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Medicine Year 3 > Week 2 - General Pathological Mechanisms > Flashcards

Week 2 - General Pathological Mechanisms Flashcards

1
Q

List the types of exudate

A
  1. Serous - usually a transudate found in pleural, pericardial or peritoneal spaces
  2. Fibrinous exudate - fluid rich in fibrin, an exudate due to high protein content - often on serosal surface, meninges
  3. Suppurative exudate - pus forming, an exudate rich in neutrophil polymorphs (abscess)
  4. Haemorrhagic - severe vascular injury or depletion of coagulatory factors
  5. Membraneous - epithelium becomes coated in membrane formed by fibrin, epithelial cells and inflammatory cells
  6. Psuedomembraneous (ulceration) - surface exudate on mucosal/epithelial sites e.g. C diff colitis
  7. Necrotising (gangrenous) - high tissue pressure leading to vascular occlusion and thrombosis
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2
Q

List the most frequently occuring causes of death, all ages, in Scotland

A
  • Neoplastic e.g. lung and breast cancer
  • Infective e.g. pneumonia
  • Vascular e.g. myocardial infarction
  • Metabolic e.g. diabetes
  • Inflammation e.g. chronic obstructive pulmonary disease
  • Traumatic e.g. road traffic collision
  • Degenerative e.g. Alzheimer’s disease
  • Iatrogenic e.g. intra-operative death
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3
Q

How prevalent is Meckel’s diverticulum?

A

Occurs in about 2% of the population

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4
Q

What is cytology?

A
  • Study of cells
  • Advantages
    • Can’t biopsy fluids e.g. pleural effusion
    • Less invasive than tissue biopsy
  • Limitations - no tissue architecture
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5
Q

Describe the process of fracture healing

A
  • Inflammation
    • Haematoma forms at site of fracture
    • Prostaglandins recruit neutrophil polymorphs, macrophages, lymphocytes and fibroblasts to the site of injury
    • Granulation tissue, ingrowth of vessels, migration of mesenchymal cells occurs
    • Nutrients and oxygen are supplied by the exposed bone and muscle
  • Repair
    • Fibroblasts lay down stroma to support ingrowing vessels
    • Collagen matrix is laid down
    • Osteoid is secreted and mineralised leading to soft callus formation
    • Callus ossified after 4-6 weeks by forming bridge of woven bone between fracture fragments
  • Remodelling
    • Occurs slowly over months and years
    • Returns bone to its original shape, structure and mechanical strength
    • Facilitated by mechanical stress
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6
Q

Describe the internal examination performed in post-mortems

A
  1. Evisceration
  • Single incision from sternal notch to symphysis pubis - allows removal of thoracic, abdominal and pelvic organs
  • Second incision around posterior part of the skulls to reflect the scalp, skull is opened and brain removed
  • Eviscerations usually performed by APTs
  1. Organ dissection
  • Pathologist inspects each organ then carefully dissects them - MACROSCOPIC ASSESSMENT
  • Pathologist may retain small amount of tissue for MICROSCOPIC ASSESSMENT
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7
Q

Define chronic inflammation

A
  • Inflammation is a physiological response to injury, defined as chronic when -
    • It is persistent and lacks resolution when the inflamed tissue is unable to overcome the effects of the injurious agent
    • It persists for weeks, months or years
    • It is characterised by infiltrates of lymphocytes, plasma cells, and macrophages
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8
Q

Describe anaplasia and dysplasia of tumours

A
  • Anaplasia = lack of differentiation of a tumour (synonymous with undifferentiated)
  • Dysplasia = disordered growth in which cells fail to differentiate fully, but are contained by the basement membrane, i.e. non-invasive
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9
Q

What are the effects of necrosis?

A
  • Functional
    • Depends on tissue/organ
  • Inflammation
    • Release of cell contents activates inflammation and causes damage
    • Either acute with removal of stimulus and then healing and repair or chronic with persistence of stimulus and chronic inflammation
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10
Q

Describe pathological calcification

A
  • Deposition of calcium salts
  • May be
    • Dystrophic - deposition in abnormal tissue with normal serum calcium
    • Metastatic
      • Deposition in normal, living tissue with raised serum calcium
      • Often in connective tissue of blood vessels
      • Can compromise tissue function
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11
Q

What are the hilar points on a chest X-ray?

A
  • Hilar points are angles formed by the descending upper lobe veins and lower lobe pulmonary arteries
  • Not always clearly visible
  • L usually higher than R
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12
Q

List the factors which influence wound healing

A
  • Local -
    • Type, size and location of wound
    • Movement within wound
    • Infection
    • Presence of foreign/necrotic material
    • Irradiation - causes formation of many fragile BVs, collagen weak
    • Poor blood supply
  • Systemic -
    • Age
    • Nutrition (vitamin C, zinc)
    • Systemic disease (e.g. renal failure, diabetes)
    • Drugs (esp. steroids)
    • Smoking
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13
Q

How is a developmental anomaly different to congenital anomaly?

A
  • Terms often used interchangeably
  • Congenital anomalies are anomalies that exist at or before birth regardless of the cause, and may be either:
    • Functional/metabolic - how the body works (inborn errors of metabolism, haemophilia, cystic fibrosis)
    • Structural - how the body is made up physically/architecturally
  • Developmental anomaly = deformity, absence or excess body parts/tissues which occur when normal growth is disturbed
    • If growth of an organ or system is disturbed = structural anomaly
    • Therefore, developmental anomaly = structural congenital anomaly
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14
Q

Describe the pathogenesis of atherosclerosis

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

Progressive endothelial dysfunction

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15
Q

Describe the pathophysiology of coronary artery disease

A
  • Atheromatous arterio-vascular disease
    • Development of atheroma/plaques
    • Progressive narrowing and stenosis of artery
      • Plaque rupture
      • Acute thrombus
        • Vascular occlusion
        • Downstream ischaemia and infarction
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16
Q

How is a post-mortem examination carried out?

A
  1. Background information
  • From medical notes
  • Past medical history
  • Summary of clinical events and treatments
  1. Autopsy
  • External examination
    • General appearances, external disease etc.
    • Medical treatment e.g. drains
  • Internal examinations
    • Body cavities and systems
    • Organs examined in turn
  1. Further examination
  • Samples taken
    • Histology, neuropathology
    • Bacteriology, biochemistry etc.
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17
Q

What is diverticulum?

A
  • Circumscribed pouch/sac caused by herniation of lining mucosa of an organ through defect in muscular coat
  • Classic examples are Meckel’s diverticulum and sigmoid colon diverticula/diverticular disease
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18
Q

How is ACS treated?

A
  • Prevent thrombus extension
    • Anti-platelet agent - aspirin, clopidogrel
    • Anticoagulant - heparin
  • Remove the thrombus
    • Thrombolysis - alteplase, tenecteplase
    • Remove clot via catheter (PCI)
  • Widen the stenotic plaque
    • Balloon angioplasty, insert coronary artery stent
  • Prevent further thrombus
    • Anti-platelet agent, statin
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19
Q

What is granulomatous inflamamtion?

A
  • Distinctive pattern of chronic inflammatory reaction
  • Predominant cell types are activated macrophages with a modified appearance (epithelioid macrophages - looks like epithelial cell) and giant cells (formed from fused epithelioid macrophages) (+CD4+ T cells)
  • Recognition of the granulomatous pattern and type of giant cells in a biopsy specimen is important because of the limited number of possible conditions that cause it and the significance of the diagnoses associated with the lesions
  • Necrosis - often in infective cases, so-called caseous necrosis is characteristic of TB (+ leprosy, blastomycosis)
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20
Q

What is the significance of the costophrenic recess on chest X-ray?

A
  • Costophrenic recess formed by the hemidiaphragm and the chest wall and contains the rim of the lung base which lies over the diaphragm
  • Angle formed by the lateral chest wall and the diaphragm is known as the costophrenic angle
    • On CXR angles should be sharp - disappears first in pleural effusions
  • Infection in base of lung - likely to be seen in recess
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21
Q

What is homeostasis?

A
  • Definition - normal cells in a steady state
  • Injury can induce changes in homeostasis
  • Injury can be either reversible or irreversible
    • Leads to either adaptation or cell death
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22
Q

Describe the final steps in the coagulation cascade, how is this clinically relevant?

A

​​Clot dissolved by plasmin to substances e.g. D-dimer

  • Typical D-dimer containing fragment contains two D domains and one E domain of the original fibrinogen molecule
  • D-dimer has long half life (8 hours) so is best for testing clotting clinically
  • Elevated D-dimer - 94% sensitivity, 95% NPV
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23
Q

How are tumours staged?

A
  • Stage of a tumour is based on the size of the primary tumour, the extent of invasion into surrounding tissue, the spread to regional lymph nodes and the presence or absence of metastases
    • Essentially, stage = how far a tumour has spread/how advanced a tumour is
  • TNM system is used, stands for:
    • Tumour - how big? Has it locally invaded?
    • Nodes - are nodes involved? How many?
    • Metastasis - distant metastases?
      • If a tumour has metastasized it is late stage or stage IV
  • Each specialty has its own dataset to stage tumours
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24
Q

What causes hypertrophy?

A
  • Increased functional demand
  • Hormonal stimulation
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25
Q

Describe the prevalence of VTE

A
  • Increases with age
  • Average incidence - 1-1.5/1,000 population per year
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26
Q

Describe the morphology of apoptosis

A
  • Cell shrinkage
  • Chromatin condensation (unlike necrosis) - packaging up of nucleus
  • Membranes of cell and mitochondria etc. remain intact, unlike necrosis
  • Cytoplasmic blebs form and break off to form apoptotic bodies which are phagocytosed by macrophages
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27
Q

Describe the morphology of neutrophil polymorphs

A

Multilobulated nucleus - 3 lobes

Limited cytoplasm

No granules

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28
Q

Define metaplasia

A
  • Reversible change from one fully differentiated cell type into another
  • Adaptation so cells sensitive to a particular stress are replaced by other cells better able to withstand the adverse environment
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29
Q

What is exposure in an X-ray?

A

Amount of X-ray going through patient, varies which differences in shape/size (smaller - less exposure, larger - more exposure)

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30
Q

What structures are visible on a normal chest X-ray?

