due to, or as a consequence of,
1c. Due to, or as a consequence of,
1d. Due, to or as a consequence of,
2. Other significant conditions contributing to death, but not related to the disease or condition causing it

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83
Q

What are the 5 most frequently occurring principal causes of death, all ages, Scotland, 3 year period in 2012-2014?

A
  1. Malignant neoplasm of bronchus & lung
  2. Acute MI
  3. Chronic ischaemic heart disease
  4. Other chronic obstructuve pulmonary disease
  5. Unspecified dementia
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84
Q

What 2 factors would you look for during a post mortem for thrombosis & infarction (vascular pathology)?

A
  1. Thrombus in coronary artery

2. Dead (necrotic) muscle

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85
Q

What are the 2 potential outcomes for an MI?

A
  1. Sudden death from arrhythmia or acute left ventricular failure
    OR
  2. Cardiac rupture through weakened necrotic muscle
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86
Q

Where else, apart from the heart, can you encounter thrombosis & infarction?

A
  • Small bowel infarction due to superior mesenteric artery thrombosis
  • Cerebral infarct
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87
Q

What is an embolus?

A

A mass of material that can move through the vascular system & is capable of blocking the lumen

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88
Q

What 4 sites can an embolus arise from?

A
  1. Thrombus
  2. Air
  3. Fat
  4. Amniotic fluid
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89
Q

What 3 sites can a thrombus arise from?

A
  1. Leg veins
  2. Carotid arteries
  3. Inside the heart
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90
Q

What 3 sites can a thrombus embolus to?

A
  1. Lungs
  2. Brain
  3. Other tissues
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91
Q

What are the 4 reasons why a blood vessel can rupture leading to haemorrhage?

A
  1. Under high pressure
  2. Congenital weakness (due to lack of elastic fibres)
  3. Weakened by disease
  4. Eroded into
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92
Q

What is a berry aneurysm?

A

Subarachnoid haemorrhage from rupture of cerebral artery aneurysm

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93
Q

What can erode a blood vessel leading to a rupture?

A

Ulcer

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94
Q

Describe lobar pneumonia?

A
  • Spread through blood
  • Largely confined to 1 lobe
  • Lung is a grey colour (grey hepatisation)
  • Severe illness
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95
Q

Describe bronchopneumonia?

A
  • Spread through airways
  • Tends to be more generalised
  • Often develops on top of chronic lung disease
  • Often terminal event in debilitated patients
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96
Q

What is endocarditis?

A

Infection of the heart valves

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97
Q

What is pyonephrosis?

A

Pus in the collecting system of the kidneys

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98
Q

Describe Meningococcus infection?

A
  • Inhaling droplets from carrier
  • Often previously healthy individual
  • Often rapid illness (< 24hrs)
  • Can occur in close communities
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99
Q

Describe pneumococcus infection?

A
  • Usually from infection in the lungs
  • More common in debilitated people
    e. g. alcoholics
  • Less rapid illness
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100
Q

Describe the post mortem appearance of peritonitis?

A
  • Purulent exudate
  • Reddening
  • Purulent fluid (pus)
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101
Q

Give 2 examples of chronic inflammation & what caused them?

A
  • Pulmonary fibrosis (from asbestos)

- Liver cirrhosis (from alcohol)

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102
Q

Describe Alzheimers disease?

A
  • Degenerative disease

- Atrophy more pronounced in the frontal & parietal lobes

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103
Q

What are the 3 normal reactions to vessel injury?

A
  1. Vasoconstriction
  2. Platelet release & aggregation
  3. Coagulation cascade
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104
Q

What does vasoconstriction result in?

A

Primary haemostatic plug –> Stable haemostatic plug

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105
Q

What does the coagulation cascade result in?

A

Thrombin –> Fibrin –> Stable haemostatic plug

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106
Q

What is the function of von Willebrand factor in primary homeostasis?

A

Binding to other proteins, in particular factor VIII & is important in platelet adhesion to wound sites

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107
Q

What is the coagulation pathway triggered by?

A

Tissue factor (TF)/factor VIIa complex

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108
Q

What does tissue factor (TF)/factor VIIa complex activate in the coagulation pathway?

A

Factor IX & Factor X

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109
Q

What does activated factor IX do in the coagulation pathway?

A

Coverts small amounts of prothrombin to thrombin which amplifies coagulation by activating factors V & VIII, platelets & platelet-bound factor XI

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110
Q

When is the coagulation pathway propagated?

A

Factor IXa binds to factor VIIIa on the surface of activated platelets, forming intrinsic tenase

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111
Q

What does intrinsic tenase activate in the coagulation pathway?

A

Factor X

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112
Q

What does activated factor X do in the coagulation pathway?

A

Binds to activated factor V to form prothrombinase, which converts prothrombin (Factor II) to thrombin (Factor IIa)

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113
Q

What happens in the final step of the coagulation pathway?

A

Thrombin converts fibrinogen to fibrin

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114
Q

In Virchow’s Triad what are the 3 broad factors that are thought to contribute to thrombosis?

A
  1. Hypercoagulable state
  2. Vascular wall injury
  3. Circulatory stasis
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115
Q

List 8 factors that could cause the hypercoagulable state in Virchow’s Triad?

A
  1. Malignancy
  2. Pregnancy
  3. Oestrogen therapy
  4. Trauma/surgery of lower extremity, hip, abdomen or pelvis
  5. IBD
  6. Nephrotic syndrome
  7. Sepsis
  8. Thrombophilia
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116
Q

List 6 factors that could cause vascular wall injury in Virchow’s triad?

A
  1. Trauma/surgery
  2. Venepuncture
  3. Chemical irritation
  4. Heart valve disease/ replacement
  5. Atherosclerosis
  6. Indwelling catheters
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117
Q

List 5 factors that could cause circulatory stasis in Virchow’s triad?

A
  1. AF
  2. Left ventricular dysfunction
  3. Immobility/paralysis
  4. Venous insufficiency/ varicose veins
  5. Venous obstruction from tumour, obesity or pregnancy
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118
Q

Describe the histopathology of arterial thrombosis?

