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Misc. 902 Flashcards > Endocrine & Metabolic Flashcards > Flashcards

Endocrine & Metabolic Flashcards

1
Q

Beckwith-Wiedemann Syndrome

A 
Unknown cause
Autosomal dominant inheritance
Characteristics:
•	Macroglossia
•	Abdominal Wall Defect
•	Organomegaly
•	Including pancreas – dump insulin causing 
        hypoglycemia & islet cell hyperplasia
•	Hypoglycemia
•	Polycythemia
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2
Q

Calcium Regulation processes:

A

• Maintenance of cell membrane permeability
• Activation of enzyme reactions for muscle
contraction
• Nerve transmission
• Blood Clotting
• Normal functioning & development of the skeletal
system

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3
Q

Calcium Regulation & the Parathyroid Hormone (PTH)

A
  • Mobilizes calcium and phosphorous from bone

* Decreases renal excretion

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4
Q 
Calcium Regulation & 1,25 Dihyroxycholecalcerferol
Vitamin D (hormone)
A

• Required for PTH to work
• Increases absorption of Calcium and Phosphorous
from the gut

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5
Q

Calcium Regulation & Calcitonin

A
  • Inhibits calcium mobilization from the bone
  • Increases calcium excretion
  • Decreases serum calcium
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6
Q

Factors that Influence Calcium Levels

A
  • Acidosis increases Ca
  • Alkalosis decreases Ca
  • Phosphorous inhibits the absorption of Calcium
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7
Q

A normal magnesium level is required for ? to work

A

• Parathyroid hormone

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8
Q

Definition of Hypocalcemia

A
  • Total Ca of < 7.0 mg/dL

* Ionized Ca < 3 - 4.4 mg/dL or < 0.75 – 1.1 mmol/L

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9
Q

Definition of Hypercalcemia

A
  • Total Ca of < 11.0 mg/dL

* Ionized Ca < 5.8 mg/dL

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10
Q

Causes of Hypercalcemia

A
  • Iatrogenic
  • Hyperparathyroidism
  • Decreases phosphate (phosphorous inhibits Ca)
  • Familial Infantile Hypercalcemia
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11
Q

Hypercalcemia Treatment

A
  • Hydrate
  • Promote excretion with Lasix
  • Decrease Ca and Vit D intake
  • Increase Phosphorous intake
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12
Q

Causes of Hypomagnesemia

A
  • Low maternal level
  • Placental insufficiency
  • Prematurity or IUGR
  • Increased losses with renal or intestinal disorders
  • Hypoparathyroidism
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13
Q

What does the Adrenal Medulla do?

A

• Secretes catecholamines (epinephrine &
norepinephrine)
• “Fight or Flight” response

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14
Q

What does the Adrenal Cortex do?

A

Production of:
• Glucocorticoids
• Mineralcorticoids
• Androgens

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15
Q

Actions of Cortisol (Glucocorticoid)

A

• Regulates blood sugar
• Important for growth
• Maintains cardiovascular function
• Releases in times of stress to increase glucose,
increase cardiac output, and maintain vascular tone.

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16
Q

Actions of Aldosterone (Mineralcorticoid)

A

• Regulates fluid and electrolyte balance
• Stimulates the reabsorption of sodium and water in
the distal collecting tubules.
• Inhibits the secretion of potassium
• Important in maintaining blood pressure,
intravascular volume, cardiac function, and
electrolytes

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17
Q

What is adrenal insufficiency?

A

• A transient phenomenon in the VLBW infant
• Related to the hypothalamic-pituitary-adrenal
immature (the pathway is immature)
• Levels of cortisol are decreased in the VLBW infant
• Levels do not increase during times of stress
• Cortisol suppression related to exogenous steroid
administration

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18
Q

Clinical Manifestations of Adrenal Insufficiency

A
  • Glucose abnormalities
  • Refractory Hypotension
  • Decreased cardiac output, acidosis, and shock
  • Decreased urinary output
  • Infection
  • Hyponatremia, Hyperkalemia
  • Tachycardia
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19
Q

What is the treatment for Adrenal insufficiency?

A
  • Hydrocortisone therapy???
  • How much????

• Recover on own by 14 days of life

20
Q

Thyroid excretes 2 hormones

A
  • Thyroxine (T4)
  • Much of T4 is converted to T3

• Triiodothyronine (T3)

• 99% are bound to protein (not able to produce
effects)
• 1% is free (able to produce effects)

21
Q

What does the pituitary secrete that stimulates the thyroid to release its hormones?

