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4th Year > Paeds - Endo (textbook + 0-finals) > Flashcards

Paeds - Endo (textbook + 0-finals) Flashcards

1
Q

What is the difference between type 1 and type 2 diabetes mellitus?

A

Type 1 is the result of an autoimmune response that causes destruction of insulin producing B cells in the pancreas = absolute insulin deficiency.

Type 2 has a strong genetic component and association with obestity and sedentary lifestyle.

Characterised by progressing inslin resistance in peripheral cells and declining pancreatic B cell function (impaired insulin secretion) resulting in relative insulin deficiency.

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2
Q

What is the bodys ideal blood glucose conc?

A

4.4 - 6.1 mmol/L

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3
Q

Describe the role of insulin and glucagon

A

Insulin is produced by the beta cells in the Islets of Langerhans in the pancreas.

  • Anabolic hormone
  • reduces sugar by causing cells to absorb glucose from blood to use as fuel
  • causes muscle and liver cells to absorb glucose from blood to store as glycogen

Glucagon is produced by alpha cells in the Islets of Langerhans

  • catabolic hormone
  • Released in response to low blood sugar levels and stress
  • makes liver break down stored glycogen to glucose (Glycogenolysis)
  • makes liver convert proteins and fats into glucose (Gluconeogenesis)
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4
Q

How would a child with T1DM present for the first time?

A
  • typically present in diabetic ketoacidosis (DKA)
  • Classic triad of polyuria, polydipsia, weight loss (mainly through dehydration)
  • secondary enuresis (bedwetting in a prev dry child)
  • Recurrent infections
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5
Q

How would you investigate a child presenting with T1DM for the first time?

A
  • Baseline FBC, U&Es, Blood glucose
  • Blood cultures if pyrexic
  • HbA1c
  • TFTs and Thyroid Peroxidase Antibodies for autoimmune thyroid disease
  • Tissue Transglutaminase (anti-TTG) antibodies for coeliac disease
  • Insulin antibodies, anti-GAD antibodies, islet cell antibodies
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6
Q

How would you manage a child with T1DM?

A

Insulin

  • Basal Bolus Insulin Regimes
    • Basal = long acting insulin like “Lantus”
    • Bolus = short acting insulin like “Actrapid” usually 3x a day before meals
    • Injecting in the same spot can cause Lipodystrophy (subcut fat hardens and prevents normal absorption of further insulin injections, so tell patients to cycle their injection sites)

OR

  • Insulin Pumps
    • ​continuous insulin infusion at different rates to control blood sugar levels
    • replaced every 2-3 days and insertion sites are cycled
    • Child must be >12 and have difficulty controlling their HbA1c
    • Pros = better blood sugar control, more flexibility with eating, less injections
    • Cons = education on use, always attached, blockages can occur, risk of infection
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7
Q

What are some symptoms of hypoglycaemia?

A
  • Severe = reduced consciousness, coma, death
  • dizziness
  • pallor
  • irritability
  • hungor
  • tremor
  • sweating
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8
Q

How would you manage someone who is hypoglycaemic? (mild and severe)

A

Mild

  • Combination of Rapid acting glucose eg. lucozade
  • AND Slower acting glucose eg. biscuits or toast

Severe (impairment of consciousness, seizures, coma)

  • IV Dextrose and IM Glucagon
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9
Q

What are some causes of hypoglycaemia?

A
  • In a diabetic:
    • too much insulin
    • not enough carbs, or not processing the carbs (eg. V&D, malabsorption)
  • Hypothyroidism
  • Glycogen storage disorders
  • growth hormone deficiency
  • liver cirrhosis
  • alcohol and fatty acid oxidation defects
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10
Q

Easy way to fix when someone is hyperglycaemic but not in DKA?

A

Increase their insulin dose.

Eventually patients will get to know their response to insulin and adminster the right dose to correct hyperglycaemia.

Be conscious that it can take a few hours to have an effect and repeated doses can lead to hypoglycaemia.

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11
Q

What is the pathophysiology of DKA?