A
  • “White thrombus”
  • Many platelets, small amounts of fibrin
  • High flow rate
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119
Q

Describe the histopathology of venous thrombosis?

A
  • “Red thrombus”
  • Many fibrin with trapped red cell
  • Slow/stagnant flow rate
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120
Q

What can be the 4 categories for differential diagnosis of a sore leg?

A
  1. Trauma
  2. Non-traumatic
  3. Vascular
  4. Skin/soft tissue infection
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121
Q

List the trauma causes of a sore leg?

A
  • Fractures
  • Dislocations
  • Muscle strain/rupture
  • Haematoma
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122
Q

List the Non-traumatic causes of a sore leg?

A
  • MSK
  • Osteoarthritis
  • Rheumatoid arthritis
  • Septic arthritis
  • Gout
  • Popliteal cyst
  • Bursitis
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123
Q

List the skin/soft tissue causes of a sore leg?

A
  • Cellulitis
  • Abscesses
  • Necrotizing fasciitis
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124
Q

List the vascular causes of a sore leg?

A
  • Venous occlusion: DVT, superficial vein thrombosis, venous insufficiency
  • Acute ischaemia: cardiac thromboembolism, peripheral arterial disease, massive DVT
  • Lymphoedema
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125
Q

List 5 causes of systemic oedema leading to bilateral leg swelling?

A
  1. Heart failure
  2. Cirrhosis
  3. Nephrotic syndrome
  4. Malnutrition
  5. Immobility
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126
Q

Describe deep vein thrombosis (DVT)?

A
  • Thrombosis in deep venous system

- Most commonly of leg

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127
Q

What is the origin of the popliteal vein?

A

Junction of the anterior tibial vein & posterior tibial vein

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128
Q

What do the superficial femoral vein & deep femoral vein join to form?

A

Common femoral vein

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129
Q

What does the common femoral vein become as it passes upwards above the groin?

A

External iliac vein

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130
Q

What is the % per-person lifetime incidence of vein thromboembolism?

A

~5%

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131
Q

Describe the 3 risk factors for DVT’s?

A
  1. VESSEL WALL: increased age, varicose veins, surgery
  2. BLOOD FLOW: obesity, pregnancy, immobilisation, IV catheters, external vein compression
  3. COMPOSITION OF BLOOD: thrombophilias, inflammatory conditions, oestrogen hormones
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132
Q

What is the likelihood of developing a vein thromboembolism in the 1st 6 weeks after surgery?

A

70x more likely

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133
Q

What 3 things help us confirm/exclude the diagnosis of DVT?

A
  1. CLINICAL DECISION RULE: determine likelihood
  2. BLOOD TESTS: fibrin D-dimer
  3. IMAGE VENOUS SYSTEM OF LEG: compression ultrasound, venography
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134
Q

What is a D-dimer?

A

Test to measure the amount of dissolved thrombus (fibrinogen degradation products)

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135
Q

What is the scoring system called to measure how likely a person is of developing a DVT in A&E?

A

Well’s Clinical Scoring System

  • DVT unlikely if <2
  • DVT possible if score >2
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136
Q

Describe the coagulation cascade?

A

Fibrinogen –> Fibrin Clot –> Fibrinogen degradation product

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137
Q

What changes fibrinogen –> Fibrin clot in the coagulation cascade?

A

Thrombin

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138
Q

What changes the fibrin clot –> Fibrinogen degradation product’s in the coagulation cascade?

A

Plasmin

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139
Q

What is the diagnosis if the wells clinical score is <2 and the D-dimer test comes back negative?

A
  • DVT very unlikely (<0.5%)
  • Consider other diagnoses
  • Issue patient information sheet
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140
Q

What is the diagnosis if the wells clinical score is <2 but the D-dimer test comes back positive?

A

Treat as DVT until confirmed or excluded by ultrasound

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141
Q

What is the diagnosis if the wells clinical score is >2 & the D-dimer test comes back either negative/positive?

A

Treat as DVT until confirmed or excluded by ultrasound

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142
Q

What are the 5 possible outcomes following a DVT?

A
  1. Painful swollen leg
  2. PE
  3. Recurrent vein thromboembolism
  4. Venous insufficiency
  5. Post thrombotic syndrome
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143
Q

At what % does compression stockings for 2 years reduce your risk of post thrombotic syndrome in DVT cases?

A

50%

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144
Q

What are the 5 possible outcomes following a PE?

A
  1. Dyspneoa, chest pain, haemoptysis
  2. Collapse (massive PE)
  3. Death (fatal PE)
  4. Recurrent venous thromboembolism
  5. Chronic thromboembolic pulmonary hypertension
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145
Q

What is the likelihood of having a recurrent PE?

A

4-fold more likely

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146
Q

What is a paradoxical embolism?

A

Embolus which is carried from the venous side of circulation to the arterial side, or vice versa (RARE)

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147
Q

What are the 4 possible means of treatment for a DVT?

A
  1. Prevent thrombus extending or embolising
  2. Remove risk factors
  3. Pain relief
  4. Graduated elastic compression stockings
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148
Q

What are the 3 preventative treatments for a DVT?

A
  1. Heparin (LMWH)
  2. Warfarin
  3. Direct Oral Anti-coagulant (direct Xa or IIa inhibitor)
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149
Q

What is the target INR for people on warfarin preventatively for DVTs?

A

2.5

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150
Q

How long would you give anticoagulation medication to prevent DVTs?

A

3-6months

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151
Q

What are the 3 oral anticoagulant agents?

A
  1. Warfarin
  2. Xa inhibitors
  3. IIa inhibitors
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152
Q

List 3 Xa inhibitor drugs?

A
  1. Rivaroxaban
  2. Apixaban
  3. Edoxaban
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153
Q

Give an example of a IIa inhibitor drug?

A

Dabigatran

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154
Q

What are the 2 parenteral anticoagulant drugs?

A
  1. Indirect Xa inhibitor

2. Indirect IIa inhibitor

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155
Q

Give 2 examples of Indirect Xa inhibitor drugs?

