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A2 ME3031 ENDO DM > 03: Childhood growth and problems; Endocrine Sx; Immunology of Endo Diseases > Flashcards

03: Childhood growth and problems; Endocrine Sx; Immunology of Endo Diseases Flashcards

1
Q

Measuring children

A

length v height (spine compr)
sitting
head circumference

bone age: left wrist; measure potential
Tanner method: puberty

*serial measurement
* mid parental height
*

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2
Q

Puberty hormones

A

lh & fsh dormant

puberty: pulsatile releases esp during sleep
= gonad hormones

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3
Q

Most significant pubertal stages

A

*breast budding (B2)
* testicular enlargement (G2)
= puberty will progress onwards normally

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4
Q

Discuss the identification and management of hypothyroidism in the newborn.

A

AMBIGUOUS GENITALIA: exclude congenital adrenal hyperplasia !adrenal crisis first 2w of life
>multidisciplinary approach
> internal ogans, gonads (USS)
> karyotyping

CONGENITAL HYPOTHYROIDISM: d/t dyshormonogenic, athyreosis, hypoplastic, no thyroid/absent

*screening = heel prick, measure TSH

> thyroid hormone replacement

ACQUIRED HYPOTHYROID: common AuIm (hashimoto’s)

*lack of growth, and poor school performance

THYROID DEF: puffiness wt gain

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5
Q

Describe the clinical features of hypopituitarism in adults and children

A

chubbier and rounder, SHORT despite chubby etc.

> diet, exercise, psychological input

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6
Q

Discuss the pathological causes of short stature (including common short stature
syndromes).

A

UNDERNUTRITION; CHRONIC ILLNESS; IATROGENIC: steroid medication

PSYCHO-SOCIAL: home v care environments

HORMONAL:
GHdef.,
>GH replacement

THYROID DEF.: growth failure/obesity
>thyroid hormone replacement

SYNDROMES
TURNER SYNDROME: short, webbed short neck, weight carried neck, short limbs

PRADER-WILLI SYNDROME: short, obese, extreme floppiness
>GH treatment

NOONAN SYNDROME:
>GH treatment

ACHONDROPLASIA: skeletal dysplasia, short limbs, XR skeletal surveys

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7
Q

Discuss the effects of obesity on childhood growth.

A

girls: grow much faster, earlier
boys:

obese children = tall, concern if obese and not growing

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8
Q

State the common causes and principles of investigation of precocious and delayed
puberty.

A

*idiopathic in nature (girls), tumours (boys)

significant pubertal changes milestones, pituitary imaging

boys commonly affected by constitutional delay of growth

GONADAL DYSGENESIS: turner (girls), klinerfelter

CHRONIC DISEASE

IMPAIRED HPG axis

> GnRH agonist (girls before age of 8)

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9
Q

Non-Path causes of short stature

A 
NON-PATH: 
familial
constitutional: puberty delay vs peers, delayed bone age
> short-term hormone boost
small gestational age (SGA): 
>GH Tx
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10
Q

Precocious pseudopuberty

A

gonadotrophin independent

abdn sex steroid secretion

virilisaing/feminanising

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11
Q

OBESITY IN CHILDREN

A

BMI = plotted, skin folds, waist measurement

OBESE + SHORT = ABNORMAL

  • hx
  • ?syndrome, axis pathology, diabetes
  • acanthosis nigricans (insulin resistance, t2DM, goitres flat pale features
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12
Q

Goitre

A

d/t genetic, iodince def., dyshormogenesis, malignancy, TSHoma

stridor (inspiratory wheeze)

> thyroidectomy !vocal cord function, hypothyroidism

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13
Q

Thyroid cancer types

A

MEDULLARY: c-cells; good prognosis

ANAPLASTIC: poor prognosis, uncontrolled dysreg growth

*FNAC

!lymph node, bone, lungs

> surgery
radio-iodine

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14
Q

Pathology of Parathyroid Glands

A

produce parathyroid hormone, which plays a key role in the regulation of calcium levels in the blood.

  • ADENOMA = XS PTH secr.
  • 2º to renal failure
  • hypovitaminosis
  • ectopic gland in chest (developmental)
  • SESTAMIBI scan = metabolic active scanning
  • USSS

> sx

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15
Q

Cushing’s Syndrome

A

xs glucocorticoids

: Weight gain, central obesity, moon facies, buffalo hump fat pad, easy bruising, thin skin, poor wound healing, purple abdominal striae, hirsutism, infertility, depression, irritability, opportunistic infections.