(How do the most dangerous aspects - dehydration, K+ imbalance, and acidosis occur)

A
  • In T1 Diabetics, DKA happens when they are not producing or injecting enough insulin to process glucose
  • Ketogenesis happens when glucose and glycogen stores are depleted eg. in prolonged fasting or low carb diets
    • Liver takes fatty acids and turns them into ketones
    • Ketones cross the blood brain barrier and can be used as fuel by the brain
  • Glucose and Ketone levels in the blood get higher and higher
  • Kidneys produce bicarbonate to buffer ketone acids and maintain normal blood pH
  • eventually ketone acids use up bicarbonate and blood becomes acidic = Ketoacidosis
  • Hyperglycaemia overwhelms kidneys so glucose becomes filtered into the urine
    • glucose in urine draws water out with it via osmotic diuresis = Polyuria = Severe Dehydration = Severe Thirst (Polydipsia)
  • Insulin usually drives potassium into cells
    • without sufficient insulin, total body K+ becomes low as no K+ is being stored in cells
    • serum K+ is high or normal as kidneys are still balancing blood K+ and urinary excreted K+
    • When treated with Insulin, patients can rapidly develop hypokalaemia = fatal arrhythmias
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12
Q

Why are children with DKA at high risk of developing cerebral oedema?

A
  • Dehydration + High blood sugar conc cause water to move from intracellular space in the brain to extracellular space
  • Brain cells shrink and become dehydrated
  • Rapid correction of dehydration and hyperglycaemia (with fluids + insulin) can Rapidly shift water from EC space back into IC space in the brain cells
  • This causes brain to swell and become oedematous
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13
Q

How would you manage and monitor for cerebral oedema?

A
  • Neurological observations (eg. GCS) should be monitored hourly
  • Look out for headaches, altered behaviour, bradycardia, changes in consciousness

Management

  • slow the IV fluids
  • IV Mannitol
  • IV Hypertonic Saline
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14
Q

How would a patient with DKA typically present?

A

Triad of…

  • Hyperglycaemia (>11mmol/L)
  • Ketosis (>3mmol/L)
  • Acidosis (HCO3 <15mmol/L, ph<7.3)

CKS

  • finger prick blood glucose >11mmol/L
  • Polydipsia
  • Polyuria
  • weight loss
  • inability to tolerate fluids
  • persistent vomiting/ diarrhoea
  • abdo pain
  • visual disturbance
  • lethargy/ confusion
  • fruity acetone smell on breath
  • acidotic breathing = Deep sighing (Kussmaul) Respiration
  • Dehydration
    • dry skin and mucous membranes, reduced skin turgor
    • Severe = sunken eyes and prolonged cap refill
    • Shock = tachycardia, hypotension, decreased consicousness showing decreased cerebral perfusion, lethargy, reduced urine output showing decreased renal perfusion
      *
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15
Q

How would you diagnose DKA?

A
  • Hyperglycaemia (blood glucose >11mmol/L)
  • Ketosis (blood ketones >3mmol/L)
  • Acidosis (pH <7.3)
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16
Q

How would you manage DKA in chidlren?

A
  • correct dehydration evenly over 48 hours
    • avoid fluid boluses unless for resus
    • too quickly = cerebral oedema
  • fixed rate insulin infusion
    • avoid hypoglycaemia with IV dextrose once blood glucose <14mmol/L
    • K+ must be greater or equal to 3.3 before insulin therapy is initiated
  • Add IV KCl to IV fluids if K+<5.3
    • monitor serum K+ ever 2 hours
  • Monitor for cerebral oedema
  • Monitor glucose, ketones, pH
  • Treat underlying triggers eg. antibiotics for sepsis
17
Q

How is congenital hypothyroidism picked up?

A

Newborn Blood Spot Screening Test (Guthrie Test)

Otherwise presents with:

  • prolonged neonatal jaundice
  • poor feeding
  • constipation
  • increased sleeping
  • reduced activity
  • slow growth and development
  • pale, cold, mottled dry skin
  • coarse facies
  • large tongue
  • hoarse cry
  • occasionally goitre
  • umbilical hernia
18
Q

What is the most common cause of acquired hypothyroidism?

A

Hashimotos Thyroiditis = Autoimmune thyroiditis

  • antithyroid peroxidase antibodies
  • antithyroglobulin antibodies
  • associated with Type 1 DM and Coeliac Disease

Symptoms

  • fatigue and low energy
  • poor growth
  • weight gain
  • poor school performance
  • Constipation
  • Dry skin and hair loss
19
Q

How would you investigate and manage hypothyroidism in children?

A
  • refer to paediatric endocrinologist
  • Thyroid Function Blood Tests (TSH, T3, T4)
  • Thyroid US
  • Thyroid antibodies

Management

  • oral Levothyroxine once a day
20
Q

What are some causes of congenital hypothyroidism?

