Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MBChB Year 3 > Week 2 - Pathological Mechanisms > Flashcards

Week 2 - Pathological Mechanisms Flashcards

1
Q

What is pathology?

A

Study of disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is a disease?

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

- Loss of homeostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is another name for the mechanisms?

A

Pathogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the levels of organisation in pathology?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the 3 normal cellular processes?

A
  1. Cell proliferation
  2. Cell growth & differentiation (specialist function)
  3. Cell death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the 3 broad tissue types for epithelia?

A
  1. Squamous
  2. Glandular
  3. Solid organs ie. liver, kidney, thyroid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is disease a combination of?

A

The causative agent & the body’s response to it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe homeostasis in normal cells?

A
  • Achieved through normal cell biological mechanisms

- Usually sense & easily adjust to mild environmental changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are some external environmental changes (stresses)?

A
  • Physical factors
  • Chemical factors
  • Infection
  • Nutrition, etc
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are some internal environmental changes (stresses)?

A
  • More/less functional demand
  • Hormones/metabolic
  • Immune response, etc
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Define cell Atrophy?

A

Smaller/fewer cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Define cell hyperplasia?

A

More cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Define cell hypertrophy?

A

Bigger cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Define cell metaplasia?

A

Change from 1 mature differentiated cell type to another

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Define cell dysplasia?

A

Abnormal genetic changes which may lead to cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A
  1. Sub-lethal cell injury

2. Cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How does the body respond to cell injury?

A

Inflammation (acute/chronic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

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

A

Neoplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the 2 possible causes of hypoxia?

A
  1. Anaemia

2. Respiratory failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What does hypoxia cause?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Define ischaemia?

A

Reduction in blood supply to tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is ischaemia caused by?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is ischaemia a depletion of what two things?

A

Oxygen & Nutrients (glucose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Describe the immunological reaction anaphylaxis?

A

Type 1 hypersensitivity: IgE mediated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

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

A
  1. Size?
  2. Shape?
  3. Colour?
  4. Texture?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Why should you establish disease diagnosis & severity?

A

Predict outcome (prognosis) & guide treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Describe inflammation?

A
  • Universal response to tissue damage

- Can be acute or chronic, continuum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What 3 things can inflammatory damage be caused by?

A
  1. Infection
  2. Necrosis
  3. Trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the purpose of inflammation?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Describe how vascular dilatation occurs?

A
  • Arterioles dilate increasing blood flow
  • Stasis of blood flow
  • Fluid passes into tissues causing swelling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What 3 chemical mediators are involved in vascular dilatation?

A
  1. Histamine (mast cells)
  2. Prostaglandins
  3. NO
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What 3 chemical mediators are involved in neutrophil activation?

A
  1. C5a
  2. Leukotriene B4
  3. Bacterial products
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Describe how neutrophil activation occurs?

A
  • Activation of neutrophils
  • Rolling, adhesion, pass between endothelial cells
  • Chemotaxis
  • Phagocytosis & bactericidal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

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

A
  1. Vascular dilatation
  2. Neutrophil activation
  3. Endothelial activation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

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

A
  1. Neutrophilic (suppurative/purulent)
  2. Fibrinous
  3. Serous
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What 3 things can result from acute inflammation?

A
  1. Resolution
  2. Healing by repair
  3. Chronic inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What clinical sign can form in acute inflammation?

A

Abscess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What results in chronic inflammation?

A

Persisting tissue damage & ongoing acute inflammation or de novo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are 3 cell infiltrates present in chronic inflammation?

A
  1. Lymphocytes
  2. Macrophages
  3. Plasma cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What 2 things does chronic inflammation usually lead to?

A
  1. Fibrosis

2. Scarring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is a subtype of chronic inflammation?

A

Granulomatous inflammation (specific histological appearance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is Granulomatous inflammation?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What are the 3 subtypes of Granulomatous inflammation?

A
  1. Necrotising
  2. Non-necrotising
  3. Foreign body granulomas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Describe granulation tissue in healing?

A

Early blood vessels which grow in the inflammed wound

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

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

A

Secondary intention has more

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is involved in wound healing leading to fibrous scarring?

A

Inflammatory cells & Fibrin –> Fibrous scar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Describe how bone heals?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What are the 2 further investigations for post mortem examinations?

A
  1. Histology, neuropathology

2. Bacteriology, biochemistry etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Describe the external examination done during post mortem’s?

A
  • Identification of deceased by pathologist
  • Height/weight/BMI
  • Skin/hair/eye colour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Who usually performs a Evisceration?

A

Anatomical pathology technicians

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is an embolus?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What 4 sites can an embolus arise from?

A
  1. Thrombus
  2. Air
  3. Fat
  4. Amniotic fluid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What 3 sites can a thrombus arise from?

A
  1. Leg veins
  2. Carotid arteries
  3. Inside the heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What 3 sites can a thrombus embolus to?