A
  1. Fondaparinux

2. Danaparoid

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156
Q

What are 3 ways to prevent venous thromboembolisms?

A
  1. Avoid risk factors
  2. Risk assess at hospital admission or surgery
  3. Provide thrombo-prophylaxis when appropriate
  4. Educate patients on risks & avoidance measures (early mobilisation)
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157
Q

What are the 5 key questions to ask regarding pain?

A
  1. Character (crushing, sharp, throbbing, dull, tight, colic-like, pleuritic)
  2. Location & Radiation (to left arm or jaw, through to back)
  3. Duration
  4. Precipitating & Relieving factors
  5. Associated features (N&V)
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158
Q

List 3 musculoskeletal causes of chest pain?

A
  1. Rib fracture
  2. Muscular
  3. Chondritis
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159
Q

List 2 cardiac causes of chest pain?

A
  1. Angina

2. MI

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160
Q

List 3 lung causes of pleuritic chest pain?

A
  1. Infection
  2. Infarction
  3. Malignant
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161
Q

List 2 vascular causes of chest pain?

A
  1. Pulmonary embolism

2. Aortic dissection

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162
Q

List 2 oesophageal causes of chest pain?

A
  1. Acid reflux (GORD)

2. Hiatus hernia

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163
Q

Describe the 6 stage pathogenesis of coronary artery disease (Atheromatous arterio-vascular disease)?

A
  1. Development of atheroma/plaques
  2. Progressive narrowing & stenosis of artery
  3. Plaque rupture
  4. Acute thrombus
  5. Vascular occlusion
  6. Downstream ischaemia & infarction
164
Q

Describe the 5 stage progression of atherosclerosis in high flow arteries?

A
  1. Monocyte adhered to epithelium
  2. Monocyte migrating into intima
  3. Monocyte becoming intimal macrophage
  4. Macrophage foam cell
  5. Dying macrophage with apoptotic bodies
165
Q

List 6 stages of the atherosclerosis timeline?

A
  1. Foam cells
  2. Fatty streak
  3. Intermediate lesion
  4. Atheroma
  5. Fibrous plaque
  6. Complicated lesion/rupture
166
Q

What are the 5 coronary arteries?

A
  1. Aorta
  2. Right coronary artery
  3. Left coronary artery
  4. Left anterior descending coronary artery
  5. Circumflex coronary artery
167
Q

List 6 risk factors for arteriosclerotic Cardiovascular Disease?

A
  1. Smoking
  2. Hypertension
  3. Hyperlipdiaemia
  4. Diabetes
  5. Obesity
  6. Family history
168
Q

What are 5 ways to diagnose MI/ Acute coronary syndrome?

A
  1. History
  2. Clinical evidence of cardiac dysfunction
  3. ECG
  4. Biochemical evidence of damage (elevated troponin)
  5. Visualisation of coronary arteries (cardiac catheterisation)
169
Q

What are the 4 possible ways to treat acute coronary syndrome?

A
  1. Prevent thrombus extension
  2. Remove the thrombus
  3. Widen the stenotic plaque
  4. Prevent further thrombus
170
Q

What are 2 ways that you can prevent thrombus extension in ACS treatment?

A
  1. Anti-platelet agent (aspirin, clopidogrel)

2. Anticoagulant (heparin)

171
Q

What are 2 ways that you can remove the thrombus in ACS treatment?

A
  1. Thrombolysis (alteplase, tenecteplase)

2. Remove clot via catheter (percutaneous coronary intervention)

172
Q

What are 2 ways that you can widen the stenotic plaque in ACS treatment?

A
  1. Balloon angioplasty

2. Insert coronary artery stent

173
Q

What are the 2 ways that you can prevent further thrombus in ACS treatment?

A
  1. Anti-platelet agent

2. Statin

174
Q

How old does a myocardial infarct have to be to be seen by the naked eye?

A

At least a day old

175
Q

When can the 1st microscopic changes be seen in myocardial infarction?

A

Around 12hrs

176
Q

What does a myocardial infarction look like after ~48hrs?

A
  • Yellow

- Soft tissue

177
Q

What does a myocardial infarction look like after ~3 days?

A
  • Haemorrhage (red) then forms yellow necrotic area

- Very soft tissue

178
Q

Describe an old myocardial infarct?

A
  • Fibrous band of tissue
  • Will not function as well
  • ~6-8 weeks after MI
179
Q

What are the 7 complications following an MI?

A
  1. Death
  2. Arrythmia
  3. Pericarditis
  4. Myocardial rupture
  5. Mitral valve prolapse
  6. Left ventricular aneurysm +/- thrombus
  7. Heart Failure
180
Q

What are the 2 possible musculoskeletal causes of limb weakness?

A
  1. Myopathy

2. Arthropathy

181
Q

What are the 3 possible neurological causes of limb weakness?

A
  1. Peripheral neuropathy
  2. Spinal lesion
  3. Cerebral lesion
    (ischaemia, inflammation, malignancy)
182
Q

How do you investigate a suspected stroke patient?

A

CT scan of brain

183
Q

What are 3 common sites for an emboli?

A
  1. Atheromatous carotid artery
  2. Left atrial thrombus
  3. Left ventricular mural thrombus
184
Q

What is the absolute stroke risk for people with AF?

A

5% per year

185
Q

What are the 2 types of AF?

A
  1. Non valvular atrial fibrillation [NVAF]

2. Valvular atrial fibrillation

186
Q

What are the 3 ways to treat stroke and AF?

A
  1. Remove thrombus (rarely)
  2. Remove/correct source of thrombus
  3. Address other CVD risk factors
187
Q

What are 2 ways to remove thrombus in the treatment of stroke & AF?

A
  1. Thrombolysis

2. Carotid end-arterectomy

188
Q

What are the 3 ways to remove / correct source of thrombus in the treatment of stroke & AF?

A
  1. Anticoagulation (warfarin or Direct Oral AntiCoagulant)
  2. Revert to sinus rhythm (cardioversion)
  3. Replace defective heart valve
189
Q

What are 2 other CVD risk factors that can be addressed in the treatment of stroke & AF?