A
  • maldescent of thyroid and athyrosis
  • Dyshormonogenesis = error of thyroid hormone synthesis
  • Iodine deficiency
  • Hypothyroidism due to TSH deficiency
    • usually associated with pituitary dysfunction (presents as GH, Gonadotrophin, and ACTH deficiency = hypoglycaemia, micropenis, undescended testes)
21
Q

What is the most common cause of hyperthyroidism?

A
  • autoimmune thyroiditis (Graves Disease)
  • secondary to the production of thyroid stimulating immunoglobulins
  • T4 and T3 are elevated, TSH is suppressed to low levels
22
Q

What are some symptoms of Hyperthyroidism?

A
  • anxiety, restlessness, palpitations
  • Tiredness and difficulty sleeping
  • sweating, sensitivity to heat
  • diarrhoea
  • weightloss despite increased appetite
  • patchy hair loss or thinning
  • Goitre
  • Eye signs less common in children
    • exophthalmos
    • opthalmoplegia
    • lid retraction
    • lid lag
23
Q

How would you manage hyperthyroidism?

A

Medication

  • Carbimazole or propylthiouracil
    • Risk of neutropenia from antithyroid medication
  • B Blockers for symptomatic relief (anxiety, tremor, tachy)
24
Q

How does neonatal hyperthyroidism occur?

A

In mothers with thyrotoxicosis, there can be transplacental transfer of Thyroid Stimulating Immunoglobulins

25
Q

What is congenital adrenal hyperplasia?

A

Autosomal Recessive congenital deficiency of 21-hydroxylase enzyme

(sometimes deficiency of 11-hydroxylase)

Results in really high Androgens (testosterone), and really low Glucocorticoids (cortisol) and Mineralocorticoids (aldosterone)

  • because there is insufficient 21-hydroxylase to convert progesterone into aldosterone and cortisol.
  • Therefore all the progesterone is being converted into testosterone instead.
26
Q

How would mild CAH present?

A

Mild typically present in childhood or after puberty due to symptoms related to high androgens

  • tall for their age
  • deep voice
  • early puberty
  • female = facial hair, absent periods
  • male = large penis, small testicles
  • Skin hyperpigmentation
    • Anterior Pituitary responds to low cortisol by increasing ACTH (a by product of ACTH is Melanocyte Stimulating Hormone)
27
Q

How would severe CAH present?

A
  • Females present at birth with virilised genetalia
    • “ambiguous genitalia” and an enlarged clitoris due to high testosterone
  • Shortly after birth:
    • Hyponatraemia
    • Hyperkalaemia
    • Hypoglycaemia
  • above leads to poor feeding, vomiting, dehydration, arrhythmias
28
Q

How would you manage CAH?

A
  • Cortisol replacement via hydrocortisone
  • Aldosterone replacement via fludrocortisone
  • Corrective surgery for females with virilised genitals
29
Q

What is primary, secondary and tertiary adrenal insufficiency?

A

Primary

  • aka Addisons disease
  • destruction of adrenal cortex, resulting in reduced secretion of cortisol and adrenaline
  • usually due to autoimmune disease

Secondary

  • inadequate secretion of ACTH from pituitary, resulting in reduced stimulation of adrenal glands
  • Causes = congenital underdevelopment (hypoplasia) of pituitary gland or damage to pituitary via surgery, infection, decreased blood flow, radiotherapy

Tertiary

  • Inadequate CRH release by the hypothalamus
  • usually the result of patients being on long term oral steroids (>3 weeks), resulting in suppression of hypothalamus
    • should taper steroids slowly to allow time for adrenal axis to regain normal function and start producing endogenous steroids again.
30
Q

How would adrenal insufficiency present in babies and children?

A

Babies

  • lethargy
  • vomiting
  • poor feeding
  • hypoglycaemia
  • jaundice
  • failure to thrive

Older kids

  • nausea and vomiting
  • poor appetitie
  • poor weight gain or weight loss
  • abdo pain
  • muscle weakness or cramps
  • developmental delay or poor academic performance
  • Hyperpigmentation due to Addisons causing high ACTH stimulation
31
Q

What investigations would you do in suspected adrenal insufficiency?