A
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31
Q

Describe reversible and irreversible cell injury

A
  • Cell injury may be reversible or irreversible
    • Reversible
      • Changes due to stress in environment
      • Return to normal once stimulus removed
    • Irreversible
      • Permanent
      • Cell death, usually necrosis, follows
  • Continuum between reversible and irreversible
    • Threshold (‘point of no return’) depends on type, duration and severity of injury
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32
Q

What are the clinical features of systemic inflammation?

A
  • Increased respiratory rate
  • Increased heart rate
  • High or low temperature
  • Low or raised white cell count
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33
Q

What is a paradoxical embolism?

A
  • Very rare
  • Venous drainage to R side of heart, in atrial septal defects blood moves R –> L and clot can form in L
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34
Q

How would the certificate of cause of death be completed from the following history:

  • 54 year old man
  • Smoker, history of angina
  • Collapsed at train station on way to work
  • Bystander CPR until ambulance arrival
  • 45 minutes of CPR in A&E with no spontaneous return of circulation
  • Pronounced dead in A&E

On post-mortem

  • Ruptured MI, ruptured aortic root
  • Necrosed myocardium - infarction
  • Left ascending coronary artery fully occluded
A
  1. Disease or condition directly leading to death
    a) Cardiac tamponade
    b) Due to, or as a consequence of, ruptured MI
    c) Due to, or as a consequence of, thrombus of left ascending coronary artery
    d) N/A
  2. Other significant conditions contributing to the death, but not related to the disease or condition causing it = smoking
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35
Q

Define hyperplasia

A
  • Increase in the number of cells in an organ or tissue
  • Adaptive response in cells capable of replication
  • Critical response of connective tissue cells in wound healing
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36
Q

What would you want to know when a 30-year-old female presents to A&E with an 18-hour history of right iliac fossa abdominal pain?

A
  • SOCRATES of the abdominal pain
    • Site
    • Onset
    • Character
    • Radiation
    • Associated symptoms
    • Time
    • Exacerbating/relieving factors
    • Severity
  • Pregnancy? - ruptured ectopic pregnancy is major concern (every woman of childbearing age presenting to A&E needs a urine pregnancy test)
  • Bowels - change, diarrhoea, constipation, blood, mucous
    • Blood - haematochezia or melena (melena = upper GI bleed), volume
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37
Q

List the risk factors for arteriosclerotic cardiovascular disease

A
  • Smoking
  • Hypertension
  • Hyperlipidaemia
  • Diabetes
  • Obesity
  • Family history
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38
Q

Give examples of endogenous and exogenous depositions

A
  • Endogenous
    • Intracellular
      • Melanin
      • Haemosiderin
      • Bile
      • Lipid, including cholesterol
      • ‘Storage disease’ especially in liver e.g. alpha-1-antitrypsin
      • ‘Degeneration products’ e.g. lipofusion
    • Extracellular
      • Amyloid
      • Fibrosis
      • Calcium
  • Exogenous
    • Intracellular
      • Tattoo pigment
      • Carbon (anthracosis)
      • Asbestos
    • Extracellular
      • Exogenous may be extracellular too
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39
Q

What is the differential diagnosis for a painful swollen leg?

A
  • Trauma
    • Fractures, dislocations, muscle strain/rupture or haematoma
  • Non-traumatic
    • Musculoskeletal causes, osteoarthritis, rheumatoid arthritis, septic arthritis, gout and pseudogout, popliteal (Baker’s) cyst, tenosynovitis, bursitis, myopathies
  • Skin/soft tissue infections
    • Cellulitis, erysipelas, abscesses, necrotising faciitis
  • Vascular causes
    • Venous occlusion - DVT, superficial vein thrombosis, venous insufficiency (post-DVT, varicose veins)
    • Acute ischaemia - cardiac thromboembolism, peripheral arterial disease, massive DVT
    • Lymphoedema
  • Causes of bilateral leg swelling
    • Systemic oedema - heart failure, cirrhosis, nephrotic syndrome, malnutrition, immobility
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40
Q

How do vascular changes occur in inflammation?

A
  • Vasodilation
    • Transient vasoconstriction then vasodilatation
    • Starts in arterioles
    • Increased blood flow
    • Due to histamine (mast cells), prostaglandins (can be produced by all nucleated cells), NO (made by nitric oxide synthase in endothelial cells)
    • Arterioles dilate increasing blood flow
  • Increased vascular permeability
    • Permits escape of protein rich fluid exudate into extravascular tissue
    • Contraction of endothelial cells
    • Increased interendothelial spaces
    • Mediated by histamine, bradykinin, substance P
  • Vascular congestion/stasis
    • Slower flow, increased concentration
  • Endothelial activation
    • By mediators produced during inflammation
    • Increased levels of adhesion molecules
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41
Q

How can you arrive at a differential diagnosis?

A
  • Location of disease
  • Think through different structures - are they normal or abnormal (systematic, like clinical history and examination)
  • Abnormality may be of quantity (more or less) or quality (different structure)
  • Consider possible causes/nature of disease
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42
Q
A
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43
Q

List physiological and pathological causes of apoptosis

A
  • Aetiology - Physiological
    • Embryogenesis - deletion of cell populations
    • Hormone dependent involution - uterus, breast, ovary
    • Cell deletion in proliferating cell populations to maintain constant number of cells e.g. epithelium
    • Deletion of inflammatory cells after an inflammatory response
    • Deletion of self-reactive lymphocytes in thymus
  • Aetiology - Pathological
    • Viral infection - cytotoxic T-lymphocytes
    • DNA damage
    • Hypoxia/ischaemia
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44
Q

Describe the hilar structures seen on chest X-ray

A
  • Each hilum contains major bronchi and pulmonary vessels
  • Lymph nodes are not visible unless enlarged
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45
Q

What causes cell injury?

A
  • If the stress is more intense, longer-lasting or of a specific type, or if the cell is very sensitive, then there may be cell injury
  • Cells directly affected may undergo
    • Sub-lethal cell injury
    • Cell death
  • The body may respond with
    • Inflammation - acute or chronic
  • Possibly, after many years, affected cells may undergo
    • Neoplasia
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46
Q

Define carcinoma in-situ

A
  • Full-thickness (severe) epithelial dysplasia extending from basement membrane to surface epithelium
  • Applicable only to epithelial neoplasms, if the entire lesion is no more advanced than CIS (carcinoma in-situ), then the risk of metastasis is zero
    • Because there are no blood vessels or lymphatics within the epithelium above the BM
  • Why cervical/bowel screening is so important
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47
Q

How does the diaphragm appear on chest X-ray?

A
  • Right hemi-diaphragm is slightly higher than the left
  • Liver is located beneath the right and stomach bubble is seen below the left
  • Cardiophrenic angles between heart and diaphragm - can have collection of fat here if obese
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48
Q

What is the right paratracheal stripe on a chest X-ray?

A
  • R edge of trachea
  • Normally less than 3mm
  • Enlargement may represent mass or nodes
  • L side of trachea not so well defined
  • Tracheobronchial angle - where azygous vein lies
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49
Q

How are histopathology samples prepared?

A
  • Pathologist examine and trim tissue
  • Tissue fixed in formalin
  • Tissue processing
    • Dehydration
    • Clearing
    • Wax impregnation
  • Tissue blocks sectioned, stained (e.g. w/ H&E)
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50
Q

Give examples of cytology samples

A
  • Exfoliative cytology
    • Fluid cytology including effusions
    • Scrape, smear and brush cytology (including cervical)
  • Fine needle aspiration
    • Direct e.g. sampling surface lumps on skin, head and neck, breast, lymph nodes
    • Under ultrasound guidance, as above plus endoscopic ultrasound (EUS) e.g. LNs, upper gastro-intestinal or respiratory tract, pancreas
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51
Q

Compare the microscopic appearance of a normal appendix vs an acutely inflamed appendix

A
  • Normal appendix wall, layers =
    • Mucosa - epithelium (columnar), lamina propria, muscularis mucosa
    • Submucosa
    • Muscularis propria (pink layer)
    • Serosa
    • Normal mucosa - uniformly arranged crypts/glands (test tube like arrangement)
  • Abnormal appendix wall:
    • Muscularis propria thicker, more blue
    • Engorged blood vessels
    • Increased cellular infiltrate
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52
Q

What molecular testing can be done for pathological diagnosis?

A
  • Immunhistochemistry
  • Flow cytometry
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53
Q

How do metastases present?

A
  • Multiple skin lesions
  • Brain - CNS lesions
  • Lungs - breathlessness/haematemesis
  • Liver - jaundice, masses
  • Bones - pathological fracture
  • Lymph nodes - e.g. neck (gastric, lung cancer)
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54
Q

Give the differential diagnosis for chest pain

A
  • Musculoskeletal
    • Rib fracture, muscular, chondritis
  • Cardiac
    • Angina, myocardial infarction
  • Lung
    • Pleuritic pain - infection, infarction, malignant
  • Vascular
    • PE, aortic dissection
  • Oesophageal
    • Acid reflux, hiatus hernia
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55
Q

How are tumours graded?

A
  • As tumours become more poorly differentiated, the higher the grade becomes
  • As tumours look less and less like the original tissue, they are really becoming worse and worse = grade
  • Poorly differentiated cancer is a high grade malignancy and a well differentiated cancer is a low grade malignancy
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56
Q

List the phases of wound healing

A
  1. Formation of blood clot
  2. Formation of granulation tissue
  3. Cell proliferation and collagen deposition
  4. Scar formation
  5. Wound contraction
  6. Connective tissue remodelling
  7. Recovery of tensile strength
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57
Q

List indications for chest X-ray

A
  • Emergency
    • Acute respiratory symptoms
    • Chest pain
    • Septic screen
    • Acute abdomen
    • Post central line/chest drain insertion
  • Elective
    • Persistent/chronic respiratory symptoms
    • Pre-operative work up
    • Metastatic screen
    • TB contacts
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58
Q

What is the function of an exudate?

A

An exudate allows delivery of nutrients, dilution of toxins, entry of antibodies and stimulates the immune response

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59
Q

How can emboli form?

A
  • Can arise within the body or out with it, including
    • Thrombus
    • Air
    • Fat
    • Amniotic fluid
  • From thrombus forming
    • In the leg veins
    • In the carotid arteries
    • Inside the heart
  • And embolising to
    • The lungs
    • The brain
    • Other tissues
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60
Q

How do defects in the immune system lead to chronic granulomatous disease?

A
  • Defect in NADPH oxidase system within phagocytes (including macrophages)
  • Heterogeneous but usually X-linked
  • Inability to kill intracellular organisms by respiratory burst
  • Patients have repeated and recurrent infections, develop granulomata of lymph nodes, skin, lungs, liver and GI tract
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61
Q

What anatomical structures are located in the right iliac fossa in a female patient which may cause pain?

