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PNP study cards > Endocrinology Pt. 2 > Flashcards

Endocrinology Pt. 2 Flashcards

1
Q

What (human leukocyte antigens)HLA haplotype is seen in 95% of patients with type 1 DM?

A

DR3 or DR4

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2
Q

What are some environmental triggers for DM type 1?

A

Viral infections (enteroviruses and rubella)

Early introduction of cow’s milk (controversial)

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3
Q

What autoimmune factors contribute to DM type 1?

A
  • Islet cell antibodies (ICA) are present in 85% of patients
    • ICA may be detected in asymptomatic patients 10 years before onset of clinical symptoms
  • Other immunologic markers
    • Antibodies against insulin and against glutamic acid decarboxylase
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4
Q

The classic presentation of DM type 1 includes several weeks of…(3)

A

Polyuria

Polydipsia

Nocturia

polyphagia, wt loss, fatigue, weakness, dysfunction of peripheral nerves

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5
Q

In what percentage of patients is Diabetic ketoacidosis the initial presentation of DM type 1?

A

25%

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6
Q

Girls who have protracted cases of _____ _________ may have early type 1 DM

A

monilial vulvovaginitis

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7
Q

What is required to diagnose patients with type 1 DM?

A

diagnostic: fasting BG >/= 126 mg/dL on 2 occations

Need to confirm with a fasting —- random blood sugar > 200 mg/dL with polyuria, polydipsia, weight loss, or nocturia

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8
Q

What is the honeymoon period of DM type 1?

A

Within a few weeks after initial diagnosis, 75% of patients exhibit a temporary progressive reduction in their daily insulin requirements; this is because of transient recovery of residual islet cell function resulting in endogenous release of insulin in response to carbohydrate exposure

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9
Q

What is the Somogyi phenomenon in DM type 1?

A

This occurs when the evening dose of insulin is too high causing hypoglycemia in early morning hours (3 am), resulting in the release of counter-regulatory hormones (epinephrine/glucagon) to counteract the insulin-induced hypoglycemia; patient then has high blood glucose and ketones in the morning

TX: reduce night time dose of insulin

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10
Q

What are some long term complications of DM type 1?

A
  • Microvascular complications: diabetic retinopathy, nephropathy, neuropathy
  • Macrovascular complications (usually seen in adults): atherosclerosis, HTN, heart disease, stroke
  • DKA: when ill or noncompliant
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11
Q

Which type of diabetes has the strongest hereditary component?

A

Type 2

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12
Q

What is likely the cause of DM type 2?

A

Combination of peripheral tissue resistance to insulin and progressive decline in insulin secretion

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13
Q

What is the clinical presentation of DM type 2?

A
  • Obesity
  • Acanthosis nigricans
  • Asymptomatic to mild DKA
  • recurrent vaginitis
  • peripheral neuropathies and blurred vision
  • chronic skin infections
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14
Q

What is the management of DM type 2?

A

Oral hypoglycemic agents if blood sugar levels are not very high (metformin) - reduced gluconeogenesis, little or no hypoglycemia

Insulin therapy may be required

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15
Q

What is the definition of DKA?

A

Hyperglycemia uually greater than 300 mg/dL with ketonuria and a serum bicarbonate level < 15 mmol/L or a serum pH < 7.3

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16
Q

What are the roles of counter regulatory stress hormones in DM type 2?

A

Hyperglycemia resulting from insulin deficiency leads to an osmotic diuresis with polyuria and eventual dehydration; counter regulatory stress hormones (glucagon, epinephrine, cortisol, GH) are released and contribute to fat breakdown (lipolysis)

Glucagon stimulates conversion of FFA to ketones and eventually leads to DKA

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17
Q

What factors regulate the hypothalamic pituitary thyroid axis?

A

Thyroxine (T4), triiodothyronine (T3), TRH, TSH

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18
Q

What is bound to T4 and T3 in circulation

A

Thyroid binding proteins, including thyroid-binding globulin (TBG) and thyroid binding prealbumin (TBPA)

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19
Q

When are T4 and T3 in their biologically active forms?

A

When they are unbound

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20
Q

What is the clinical presentation of hypothyroidism?

A
  • Suboptimal growth velocity with delayed bone age
  • Goiter
  • Myxedema (puffy skin)
  • Amenorrhea or oligomenorrhea in adolescent girls
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21
Q

What maternal factors may lead to transient congenital hypothyroidism?

A

Use of PTU during pregnancy for maternal Graves’ disease may result in transient hypothyroidism (PTU crosses placenta)

Maternal autoimmune thyroid disease - maternal thyroid blocking antibodies may cross the placenta and block TSH receptors on the newborn thyroid gland

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22
Q

How do most newborns with hypothyroidism present?

A

Asymptomatic and unremarkable physical examination (T4 is not essential for fetal growth)

23
Q

What are classic physical examination findings of congenital hypothyroidism?

A

Large anterior and posterior fontanelles, protruding tongue, umbilical hernia, myxedema, mottled skin, hypothermia, delayed neurodevelopment, poor growth

24
Q

What are the 2 classic symptoms of congenital hypothyroidism?

A

Lethargy and constipation

25
Q

What is the management of congenital hypothyroidism?

A

Thyroid hormone replacement should begin immediately with L-thyroxine

26
Q

What is measured to diagnose hypothyroidism?