A
  1. High blood pressure

2. Hyperlipidaemia

190
Q

What do atheroma look like in post-mortems?

A

Yellow plaques attached to interior of vessel wall

191
Q

What does a recent cerebral infarct look like?

192
Q

What does a cardiac abscess look like macroscopically?

A

Green area

193
Q

What is margination of leucocytes?

A

Free-flowing leukocytes exit the central blood stream & initiate leukocyte & endothelial cell interactions by close mechanical contact

194
Q

Describe Vasodilatation during acute inflammation?

A
  • Increased flow
  • Allows mediators in
  • Due to Nitric oxide & histamine
195
Q

Describe increased vascular permeability in acute inflammation?

A
  • Endothelial contraction
  • Mediated by bradykinin, histamine & substance P
  • Quick & transient
196
Q

What does exudate fluid do during acute inflammation?

A

Takes cells & mediators to the site of injury

197
Q

What is exudate rich in?

198
Q

Describe the vascular changes which occur in acute inflammation?

A

Chemotaxis –> Margination –> Rolling –> Adhesion –> Migration

199
Q

What are the inflammatory chemicals adhered to?

200
Q

What migrates during the vascular changes of acute inflammation?

201
Q

What 4 inflammatory markers are attracted during chemotaxis in acute inflammation?

A
  1. Neutrophils
  2. Bacterial products
  3. Complement
  4. Chemokines
202
Q

What are the 5 cellular derived (intracellular granules or synthesised) chemical mediators in inflammation?

A
  1. Vasoactive amines (histamine & serotonin)
  2. Arachidonic acid metabolites (prostaglandins)
  3. Nitric oxide
  4. Cytokines (TNF, IL-1 – acute phase response)
  5. Interferons (macrophages)
203
Q

What are the 2 functions of nitric oxide in inflammation?

A
  1. Inhibits platelet aggregation

2. Blocks mast cell degranulation

204
Q

What are the 2 plasma protein derived (secreted from liver in inactive state) chemical mediators in inflammation?

A
  1. Complement (opsonisation/membrane attack complex)

2. Coagulation & Kinin Systems

205
Q

What are the 5 other chemical mediators in inflammation?

A
  1. Cascades
  2. G-coupled protein receptors to bacterial products
  3. Opsonisation
  4. Phagocytosis
  5. Termination
206
Q

What do toll-like receptors do?

A

Bind bacterial & viral components & then cause further chemical stimulation

207
Q

Describe the 3 factors in inflammation termination?

A
  1. Short-lived mediators
  2. Anti-inflammatory cytokines
  3. Neural impulses
208
Q

How can a local infection spread?

A
  • Remain at initial site
  • Spread to local lymph nodes via draining lymphatics
  • Five cardinal signs!
209
Q

What 2 ways can a systemic infection spread?

A
  1. Haematogenous: spread through blood/lymph to cause SIRS

2. Track through tissue to form abscess/infection elsewhere ie. psoas abscess

210
Q

What is the spreading of infection controlled by?

A

How virulent the organism is, the host condition i.e. immunosuppression, low protein levels, poor vascular supply & treatment given

211
Q

List the factors testing in the NHS Sepsis screening tool?

A
  • Is infection known/ suspected?
  • Resp rate >20 bpm
  • Heart rate > 90 bpm
  • Temp <36oC or >38oC
  • WCC <4x109/l or >12x109/l
  • Altered mental state?
  • Glucose >7.7mmol/L
212
Q

What are the 3 outcomes of acute inflammation?

A
  1. Resolution (complete restoration or tissue to normal)
  2. Healing by fibrosis
  3. Progression to chronic inflammation
213
Q

List what 4 factors can result in the resolution of acute inflammation?

A
  1. Minimal tissue damage
  2. Occurs in tissue with regenerative capacity i.e. skin
  3. If cause is rapidly removed or destroyed
  4. Good vascular drainage
214
Q

List what 3 factors can result in acute inflammation healing by fibrosis?

A
  1. After substantial tissue damage
  2. Tissue incapable of regeneration
  3. Abundant fibrin exudate
215
Q

List what 2 factors can result in acute inflammation progressing to chronic inflammation?

A
  1. Persistent stimulus

2. Tissue destruction leading to ongoing inflammation

216
Q

What are 3 possible causes of an inflammatory infiltrate rich in eosinophils?

A
  1. Parasitic infection
  2. Drug reactions
  3. Allergy
217
Q

Describe what excess production of eosinophils causes in hypereosinophilia syndrome?

A
  • Drive inflammatory process within the myocardium which damages the myocytes in subendocardial distribution
  • Fibrosis ensues
218
Q

What does hypereosinophilia syndrome present with clinically?

A

Restrictive cardiomyopathy

219
Q

What can neutrophil polymorphs be due to?

A

Tissue damage leading to ischaemia

220
Q

What are the 5 beneficial effects of acute inflammation?

A
  1. Dilution of toxins by oedema fluid
  2. Increased entry of antibodies & drug transport
  3. Fibrin traps micro-organisms
  4. Delivery of nutrients
  5. Stimulation of immune response
221
Q

What are the 3 detrimental effects of acute inflammation?

A
  1. Digestion of normal tissues
  2. Swelling e.g. epiglottitis
  3. Inappropriate response e.g. type I hypersensitivity response
222
Q

What could the diagnosis be for someone with moderate erythema & granularity in the distal large bowel during a colonoscopy?

223
Q

How can we define chronic inflammation?

A
  • Persistent & lacks resolution when inflamed tissue is unable to overcome the effects of the injurious agent
  • Persists for weeks, months, or years
224
Q

What is chronic inflammation characterised by?

A

Infiltrates of lymphocytes, plasma cells & macrophages

225
Q

What is the histological difference between Crohn’s disease & Ulcerative colitis?

A
  • CROHNS: granulomas

- UC: architectural changes

226
Q

What are the 2 predominant cell types in granulomatous inflammation?

A
  1. Activated macrophages with a modified appearance (epithelioid macrophages)
  2. Giant cells (formed from fused epithelioid macrophages)
227
Q

What disease is so-called caseous necrosis characteristic of?