A
  • U&Es (hyponatraemia, hyperkalaemia)
  • Blood glucose (hypoglycaemia)
  • Adrenal antibodies
  • CXR may show TB and calcified adrenal glands
  • Measure Random serum Cortisol, 0900 levels of ACTH, Serum Aldosterone, Renin levels before steroids
    • Addisons = low cortisol, high acth, low aldosterone, high renin
    • Secondary = low cortisol, low acth, normal aldosterone, normal renin
  • Short Synacthen Test
    • give synthetic ACTH (synacthen) in the morning
    • measure baseline cortisol 30-60 mins after administration
    • synacthen should stimulate cortisol levels to at least double
    • Measurement of less than double baseline cortisol = primary adrenal insufficiency
32
Q

How would you manage adrenal insufficiency?

A
  • Hydrocortisone to replace cortisol
  • Fludrocortisone to replace aldosterone
  • Give patients a steroid card and emergency ID tag to inform emergency services they are dependent on steroids
  • Monitored by paediatric endocrinologist (Group and development, BP, U&Es, Glucose, Bone profile, Vit D)
33
Q

What are the sick day rules for adrenal insufficiency and steroid treatment?

A

Sick Day rules (temp over 38 or D&V)

  • increase dose of steroid and given more regularly until illness has resolved
  • eat more carb containing foods, measure blood sugar closely
  • IM injection of steroid at home if D&V, may need admission for IV steroids
34
Q

What is an addisonian crisis?

A

an acute presentation of severe addisons - the absence of steroid hormones has resulted in a life threatening presentation

  • reduced consciousness
  • hypotension, hypovolaemic shock
    • due to the aldosterone deficiency
  • fever, vomiting
  • abdo pain
  • hypoglycaemia
  • hyponatraemia
  • hyperkalaemia

Can be first presentation of Addisons, or established Addisons triggered by infection/ illness/ trauma/ abrupt steroid cessation in someone whose natural steroid production has been suppressed by exogenous steroids.

35
Q

How would you manage an addisonian crisis?

A
  • intensive monitoring and emergency admission
  • Hydrocortisone IM or IV
  • IV fluid resuscitation
  • Correct hypoglycaemia
  • Monitor Electrolytes and fluid balance
36
Q

What is Cushings Syndrome?

A

A state of excess free circulating glucocorticoid (cortisol).

In kids it is usually a SE of Long term glucocorticoid treatment for conditions like nephrotic syndrome or asthma.

can also be due to:

  • ACTH producing tumours (eg. in pituitary or small cell lung cancer etc)
    • Cushings Disease = Cushings Syndrome due to pituitary adenoma
  • Adrenal Tumours
    • usually in young children (may also be virilisation)
37
Q

What are some features of Cushings Syndrome

A

Symptoms

  • slow growth
  • red cheeks
  • weight gain
  • thin skin, easy bruising
  • amenorrhoea/oligomenorrhoea
  • polyuria
  • dyspepsia
  • acne
  • reduced libido
  • back pain

Signs

  • round “Moon face”
  • hirsutism
  • pigmentation (In ACTH dependent causes like pituitary adenoma)
  • HTN
  • Osteoporosis/osteopenia
  • dorsal fat pad = “buffalo hump”
  • Kyphosis = hunch back
  • Purple or red striae on abdo
  • Supraclavicular fat pads
  • oedema
  • proximal myopathy
  • Glycosuria
  • Diabetes/ impaired glucose tolerance
    *
38
Q

How would you investigate suspected Cushings?

A
  • Consider in children with obesity
    • a child who was obese due to dietary excess woud be tall compared with their midparental height
    • Cushings syndrome children would be short
  • Midnight cortisol level is high
    • normal diurnal variation of cortisol is high in morning, low at midnight
  • 24 hour urine free cortisol is high
  • 1mg overnight dexamethasone suppression test
    • After administering dexamethasone at night, there is failure to suppress plasma 0900 cortisol levels the next morning
    • OR 48 hour low dose dexamethasone test
      • Cushings patients will fail to suppress cortisol level to <50nmol/L
  • CT or MRI of abdo will show adrenal tumour
  • MRI brain will show pituitary adenoma
  • CXR to show carcinoma of bronchi
39
Q

How would you manage Cushings?

A

Control cortisol hypersecretion medically first

  • metyrapone

Cushings Disease

  • Radiotherapy = External Pituitary Irradiation (preferred in children)
  • Medicine = Bromocryptine (try to reduce ACTH secretion)
  • Surgery = transphenoidal removal of tumour
    • Bilateral adrenalectomy as last resort
      • Can result in Nelsons syndrome (hyperpigmentation due to high ACTH)

Remove ectopic ACTH Tumours .

Radiotherapy and surgical removal of adrenal carcinoma.

4th Year (17 decks)

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