A
  • Anatomical structures
    • Skin - sebaceous cyst
    • Subcutaneous fat - lipoma
    • Appendix - appendicitis
    • Ovary - cyst
    • Fallopian tube - ectopic pregnancy
  • If there is GI bleeding - aetiology unlikely to be gynaecological
  • Gynaecological disease may cause GI upset by impinging bowel
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62
Q

Describe the coagulation cascade

A
  • Tissue injury causes the coagulation system to be triggered by the tissue factor/factor VIIa complex, which activates FIX and FX
  • Activated FIX converts small amounts of prothrombin to thrombin, which is sufficient to amplify coagulation by activating factors V and VIII, platelets, and platelet-bound factor XI
  • Coagulation is propagated when FIXa binds to FVIIIa on the surface of activated platelets, forming intrinsic tenase, which activates FX
  • Activated FX binds to activated factor V to form prothrombinase, which converts prothrombin (factor II) to thrombin (factor Iia)
  • In the final step, thrombin converts fibrinogen to fibrin
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63
Q

Describe the covering of the lungs

A
  • Lungs covered by pleura - two layers
    • Inner layer = visceral pleura
    • Outer layer = parietal pleura
  • Fissures formed by invagination of the visceral pleura
  • Two layers separated by a potential space which may contain up to 15mls of fluid normally
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64
Q

Give examples of ectopia

A
  • Ectopia cordis = displacement of heart outside of body
  • Ectopic thyroid tissue = nodules of mature thyroid tissue located elsewhere in the neck
  • Ectopic pregnancy = implantation occurring in fallopian tube rather than endometrium (more often seen in the context of pelvic inflammatory disease or previous surgery)
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65
Q

What is the importance of differentiation in tumours?

A
  • Site of origin in metastatic disease
    • E.g. Squamous carcinoma in a lymph node - sites of origin would include lungs, respiratory tract, gynae tract, skin
  • Prognosis
    • Well differentiated often better prognosis than poorly differentiated (unpredictable)
  • Treatment
    • Treatment varies e.g. adenocarcinoma vs squamous
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66
Q

Why are mastectomy specimen edges stained?

A
  • When examined under microscope can measure distance between edge of tumour and stained edge of specimen - gives surgical margin
  • >1mm clear surgical margin - doesn’t require further treatment (can ensure that all of tumour has been removed)
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67
Q

Describe the gross pathological appearance of the terminal ileum in Crohn’s

A
  • Large BVs - vasodilation due to inflammation
  • Stricture - narrowing of the terminal ileum due to fibrosis (from inflammation)
  • Opened specimen
    • Colour - red due to engorged blood vessels
    • Thickness of intestinal of wall - thickened due to inflammation, lumen is narrower (strictures form), causes outflow obstruction
    • Strictures - outflow obstruction, perforation, peritonitis (area of stricture has to be removed)
    • Appearance of mucosal surface - irregular, cobbled
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68
Q

What are the functions of neutrophil polymorphs?

A
  • Phagocytosis of cells which have been targeted by opsonisation
  • Intracellular killing of micro-organisms (bactericidal components)
    • Oxygen dependent
    • Oxygen independent
  • Release lysosomal products, propagating the response
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69
Q

List the types of malignant tumours

A
  • Carcinoma - epithelial origin (squamous cell carcinoma, basal cell carcinoma, renal cell carcinoma, adenocarcinoma)
  • Sarcoma - mesenchymal origin (osteosarcoma, liposarcoma, pleomorphic sarcoma)
  • Melanoma - melanocytic origin
  • Lymphoma - haemopoeitic origin (Hodgkin or non-Hodgkin lymphoma, high grade or low grade)
  • Germ cell tumours
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70
Q

What is the significance of the aortic knuckle on chest X-ray?

A
  • Represents the left lateral edge of the aorta as it arches backwards over the left main bronchus, continues as the descending aorta
  • Older people - bulging
  • Teenagers - small aortic knuckle, big hila
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71
Q

What bloods are done in tumour investigation?

A
  • FBC, U+E, LFTs, calcium
  • Protein electrophoresis
  • Tumour ‘markers’ as appropriate: AFP, HCG, PSA, CEA, Ca 19.9 (pancreatic Ca), Ca 125 (ovarian Ca) - non-specific
  • Clinical context crucial
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72
Q

Which important structres are not visible on a chest X-ray?

A
  • Sternum
  • Oesophagus
  • Spine - can see spinous processes usually
  • Fissures
  • Pleura
  • Aorta
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73
Q

How is a post-mortem completed?

A
  • All organs returned to patient’s body cavity (minus tiny amount of tissue taken for microscopic assessment)
  • If no death certificate has been issued before the PM, the pathologist will write a death certificate
  • The report prepared by the pathologist is sent to the PF, or for consented/hospital cases, to the patient’s GP and the clinician in charge of care
  • Patient’s body is then reconstructed to permit viewing of the deceased by their family
  • Body released for burial or cremation as specified by the deceased/family
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74
Q

Describe the morphology of macrophages

A
  • Elongated, large nucleus
  • Voluminous cytoplasm
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75
Q

What is neoplasia?

A
  • Literally = new growth
  • An abnormal tissue mass, the growth of which is excessive (i.e. not an adaptation to physiological demands) and uncoordinated compared to adjacent normal tissue
  • Persists even after cessation of the stimuli that caused it
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76
Q

How does a normal lymph node aspirate compare to an abnormal lymph node aspirate?

A

Normal:

  • Lymphocytes are pleomorphic
  • Vary in size, shape, colour
  • Clonal expansion is bad - monomorphic, suggests cancer (lymphoma)

Abnormal:

  • Non-Hodgkin’s lymphoma
    • Monomorphic cell population (lymphocytes)
    • All same colour, size, shape
  • Low grade B-cell lymphoma - small to medium lymphocytes
    • Very difficult or impossible to distinguish from normal reactive lymph nodes
  • Metastatic squamous cell carcinoma
    • Squamous epithelial cells are larger than lymphocytes, with more cytoplasm - which is usually pink (keratin)
    • Epithelial cells generally cohesive (form protective coverings) so stick together - appear in sheets and lumps rather than dispersed (like lymphocytes)
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77
Q

Give examples of local effects of tumours

A
  1. Oesophagus - dysphagia/odynophagia
  2. Sigmoid colon - altered bowel habit/blood PR
  3. Bronchus - pneumonia/haemoptysis
  4. Head of pancreas - obstructive jaundice
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78
Q

What vascular pathology can be seen on post-mortem?

A
  • Thrombosis and infarction
    • Dead (necrotic) heart muscle due to infarction - takes 2-3 days to be visible
      • Feels soft at first
      • Turns yellow/grey
    • Bowel infarction
    • Cerebral infarct
  • Embolism
  • Haemorrhage
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79
Q

How are tumours named based on their tissue of origin?

A
  • Lipo- = fat
  • Rhabdo- = skeletal muscle
  • Leio- = smooth muscle
  • Osteo- = bone
  • Chondro- = cartilage
  • Adeno = gland
  • Meningo- = meninges
  • Angio- = vascular
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80
Q

How are post-mortem examinations done in the UK?

A
  • Hospital ‘consented’ PM
    • Usually done at the request of clinicians to answer questions about the patient’s pathology or treatment
    • Requires specific consent of the family
    • Few cases per year (e.g. 40-50 in Glasgow)
  • Medico-legal PM
    • At the instruction of the Procurator Fiscal (Scotland) or Coroner (England and Wales)
    • Does not require consent of the family
    • Constitute the vast majority of PMs performed in the UK (110,000 per year in England and Wales, 6500 in Scotland)
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81
Q

List the causes of atrophy

A
  • Loss of innervation
  • Diminished blood supply
  • Inadequate nutrition
  • Decreased workload
  • Loss of endocrine stimulation
  • Aging (senile atrophy)
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82
Q

What is metastasis? How can metastasis occur?

A
  • Tumour implants discontinuous from the primary tumour
  • Spread of tumour to distant sites can occur by:
  1. Lymphatic spread - most common pathway for dissemination of carcinomas (+ sarcomas). Pattern of lymph node involvement follows the natural routes of drainage.
  2. Haematogenous spread - typical of sarcomas. Arteries are more difficult for tumour to penetrate than veins. With venous invasion, the blood-borne cells follow the venous flow draining the site of the tumour. Liver and lungs are frequently involved.
  3. Seeding of body cavities (transcoelomic spread) - occurs when a malignant neoplasm penetrates into a natural ‘open field’ such as peritoneal cavity, pleural space, pericardial cavity etc. Most common examples - ovarian carcinoma, gastric carcinoma.
  4. Perineural
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83
Q

Describe prevention of DVT thrombus extending or embolism

A
  • Anticoagulation for 3-6 months
    • Heparin (LMWH)
    • Warfarin (target INR 2.5)
    • Direct oral anti-coagulant (direct Xa or IIa inhibitor)
  • Remove risk factors - smoking, OCP etc.
  • Graduated elastic compression stockings
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84
Q

How sensitive/specific is the Wells clinical score?

A
  • 5.5% of those with score <2 actually had DVT or PE
  • 27.9% of those with score >/= 2 had a DVT or PE confirmed
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85
Q

How does the acute inflammatory response terminate?

A
  • Removal of stimulus
  • Neutrophils have a short half life
  • Variation in cytokine stimuli
  • Neural impulses
  • Macrophages are activated to perform different functions
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86
Q

What are the affects of acute inflammation?

A

Beneficial -

  • Dilation of toxins by oedema fluid
  • Increased entry of antibodies and drug transport
  • Fibrin mesh traps microorganisms
  • Delivery of nutrients
  • Stimulation of immune response

Detrimental -

  • Digestion of normal tissue
  • Swelling e.g. epiglottitis (bacterial infections, obstructs airways)
  • Inappropriate response e.g. type I hypersensitivity response (allergic rhinitis)
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87
Q

What is intussusception? When does it commonly occur?

A
  • Elderly - usually in context of tumour
  • Peristalsis of proximal bowel over next part
  • –> ischaemic bowel disease, colitis
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88
Q

Describe the pathological appearance of an old cerebellar infarct

A
  • Depressed area - colliquitive necrosis (liquifies)
  • Brain has no fibroblasts - glial cells
    • Gliosis = cerebral scar
    • Indentation, loss of tissue, feels firm
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89
Q

How is MI/ACS diagnosed?