A

Tuberculosis

228
Q

What is the formation of granulomas a manifestation of?

A

T cell mediated immune reaction (delayed hypersensitivity reaction)

229
Q

What results in macrophage activation during an inflammatory response?

A

Antigen is presented to CD4+ T cells which in turn produce IFN gamma & other cytokines

230
Q

What are the 5 important factors to consider in the clinical history of a patient with oral ulceration?

A
  1. Drugs
  2. Trauma
  3. Viral infection
  4. Connective tissue disorder
  5. Immunosuppression
231
Q

What is syphilis caused by?

A

Treponema pallidum

232
Q

What is predominant histologically in syphilis?

A

Plasma cell rich infiltrate

233
Q

What is the acute response to syphilis driven by?

A

Neutrophils, complement & IgG, IgA, IgM immune complexes (derived from plasma cells)

234
Q

What 2 immune cells are important in chronic disease?

A
  1. CD4+ T cells

2. Macrophages

235
Q

What is the response to syphilis if CD4+ T cells are low (HIV)?

A

Relatively poor response

236
Q

Describe the histological appearance of oesophageal candidiasis?

A
  • Exudate
  • Ulceration
  • Plasma cell infiltrate
  • Inflammatory debris on surface
  • Neutrophil polymorphs in keratin layer
237
Q

What are pleomorphic cells?

A

Cells with variation in their size

238
Q

Describe how tumours can evolve in the presence of Epstein-Barr virus (EBV) infection?

A
  • Inflammatory cells recruited in response to EBV infection
  • Ligands on the tumour cells (PDL1) allow them to evade this inflammatory response
  • CD8+ T cells bind to the tumour cells via ligand & negatively regulates their activation & proliferation
239
Q

Why is there an increase in histamine during anaphylaxis?

A

Because its being released by mast cells

240
Q

What is Systemic mastocytosis?

A

Mast cells accumulate in internal tissues & organs which release histamine and cause symptoms of rash & itch

241
Q

What happens when mast cells infiltrate the bone marrow, spleen, liver & lymph nodes?

A

Lead to suppression of the normal functions of these organs

242
Q

What can Systemic mastocytosis be caused by?

A

Mutation in CD117

243
Q

What can Systemic mastocytosis be treated with?

A

Imatininb (CD117 inhibitor)

244
Q

List 7 potential causes of cell injury?

A
  1. Physical agents
  2. Chemicals/drugs
  3. Infections
  4. Hypoxia/ischaemia
  5. Immunological reactions
  6. Nutritional imbalance
  7. Genetic disease
245
Q

Cell injury may be ______ or ______?

A
  • Reversible

- Irreversible

246
Q

Describe reversible causes of cell injury?

A
  • Changes due to stress in environment

- Return to normal once stimulus removed

247
Q

Describe irreversible causes of cell injury?

A
  • Permanent

- Cell death, usually necrosis, follows

248
Q

What 3 factors does the threshold between reversible & irreversible cell injury depend on?

A
  1. Type
  2. Duration
  3. Severity of injury
249
Q

What can damage to the mitochondria cause?

A

Disrupted aerobic respiration/ATP synthesis

250
Q

What can damage to the cell membrane cause?

A

Disrupted ion concentrations esp. increased calcium ions

251
Q

What can damage to the cytoplasm (including ribosomes) cause?

A

Disrupted enzyme & structural protein synthesis & architecture

252
Q

What can damage to the nucleus cause?

A

Disrupted DNA maintenance & DNA damage

253
Q

What is oxidative stress caused by?

A

Reactive oxygen species (free radicals)

254
Q

Describe the 2 ways in which oxidative stress can occur?

A
  1. Normally formed in small amounts as a by- product of respiration
  2. Formed pathologically by absorption of radiation, toxic chemicals, hypoxia etc
255
Q

What makes oxidative stress more damaging?

A

Lack of antioxidants

256
Q

List the 5 different types of reversible (less severe) cell injury?

A
  1. “Cloudy swelling”
  2. Cytoplasmic blebs
  3. Disrupted microvilli
  4. Swollen mitochondria
  5. “Fatty change”
257
Q

Describe the reversible “Cloudy swelling” type of cell injury?

A

Osmotic disturbance, loss of energy-dependent Na pump leads to Na influx & build up of intracellular metabolites

258
Q

Describe the reversible “Fatty change” type of cell injury?

A

Accumulation of lipid vacuoles in cytoplasm caused by disruption of fatty acid metabolism, especially in liver

259
Q

List the 5 difference types of irreversible cell injury?

A
  1. Swelling of endoplasmic reticulum & loss of ribosomes
  2. Lysosome rupture
  3. Membrane blebs
  4. Swelling of mitochondria
  5. Nuclear condensation
260
Q

Describe the 2 different forms of cell death?

A
  1. NECROSIS which is uncontrolled & due to external stimuli (always pathological)
  2. APOPTOSIS which is “programmed” & controlled (usually physiological, can be pathological)
261
Q

What is the main difference between necrosis and apoptosis?

A

Whether cell contents leak out or not

262
Q

Give an example of necrosis?

A

Infarction (loss of blood supply)

263
Q

Describe the histological changes during necrosis?

A
  • Cell swelling, vacuolation & disruption of membranes of cell & its organelles including mitochondria, lysosomes & ER
  • Release of cell contents including enzymes –> adjacent damage & acute inflammation
  • DNA disruption & hydrolysis
264
Q

What is Karyolysis?

A
  • Nuclear fading

- Chromatin dissolution due to action of DNAases & RNAases

265
Q

What is Pyknosis?

A
  • Nuclear shrinkage

- DNA condenses into shrunken basophilic mass

266
Q

What is Karyorrhexis?

A

Pyknotic nuclei membrane ruptures & nucleus undergoes fragmentation

267
Q

Describe early necrosis morphology under the microscope?

A
  • Nuclei are papers & more ill-defined
  • Cytoplasm looks bigger & paler
  • Immune cells are present
268
Q

Describe late necrosis morphology under the microscope?