A
  1. Lungs
  2. Brain
  3. Other tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What is a berry aneurysm?

A

Subarachnoid haemorrhage from rupture of cerebral artery aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What can erode a blood vessel leading to a rupture?

A

Ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Describe lobar pneumonia?

A
  • Spread through blood
  • Largely confined to 1 lobe
  • Lung is a grey colour (grey hepatisation)
  • Severe illness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What is endocarditis?

A

Infection of the heart valves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What is pyonephrosis?

A

Pus in the collecting system of the kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Describe Meningococcus infection?

A
  • Inhaling droplets from carrier
  • Often previously healthy individual
  • Often rapid illness (< 24hrs)
  • Can occur in close communities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Describe pneumococcus infection?

A
  • Usually from infection in the lungs
  • More common in debilitated people
    e. g. alcoholics
  • Less rapid illness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Describe the post mortem appearance of peritonitis?

A
  • Purulent exudate
  • Reddening
  • Purulent fluid (pus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Give 2 examples of chronic inflammation & what caused them?

A
  • Pulmonary fibrosis (from asbestos)

- Liver cirrhosis (from alcohol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Describe Alzheimers disease?

A
  • Degenerative disease

- Atrophy more pronounced in the frontal & parietal lobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What are the 3 normal reactions to vessel injury?

A
  1. Vasoconstriction
  2. Platelet release & aggregation
  3. Coagulation cascade
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What does vasoconstriction result in?

A

Primary haemostatic plug –> Stable haemostatic plug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What does the coagulation cascade result in?

A

Thrombin –> Fibrin –> Stable haemostatic plug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What is the coagulation pathway triggered by?

A

Tissue factor (TF)/factor VIIa complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

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

A

Factor IX & Factor X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

When is the coagulation pathway propagated?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What does intrinsic tenase activate in the coagulation pathway?

A

Factor X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What happens in the final step of the coagulation pathway?

A

Thrombin converts fibrinogen to fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Describe the histopathology of arterial thrombosis?

A
  • “White thrombus”
  • Many platelets, small amounts of fibrin
  • High flow rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Describe the histopathology of venous thrombosis?

A
  • “Red thrombus”
  • Many fibrin with trapped red cell
  • Slow/stagnant flow rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

List the trauma causes of a sore leg?

A
  • Fractures
  • Dislocations
  • Muscle strain/rupture
  • Haematoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

List the Non-traumatic causes of a sore leg?

A
  • MSK
  • Osteoarthritis
  • Rheumatoid arthritis
  • Septic arthritis
  • Gout
  • Popliteal cyst
  • Bursitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

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

A
  • Cellulitis
  • Abscesses
  • Necrotizing fasciitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Describe deep vein thrombosis (DVT)?

A
  • Thrombosis in deep venous system

- Most commonly of leg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What is the origin of the popliteal vein?

A

Junction of the anterior tibial vein & posterior tibial vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

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

A

Common femoral vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

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

A

External iliac vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

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

A

~5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

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

A

70x more likely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What is a D-dimer?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Describe the coagulation cascade?

A

Fibrinogen –> Fibrin Clot –> Fibrinogen degradation product

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

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

A

Thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

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

A

Plasmin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

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

A

50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

What is the likelihood of having a recurrent PE?

A

4-fold more likely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

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

A

2.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

How long would you give anticoagulation medication to prevent DVTs?

A

3-6months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

What are the 3 oral anticoagulant agents?

A
  1. Warfarin
  2. Xa inhibitors
  3. IIa inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

List 3 Xa inhibitor drugs?

A
  1. Rivaroxaban
  2. Apixaban
  3. Edoxaban
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

Give an example of a IIa inhibitor drug?

A

Dabigatran

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

What are the 2 parenteral anticoagulant drugs?

A
  1. Indirect Xa inhibitor

2. Indirect IIa inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

Give 2 examples of Indirect Xa inhibitor drugs?

A
  1. Fondaparinux

2. Danaparoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

List 3 musculoskeletal causes of chest pain?

A
  1. Rib fracture
  2. Muscular
  3. Chondritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

List 2 cardiac causes of chest pain?

A
  1. Angina

2. MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

List 3 lung causes of pleuritic chest pain?

A
  1. Infection
  2. Infarction
  3. Malignant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

List 2 vascular causes of chest pain?

A
  1. Pulmonary embolism

2. Aortic dissection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

List 2 oesophageal causes of chest pain?

A
  1. Acid reflux (GORD)

2. Hiatus hernia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

A

Red

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?

A

Proteins

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?

A

Selectins

200
Q

What migrates during the vascular changes of acute inflammation?

A

Integrins

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?

A

IBD

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?

A

Carina

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?

A

15mls

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?

A

3mm

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?

A

Left side

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?

A

<1 week

388
Q

What is the turnaround timescale for other pathological problems?

A

<4 weeks

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions