Week 20 Pathology - Environmental

Question 1

What are the non-malignant effects of smoking?

Answer 1

COPD
Atherosclerosis
Pre-term labour
Gastric ulcers

Question 2

What are the malignant effects of smoking?

Answer 2

Lung, oesophagus, pancreas, kidney, bladder, cervix

Question 3

What is the clinical presentation of lead poisoning in children vs adults

Answer 3

Children = intellectual impairment, behavioural problems subclinically, can result in encephalopathy, abdominal pain, tubulointersitial disease, radio dense deposits in epiphyses

Adults = headache, memory loss, peripheral nerve demyelination, (classic wrist drop) as well as the above with children, including anaemia with basophilic stippling (microcytic, hypo chromic) - differential diagnosis for microcytic anaemia

Question 4

Describe the different pathways of metabolism of alcohol? What is the main one? Where is each located?

Answer 4

Common pathway (3 different mechanisms) metabolises EtOH to acetaldehyde.

1. Alcohol dehydrogenase (Main) - Cytosol
2. Microethanol-oxidising system (MEOS) - Microsome
3. Catalse - Peroxisome

Question 5

How does ADH work to metabolise EtOH?

Answer 5

Cytosolic ADH catalyses the reduction of NAD to NADH, with the byproduct of acetaldehyde formation.

Within mitochondria, acetaldehyde is acted on by acetaldehyde dehydrogenase to form acetic acid, which is then used in mitochondrial respiratory chain

Question 6

What are the biggest life threats associated with thermal burns?

Answer 6

1. Fluid shift and shock (movement of fluid into interstitial space both locally and systemically due to SIRS, including APO)
2. Airway burns
3. Infection/sepsis

Question 7

What is the body’s most sensitive tissue to ionising radiation?

Answer 7

Lymphoid

Question 8

What are the neurohormones that signal to hypothalamus satiety?

Answer 8

Leptin, Adiponectin, Pyy = satiety

Ghrelin = hunger hormone

Question 9

What type of hypersensitivity reaction is urticaria?

Answer 9

Type 1

Question 10

What causes the characteristic wheals in urticaria?

Answer 10

Mast cell degranulation causing dermal microvascular hyper permeability

Question 11

What is the pathogenesis of urticaria?

Answer 11

Antigen induced release of vasoactive mediators from mast cell granules, IgE antibodies. Also can have IgE independent urticaria from drugs that act directly on mast cells (opioids, contrast, antibiotics)

Question 12

What hypersensitivity reaction is involved in psoriasis?

Answer 12

Type IV

Question 13

What is the pathophysiology of psoriasis?

Answer 13

Hyperproliferative disorder resulting from cascade of inflammatory mediators, with increased mitotic activity of basal cells, and increased migration to status corneum. Strong genetic + environmental factors

Question 14

What are the different types of psoriasis?

Answer 14

Plaque: commonest, raised, inflamed plaques with scaly eruptions

Inverse: occurs in moist areas (axilla, groin, submammary, still well demarcated but not classic scale)

Guttate: children, widespread, fine and scaly often after URTI

Pustular

Psoriatic

Question 15

What layer of the skin are dermatophytes confined to?

Answer 15

Stratum corneum

Question 16

What are the mechanisms of spread of osteomyelitis?

Answer 16

1. Haematogenous (most common in children, long bones)
2. Extension from contiguous site (adults, open fracture, DM wound)
3. Direct implantation

Question 17

What are the common causative organisms in OM?

Answer 17

Staph. aureus 80-90%

E. coli, klebsiella, pseudomonas (concurrent UTI, IVDU)

Question 18

What is the sequence of events/progression of OM?

Answer 18

Bacteria seeded, proliferate and induce inflammatory reaction - entrapped bone undergoes necrosis and bacteria spread throughout Haversian system to periosteum –> lifting of periosteum and suppurative ischaemic injury

Question 19

What is the natural progression of rheumatoid arthritis?

Answer 19

Chronic inflammatory disorder producing non-suppurative and proliferative synovitis.

Progressed to destruction of articular cartilage and ankylosis

Question 20

What is the pathophysiology of RA?

Answer 20

Antibodies directed against self antigen and cytokine mediated inflammation, primarily by CD4 T cells.

Resident synovial macrophages secrete proteases, as well as sensitised plasma cells, which produced autoantibodies for cartilage/connective tissue antigens

Question 21

What is the pattern of joint pain in RA?

Answer 21

Symmetrical, polyarticular, often MCP joints classically

Question 22

What increases susceptibility to septic arthritis?

Answer 22

Immunodeficiency
Joint trauma
IVDU

Question 23

What are the common causative organisms in septic arthritis?

Answer 23

Children < 2 HiB
Aged > 2 Staph aureus
Teens/young adults = gonococcus

Question 24

What viruses can lead to a reactive arthritis?

Answer 24

Parvovirus
Rubella
EBV
Hep B, C

Question 25

What are the two endogenous forms of crystal arthritis?

Answer 25

Gout - monosodium urate

CPPD - calcium phosphate

Question 26

What is the pathogenesis of gout?

Answer 26

Either increased production or decreased excretion of urate.

(Urate = end product of purine catabolism)

Precipitation of monosodium urate crystals into joints, resulting in cytokine mediated recruitment of leukocytes.

Question 27

What are risk factors for gout?

Answer 27

Genetic predisposition
EtOH
Obesity
Drugs ( thiazides) that reduce urate excretion