HY, DM, impaired glucose tolerance

> Transabdominal Laparoscopic Adrenalectomy

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16
Q

Conn’s Syndrome

A

xs aldosterone

Increased Na reabsorption by distal tubule and collecting duct of the nephron & Increased K/H excretion
Increased ECF volume
Hypertension +/- Hypokalemia

17
Q

phaeochromocytoma

A

xs Catecholamines

*tumour

Tachycardia, palpitations, pallor, tremor, headache & sweating / Hypertensions, Orthostatic hypotension, Pallor, Retinopathy, Fever & Tremor

  • urine metanephrines
  • MIBG scans
18
Q

Neuroendocrine Tumours

A

gut endocrine cells (origin)

MEN1

  • insulinoma = hypo
  • gastrinoma = peptic ulcers
  • glucagonoma = DM

FUNCTIONAL: SEROTONIN & CHROMOGRANIN SECRETION

  • asymp
  • intestinal obstruction/bleeding

*urinary 5-HIAA serum chromogranin

19
Q

Describe common organ specific and non-organ specific autoimmune disease.

A

organ-specific Vs non-organ specific

TSH R = hyper/hypo
insulin R = hyperglc/hypoglc
myasthenia gravis (ACh R)

NON-SPEC
haemolytic anaemia = TBC ag (multiple)

20
Q

Illustrate the multifactorial aetiology of autoimmune disease.

A

Antigens that induce tolerance are called tolerogens, or tolerogenic antigens = self-tolerance = failure = AuIm disease

*T and B cells bearing these self-reactive
molecules must be either eliminated or downregulated so that the immune
system is made specifically tolerant to self-antigens.

CENTRAL TOLERANCE: THYMUS, eliminating T cells high affinity to self-ag, BM site regulating b cell tolerance

PERIPHERAL TOLERANCE:
- removal/apoptosis of identified mature self-reactive lymphocytes

  • Treg suppress activation of self-reactive lymphocytes
  • sequestration of self-ag from immune system (immune privelege sites)
    •CNS, testes and eyes, and thus cannot engage
    antigen receptors
  • induction of peripheral tolerance is antigen
    recognition without co-stimulation or “second signals.
  • WIDELY VARIABLE GENETIC FACTORS: HLA associations
  • infections (Coxsackie B/mumps for DM1)
  • drugs
  • UV radiation
21
Q

Describe the immuno-pathological mechanisms involved in causation of
autoimmune disease.

A
  • inapt access of self-ag
  • ⇧local expression of co-stimulatory molecules
  • dysregulated presentation of self-molecules to immune system
  • inflamm. = ⇧proteolytic enzymes = non-sepcific breakdown = cryptic epitope creation presented to responsive T cells
  • self-ag altered by viruses, FR, ionising radiation
22
Q

Illustrate the roles of cell mediated and humoral immune mechanisms in
autoimmune thyroid disease (as an illustration of all autoimmune endocrine
disorders).

A

SELF-REACTIVE T CELLS require COSTIMULATION FROM DENDRITIC CELLS to induce autoimm. but if COSTIMULATION is deficient in resting APC = peripheral tolerance via anergy (via SEQUESTRATION)

APC activated by MICROBES = expression of costimators = activating self-toleranct immune cells

23
Q

Define and classify autoimmune polyendocrine syndromes

A

group of clinical conditions characterized by functional
impairment of multiple endocrine glands due to loss of immune tolerance.

alopecia, vitiligo, celiac disease, and autoimmune gastritis with vitamin B12 deficiency that affect nonendocrine organs.

  • genetic factor + env.
  • eventually leads to organ failure
  • early infancy to old age
APS-1: auim regulator gene mutations 
*chronic mucocutaneous candidiasis
*hypoparathyroidism
*addison's disease
\+enamel hypoplasia
APS-2: commoner than APS-1
*DM1, AuIm Thyroid, Addison's Disease
*F>M
*young adulthood (later than APS-1 onset)
\+celiac, alopecia, vitiligo etc.

IPEX: inherited.
*DM1 early
* enteropathy with intractable diarrheal and malabsorption
* Dermatitis that may be eczematiform, ichthyosiform, or psoriasiform.
*earlier dev than APS1
IgE (eosinophillia)
kidney disease

24
Q

Illustrate the importance of endocrine autoantibodies as primary pathogenic agents or as secondary non-pathogenic markers of disease.

A

Mediate pathogenesis of AuIm disease as well as providing speciifc phenotypic info for screening/dx

25
Q

Hashimoto Thyroiditis

A

common cause of acquired hypothyroid, F>M

inital: transient thyrotox. + enlargement
AuIm nature

A2 ME3031 ENDO DM (11 decks)

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