A

• Thyroid Stimulating Hormone (TSH)

22
Q

Congenital Hypothyroidism: Causes

A

• Dysgenic or absent thyroid gland
• Deficient synthesis of thyroid hormones
• Maldevelopment or absence of the anterior
pituitary

23
Q

Congenital Hypothyroidism: Clinical Manifestations

A 
•	Often asymptomatic
•	Symptoms are often subtle and nonspecific
•	May be associated with chromosomal defects (. 
         Downs)
•	Post dates / LGA
•	Defective skeletal maturation & growth
•	Hypotonia
•	Large tongue
•	Umbilical hernia
•	Temperature instability
•	Poor feeding
24
Q

Congenital Hypothyroidism: Diagnosis

A

• State metabolic screen

  • T4 is low
  • TSH is elevated

• Anterior pituitary sees the low T4 and cranks out
the
• TSH to stimulate the thyroid

25
Q

Congenital Hypothyroidism: Treatment

A
  • L-thyroxine (a synthetic T4)
  • Monitor levels
  • Irreversible mental retardation if not treated
26
Q

Hypothyroxinemia of Prematurity

What is it?

A
  • A transient phenomena due to immaturity
  • Fetal thyroid hormones not made until 30 weeks
  • Severity is dependent on gestational age
  • Persists for 4-6 weeks
  • No proven benefit with treatment.
  • Low T4
  • Normal TSH
27
Q

Hyperthyroidism

Neonatal Thyrotoxicosis

A

• Thyroid gland secretes excessive thyroid hormone
• 90% are due to Maternal Graves disease
• Transplacental transfer of thyroid stimulating
immunoglobulins (Mom has thyroid stimulating
immunoglobulins that cross the placenta and
stimulate the babies thyroid)
• May be transient or prolonged
• Considered a medical emergency

28
Q

Hyperthyroidism: Clinical Manifestations

A
  • IUGR
  • Irritability
  • Tachycardia & tachypnea
  • Cardiac failure
  • Hyperthermia
  • Vomiting & diarrhea (due to overeating)
  • Failure to thrive
  • Goiter
29
Q

What is the best position to exam the neonatal thyroid?

A

• Sitting up

30
Q

Hyperthyroidism: Diagnosis

A

• High T4
• Because the maternal immunoglobulins are
stimulate the infants thyroid
• Low TSH
• Because the anterior pituitary sees the high T4 level
and is trying not to stimulate the thyroid anymore.

31
Q

Hyperthyroidism: Treatment

A

Acute treatment:
• PTU (Prophlthiouracil) – blocks the thyroid from
making hormones

Chronic treatment:
• Lugol’s solution – iodine solution

32
Q

Osteopenia of Prematurity: What is it?

A
  • Thinning and undermineralization of the bone
  • Occurs in 50% of infants < 1000 grams
  • Peaks in 2-3 months of age
33
Q

Osteopenia of Prematurity and Prematurity

A

• 80% of bone mineralization occurs during 3rd
trimester
• Intrauterine mineral accretion is much greater than
extrauterine
• Inadequate postnatal bone mineralization

34
Q

Osteopenia of Prematurity: Causes

A

• Inadequate calcium, phosphorus, & Vit D intake
• Feeding intolerance
• Lasix
• Increases renal calcium loss
• Stimulates calcium reabsorption from bone
• Aminophylline – calcium excretion in urine
• Phenobarbital & Dilantin – enhanced Vit D
metabolism

35
Q

What do you need to make bones?

A 
Vitamin D
o	1,25 dihyroxyvitamin D
o	Stimulates absorption of calcium & phosphorous 
        from the intestines
Phosphorous
o	Stimulates bone formation
o	Inhibits reabsorption of bone
Calcium
36
Q

Clinical Manifestations of Osteopenia of Prematurity

A
  • Normal calcium levels
  • Normal to low phosphorous (< 3.5 mg/dL)
  • Increased alkaline phosphate (> 499)
  • Enzyme released due to bone breakdown
  • Cupping & fraying of the metaphysic
  • Decreased bone density
  • Fractures of the long bones & ribs
37
Q

Osteopenia of Prematurity: Treatment

A
  • Prevention!
  • Adequate amounts of calcium & phosphorous
  • Adequate kcal & protein
  • 400 IU of vitamin D
  • Fortify breastmilk / use of premature formulas
38
Q

Osteopenia of Prematurity: Prognosis

A
  • Self-resolving

* Increased incidence of BPD

39
Q

When are the gonads formed?

A

6 – 7 weeks gestation

40
Q

When is testosterone first released?

A

6 – 7 weeks gestation

41
Q

When is sexual differentiation?

A

8 – 9 weeks gestation

42
Q

Klinefelter’s Syndrome

A
  • 47xxy
  • hypogonadism
  • dysgenesis of the seminiferous tubules
  • Not generally diagnosed in the neonatal period
43
Q

Hermaphrodite

A
  • 46xx or 46xy mosaic

* Both ovaries and testes in one individual

44
Q

What is an inborn error in metabolism?

A

• Autosomal recessive genetic defect
• Due to the absence of an enzyme, cofactor, or
transport
• protein which either degrades or converts one
substance into another.
• This absence results in either a toxic accumulation
of the substrate or the deficiency itself can be toxic

45
Q

Inborn Error of Metabolism (Pathway)

A

• The lack of the enzyme leads to an excess (elevation) of the precursor and a deficiency (decrease) in the substrate.

Misc. 902 Flashcards (3 decks)

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