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Clinical Conditions > 2. TOB > Flashcards

2. TOB Flashcards

1
Q

What is an ectopic pregnancy?

A

Implantation of the embryo in Fallopian tube or another site not the posterior uterine wall.

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2
Q

What are the complications of ectopic pregnancies?

A

Rupturing can lead to miscarriage and haemorrhage.

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3
Q

What is placenta praevia?

A

Implantation of the embryo in lower segment of uterine wall, blocking the cervix.

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4
Q

How are placenta praevia pregnancies dealt with?

A

Perform C-section to avoid haemorrhage.

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5
Q

What causes Marfan’s syndrome?

A

Autosomal dominant causes misfolding of fibrillin so there is more elastic connective tissue.

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6
Q

What is the presentation of Marfan’s syndrome?

A

Very tall, long digits, high arched palate.

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7
Q

What is the risk of Marfan’s syndrome?

A

Often die from aortic rupture around 40 years old.

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8
Q

What is Ehlers-Danlos syndrome?

A

Type III collagen deficiency leading to a loss of structure.

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9
Q

What is the presentation of Ehlers-Danlos syndrome?

A

Stretchy skin, unstable joints, etc.

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10
Q

What is vitiligo?

A

An autoimmune condition that attacks melanocytes causing loss of pigmentation in the skin.

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11
Q

In what population does vitiligo have a more obvious effect?

A

Dark skinned.

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12
Q

What is alopecia?

A

Autoimmune destruction of hair follicles causing hair loss.

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13
Q

What is alopecia worsened by?

A

Stress.

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14
Q

What is psoriasis?

A

Extreme overproduction of skin cells causing too much corneum and scaling.

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15
Q

What is the presentation of psoriasis?

A

Scaling on skin.

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16
Q

How is psoriasis managed?

A

Give steroids.

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17
Q

What causes malignant melanoma?

A

Excessive UV radiation causing melanocyte mutation.

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18
Q

What is malignant melanoma?

A

An aggressive skin cancer.

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19
Q

What affects the prognosis of malignant melanoma?

A

If it has penetrated through the basement membrane, then it’s a poorer prognosis. Also metastases give a poor prognosis.

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20
Q

What is osteogenesis imperfecta?

A

An autosomal dominant condition where type I collagen is deformed or deficient.

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21
Q

What is the most severe presentation of osteogenesis imperfecta?

A

No conversion of foetal skeleton to solid bone.

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22
Q

What is the normal presentation of osteogenesis imperfecta?

A

Lots of fractures, bowed long bones, blue sclerae.

23
Q

What can vitamin D deficiency lead to?

A

Less Ca2+ absorbed so less rigid bones -> rickets of osteomalacia.

24
Q

What is Rickets?

A

Vitamin D deficiency in children when they are still growing leads to bowed bones.

25
Q

What is osteomalacia?

A

Vitamin D deficiency in adults that causes bone and back ache.

26
Q

What is osteoporosis?

A

Where osteoclast activity is greater than osteoblast activity.

27
Q

What is type I osteoporosis?

A

Menopausal, oestrogen no longer mediates osteoclast function.

28
Q

Which fractures are common in type I osteoporosis?

A

Hip and vertebrae fractures.

29
Q

What is type II osteoporosis?

A

Old age, osteoblast action is less so no bone remodelling.

30
Q

What is acromegaly and gigantism caused by?

A

Excess growth hormone causing increased bone deposits.

31
Q

What causes acromegaly?

A

Excess growth hormone if epiphyseal growth plates are closed (in adults) then there is more intramembranous ossification so larger flat bones.

32
Q

What causes gigantism?

A

Excess growth hormone if epiphyseal growth plates are open (in growing children) so there is more intramembranous and endochondral ossification causing long bones to get longer and tall stature.

33
Q

What is a complication of neonatal hypothyroidism?

A

Cretinism - retardation and short stature.

34
Q

How is cretinism avoided in neonates with hypothyroidism?

A

Thyroxine is given before aged 3 weeks to prevent irreversible change.

35
Q

What causes achondroplasia?

A

An autosomal dominant defect causing deformed fibroblast growth factor receptor and so less endochondral ossification.

36
Q

What are the features of achondroplasia?

A

Short limbs, enlarged forehead, normal trunk, 4ft tall.

37
Q

What is myasthenia gravis?

A

An autoimmune condition with destruction of end plate ACh receptors.

38
Q

What is the presentation of myasthenia gravis?

A

Droopy eyelids, fatigue, sudden collapse.

39
Q

How is myasthenia gravis managed?

A

With immunosuppression and AChesterase inhibitors so ACh stays in the synapse for longer.

40
Q

What is muscular dystrophy?

A

X linked recessive disorders with absent or truncated dystrophin causing muscle fibres to tear on contraction.

41
Q

What is the difference between Duchenne’s and Becker’s muscular dystrophy?

A

Duchenne’s has absent dystrophin, Becker’s has truncated dystrophin.

42
Q

What is a sequelae of muscle fibres tear in muscular dystrophy?

A

Ca2+ induced necrosis.

43
Q

What are the clinical features of muscular dystrophy?

A

Fat and connective tissue laid down, Gower’s sign (brace thighs with arms), chest muscles destroyed.

44
Q

How can muscular dystrophy lead to death?

A

The chest muscles can be destroyed leading to respiratory collapse and death.

45
Q

What is the effect of botulinum toxins?

A

They block ACh release so there is no muscle contraction.

46
Q

How is botulism used clinically?

A

In botox to stop facial muscles contraction and therefore to prevent wrinkles.

47
Q

What is thyrotoxicosis?

A

Increased BMR leads to protein catabolism and atrophy.

48
Q

What is hypoparathyroidism?

A

Lack of parathyroid hormone causes lack of Ca2+ absorption and tetany.

49
Q

What is malignant hyperthermia?

A

An autosomal dominant life threatening reaction to general anaesthesia.

50
Q

How is malignant hyperthermia life threatening?

A

It releases Ca2+ from al SR stores in response to general anaesthesia, which causes a huge spike in oxphor in skeletal muscle, causing a huge temperature spike and death.

51
Q

How is malignant hyperthermia dealt with?

A

Manage symptoms with paracetamol. Dantrolene to prevent Ca2+ release.

52
Q

What is multiple sclerosis?

A

Autoimmune destruction of myelin sheath and Schwann cells causing reduced conduction and loss of function.

53
Q

How is multiple sclerosis managed?

A

B interferon or steroids to mediate immune function.

Clinical Conditions (13 decks)

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