A
  • No structure

- Wasted away tissue

269
Q

Describe coagulative necrosis?

A

Firm, tissue outline retained

270
Q

What are the 2 types of coagulative necrosis?

A
  1. Haemorrhagic: due to blockage of venous drainage

2. Gangrenous: larger area especially lower leg

271
Q

Describe Colliquitive necrosis?

A

Tissue becomes liquid & its structure is lost

e.g. infective abscess, cerebral infarct

272
Q

Describe Caseous necrosis?

A
  • Combination of coagulative & colliquitive, appearing “cheese-like”
  • Classical for granulomatous inflammation, esp TB
273
Q

Describe fat necrosis?

A

Due to action of lipases on fatty tissue

274
Q

What are the 4 different types of necrosis?

A
  1. Coagulative
  2. Colliquitive
  3. Caseous
  4. Fat
275
Q

What are the 2 types of effects of necrosis?

A
  1. Functional (depends on the tissue/organ)

2. Inflammation (release of cell contents activates inflammation & causes damage)

276
Q

Describe the 2 types of inflammatory effects that necrosis has?

A
  1. ACUTE with removal of stimulus & then healing and repair
  2. CHRONIC with persistence of stimulus & chronic inflammation
277
Q

What does apoptosis require?

A

Energy & distinct pathways involved

278
Q

What does apoptosis NOT cause?

A

Inflammation but may be caused by immunological mechanisms

279
Q

List the 5 different types of apoptosis physiological aetiologies?

A
  1. Embryogenesis
  2. Hormone dependent involution
  3. Cell deletion in proliferating cell populations to maintain constant cell number (epithelium)
  4. Deletion of inflammatory cells after inflammatory response
  5. Deletion of self-reactive lymphocytes in thymus
280
Q

List the 3 different types of apoptosis pathological aetiologies?

A
  1. Viral infection (cytotoxic T-lymphocytes)
  2. DNA damage
  3. Hypoxia/ischaemia
281
Q

Describe the morphology of apoptosis?

A
  • Cell shrinkage
  • Chromatin condensation (unlike
    necrosis)
  • Membranes of cell & mitochondria remain intact (unlike necrosis)
  • Cytoplasmic blebs form & break off to form apoptotic bodies which are phagocytosed by macrophages
282
Q

What is Chromatin condensation?

A

Packaging up of nucleus

283
Q

What is the pathway of necrosis?

A

Normal –> Reversible swelling –> Irreversible swelling –> Disintegration

284
Q

What is the pathways of apoptosis?

A

Normal –> Condensation (cell blebbing) –> Fragmentation –> Secondary necrosis

285
Q

Define depositions?

A

Abnormal accumulation of substances

286
Q

What are the 3 potential locations for depositions?

A
  1. Intracellular
  2. Extracellular
  3. Connective tissue
287
Q

What are the 2 different compositions of depositions?

A
  1. Normal endogenous substances

2. Exogenous (foreign) material

288
Q

What are 2 normal endogenous substances?

A
  1. Normal products of metabolism, including protein, lipid, & carbohydrate
  2. Pigments (some deposits are both product & pigment)
289
Q

What are 2 Exogenous (foreign) materials?

A
  1. Pigments

2. Industrial material

290
Q

What are 5 examples of intracellular endogenous depositions?

A
  1. Melanin
  2. Haemosiderin
  3. Bile
  4. Lipid, including cholesterol
  5. “Storage diseases” especially in liver e.g. alpha-1-antitrypsin
291
Q

What are 3 examples of extracellular endogenous depositions?

A
  1. Amyloid
  2. Fibrosis
  3. Calcium
292
Q

What are 3 examples of intracellular exogenous depositions?

A
  1. Tattoo pigment
  2. Carbon (anthracosis)
  3. Asbestos
293
Q

Describe the nature of amyloid endogenous depositions?

A

Organisation (abnormal folding) of soluble protein fibrils into specific abnormal, insoluble aggregates

294
Q

What does amyloid depositions resemble on morphology?

A

Fibrosis but without prior inflammation

295
Q

What can amyloid depositions be stained by & how does it appear?

A

Congo Red: fibrils have a specific structure which the stain intercalates & shows pink

296
Q

How does the congo red stain of amyloid appear under polarised light?

A

“Apple- green birefringence”

297
Q

What are the 2 forms of amyloid accumulation?

A
  1. Systemic: widespread

2. Localised: one place

298
Q

What are 3 ways that amyloid can occur?

A
  1. Excessive production/ accumulation of a normal
    protein
  2. Production/accumulation of an abnormal protein
  3. Tendency of protein to misfold (i.e. abnormal)
299
Q

What is amyloid deposition an example of?

A

Accumulation of abnormal protein (alzheimer’s, genetic variants)

300
Q

What is AL amyloid?

A

Immunoglobulin light chain

- Produced in B-cell neoplasms e.g. multiple myeloma

301
Q

What is AA amyloid?

A

Serum amyloid associated protein (anormal

acute phase protein)

302
Q

Where is AA amyloid produced?

A
  • In liver

- In prolonged chronic inflammation e.g. rheumatoid arthritis

303
Q

Give 3 examples of the clinical effects of amyloid on specific organs (kidney, heart, brain)?

A
  1. Kidney: renal impairment or failure
  2. Heart: heart failure
  3. Brain: dementia
304
Q

What is amyloid important in?

A

Systemic pathology especially in kidney, osteo-articular system & brain

305
Q

Give an example of an acute sub-lethal cell injury (deposition)?

A

Steatosis in liver caused by alcohol & reversible on abstinence

306
Q

What is lipofuscin?

A
  • Brown “wear & tear” or “age” pigment in liver
  • Endogenous breakdown product
  • May also deposit in heart & other organs
307
Q

Describe the stained appearance of excess iron deposited in the liver?

A

Stained blue with Perl’s stain (“Prussian blue reaction”)

308
Q

What is excess iron in the liver called?

A

Haemosiderosis

309
Q

What 2 circumstances would Haemosiderin (iron, brown) be deposited in macrophages?