A
  • Suggestive history
  • Clinical evidence of cardiac dysfunction
  • ECG findings
  • Biochemical evidence of myocardial damage (ischaemia)
    • Elevated troponin (biochemical marker)
  • Visualisation of coronary arteries
    • Cardiac catheterisation
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90
Q

Gives examples of atrophy - physiological and pathological

A
  • Uterus - menopause causes atrophy (physiological)
  • Brain atrophy seen with age (physiological) or with degenerative conditions e.g. Alzheimer’s (pathological)
  • Kidney atropy due to renal artery stenosis e.g. due to high BP (pathological)
  • Intestinal villous atrophy in coeliac disease (T cell mediated resposne - pathological)
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91
Q

Describe the deposition of haemosiderin in macrophages

A

Haemosiderin (iron - brown) may be deposited after haemorrhage or if there is congestion of blood vessels

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92
Q

How do we confirm or exclude the diagnosis of DVT?

A
  • Clinical decision rule
    • Determine likelihood of DVT
  • Blood tests
    • Fibrin D-dimer, a measure of dissolved thrombus
  • Image venous system of leg
    • Compression ultrasound, venography
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93
Q

List the types of necrosis

A
  • Coagulative
    • Firm, tissue outline retained
      • Haemorrhagic - due to blockage of venous drainage
      • Gangrenous - larger area especially lower leg
  • Colliquitive
    • Tissue becomes liquid and its structure is lost e.g. infective abscess, cerebral infarct
  • Caseous
    • Combination of coagulative and colliquitive appearing ‘cheese-like’ (caseous)
    • Classical for granulomatous inflammation esp. TB
  • Fat
    • Due to action of lipases on fatty tissue
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94
Q

Describe differentiation of tumours

A
  • Tissue type represented by the tumour
  • The extent to which the tumour cell resembles the original cell
  • Ranges of differentiation - well, moderately, poorly, undifferentiated
  • Well differentiated tumours resemble identifiable tissue types
  • Undifferentiated tumours do not resemble anything, ICC (immunocytochemistry) may be needed to know where it came from
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95
Q

What histopathology sample types are taken?

A
  • Small biopsies
    • Mucosal (e.g. colonic biopsy)
    • Needle core (e.g. liver biopsy)
    • Incisional (e.g. skin punch biopsy)
  • Excision biopsy (e.g. suspected melanoma) - whole thing removed
  • Resections
    • Small e.g. appendicectomy
    • Large e.g. pneumonectomy
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96
Q

Describe prevention of DVT

A
  • Avoid risk factors if possible
  • Risk assess at hospital admission or surgery
  • Provide thrombo-prophylaxis when appropriate
    • Anti-embolism stockings
    • Heparin (LMWH daily SC)
  • Education of patients on risks and avoidance measures e.g. early mobilisation
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97
Q

What can the outcome of acute inflamamtion be?

A
  • Resolution - complete restoration of tissue to normal
    • If minimal tissue damage
    • If occurs in tissue with regenerative capacity i.e. skin
    • If cause is rapidly removed or destroyed
    • If there is good vascular drainage
  • Healing by fibrosis
    • After substantial tissue damage
    • Tissue incapable of regeneration e.g. brain
    • Abundant fibrin exudate
  • Progression to chronic inflammation
    • Persistent stimulus
    • Tissue destruction leading to ongoing inflammation
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98
Q

Which cardiac contours are seen on a normal chest X-ray?

A
  • RA and LV cardiac contours seen
  • Can’t see RV (front) or LA (back)
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99
Q

What is deep vein thrombosis?

A
  • Thrombosis in deep venous system
  • Most commonly of leg
  • Compromises 2/3rd of all venous thrombosis
100
Q

How is a PA projection X-ray taken?

A
  • Taken in X-ray department rather than on ward
  • Tube is set distance from patient/detector (traditionally 6 feet)
  • PA is the standard projection but not always possible
  • Heart is closer to the film and less magnified
    • Gives assessable heart size
  • Well inspired - lots of lung visible
101
Q

Describe the formation of granulomas in the colonic mucosa

A
  • Multinucleated giant cell, made of fusion of epithelioid neutrophils
  • Eventually forms granuloma - necrosis and inflammation
    • Can be caseous e.g. in TB (caseating epithelioid granuloma)
    • Crohn’s
102
Q

List the stages of cutaneous wound healing

A
  1. Inflammation
  2. Proliferation
  3. Maturation
103
Q

Why is a post-mortem performed?

A

‘Medical’ Questions:

  • Confirm a diagnosis or its extent - audit of medical care
  • Revealing a diagnosis or explaining unexplainable findings - diagnostic tool
  • Investigating possible failings in surgery or other medical care - monitor of medical care

‘Medico-legal’ Questions:

  • A wide range of circumstances including deaths that may involve potential criminality, ‘violent’ deaths, accidental deaths, unexplained deaths, occupation related deaths, suicide, deaths in custody etc.
104
Q

What scopes can be used in the diagnosis of tumours?

A
  • ENT
  • Bronchoscopy
  • Upper GI/colonoscopy
  • Cystoscopy (urethra to bladder)
  • Colposcopy (cervix)
105
Q

Describe LIGHTs criteria

A
  • Exudate is extra-cellular fluid with a HIGH protein and cellular content
  • Transudate is extra-cellular fluid with a LOW protein and cellular content - serous exudate
106
Q

Describe the function of mast cells

A
  • Reside in tissues
  • Contain histamine and heparin in preformed granules
  • Stimulated to release contents by injury, complement, IgE
  • Role in allergy/anaphylaxis
  • Also make eicosanoids to propagate immune response
107
Q

What is Virchow’s triad?

A
  • Three braod categories of factors that contribute to thrombosis
  • Hypercoagulable state
    • Malignancy
    • Pregnancy and peri-partum period
    • Oestrogen therapy
    • Trauma or surgery of lower extremity, hip, abdomen or pelvis
    • Inflammatory bowel disease
    • Nephrotic syndrome
    • Sepsis
    • Thrombophilia
  • Vascular wall injury
    • Trauma or surgery
    • Venepuncture
    • Chemical irritation
    • Heart valve disease or replacement
    • Atherosclerosis
    • Indwelling catheters
  • Circulatory stasis
    • Atrial fibrillation
    • Left ventricular dysfunction
    • Immobility or paralysis
    • Venous insufficiency or varicose veins
    • Venous obstruction from tumour, obesity or pregnancy
108
Q
  1. Disease or condition directly leading to death
    a) Pulmonary thromboembolism
    b) Due to, or as a consequence of, DVT of leg
    c) N/A
    d) N/A
  2. Other significant conditions contributing to the death, but not related to the disease or condition causing it - immobility/surgery/OCP etc. (?)
A
109
Q

Describe the external examination performed in post-mortems

A
  • Identification of the deceased by the pathologist
  • Height, weight, BMI
  • Skin, hair, eye colour
  • Iatrogenic - scars, drains, IV lines
  • Evidence of trauma?
  • Jaundice cyanosis, finger clubbing, oedema, lymphadenopathy
110
Q

What are the types of excessive growth?

A
  • Neoplastic - benign or malignant
    • Uncontrolled and irreversible
  • Non-neoplastic
    • Controlled and reversible
111
Q

What initial investigations would you do in a 50 y/o patient presenting with a 6 week history of a neck lump?

A
  • FBC - WCC
  • If lump isn’t pulsatile (aneurysm?) then aspirate to test sample
  • Temperature, BP, HR etc.
112
Q

What is the function of plasma cells?

A

Antibody production

113
Q

Describe the appearance of the muscularis and serosal (peritoneal) surface in an abnormal appendix

A
  • Collection of inflammatory cells = granuloma
  • Adipose tissue
  • At the peritoneal surface, there is congestion and inflammation - causes peritonitis (rebound tenderness)
114
Q

Describe the appearance of the muscularis propria in an abnormal appendix

A
  • Blue = neutrophils
    • Abnormal cellular inflammatory infiltrate has reached muscularis propria (transmural)
  • Red = congestion with injured and dead muscle cells
    • In most severe form this can be described as gangrenous
  • Muscle will be weakened due to damage from inflammatory cells - risk of perforation of infected appendix (= peritonitis)
115
Q

How does the histology of the heart change following MI?

A
  • Normal myocardium - pink strands of myocytes, white interstitium (scaffold)
  • 24 hours post MI -
    • Myocytes atrophied - smaller and thinner
    • Hyper-eosinophilia - darker pink, due to cytoplasmic changes which occur as myocytes die
    • Interstitium larger due to oedema (inflammation)
116
Q

How can the pulmonary arteries be seen in chest X-ray?

A

Catheter through vein at cubital fossa –> axillary v –> subclavian v –> SVC –> RA, contrast to pulmonary arteries

117
Q

Describe the major airways which can be seen on a normal chest X-ray

A

​

  • The trachea and the main bronchi are visible branching at the carina
  • Trachea passes to the right of the aorta, may be slightly off midline to R
  • R main bronchus is more vertically orientated and straighter than L, therefore aspiration occurs more commonly on R
118
Q

What is a hamartoma?

A
  • Hamartion = bodily defect, + -oma = tumour
  • Malformation that may resemble a neoplasm that results from faulty growth of an organ
  • Composed of a mixture of mature tissue elements which would normally be found at that site which develop and grow at the same rate as the surrounding tissue
  • = ‘overgrowth of tissues normally found there’
119
Q

What are the local effects of tumours?

A
  • Lumps occupy space - pressure effects
    • Depend on site (pituitary adenoma/meningioma)
  • Locally destructive
  • Ulcerate/bleed - anaemia
  • Induce stromal reaction/fibrosis - stenosis/obstruction (renal failure in cervical cancer)
  • Pain - invasion of nerves
120
Q

Describe the types of neoplasms

A
  • Benign neoplasm
    • A neoplasm that grows without invading adjacent tissue or spreading to distant sites
    • Usually well-circumscribed due to the lack of invasion of surrounding tissues
  • Malignant neoplasm
    • A neoplasm that invades the surround normal tissue
    • Can spread to distant sites (metastasize)
    • Usually is not well circumscribed
    • Malignant tumour and cancer are synonyms
121
Q

What would you want to know in the clinical history of a 50 y/o man presenting with a 6 week history of a neck lump?

