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Neville and Damm > Ch 17 Systemic Diseases 4 > Flashcards

Ch 17 Systemic Diseases 4 Flashcards

1
Q

What two hormones regulate calcium levels in extracellular tissues? What are the two target tissues/cells for these hormones?

A

PTH (kidney to increase ca reabsorption and phostphate excretion) and Vit D (gut to increase ca absorption)

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2
Q

What is hypoparathyroidism “usually” caused by? What is it “sometimes” caused by? (dont you love how specific Neville is?)

A

usually inadvertant removal of the parathyroid glands during thyroidectomy….sometimes autoimmune destruction

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3
Q

What 2 syndromes have been associated with hypoparathyroidism?

A
  1. DiGeorge Syndrome 2. Autoimmune polyendocinopathy-candidiasis-ectodermal dystrophy syndrome (I’m gonna call it “APCEDS” lol)
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4
Q

Name the test of tapping the facial nerve just below the zygomatic process for a patient with hypoparathyroidism….what does a positive result indicate?

A

CHVOSTEK sign: twitching of the upper lip when the facial nerve is tapped below the zygomatic process… Positive response = latent degree of tetany (hypocalcemia)

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5
Q

What are 3 oral manifestations of hypoparathyroidism?

A
  1. pitting enamel hypoplasia (hypo PTH early in life) 2. failure of tooth eruption (hypo PTH early in life) 3. Persistent candidiasis in young pt (onset of APCEDS)
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6
Q

What are the 4 serum markers used to diagnose hypoparathyroidism? (one is not a specific marker)

A
  1. decreased PTH 2. decreased calcium 3.elevated phosphate 4. normal renal function
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7
Q

Lol: what are the two alternate names for PSEUDOhypoparathyroidism?

A
  1. Albright Hereditary Osteodystrophy (yes, the same Albright as McCune-Albright) (Oh also, McCune was a Columbia attending for 20 years) 2. Acrodysostosis
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8
Q

Term for normal parathyroid hormone (PTH) is present in adequate amounts but the biochemical pathways responsible for activating the target cells are not functioning properly

A

pseudohypoparathyroidism

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9
Q

What is the most common mode of inheritance for pseudohypoparathyroidism (some cases are sporatic)? Which critical metabolic molecule is affected in multiple types of the disease?

A

AD…cAMP (Gs-Delta alteration leading to non-functioning or does not make cAMP)

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10
Q

This plus oseoma cutis

A

pseudohypoparathyroidism type 1a or 1c (Type 1b or II patients appear normal)

Types Ia or Ic have a characteristic array of features

Mild intellectual disability

Obesity

Round face

Short neck

Short stature

Midfacial hypoplasia

Short thick fingers

Osteoma cutis

Hypogonadism, hypothyroidism

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11
Q

What are the 5 dental manifestations of pseudohypoparathyroidism? What is the radiographic buzzword for the intrapulpal calcifications?

A
  1. Generalized enamel hypoplasia
  2. Widened pulp chambers with “DAGGER” shaped intrapulpal calcifiactions
  3. Oligodontia
  4. Delayed eruption
  5. Blunting the apicies of the teeth
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12
Q

What are the 4 serum markers for the diagnosis of pseudohypoparathyroidism? (again, one of the 4 is a generalization)

A
  1. Elevated PTH
  2. Hypocalcemia
  3. Hyperphosphatemia
  4. Normal renal function
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13
Q

What is the cause of 90% primary hyperparathyroidism cases? What about 10%? And what is a rare cause?

A

90% parathyroid adenoma, 10% parathyroid hyperplasia, Rare parathyroid carcinoma

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14
Q

What are three syndromes that can cause hyperparathyroidism?

A
  1. MEN1
  2. MEN2a
  3. Hyperparathyroidism-Jaw tumor syndrome
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15
Q

Which jaw lesion develops in Hyperparathyroid-Jaw Tumor syndrome? (usually multiple)

A

Central ossifying fibromas

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16
Q

What type of cancer are patients with Hyperparathyroid-Jaw Tumor syndrome at an increased risk of developing?

A

parathyroid carcinoma

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17
Q

What is the typical cause for secondary hyperparathyroidism?

A

chronic renal disease (Vit D not being produced by kidney so no absorption of calcium from the gut)

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18
Q

What is the age range, gender for hyperparathyroidism?

A

older than 60 years, women 4x more than men

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19
Q

What is the classic saying for the triad of symptoms associated with hyperparathyroidism? What does it mean?

A

“stones, bones, and abdominal groans”

stones = kidney stones

bones= resorption of the index/mid fingers, loss of lamina dura, alteration in trabecular pattern “GROUND GLASS”, Brown tumors, osteitis fibrosa cystica, jaw enlargment in secondary hpth pts

abdominal groans = duodenal ulcers, lethargy, weakness, confusion, dimentia

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20
Q

What 4 bones are most often affected by Brown tumors?

A
  1. Mandible
  2. Clavicles
  3. Ribs
  4. Pelvis
21
Q

What is the term for the changes seen in a longstanfing brown tumor of HPTH?

A

osteitis fibrosa cystica

22
Q

What is the nuclear medicine element used to label the hyperplastic parathyroid tissue?

A

technetium-99

23
Q

What organ usually shows the first signs of secondary hyperparathyroidism?

A

kidney (stones or osteodystrophy)

24
Q

What is the alternate name for hypercortisolism? What is the alternate name specific for?

