TAS > Chapter 11-15 > Flashcards

Chapter 11-15 Flashcards

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1
Q

Most destructive type of burn?

A

Wet (scalding)
Most common

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2
Q

Contact burn greater than? (what temperature)

A

49C

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3
Q

Uniform shape and depth

A

More likely NAI

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4
Q

Superficial burn

A

Epidermis e.g. suburn

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5
Q

Partial thickness

A

Epidermis and inner dermis

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6
Q

Superficial partial thickness

A

Entire epidermis + upper 1/3 dermis

Micro-vessels injured
Blister formation
Nerve endings exposed
Pink and wet

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7
Q

Deep Partial thickness burn

A

Most of dermal layer
Some epidermal cells remain
White and dry. No blisters
Less painful, sensation remains

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8
Q

Full Thickness burn

A

Complete destruction of dermis + epidermis
Painless

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9
Q

Subdermal burn

A

Epidermis, dermis and tissues below, including fat, tendons, muscle, bone.

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10
Q

Thermal injury
3 zones

A
  1. Zone of Hyperaemia = warm and red
  2. Zone of Stasis = Fliod leak from vasculature
  3. Zone of coagulation = deepest, heat damaged cells collude blood vessels. Immune response is blocked.
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11
Q

Rete Pegs

A

Destruction in epidermis has led to blistering

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12
Q

Things to rule out in short stature

A

Malnutrition
Renal disease
Asthma
Neglect
Thyroid
Karyotype for Turners

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13
Q

Genetic short stature

A

Turners
Short stature homeobox gene (SHOX)
Prader Willi
Trisomy 21
Russell Silver Syndrome

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14
Q

Skeletal dysplasia

A

Achondroplasia
FGFR3 mutations

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15
Q

Environmental short stature

A

IUGR
Neglect
Malnutrition

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16
Q

Chronic disease short stature

A

IBD
Coeliac
CKD
Liver disease

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17
Q

Iatrogenic

A

High dose steroids
Methylphenidate (ADHD)

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18
Q

Endocrine short stature

A

Hypothyroid
Isolated GH deficiencies e.g. GH1
Multiple pituitary hormone deficiency
IGF-1 deficiency
Cushing’s
Hypoparathyroidism

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19
Q

Other short stature

A

Familial short stature
Constitutional short stature

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20
Q

Growth Hormone def

Causes

A

Often no cause found
Multiple pituitary hormone deficiency or brain tumour need to be ruled out

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21
Q

Regulated growth from after infancy to puberty

A

Growth Hormone

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22
Q

Early growth

A

Nutritionally regulated
Mediated by insulin and insulin-like growth factors

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23
Q

Growth Hormone synthesised….where?

A

Anterior pituitary

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24
Q

GH regulated by?

A

Growth hormone releasing hormone (GHRH) (stimulate)
Somatastatin (inhibit)

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25
Pattern GH release
Pulsatile Low during day Maximal early part of night Triggers: Stress, fasting, vigorous exercise, hypoglycaemia
26
GH stimulation test?
Insulin tolerance test
27
GH stimulates release of...
Insulin-like growth factor 1 Insulin - like growth factor 3
28
IGF -1 action sites
Action at bone growth plates Liver Fat Muscle Negative feedback
29
IGF-1 function
growth of bone Cartilage connective tissue Stimulate protein synthesis Cell proliferation Lipolysis
30
Features of GHD
Low muscle bulk Increased s/c fat Mid-facial crowding Delayed dentition
31
Assessing Bone age
Delayed in GHD Rating epiphyseal centres in wrist Rate of ossification Left hand XR Bone age +/- 1 year abnormal
32
Assessing tall stature (4 questions)
Growth velocity normal? Expected genetic target height? Obesity? Is child proportionate?
33
Increased heigh velocity (sudden) without obesity
Hyperthyroid GH excess CAH Precocious puberty
34
Mid parental height
Girls: (Dad + Mum)/2 -7cm Boys: (Dad + Mum)/2 +7cm
35
Marfans
Autosomal dominant Can be disguised as constitutional tall stature Increased arm span vs standing height
36
Developmental delay/ LD with tall stature
Homocystinuria Klinefelter's Sotos
37
Abnormal sitting height: height ration
Long legs + short back Marfans Klinefelter's Gonadotrophin def
38
Beckwith wiedemann
Macroglossia Omphalocele Tall stature/ Macrosomia at birth
39
Long term steroids + cushingoid appearance
Iatrogenic adrenal insufficiency likley Downregulation of glucocorticoids + atrophy of adrenals Low ACTH, low cortisol, low CRH
40
Cortisol secreted from where?
Adrenals Zona fasciculata
41
Cortisol secretion regulated by
Hypothalamo-pituitary axis
42
Cortisol secretion triggered by?
ACTH
43
ACTH released from?
Anterior pituitary gland In response to CRH Negative feedback from Cortisol
44
Function of cortisol
Counters effects of insulin Vascular function INflammatory response Cardiac/ skletal muscle Water excretion
45
Signs of adrenal insufficiency
Anorexia Headache Malaise Nausea Vomiting Hypotension Hypoglycaemia in infants
46
Sick day rules steroids
Double oral dose
47
Ideal timing of steroids
Early morning Alternate days Stop by tapering if >3 weeks
48
Short synacthen test
Ability of adrenal cortex to produce cortisol after stimulation by ACTH (synthetic) 0, 30, 60 mins Morning test
49
CAH caused by
Deficiency in one of five enzymes needed for steroidogenesis Biosynthesis of cortisol from cholesterol 90% by 21-hydroxylase deficiency
50
CAH clinical features (caused by)
Inability to produce Cortisol = hypoglycaemia + hypotension Aldosterone (hyponatrameia + Hyperkalaemia) Accumulation of steroid precursors = virilisation
51
21-hydroxylase deficiency
17-OHP accumulates (downstream part of progesterone metabolism) In excess, converted to androgens = virilisation Deficiency of Cortisol and aldosterone, means ACTH released unchecked = hyperplasia of adrenal glands
52
CAH presentation
Not obvious at birth Range of phenotypes Adrenal insufficiency day 7-14 Girls more obvious due to virilisation
53
CAH investigation at birth
Immediate Karyotype 17-OHP after 72 hours monitor K+, Na2+, Glucose + BP
54
First component of Salt/Sugar/Sex hormones
Cholesterol
55
Zones of Adrenal glands
Zona Glomerulosa Zona Fasciculata Zona Reticularis
56
Way to remember Adrenal products
Go Find Rex (GFR layers) Make Good Sex (mineral, Glucocortico, Sex hormones) Salt, Sugar, Sex
57
Zona Glomerulosa
'Salt' Aldosterone Blood pressure Electrolytes
58
Zona Fasciculata
'sugar' Cortisol Glucose control Blood pressure
59
Zona reticularis
Sex Androgens sexual differentiation
60
Adrenal Medulla
Epinephrine Norepinephrine
61
Treatment CAH
Hydrocortisone Fludrocortisone Salt replacement
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