A
  • Alcohol/smoking history
  • Family history of cancer
  • PMH of malignancy, thyroid/vascular problems etc.
  • Weight loss?
  • Recent upper respiratory infection, dental problems, mouth pain, swallowing pain?
  • Thyroid symptoms - sweating, shaking, lethargy, depression, hair/skin changes, constipation/diarrhoea
122
Q

Describe the inflammatory pathogenesis of rheumatoid arthritis

A
  • Non-suppurative, proliferative synovitis
  • Destruction of articular cartilage
  • Inflammatory infiltrate includes lymphocytes, plasma cells, dendritic cells, macrophages
  • Increased vascularity due to vasodilatation and angiogenesis
  • Aggregation of fibrin
  • Pannus formation leading to erosion of cartilage and bone
  • Neutrophils in synovial fluid
123
Q

What are the clinical signs of inflammation?

A
  1. Redness - caused by hyperaemia
  2. Swelling - caused by fluid exudate and hyperaemia
  3. Heat - caused by hyperaemia
  4. Pain - caused by release of bradykinin and PGE2
  5. Loss of function - caused by combination of above
124
Q

When does environmental change become a cell stress become a cell injury?

A
  • Change/stress factors
    • Type of change
    • Intensity of change
  • Cell factors
    • Sensitivity of cell due to its natures - inherent susceptibility, lack of protective factors
    • Sensitivity of cell due to timing
125
Q

Describe the deposition of lipfuscin in the liver

A
  • Brown lipofuscin ‘wear and tear’ or ‘age’ pigment in liver
  • Endogenous breakdown product
  • May also deposit in heart and other organs
126
Q

How is a medical certificate of cause of death completed?

A
  1. Disease or condition directly leading to death e.g. myocardial infarction
  • Due to, or as a consequence of ,e.g. severe coronary artery atheroma
  • Due to, or as a consequence of,
  • Due to, or as a consequence of,
  1. Other significant conditions contributing to the death, but not related to the disease or condition causing it, e.g. diabetes
127
Q

How can clots formed in life and the normal clotting which occurs in death be distinguished in a post mortem?

A
  • Normal coagulation after death - dense blood components e.g. RBC fall to bottom of vessel, liquid component (plasma) floats on top (‘chicken fat’)
  • Thrombus formed in life - granular, adheres to vessel wall
128
Q

Can the pleural fissures be seen on chest X-ray?

A
  • Oblique fissures overlie each other on the lateral view and are not always seen in their entirety
  • Accessory fissure
    • Anatomical variants
    • Most common accessory fissure is the azygous fissure (1-2%) contains the azygous vein w/ pleura wrapped around it
    • Azygous/hemi-azygous v drain posterior chest wall (lung apex –> T4)
    • Not much pathological relevance
129
Q

What is immunohistochemistry?

A
  • Method of localising specific intra-cellular or surface antigen (protein) expression
  • Based on antibody-antigen reaction
  • Specific labelled antibodies applied to tissue
  • Site of antibody binding identified by tagging the antibody (directly or indirectly) with a visible label
  • Label visualised under microscope
  • Use of ‘blocking buffers’ prevents non-specific binding - reducing background staining
130
Q

What features are seen in reversible cell injury?

A
  • Nature of changes are same whether reversible or irreversible
  • But reversible are less severe and include particularly:
    • ‘Cloudy swelling’ - osmotic disturbance, loss of energy dependent Na pump leads to Na influx and build up of intracellular metabolites
    • Cytoplasmic blebs, disrupted microvilli, swollen mitochondria
    • ‘Fatty change’ - accumulation of lipid vacuoles in cytoplasm caused by disruption of fatty acid metabolism, especially in liver
131
Q

List the cell types in chronic inflammation

A
  • Macrophages
  • Plasma cells
  • Lymphocytes
132
Q

What are the potential outcomes following DVT?

A
  • Painful swollen leg
  • Pulmonary embolism
    • 50% cases of DVT will have asymptomatic PE
  • Recurrent VTE
    • 20-30% at 8-10 years
  • Venous insufficiency
    • 40-60% have residual thrombus on US at 6-12 months
  • Post thrombotic syndrome - lower leg ulcers due to reduced venous return
    • 25% at 2 years (4% severe)
    • 2.4-fold higher after recurrent DVT
    • Reduce risk by 50% with compression stockings 2 years
133
Q

Give examples of developmental anomalies

A
  • Ventricular septal defect
  • Spina bifida
  • Less severe developmental anomalies - syndactyly, polydactyly, uneven hips and scoliosis
134
Q

How is an AP projection X-ray taken?

A
  • Done on ward/ICU - distance variable
  • Patient faces towards tube
  • Heart size should not be considered enlarged on an AP film
135
Q

Describe the formation of thrombosis in DVT

A
  • Sluggish flow of blood e.g. post op
  • Minute clot forms, caught behind valves of deep veins of legs
  • Thrombus grows
136
Q

What imaging can be done in the diagnosis of a DVT?

A
  • Venography - contrast injected and X-ray
  • Ultrasound
137
Q

Describe the process of inflammation

A
138
Q

Describe the gross appearance of the mucosal surface of the terminal ileum in Crohn’s disease

A
  • Red = cobblestone mucosa
    • Typical of Crohn’s disease
    • Due to fibrosis of mucosa - some parts protrude
    • = polyps (abnormal tissue growths, small flat lumps)
  • Black = ulcers
    • Ulcer - break in integrity of the mucosal surface which fails to heal
    • In Crohn’s can be deep
139
Q

Who performs post-mortem examinations?

A
  • Both types of PMs performed by general pathologists
  • Forensic pathologists are a sub-speciality within pathology who perform PMs required in certain circumstances e.g. homicide (more training)
  • Assisted by Anatomical Pathology Technicians (APTs)
140
Q

How would the certificate of cause of death be completed in the following patient:

  • 72 year old man
  • No past history of note
  • Sitting at home, chatting to daughter when he suddenly collapses
  • In PEA (pulseless electrical arrest) on arrival of ambulance crew
  • CPR started by crew and continued in A&E. No return of circulation. Pronounced dead 50 minutes after arrival in A&E

On post-mortem:

Saddle embolus - PE

A
141
Q

How can structure be examined in pathology?

A
  1. Levels of magnification
  2. Levels of organisation - cells to systems
  • Molecules –> cell –> tissue –> organ –> organ system –> organism
142
Q

Why can it be difficult for pathologists to estimate the volume of blood lost through haemorrhage?

A

Can be large volume lost to environment

143
Q

List the types of wound healing

A
  • Healing by primary/first intention e.g. incised wound/laceration - simple incision
  • Healing by secondary intention e.g. abrasion - dirty/infected wound (can’t bring edges together)
    • Need granulation tissue
    • If no infection/damage causing inflammation - replaced by scar tissue
    • Area of fibrosis (scarring) - collagen deposition
  • Bone heals by regeneration rather than repair, callus formation
144
Q

Describe the morphology of mast cells

A

Granules in cytoplasm

145
Q

Give examples of metaplasia

A
  • Cigarette smokers - normal ciliated columnar epithelial cells of trachea and bronchi are replaced by stratified squamous epithelial cells
  • Chronic gastric reflux - normal stratified squamous epithelium of the lower oesophagus may undergo metaplasia to gastric columnar epithelium (= Barrett’s oesophagus)
146
Q

How are cytology samples prepared?

A
  1. Received and washed
  2. Spun and fixed (preserved) - can last for 30 years
  3. Spun onto slide
  4. Stained
  5. Slide cover applied
147
Q

Describe the movement of white blood cells in inflammation

A
  • Margination
    • White blood cells situation peripherally due to stasis
  • Rolling
    • White blood cells stick and detach from wall
    • Mediated by selectins
    • Upregulated by IL-1 and TNF (from macrophages/polymorphonuclear neutrophils)
      • Histamine, thrombin, PAF
      • Binds L-selectin on leukocytes
  • Adhesion
    • Mediated by integrins
    • Stimulated by IL-1 and TNF
    • Chemokines also facilitate binding
  • Migration (diapedesis)
    • Chemokines act on leucocytes to stimulate across endothelium
  • Chemotaxis
    • Travel along a chemical gradient, attracted by
      • Bacterial products
      • Cytokines IL-8
      • Complement
      • Leukotriene B (from arachidonic acid)
148
Q

What causes haemorrhage?

A
  • From rupture of a blood vessel
    • Under high pressure - e.g. cerebral haemorrhage in hypertension
    • Congenital weakness - e.g. subarachnoid haemorrhage from rupture of cerebral artery aneurysm (berry aneurysm)
    • Weakened by disease - e.g. atheroma in the abdominal aorta causing weakness of the wall
    • Eroded into - e.g. bleeding from duodenal ulcer
149
Q

Why are post-mortem examinations required when there are imaging techniques e.g. CT/MRI scans and scopes?

A
  • Repeated studies show major disagreements in cause of death as listed on the Medical Certificate or Cause of Death (MCCD) and as revealed at PM in 10-20% of cases
  • Disagreements vary between specialities (esp. orthopaedics - old patients, complex medications/comorbidities)
150
Q

Describe the types of hyperplasia

A
  • Physiological hyperplasia
    • Hormonal (normal proliferative endometrium)
    • Compensatory - hyperplasia that occurs when a portion of a tissue is removed or diseased
  • Pathological hyperplasia
    • Caused by excessive hormonal or growth factor stimulation (androgens: BPH, oestrogen: atypical endometrial hyperplasia)
151
Q

List the symptoms of spina bifida

A
  • Muscle weakness or paralysis
  • Bowel and bladder problems
  • Seizures
  • Orthopedic problems, such as deformed feet, uneven hips and scoliosis
  • Hydrocephalus
152
Q

How are developmental anomalies classified?

A

Classified according to the organ system affected (e.g. congenital heart defect) or according to the way the defect occurred (developmental failure/arrest, failure to atrophy or subdivide, fusion, misplacement etc.)

153
Q

Describe the appearance of the ribs on a normal chest X-ray

A
  • Posterior ribs run horizontal, anterior ribs are less obvious and run at an angle
  • Can only see costosternal junction in old people - calcified
  • 1st costosternal joint often calcifies, lung cancer can be mistaken for (asymmetry suggests lung cancer)
154
Q

What are the components of pathology?