A

Cushing Syndrome: clinical condition that results from a
sustained increase in glucocorticoid levels. In most cases this
increase is due to corticosteroid therapy that is prescribed for
other medical purposes.

If a pituitary adenoma is responsible,
then the term Cushing disease is applied. This condition is
rather rare and usually affects young adult women.

25
Q

What are most cases of hypercortisolism due to? What are two other causes?

A

Most common: prescribed corticosteriod therapy

Others: an adrenal tumor

or

a pituitary adenoma (Cushing DZ)

causing an increase in ACTH hormone

26
Q

What is the age and gender demographic for Cushing DISEASE?

A

young adult women

27
Q

Name that condition

A

Cushing Syndrome (Buffalo hump, moon face, red-purple abdominal striae, hirsutism, etc)

28
Q

What is the threshold for a “large” amount of corticosteriod therapy?

A

greater than the equivalent 20mg prednisone on a daily basis for several months

29
Q

What test is used to determine if a patient has hyperadrinocorticoism due to a tumor?

A

a dexamethasone assay: ACTH and cortisol do not decrease in the serum (normally administration of dexa would cause a decrease in ACTH and cortisol)

30
Q

What is an addisonian crisis? How is it treated?

A

An addisonian crisis is a life-threatening situation that results in low blood pressure, low blood levels of sugar and high blood levels of potassium.

theraputic corticosteriods suppress production of ACTH by the pituitary, in times of stress the pituitary may not be able to produce ACTH

If a dental or surgical procedure (potentially stressful) is planned, an increase in corticosteriod dose to cover the body’s increased need for cortisol

31
Q

What is the alternate name for Addison Disease?

A

Hypoadrenocorticism

32
Q

What are the three general categories for the cause of primary hypoadrenocorticism?

A

Destruction of the adrenal cortex via:

  1. Autoimmune destruction (most common in Western societies)
  2. Infection (TB, Fungal, esp w AIDS pts)
  3. Metastatic tumors / sarcoidosis / hemochromatosis / amyloidosis
33
Q

What is the cause of secondary hypoadrenocorticism?

A

pituitary gland dysfunction resulting in less ACTH production

34
Q

What % of the adrenal cortext is usually destroyed before clinical features appear? What are some clinical features of Addison Disease?

A

90% destruction

  1. fatigue
  2. irritability
  3. depression
  4. weakness
  5. hypotension
  6. BRONZING of the skin
  7. GI upset / anorexia /nausea / vomiting / diarrhea / weight loss
  8. Craving for salt (due to lack of aldosterone)
35
Q

What is the mechanism behind the bronzing of the skin in Addision Disease?

A

Increased levels of beta-LipoTropin or ACTH each can stimulate melanocytes

36
Q

What is the triad of conditions that should encourage a clinician to consider APCEDS? (autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy syndrome)

A
  1. Hypoadrenocorticism
  2. Hypoparathyroidism
  3. Mucocutaneous candidiasis
37
Q

What typically comes first in a Addison patient: the oral pigmentation or the skin? What is a good indicator that the oral pigmentation is NOT physiologic?

A

Oral..recent onset

38
Q

What are the lab findings in Addison Dz?

A
  1. Serum cortisol levels below 18ug/dL (adrenal insufficency)
  2. Plasma ACTH levels (primary: increased >100ng/L, secondary: normal 9-52ng/L or low)
39
Q

In order to avoid Addisonian crisis, a pt with Addison Dz may need to alter their doses of corticosteriod, however dental procedures using ______ (type of anesthesia) and under ____ (time) adjustment is generally not required

A

local anesthesia, 1 hour

40
Q

Why is ‘juvenile onset’ not an appropriate name for type 1 DM?

A

5% to 10% of type 1 diabetics
develop their disease after 30 years of age.

41
Q

Which type of DM is more at risk for developing ketoacidosis?

A

Type 1 (rare in type 2)

42
Q

Of the 26 million Americans with DM, what % is type 1 DM?

A

5-10%

43
Q

What 3 tissues are affected the most by peripheral vascular disease as a complication of DM?

A

kidneys, limbs, and eyes

44
Q

The hormone insulin is produced by the _____ cells of the
pancreatic islets of Langerhans

A

beta

45
Q

What are the three “poly”s of the signs/symptoms of Type 1 DM/hyperglycemia?

A
  1. Polyphagia (increased food intake, despite weight loss)
  2. Polyurea (increased osmolarity of the blood and urine)
  3. Polydipsia (thirst leading to increased water intake)
46
Q

The oral manifestations of diabetes mellitus are generally
limited to patients with which type?

A

type I diabetes

47
Q

What are the 7 oral manifestations of diabetes?

A
  1. periodontal disease (more freq/rapid)
  2. delayed healing / infection post procedure
  3. diabetic sialadenosis (bilateral parotid swelling - type 1 or 2)
  4. Erythema of attached gingiva
  5. Fungal: Oral candidiasis (erythematous candidiasis on tongue) / Mucormycosis
  6. Geographic tongue (type 1, but debated)
  7. Xerostomia (subjective symptom, actual salivary flow in these patients is debated)
48
Q

What is the term for lack of adequte dietary carbs following use of insulin for a type 1 diabetic? What is the dangerous threshold for blood glucose in this situaiton?

A

“insulin shock” = blood glucose below 40mg/dL

49
Q
A

Neville and Damm (72 decks)

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