A
  1. After haemorrhage

2. Congestion of blood vessels

310
Q

Describe the appearance & location of carbon depositions in the lungs?

A

Black carbon in lines on lung serosal surface, in lymphatics

311
Q

When would carbon depositions be higher in the lungs?

A

If smoker or from a city

312
Q

What are the 2 pathological types of calcification (deposition of calcium salts)?

A
  1. Dystrophic

2. Metastatic

313
Q

Describe dystrophic calcification?

A

Deposition in abnormal tissue with normal serum calcium

314
Q

Describe metastatic calcification?

A
  • Deposition in normal, living tissue with raised serum calcium
  • Often in connective tissue of blood vessels
  • Can compromise tissue function
315
Q

What are 2 potential causes of raised serum calcium?

A
  1. Increased levels of parathyroid hormone

2. May be systemic effect with cancer

316
Q

What are the primary & secondary causes of increased levels of parathyroid hormone?

A
  • Primary: parathyroid gland tumour

- Secondary: kidney disease

317
Q

What do depositions cause?

A

Cell degeneration

318
Q

What 3 things are present in the lung hilum?

A
  1. Pulmonary arteries
  2. Pulmonary veins
  3. Main bronchi
319
Q

Describe the anatomy of the left lung?

A

Divided into 2 lobes by the oblique fissure

320
Q

Describe the anatomy of the right lung?

A

Divided into 3 lobes by the horizontal & oblique fissures

321
Q

What is the branching of trachea called?

322
Q

Describe the lung coverings?

A
  • Pleura
  • 2 layers
  • Inner layer: visceral
  • Outer layer: parietal
323
Q

How are lung fissures formed?

A

Invagination of the visceral pleura

324
Q

How much fluid may the space between visceral & parietal pleura contain?

325
Q

What does the bronchi divide further into?

A

Bronchopulmonary segments

326
Q

List the 6 important invisible/obscure structures in a chest X-ray?

A
  1. Sternum
  2. Oesophagus
  3. Spine
  4. Fissures
  5. Pleura
  6. Aorta
327
Q

Describe the location of the trachea compared to the aorta?

A

Passes to the right of the aorta so may be slightly off midline to the right

328
Q

What bronchus is more vertical?

A

Right main bronchus (aspiration)

329
Q

Describe the appearance of oblique fissures in a lateral view?

A

Overlie each other & are not always seen in their entirety

330
Q

What is another name for the accessory fissure in the lung?

A

Azygous fissure

331
Q

How common is the accessory/azygous fissure?

A

1-2% of individuals

332
Q

What is contained within the azygous fissure?

A

Azygous vein with pleura wrapped around it

333
Q

When is the pleura visible on X-ray?

A

When abnormal

334
Q

What is the costophrenic recess formed by?

A

Hemidiaphragm & the chest wall

335
Q

What does the costophrenic recess contain?

A

Rim of the lung base which lies over the diaphragm

336
Q

What is the costophrenic angle formed by?

A

Lateral chest wall & the diaphragm

337
Q

Is the right or left hemidiaphragm slightly higher than the other?

A

Right is higher

338
Q

Where is the liver located?

A

Beneath the right hemidiaphragm & the stomach bubble is seen below the left

339
Q

What makes up the right border of the heart?

A

Right atrium

340
Q

What makes up the left border of the heart?

A

Left ventricle

341
Q

What is the normal heart volume no more than?

A

60% cardio thoracic ratio

342
Q

What is the aortic knuckle?

A

The left lateral edge of the aorta as it arches backwards over the left main bronchus

343
Q

What does the aortic knuckle continue as?

A

Descending aorta

344
Q

Where does the aorto-pulmonary window lie?

A

Between the arch of aorta & the pulmonary artery

345
Q

What is the right edge of the trachea seen as?

A

Right para-tracheal stripe

346
Q

What is the right para-tracheal stripe normally less than?

347
Q

Where is a common place for lung cancer/mass/nodes?

A

Right para-tracheal stripe

348
Q

What side of the trachea is less well defined?

349
Q

What are hilar points formed by?

A

Descending upper lobe veins & the lower lobe pulmonary arteries (not always clearly visible)

350
Q

When are hilar lymph nodes visible in chest X-rays?

A

Only when enlarged

351
Q

Where can lung cancer pain occur?

A

In the shoulder

352
Q

Describe the appearance of posterior and anterior ribs on a chest X-ray?

A
  • POSTERIOR: run horizontal

- ANTERIOR: less obvious & run at an angle

353
Q

What are the 5 emergency indications for chest X-rays?

A
  1. Acute respiratory symptoms
  2. Chest pain
  3. Septic Screen
  4. Acute abdomen
  5. Post central line / chest drain insertion
354
Q

What are the elective indications for chest X-rays?

A
  1. Persistent/chronic respiratory symptoms
  2. Pre-operative work up
  3. Metastatic screen
  4. TB contacts
355
Q

What are the 4 technical factors to take into consideration when interpreting an X-ray?

A
  1. PA vs AP
  2. Rotation
  3. Inspiration
  4. Penetration
356
Q

Describe a PA X-ray?

A
  • X-rays penetrated through the back to the front of the patient
  • Standard projection
  • Heart is closer to the film & less magnified
357
Q

What are all X-rays in the PICU?

A
  • Portable

- AP view

358
Q

How do you work out the degree of inspiration from a chest X-ray?

A
  • Count the ribs
  • Highlight anterior versus posterior
  • Should be 9- 10 posterior ribs & 6 anterior ribs
359
Q

How do you tell if a patient is rotated on a chest X-ray?

A

Highlight tear drops ie spinous processes & that they are equidistant from clavicles

360
Q

What indicates good chest X-ray exposure?

A

Not being able to see the vertebra through the heart shadow

361
Q

Describe how the silhouette sign in chest X-rays are formed?

A

Normal adjacent anatomical structures of differing densities form a crisp silhouette or contour

362
Q

What does a loss of specific contour (silhouette sign) in a chest X-ray help to determine?

A

Position of the disease process

363
Q

What lobe lie adjacent to the right heart border?

A

Right lung middle lobe

364
Q

What can determine the heart size?