A
  • Cytopathology (cells)
  • Histopathology (tissues)
  • Autopsy (post-mortem examination)
155
Q

Describe the appearance of a normal appendix vs an acutely inflamed appendix

A
  • Normal appendix:
    • Small - pinky finger width, 7cm length
    • Pale
    • Small BV visible on surface
    • Covered by layer of fat - mesoappendix
  • Acutely inflamed appendix
    • Red/purple - engorged with blood due to vasodilation
    • Larger - oedematous due to inflammation (vasodilation and extravasation of blood vessels)
    • Covered in pus = neutrophils (fibrino-purulent exudate)
156
Q

Describe the clinical scoring system for DVT

A

Wells Clinical Score - 1 point each:

  • Active cancer (treatment ongoing or within previous 6 months or palliative)
  • Paralysis, paresis, or recent plaster immobilisation of lower extremities
  • Recently bedridden for >3 days, or major surgery within 12 weeks
  • Localised tenderness along distribution of deep venous system
  • Entire leg swollen
  • Calf swollen by >3cm compared to asymptomatic leg (10cm below tibial tuberosity)
  • Pitting oedema (greater in symptomatic leg)
  • Collaterial superficial veins (non-varicose)
  • Previously documented DVT
  • Alternative diagnosis as likely or greater than that of DVT

DVT unlikely if score <2, DVT possible if score >2

157
Q

What are the potential outcomes following PE?

A
  • Dyspnoea, chest pain, haemoptysis
  • Collapse (massive PE) - 5%
  • Death (fatal PE)
    • 90% of PE deaths diagnosed post mortem
    • 12% risk after massive PE, lower risk if smaller
  • Recurrent VTE
    • As after DVT but 4x more likely to be recurrent PE
  • Chronic thromboembolic pulmonary hypertension
158
Q

What levels of magnification can be used to look at pathology?

A
  • Gross (naked-eye)
  • Light microscopy
  • Electron microscopy
  • Molecular cell biology

Changes happen first at molecular level, then EM level and so on - but may be easier to see at gross or microscopic levels

159
Q

What is pathology?

A
  • Pathology = study of disease
    • Disease = abnormality of cell/tissue structure and/or function
  • Pathology can be divided into
    • General - disease causes and processes in general e.g. inflammation
    • Systemic - general processes occurring in each system e.g. cardiovascular etc.
  • Includes
    • Broad patterns - epidemiology
    • Causes - aetiology
    • Mechanisms - pathogenesis
    • Nature of disease
      • Morphology and underlying molecular changes
      • Functional changes
    • Complications - sequelae
    • Plus clinical presentation associated with function i.e. symptoms and clincial management i.e. treatment
160
Q

List the classifications of organ systems in pathology

A
  • Cardiovascular
  • Respiratory
  • Gastrointestinal
  • Genitourinary
  • Haematolymphoid
  • Skin
  • Breast
  • Musculo-skeletal
  • Neurological
  • Ear, nose and throat/head and neck
  • Eye/ophthalmic
161
Q

What are the causes of limb weakness?

A
  • Musculoskeletal
    • Myopathy
    • Arthropathy
  • Neurological
    • Peripheral neuropathy
    • Spinal lesion
    • Cerebral lesion

(Ischaemia, inflammation, malignancy)

162
Q

What is local invasion? Which tumours locally invade?

A
  • Growth into the surrounding tissue by direct extension/expansion
  • Benign tumours never locally invade
  • Malignant tumours always invade the surrounding tissues
163
Q

Describe the venous supply of the leg

A
  • The junction of the anterior tibial vein and posterior tibial vein defines where the origin of the popliteal vein will occur
  • Popliteal vein becomes the superficial femoral vein as the popliteal vein leaves the adductor canal, which is also known as Hunter’s canal
  • In the proximal thigh, the SFV and DFV join to form the common femoral vein (CFV), which passes upwards above the groin crease to become the external iliac vein
164
Q

Describe the DVT diagnosis decision algorithm

A
165
Q

Describe the types of hypertrophy

A
  • Physiological
    • Muscle training
    • Uterus during pregnancy
    • Heart hypertrophy in athletes (up to 500g)
  • Pathological
    • Left ventricular hypertrophy - heart pumping harder against peripheral resistance (pathological)
166
Q

What can cause raised serum calcium leading to pathological calcification?

A
  • Increased levels of parathyroid hormone
    • Primary - parathyroid gland tumour
    • Secondary - kidney disease
  • May be systemic effect with cancer
167
Q

What is a chondroid hamartoma?

A
  • Lung lesion which may be seen as a ‘coin lesion’ on X-ray
  • Can mimic malignancy clinically if endobronchial
  • Composed of a mixture of epithelium, cartilage, fat, smooth muscle
  • BENIGN
168
Q

How are cytology samples morphologically assessed?

A
  • Are they normal? Signs of dysplasia/malignancy:
    • Quantity
    • Pleomorphism - look different
    • Hyperchromasia - more DNA, darker staining
    • Increased nuclear:cytoplasm ratio
  • Specific features
    • Nuclear molding - cells attach to one another
    • Chromatin/DNA speckles - salt and pepper chromatin ( = small cell carcinoma)
    • Orange cytoplasm - keratin (squamous cells)
    • White blobs - mucin (glandular cells - adenocarcinoma)
169
Q

How are leucocytes activated and microbes recognised at the site of inflammation?

A
  • Toll-like receptors
    • Receptors for microbial products on surface of leucocytes
    • Stimulate microbe killing and cytokine production
  • G-protein coupled receptors on PMNs and macrophages
    • Recognise products of short bacterial peptides, complement, prostaglandins
    • Induce migration of cells and production of respiratory burst
  • Receptors for opsonins on surface of leucocytes
    • Coating a particles to target for ingestion
    • Coating included antibodies and complement
  • Receptors for cytokines on surface of leucocytes
    • E.g. IFN-gamma activates macrophages
170
Q

Describe the process of phagocytosis

A
  1. Opsonisation
  2. Engulfment using pseudopodia
  3. Formation of phagosomes
  4. Fusion with lysosomes containing enzymes to form phagolysosomes
  5. Material destroyed and removed from cell by pinocytosis
171
Q

Describe the pathogenesis of amyloid

A
  • Excessive production/accumulation of a normal protein
  • Production/accumulation of an abnormal protein
    • tendency of protein to misfold (i.e. abnormal)
172
Q

Are the pleural visible on a normal chest X-ray?

A
  • Pleura is only visible when abnormal
  • Lung markings should reach the thoracic wall
  • Around entire edge of lung except hila
173
Q

What are the complications of untreated appendicitis?

A
  • Appendix rupture
    • Peritonitis (can be fatal)
    • Abscesses
174
Q

What is an ectopia?

A

An abnormal location or position of an organ or a tissue, most often occurring congenitally but can occur as a result of injury

175
Q

What are the differences between Crohn’s and UC?

A
  • UC is only mucosal, Crohn’s is transmural
    • Stricture formation in Crohn’s - often need areas of bowel resected
  • Because Crohn’s usually results in bowel resections, more risk of cancer in UC, more bowel left to be dysplastic
  • Crohn’s has patchy distribution, often in terminal ileum, UC has moth to anus distribution
  • Typical morphological features of Crohn’s - cobble-stoning, granulomas, transmural
  • Both are episodic chronic inflammatory conditions

Transmural = extends across entire wall of an organ or blood vessel (e.g. through whole wall of bowel)

176
Q

Which cells are involved in chronic granulomatous inflammation?

A
  • Epithelioid macrophages
    • Modified macrophages arranged in small nodules or clusters
    • Have a mainly secretory role rather than phagocytosis
    • Multinucleated giant cells form where material is difficult to digest
  • Lymphocytes - CD4 and CD8
    • Formation of granulomas is a manifestation of T cell mediated immune reaction (delayed type hypersensitivity)
    • Antigen is presented to CD4+ T cells which in turn produce IFN gamma and other cytokines resulting in macrophage activation
177
Q

What ECG changes are seen in ACS

A
178
Q

Describe the pathogenesis of the mechanisms of cell inury

A
  • Damage to:
    • Mitochondria: disrupted aerobic respiration/ATP synthesis
    • Cell membrane: disrupted ion concentration, esp. increased calcium 2+ ions
    • Cytoplasm including ribosomes etc.: disrupted enzyme and structural protein synthesis and architecture
    • Nucleus: disrupted DNA maintenance and DNA damage
  • Oxidative stress:
    • Oxidative stress caused by reactive oxygen species (free radicals)
    • Normally formed in small amounts as a by-product of respiration
    • Formed pathologically by absorption of radiation, toxic chemicals, hypoxia etc.
    • Lack of antioxidants makes damage more likely (nutritional deficiency) - mop up toxic metabolites
179
Q

Describe the process of necrosis

A
  • Unprogrammed cell death
    • E.g. infarction = necrosis caused by loss of blood supply
  • Histological changes
    • Cell swelling, vacuolation and disruption of membranes of cell and its organelles including mitochondria, lysosomes and ER
    • Release of cell contents (cell lysis) including enzymes causes adjacent cell damage and acute inflammation
    • DNA disruption and hydrolysis
180
Q

What is Meckel’s diverticulum?

A
  • Congenital
  • Two inches long usually and present at terminal ileum
  • Blind ending duct that is a remnant of the yolk sac (nourishes embryo) which failed to involute
  • Contains all layers of the intestine and often has ectopic tissue within it (pancreatic/gastric)
181
Q

How would you examine a 50 y/o patient presenting with a 6 week history of a neck lump?

A
  • Bilateral lymph node enlargement?
  • Is the lump tender, soft etc.
  • Other lymph nodes enlarged? - axillary, groin (would suggest lymphoma)
  • Is the lump pulsatile?
182
Q

Define spina bifida

A

Defect of the neural tube (i.e. the embryonic structure that develops into the spinal cord and brain) wherein a portion of the neural tube fails to develop or close properly

183
Q

Describe the morphology of plasma cells

A
  • Area of pallor around nucleus - paranuclear hof
  • Eccentric nucleus - to one side
  • Stippled quality to nucleus (clock face nucleus)
  • Bi/trinucleic
184
Q

Give an example of pathological calcification

A

Calcification of the mitral valve

185
Q

Describe the histopathology of arterial vs venous thrombosis

A
  • Arterial - ‘white thrombus’
    • Many platelets, small amounts of fibrin (reflects high flow)
  • Venous - ‘red thrombus’
    • Many fibrin with trapped red cells (reflects indolent flow)
186
Q

Are tumours and neoplasms synonymous?