A
  • TSH (neonatal screening tests)
  • Increased TSH
  • Low T4 level
  • Antithyroid antibodies (thyroid antiperoxidase antibodies)
27
Q

What clinical features of hyperthyroidism are seen in the eye, the skin, and the CNS evaluations?

A
  • Eye: Lid lag and exophthalmos
  • Skin: Warm and flushed (presence of vitiligo or alopecia suggests the possible coexistance of other autoimmune polyendocrinopathies)
  • CNS: nervousness, fine tremors, history of fatigue and difficulty concentrating in school
28
Q

What is Graves’ disease?

A

Autoimmune disorder characerized by produciton of excessive thyroid hormone by the thyroid gland mediated by a TSH look-alike antibody

29
Q

What antibody is associated with Graves’ disease?

A

Thyroid-stimulating immunoglobulin (TSI), an IgG antibody that cross reacts with TSH and binds to and stimualtes the TSH receptors in the thyroid gland

30
Q

What are the laboratory findings in Graves disease?

A

Increased T3 and T4 levels with suppressed TSH level in the presence of TSI

31
Q

What is the management of Graves’ disease?

A
  • Antithyroid medications: PTU and methimazole (PTU also impairs peripheral conversion of T4 to T3)
  • Subtotal thyroidectomy
  • Radioactive iodine
32
Q

Both _______ and ______ release calcium and phosphorous from bone

A

Vitamin D; PTH

33
Q

PTH helps maintain normal serum calcium level by…

A

Releasing calcium from bone and reabsorbing calcium from the kidneys

34
Q

What enzyme converts 25-(OH) vitamin D (made in liver) into active vitamin D metabolite (1,25-(OH) vitamin D)?

A

1ß-hydroxylase vitamin D

35
Q

What is the main source of calcium absorption and how is it regulated?

A

Gastrointestinal tract due to 1,25-(OH) vitamin D (most potent form of vitamin D)

36
Q

What are the clinical features of hypocalcemia?

A
  • Tetany
    • Carpopedal spasm
    • Laryngospasm
    • Paresthesia
  • Seizures
37
Q

What laboratory evaluation is done for hypocalcemia?

A
  • Serum ionized calcium and phosphorous
  • Serum magnesium
  • Electrocardiogram demonstrating a prolonged QT interval
  • PTH level
  • Vitamin D level
  • Radiograph of wrists or knees to evaluate for rickets
38
Q

How is hypocalcemia managed?

A
  • If mild: no treatment
  • Calcium correction in kids to prevent CNS hyperexcitability
  • Calcium supplementation (Oral or IV calcium gluconate)
  • Calcitriol (Vitamin D analog) for patients with chronic hypoparathyroidism
39
Q

What enzyme is deficient in vitamin-D dependent rickets? What is its inheritance pattern?

A

1ß-hydroxylase

Autosomal recessive (very rare)

40
Q

When does rickets usually occur (2)?

A
  • First 2 years of life
  • Adolescence when bone growth is most rapid
41
Q

What are some clinical features of Rickets?

A
  • Weight bearing bones become bowed
  • Short stature
  • Rachitic rosary (prominent costochondral junctions)
  • Craniotabes (thinning of outer skull)
  • Frontal bossing, delayed suture closure
42
Q

What is diabetes insipidus?

A

Inability to maximally concentrate urine because of either low levels of ADH or renal unresponsiveness to ADH

43
Q

What is ADH?

A

An octapeptide synthesized in the hypothalamus and transported via axons to the posterior pituitary; increases permeability of the renal collecting ducts to water, leading to increased water reabsorption

44
Q

What is central vs nephrogenic DI?

A

Central: ADH deficient

Nephrogenic: ADH resistant

45
Q

What are the possible etiologies of central DI?

A
  • Autoimmune
  • Trauma
  • Hypothalamic tumors
  • Langerhans cell histiocytosis
  • Granulomatous disease (sarcoidosis)
  • Vascular (aneurysms)
  • Genetic (autosomal dominant)
46
Q

How is nephrogenic DI inherited?

A

X-linked recessive disorder

47
Q

What are the clinical features in children with DI?

A

Nocturia, enuresis, poor weight gain, polydipsia, and polyuria

48
Q

Patients with DI present with hypernatremic dehydration and inappropriately dilute urine in the face of increased serum ______ and increased serum osmolality

A

sodium

49
Q

An early monring urine specimin with a specific gravity greater than ______ rules out the diagnosis of DI

A

specific gravity > 1.018

50
Q

What test can be used to diagnose DI?

How can it be determined whether the DI is central or nephrogenic?

A

Water deprivation test: Rising serum osmolality in the presence of persistent urine output and an inappropriately low urine osmolality is diagnostic

At the end of the test, if the patient does not respond to administered ADH, the patient has nephrogenic DI

51
Q

What is the drug of choice for central DI?

A

DDAVP (synthetic ADH)

52
Q

What are the symptoms of hypoglycemia in newborns/infants? In older children?

A
  • Newborns: Lethargy, myoclonic jerks, cyanosis, apnea, or seizures
  • Older children: Tachycardia, diaphoresis, tremors, headaches or seizures
53
Q

What ingestions can lead to hypoglycemia?

A
  • Alcohol (depletes essential cofactors needed for adequate gluconeogenesis)
  • Oral hypoglycemic agents

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