A

PA radiograph

365
Q

What are the 3 types of cellular pathology?

A
  1. Autopsy (post-mortem exanimation)
  2. Histopathology (tissues)
  3. Cytopathology (cells)
366
Q

What are the 2 types of specimens taken in cytology?

A
  1. Smears

2. Aspirates

367
Q

What are the 3 types of specimens taken in small tissue biopsies?

A
  1. Prostate chips
  2. Bladder chips
  3. Punch biopsies
368
Q

What is the purpose of specimens?

A

Diagnostic and/or treatment (e.g. removal of effusion, colectomy)

369
Q

Describe the types of exfoliative cytology?

A
  • Fluid cytology including effusions

- Scrape, smear & brush cytology (including cervical)

370
Q

Describe the types of fine needle aspiration cytology sample (FNA)?

A
  • Direct ie. sampling surface lumps on skin,
    head & neck, breast, lymph nodes
  • Under ultrasound (US) guidance, as above plus endoscopic ultrasound (EUS)
371
Q

What are the 3 different types of pathology specimens?

A
  1. Cytology samples
  2. Small tissue biopsies
  3. Larger tissue resections
372
Q

What are the 2 different types of cytology samples?

A
  1. Exfoliative cytology

2. Fine needle aspiration (FNA)

373
Q

What are the 3 different types of histology samples?

A
  1. Small biopsies
  2. Excision biopsy
  3. Resection
374
Q

What are the 3 different types of small biopsy histology samples?

A
  1. Mucosal
  2. Needle core
  3. Incisional ie. skin punch
375
Q

What 2 things can needle core biopsy sample (histology)?

A
  1. Diffusely abnormal organ e.g. liver

2. Focal lesion e.g. liver, breast, prostate

376
Q

What can excision biopsy sample (histology)?

A

Full skin lesion

377
Q

Give an example of a smaller histological resection?

A

Appendicectomy

378
Q

Give examples of a larger histological resection?

A

Lung, limb amputation, hysterectomy & oophorectomy, prostatectomy

379
Q

Describe how the small and large specimens are examined & described?

A
  • LARGE: gross examination & macroscopic description

- SMALL: trimmed & described by biomedical scientist then placed in cassettes

380
Q

Describe the gross examination, description & trim of larger specimens?

A
  • Includes “inking” of specimen “resection margins”
  • Orientation
  • Macroscopic description aided
    by Biomedical Scientist
381
Q

Describe tissue processing in diagnostic pathology?

A
  • From water-based formalin through graded alcohols to xylene then wax
  • Different cycles used (2hr, 4hr, 15hr, Brain & Breast)
382
Q

What does formalin do during tissue processing?

A

Fixes tissue

383
Q

What does H&E stand for?

A

Haematoxylin & Eosin

384
Q

Describe the appearance of Haematoxylin stain?

A
  • Dark blue

- Nuclei

385
Q

Describe the appearance of Eosin stain?

A
  • Pink

- Cytoplasm

386
Q

What are 3 other stains which may be required during diagnostic pathology of a specimen?

A
  1. Special stains
  2. Immunohistochemistry (IHC)
  3. Molecular test (FISH)
387
Q

What is the turnaround timescale for an urgent pathological problem?

388
Q

What is the turnaround timescale for other pathological problems?

389
Q

What is the most routine diagnostic stain?

A

Standard H&E

390
Q

Describe the 4 particular features that “special” stains are used to demonstrate?

A
  1. Mucin in epithelial cells for adenocarcinoma classification
  2. Normal elastic tissue in vessels
  3. Depositions e.g. fibrous tissue
  4. Infections e.g. bacterial, fungal
391
Q

Describe Immunohistochemistry (IHC)?

A

Staining technique which yields brown staining of specific proteins (may be cytoplasmic, membranous &/or nuclear)

392
Q

List the 4 applications of Immunohistochemistry (IHC)?

A
  1. Tumour diagnosis & classification
  2. Prediction of cancer prognosis
  3. Prediction of cancer treatment benefit e.g. ER & HER2 in breast cancer
  4. Diagnosis of infectious disease
393
Q

What are the 3 comparisons to look at in molecular pathology?

A
  1. Somatic (tumour) versus germ-line (blood)
  2. Tissue sections versus tissue extracts, for different techniques
  3. Quantitative changes versus qualitative changes
394
Q

What does FISH demonstrate?

A

Large-scale qualitative changes in DNA ie. chromosomal translocations, amplifications, deletions

395
Q

What is FISH useful for in somatic (tumour) DNA?

A

Tumour classification & prediction of treatment benefit

396
Q

What does PCR stand for?

A

Polymerase chain reaction

397
Q

What type of tissue sample can FISH technique be used on?

A

Tissue sections

398
Q

What does PCR demonstrate?

A

Large-scale quantitative changes in DNA ie. clonality in lymphoma for diagnosis and classification

399
Q

What type of tissue sample can PCR technique be used for?

A

Tissue extracts

400
Q

What does NGS stand for?

A

Next generation sequencing

401
Q

What does NGS demonstrate?

A

Small-scale qualitative or quantitative changes in DNA ie. sequence mutations including “actionable mutations”

402
Q

What type of tissue sample can NGS technique be used for?

A

Tissue extract

403
Q

What are the 5 categories for classifying breast lesions?

A
  1. Palpation
  2. Mammography
  3. Ultrasound
  4. FNA (fine needle aspiration cytology)
  5. Core biopsies
404
Q

Breast tumours which have a ____ lesion are at a worse prognosis?

A

HER2 positive

405
Q

What does ER and PR stand for in regards to breast lumps?

A
  • ER: Oestrogen receptor

- PR: Progesterone receptor

406
Q

What would be the 3 forms of treatment plan for someone with infiltrative carcinoma with ductal carcinoma & widespread infiltration of lymphovascular channels?

A
  1. Neoadjuvant systemic chemotherapy
  2. Left mastectomy with left axillary clearance
  3. Adjuvant chemotherapy +/- radiation therapy +/- Herceptin +/- endocrine therapy

MBChB Year 3 (15 decks)

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