A
  • Tumour and neoplasm are not synonymous
  • Tumour = swelling/lump, not all swellings are tumours (e.g. hamartomas) and not all neoplasms cause swelling (MF, leukaemia, some lymphomas)
187
Q

What are the potential complications of Meckel’s diverticulum?

A
  • Complications include inflammation, bleeding (from ulcerated gastric tissue), perforation and obstruction/intussusception (one segment of intestines ‘telescopes’ inside another)
  • Inflammation mimics appendicitis due to location
188
Q

Describe deposition of excess iron in the liver

A
  • Iron is brown but stained blue with Perl’s stain (Prussian blue reaction)
  • Called haemosiderosis
  • Can be due to genetic haemochromatosis
189
Q

What is the most common congenital anomaly?

A

Congenital heart anomalies represent the most common congenital anomalies, ventricular septal defects being the most common

190
Q

How should pathology specimens be described?

A
  • Broadly, what is the magnification (low vs high power image)?
  • What is the organ/tissue?
  • And/or how and what is sampled?
  • Is it normal or abnormal?
  • If abnormal, describe abnormality (including whether it is focal or diffuse)?

Gross:

  • Size?
  • Shape?
  • Colour?
  • Texture?
  • Resemblance e.g. to food/fruit
  • For both normal and abnormal

Microscopic:

  • Go through a systematic description
    • Exists for each tissue/organ
    • If not sure, consider which tissues are present, where and whether normal or abnormal
      • Epithelium (and what type)?
      • Connective tissues
      • Haemato-lymphoid tissues
      • Neural tissue/melanocytes
  • Abnormal quantitative or qualitative
  • Go through systematically first if no obvious abnormality, or after even if obvious abnormality to ensure nothing missed
191
Q

How are tumours diagnosed?

A
  • History and clinical examination
  • Imaging - X-ray, ultrasound, CT, MRI
  • Tumour markers laboratory analysis - CEA, AFP, Cal25 (ovarian malignancy - sensitive but not specific)
  • Cytology - pap smear, FNA, flow cytometry
  • Biopsy - histopathology, ICC
  • Molecular - gene detection
192
Q

What are depositions? Where are they found? Of what are they composed?

A
  • Abnormal accumulation of substances
  • Location may be intracellular or extracellular (in connective tissue)
  • Composition may be of
    • Normal endogenous substances e.g.
      • Normal products of metabolism including protein, lipid, carbohydrate
      • Pigments (some deposits are both products and pigment)
    • Exogenous (foreign) material e.g.
      • Pigments
      • Industrial material
193
Q

Describe the histological appearance of the terminal ileum in Crohn’s disease

A
  • Inflammatory infiltrate - blue
  • Break in integrity of mucosa - ulceration
  • Muscularis layer infiltrated - transmural
194
Q

Define atherosclerosis

A

Atherosclerosis (also known as arteriosclerotic vascular disease) is a specific form of arteriosclerosis in which an artery wall thickens as a result of the accumulation of fatty materials such as cholesterol and triglycerides

195
Q

Describe the role of inflammation in pathology/physiology

A
  • Universal response to tissue damage
  • Damage can be caused by infection, necrosis, trauma
  • Purpose is to destroy or control the harmful stimulus, initiate repair and restore function
  • Can be acute or chronic (continuum between)
  • Inflammatory process also has a role in AI disease, atheroma, cancer progression and treatment
196
Q

What causes chronic granulomatous inflammation?

A
  • Infectious agent - TB, leprosy, toxoplasmosis
  • Foreign material e.g. talc
  • Sarcoidosis, Crohn’s disease
  • Response to tumour e.g. Hodgkin lymphoma
  • More commonly recently - lip fillers
197
Q

List the possible causes of disease

A
  • Physical agents
    • Mechanical trauma - stricture, adhesions, hernia, criminal
    • Temperature extremes - heat or cold
    • Ionising radiation - causes DNA damage
    • Electric shock
  • Chemicals/drugs
    • May damage various cell organelles and processes e.g. disruption of cell membranes (osmotic damage), protein production/folding
    • Includes
      • Drugs e.g. chemotherapy (cytotoxic by definition), paracetamol
      • Poisons (cyanide)
      • Environmental (insecticides)
      • Occupational hazards (asbestos)
  • Infections
  • Hypoxia/ischaemia
    • Hypoxia definition - deficiency of oxygen
      • Causes - anaemia, respiratory failure
      • Disrupts oxidative respiratory process (in mitochondria) in cell and so decreases ATP
    • Ischaemia definition - reduction in blood supply to tissue
    • Caused by blockage of arterial supply or venous drainage e.g. atherosclerosis
    • Depletion of not just oxygen (as with hypoxia alone) but also nutrients e.g. glucose
    • Damage therefore more rapid and severe
  • Immunological reactions
    • Anaphylaxis - type 1 hypersensitivity: IgE mediated
    • Autoimmune reactions
      • Type 2: antibodies directed towards antigens on cells
      • Type 3: antigen-antibody complexes and their deposition
  • Nutritional
  • Endocrine/metabolic
  • Genetic disease
    • Abnormalities of gene structure or number (too many or too few)
    • Leads to abnormal protein or too much/not enough protein e.g.
      • Sickle cell anaemia - abnormal haemoglobin chain
      • Inborn error of metabolism (lack of enzyme causes build up of enzyme substrate)
198
Q

What are the outcomes of myocardial infarction?

A
  • Sudden death from arrhythmia or acute left ventricular failure
  • Cardiac rupture through weakened necrotic muscle
    • Blood collects in pericardium –> tamponade –> stops heart beating
199
Q

Describe the cellular changes which occur in inflammation

A
  • Neutrophil activation
    • C5a, leukotriene B4, bacterial products
    • Activation of neutrophils
    • Rolling, adhesion, pass between endothelial cells
    • Chemotaxis
    • Phagocytosis and bactericidal effects
  • Endothelial activation
    • 5-HT, histamine, C3a, C5a, bradykinin, leukotriene
    • Activates vascular endothelium
    • Increased cell adhesion molecules
    • Increased leakiness of endothelium
    • Plasma proteins travel into tissues including immunoglobulins, complement, fibrinogen (provide nutrients to site of inflammation)
200
Q

Describe the pathological appearance of a recent MI with mural thrombus

A
  • Loss of thickness of wall, loss of muscle mass
  • Brown –> white
  • Consequence to LV - hyperkinetic segments (don’t move well), less blood flow, predisposes to developing thrombus
  • At risk of developing arrhythmias
201
Q

What is the role of Von Willebrand’s factor in primary haemostasis?

A
  • Binds platelets and endothelial wall to form platelet plug
  • Also binds to factor 8
202
Q

What are the possible complications of Crohn’s disease?

A
  • Stricture formation due to inflammation/fibrosis
    • Causes obstruction, perforation
    • Problems with pain, obstructive symptoms as consequence
  • Ulcers
  • Fistula formation
    • E.g. with bladder - pass air/faeces in urine, pain
  • Dysplasia/cancer in future
    • Need surveillance scope every 3 years
203
Q

Describe the aetiology of amyloid

A
  • Accumulation of excessive amount of normal protein: two main types (systemic deposition)
    • AL amyloid
      • Immunoglobulin light chain
      • Produced in B-cell neoplasms e.g. multiple myeloma
    • AA amyloid
      • Serum amyloid associated protein (a normal acute phase protein), produced in liver
      • Produced in prolonged inflammation e.g. rheumatoid arthritis
  • Accumulation of abnormal protein: multiple types (often localised deposition)
    • E.g. Alzheimer’s, genetic variants
204
Q

List the methods of spread of infection

A
  • Natural barriers
  • Air borne
  • Blood borne
  • Immune factors
205
Q

Where is the primary site of a squamous cell carcinoma likely to be?

A

Head/neck - squamous cell covering

Significance of smoking/alcohol history - leads to dysplasia esp. in head and neck

206
Q

How can the degree of rotation be determined in a chest X-ray?

A
  • Distance between spinous processes and clavicles should be same on both sides - if not there is degree of rotation
  • Badly rotated film - compare, get another example
    • Difference in how ribs look, posterior rib ends have different orientations/lengths
207
Q

How are benign tumours named?

A
  • Usually end with the suffix -oma
  • E.g.
    • Fibroma- fibrous
    • Chondroma - cartilaginous
    • Osteoma - bone
    • Lipoma - fat
    • Adenoma - glandular
    • Cystadenoma - cystic glandular
    • Papillary cystadenoma
  • Big exceptions include sarcoma, melanoma, lymphoma which are all malignant
208
Q

What bones are seen on chest X-ray?

A
  • Clavicles
  • Spinous processes of the vertebrae
  • Ribs
  • Sternoclavicular joint medially - manubrium of sternum articulates with head of clavicle
  • Distal clavicle articulates with the acromion of the scapula at the acromioclavicular joint
  • Glenoid fossa of scapula + humoral head - glenohumeral joint
209
Q

What are the risk factors for DVT?

A
  • Vessel wall
    • Increasing age, varicose veins, surgery
  • Blood flow
    • Obesity, pregnancy, immobilisation, intravenous catheters, external vein compression
  • Composition of blood
    • Thrombophilias (including family history), inflammatory conditions, oestrogen hormones
210
Q

What environmental changes can occur which affect cell homeostasis?

A
  • External
    • Physical factors
    • Chemical factors
    • Infection
    • Nutrition
  • Internal
    • More or less functional demand
    • Hormones/metabolic
    • Immune response
211
Q

Describe the circumstances which may lead to chronic inflammation

A
  • Acute inflammation can terminate either by
    • Complete resolution
    • Continuing chronic inflammation, then resolution
  • Chronic inflammation will always lead to a degree of organisation (granulation tissue formation) and scarring
  • Many factors important e.g.
    • Site affected
    • Type of wound
    • Presence of infection and type of organism involved
    • Presence of indigestible material - foreign body e.g. sutures
    • Treatment given
    • Background disease
212
Q

Describe the nature of amyloid

A
  • In general, accumulation of abnormal substance outside cells
  • For amyloid, organisation (abnormal folding) of soluble protein fibrils into specific abnormal insoluble aggregates
  • Morphology resembles fibrosis but without prior inflammation
  • Can be stained by Congo Red: the fibrils have a specific structure into which the stain intercalates and shows pink
  • E.g. in kidney disease
213
Q

How do cells adapt to stress?

