QNA 3 Flashcards

1
Q

Pathophys diverticulosis

A
  1. Low fibre diet -> chronic constipation -> increased pressure
  2. Connective tissue disorders

1 + 2 ->muscular hypertrophy
herniation of mucosa through wall

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2
Q

Why no diverticularis within small intestine

A

As neurovascular bundle enters the muscularis propria, points of weakness are created

These are re-enforced with a longitudinal layer of muscle in small intestine

In large intestine, these longitudinal muscles form 3 bands only (taeniae coli)

Could herniate through between these bands

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3
Q

Why endometriosis cause pain

A

intrapelvic bleed
Peri-uterine adhesions

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4
Q

Endometriosis cancer risk

A

3times risk of ovarian cancer

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5
Q

Types of graft rejection

A

Hyperacute: Immediate

Acute:
- Accelerated acute: within 7 days
- within 100 days
- treated with high-dose steroids

Chronic:
- T cell
- months-years

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6
Q

3 separate gene mutations for insulinoma

A
  1. MEN 1
  2. PTEN/TSC2 tumour suppressor genes
  3. ATRX and DAXX ->maintenance of telomere
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7
Q

MRSA decol

A

Mupirucin nasal cream
Chlorhexadine body wash

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8
Q

Causative agents for osteomyelitis

A

G +:
Staph aureus
Strep pneumonia

G -:
E coli
H influenza

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9
Q

Pathogenesis of osteomyelitis

A
  1. Inflammation
    - microbial invasion -> inflammation ->increased interosseus pressure -> pain and obstruction of
  2. Suppuration
    - Pus appears in the medulla and spread along Volkmanns canal
    - Lifts periosteum, spreads along the shaft, and forms subperiosteal abscess
    - pus could re-enter at a different point
  3. Necrosis
    - raised pressure, vascular stasis, infective thrombosis comprises blood supply to bone, resulting in death and formation of SEQUESTREUM
  4. New bone formation
    - 10-14 d after
    - deep layer of periosteum forms new bone becoming INVOLUCRUM (enclosing infected tissue and sequestra)
  5. a : Resolution
    - if infection is controlled, intraosseus pressure decreases and bone will heal

5.b. Chronic OM
- if not controlled, pus may break through the involucrum, and track by sinus to skin surface

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10
Q

MEN I

A
  • pancreas insulinoma
  • parathyroid hyperplasia
  • pituitary adenoma
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11
Q

MEN II

A

Phaeochromo
Parathyroid hyperplasia
Thyroid medullary carcinoma

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12
Q

MEN IIb

A

MEN II + Marfinoid habitus + Mucosal neuroma

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13
Q

MEN 1 vs MEN2 mutation

A

Autosomal dominant
MEN 1:
- Menin gene
MEN 2:
- RET protoconcogene

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14
Q

Where is carcinoid tumour commonly found

A

Small intestine
Appendix

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15
Q

Origin cells of carcinoid

A

Enterochromaffin cells

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16
Q

Secretion of carcinoid

A

serotonin

17
Q

Sx of carcinoid tumour

A

Flushing
Diarrhoea

Cadiac: valvular abnormality, fibrosis of endocardium

Wheeze (bronchial constriction)

18
Q

Met site of carcinoid

A

Liver

19
Q

Why carcinoid present after met to liver

A

Seretonin produced by bowel passes through liver and gets broken down before spreading

But when produced by liver, enters the systemic circulation

20
Q

Dx of carcinoid

A

Chromagranin A blood

5HIAA 24hr urinary test

21
Q

Haemorrhoids def

A

swollen anal cushions

22
Q

Pathogenesis of haemorroids

A

Anal cushions fixed by fibromuscular ligaments

Repeated strained defecation -> downward stress tears the fibromuscular ligaments

Can become engorged with blood/prolapse

23
Q

What is TNF

A

a cytokine in systemic inflammation

24
Q

Anti TNF drugs

A

IgG antibodies against TNF
Infliximab
Adalimumab

25
Q

Difference between proto-oncogene and oncogene

A

Proto-oncogene: normal genes promoting cellular proliferation

Oncogene: mutated or over expressed protooncogenes resulting in abnormal proliferation