A
  • Adaptations are reversible changes in the number/size/type of cells in response to changes in their environment
  • Physiological adaptations are responses of cells to normal stimulation by hormones or endogenous chemical mediations
  • Pathological adaptations are responses to stress that allow cells to modulate their structure/function and avoid injury
214
Q

Compare localised and systemic infection

A
  • Localised infection
    • Remain at initial site
    • Spread to local lymph nodes via draining lymphatics
    • Five cardinal signs
      • Redness, heat, loss of function, pain, swelling
  • Systemic infection
    • Haematogenous - i.e. spread through blood/lymph to cause systemic inflammatory response
    • Track through tissues to form abscess/infection elsewhere e.g. psoas abscess
  • Controlled by how virulent the organism is, the host condition i.e. immunosuppression, low protein levels, poor vascular supply and treatment given
215
Q

Describe the normal anatomy seen on a chest X-ray

A
  • Lung lobes and fissures
    • Left lung divided into two lobes (upper = green and lower = yellow) by the oblique fissure
    • Right lung divided into three lobes (upper = green, middle = purple, lower = yellow) by the horizontal (between middle and upper) and oblique (between middle and lower) fissures
    • R is bigger because L has cardiac impression where heart lies
  • Airways
    • Midline trachea branches at the carina into right and left main bronchi
  • Hilum
    • Pulmonary arteries
    • Pulmonary veins
    • Main bronchi
  • Heart and mediastinum
216
Q

List the current and new anticoagulants and their mechanisms of action

A
  • Oral
    • Warfarin - vitamin K antagonist (VIIa/TF, IXa, Xa, IIa inhibition)
    • Xa inhibitors - Rivaroxaban, Apixaban, Edoxaban
    • IIa inhibitors - Dabigatran
  • Parenteral
    • Indirect Xa inhibitors (antithrombin) - Fondaparinux, Danaparoid, LMWH, UFH
    • Indirect IIa inhibitors (antithrombin) - UFH, LMWH
217
Q

What are the clinical effects of amyloid?

A
  • Depend on site of amyloid deposition
  • Outcomes in specific organs similar but of varying severity
  • Examples
    • Kidney - renal impairment or failure
    • Heart - heart failure
    • Brain - dementia
  • Important in systemic pathology especially in kidney, osteoarticular system and brain
218
Q

Define atrophy

A
  • Shrinkage in the size/numbers of the cell by the loss of cell substance
  • Results from decreased protein synthesis and increased protein degradation
219
Q

What are the broad classifications of tissue types?

A
  • Epithelial
    • Squamous
    • Glandular
    • Solid organs e.g. liver, kidney, thyroid
  • Connective tissue
    • Fibrous
    • Blood vessel
    • Fat
    • Muscle
    • Bone
    • Cartilage
  • Haematolymphoid
  • Neuro-glial
  • Melanocytic
  • Germ cell
220
Q

What is the aorto-pulmonary window on chest X-ray?

A
  • Lies between the arch of the aorta and the pulmonary artery
  • Can be straight
  • Bulge = mediastinal mass (lymph nodes, lung cancer)
221
Q

What are the pathological consequences of diverticular disease?

A
  • Effects include inflammation, bleeding, perforation, fistulation
    • When there is chronic inflammation and healing, there will be fibrosis which in turn will cause hypertrophy of the muscle which may ultimately exacerbate the problem and lead to stenosis and eventually large bowel obstruction
    • Low fibre, weakening of muscle wall - sac pushed out
    • Becomes inflamed, peritonitis, perforation, localised abscess, fistulate (bladder, upper vagina)
222
Q

Describe the deposition of carbon in the lungs

A
  • Black carbon in lines on lung serosal surface, in lymphatics
  • Carbon from breathing atmosphere
  • Would be more marked if smoker or from city
223
Q

What is the significance of the cardio-thoracic ratio on chest X-ray?

A
  • Normal adult, ratio 50% or less
  • Babies can be 60%, 6 month old can be 55%
  • Afro-Caribbean origin can be 55%
224
Q

How does lobar pneumonia appear pathologically?

A
  • Largely confined to one lobe
  • Gives lung a grey colour (grey hepatisation)
225
Q

What complications can occur following an MI?

A
  • Death
  • Arrhythmia
  • Pericarditis
  • Myocardial rupture
  • Mitral valve prolapse
  • LV aneurysm +/- thrombus
  • Heart failure
226
Q

List the classifications of disease

A
  • Vascular
  • Infective/inflammatory
  • Traumatic
  • Autoimmune
  • Metabolic
  • Iatrogenic/idiopathic
  • Neoplastic
  • Congenital
  • Degenerative/developmental
  • Endocrine/environmental
  • Functional

VITAMIN CDEF

227
Q

What are the functions of lymphocytes?

A
  • Antigen presentation
  • Antibody production
  • Cytokine production
228
Q

What causes developmental anomalies?

A

Caused by genetic mutations, chromosomal aberrations, teratogens and environmental factors (smoking/alcohol)

229
Q

What is amyloid?

A
  • Amyloid is a general pattern/appearance which can be produced by multiple different proteins, due to multiple different causes (e.g. cirrhosis)
  • Amyloid accumulation may be
    • Systemic - widespread
    • Localised - one place
230
Q

Describe the appearance of the mucosa of an abnormal appendix

A
  • Blue cells (main cell type) = neutrophils
    • Inflammatory infiltrate
  • Areas in red - necrosis due to inflammatory cells
    • eosinophils, plasma cells
  • Pathological process = acute inflammation (appendicitis is diagnosis)
  • R - residual epithelial cells are mildly abnormal (swollen and degenerate) and thus show sub-lethal injury
231
Q

What is apoptosis?

A
  • Apoptosis = genetically programmed/activated cell death
  • Requires energy and distinct pathways involved
  • Important physiological role, but can occur in pathological situations
  • Does not cause inflammation but may be caused by immunological mechanisms
  • Different morphology from necrosis
232
Q

How is fluoescence in-situ hybridisation used for pathological analysis?

A
  • Determines presence/absence of DNA/RNA sequences - typically gene(s)
  • Can localise these to a specific chromosomal sites
  • Labeled probes (lengths of complementary DNA or RNA) hybridise to specific areas of interest following denaturation
  • Annealed hybrids then visualised using fluorescence microscopy
233
Q

How is the degree of inspiration in a chest X-ray be determined

A
  • Count the ribs
    • Should be 9-10 posterior ribs and 6 anterior ribs (5 in children)
234
Q

Compare necrosis and apoptosis

A
  • Cell death following injury is usually necrosis - uncontrolled and due to external stimuli
    • Always pathological
  • Other form of cell death is apoptosis - ‘programmed’ and therefore controlled
    • Apoptosis is usually physiological e.g. during embryogenesis and development
    • It can be pathological e.g. in viral infection
  • Main difference is whether cell contents leak out or not - leak = apoptosis
235
Q

Compare the normal appearance of the colonic mucosa to the abnormal appearance seen in Crohn’s disease

A

Normal:

  • Uniformly arranged crypts
  • Produce mucous for lubrication (allows peristalsis)
  • Normal number of neutrophils in underlying lamina propria

Abnormal:

  • Loss of structure/arrangement of crypts
  • Bifid - branched glands
  • Architectural abnormality - long-standing damage healing
  • Increased infiltration of neutrophils/other inflammatory cells e.g. eosinophils (mainly in lamina propria), congestion of blood vessels
236
Q

Define hypertrophy

A
  • Increase in the size of cells and therefore increase in the size of an organ
  • Enlargement is due to an increased synthesis of structural proteins and organelles
  • Occurs when cells are incapable of dividing
237
Q

Describe the function of macrophages

A
  • Macrophages = tissue resident, monocytes = circulating
  • Chemotaxis
  • Synthesise TNF, IL-1, IL-6
  • Phagocytosis
  • Antigen-presenting cells, link between innate and adaptive immune response
238
Q

What is the silhouette sign?

A
  • Normal adjacent anatomical structures of differing densities form a crisp silhouette or contour
  • Loss of a specific contour can help determine the position of the disease process
239
Q

What imaging can be done in tumour diagnosis?

A
  • Plain X ray, CT, CT/PET
  • MRI, ultrasound
  • Contrast studies
    • Angiography, Barium swallow
    • Barium enema
  • Diagnosis and staging
240
Q

What specimens are used for pathology?

A
  • Cytology samples
    • Smears, aspirates
  • Small tissue biopsies
    • Prostate chips, bladder chips, punch biopsies
  • Larger tissue resections
    • Colectomy, oesophagectomy etc.

Specimen purposes

  • Diagnostic only
  • Diagnostic and/or treatment e.g. removal of effusion, colectomy
241
Q

What is an embolism?

A

Mass of material that can move through the vascular system and is capable of blocking the lumen

242
Q

What is a developmental anomaly?

A
  • Any congenital (present since birth) defect that occurs when normal growth and differentiation of the foetus is disturbed
  • Arise at any stage of embryonic development and vary greatly in type/severity
243
Q

Describe the microscopic appearance of papillary carcioma of the thyroid

A
  • V cellular specimen in which there are numerous groups of three dimensional aggregates of epithelial cells
  • Frequent nuclear grooves and occasional nuclear inclusions are seen
  • Background colloid is scant
244
Q

What features are seen in dysplasia?

A
  • Recognised by alterations in the appearance of cells
    • Cell nuclei become hyperchromatic
    • Nuclear membranes become irregular
    • Nuclear to cytoplasmic ratio increases
    • Dysplasia may regress, persist or progress
245
Q

What nuclear changes are seen in necrosis?

A
  • Nuclear fading - chromatin dissolution due to action of DNAases and RNAases
  • Nuclear shrinkage - DNA condenses into shrunken basophilic mass
  • Nuclear fragmentation - pyknotic nuclei membrane ruptures and nucleus undergoes fragmentation

= Nuclear dissolution - anuclear necrotic cell

246
Q

Describe the presentation of ventricular septal defects

A
  • Ventricular septal defects often associated with other syndromes, such as Down’s
  • Ventricular septal defect (VSD) usually symptomless at birth and manifests a few weeks after birth
  • Acyanotic congenital heart defect, aka left-to-right shunt, so there are no signs of cyanosis in the early stage but uncorrected VSD can increase pulmonary resistance leading to the reversal of the shunt and corresponding cyanosis
247
Q

Describe the types of chest X-ray views

A
  • PA - the X-rays penetrate through the back of the patient on to the film
  • AP - the X-rays penetrate through the front of the patient on to the film

All X-rays in the PICU are portable and are AP view

Medicine Year 3 (15 decks)

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