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Endocrine Disorders > Conditions > Flashcards

Conditions Flashcards

1
Q

Maximum terminal tuft size?

A

12mm in Men

10mm in Women

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2
Q

Increased Joint spaces

A

Acromegally

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3
Q

What are potential causes of hypopituitarism?

A

Neoplasm

Infection

Granulomas

Hemochromatosis

Injury / iatrogenic

Vascular insult

familial / idiopathic

Hypothalamic neoplasm

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4
Q

MCC of hypopitutarism?

A

Familial (~10%)

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5
Q

Radiographic appearance of hypopituitarism?

A

Delay in the appearance and growth of ossification centers, and a similar delay in their fusion and disappearance.

Growth rate is 50-60% of normal

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6
Q

Rare side effect of treatment of with GH in hypopituitarism?

A

SCFE

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7
Q

Causes of thyrotoxicosis (hyperthyroidism)?

A

MCC: 1. Toxic diffuse goiter (Graves’, Basedow’s)

  1. Toxic nodular goiter produced by adenomas

Other:

Toxic adenoma

Trophoblastic diseases

Iodine induced

Thyroiditis (subacute, chronic)

Ectopic thyroid tissue

Thyrotoxicosis factitia

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8
Q

Increased (bone related) lab values with hyperthyroidism?

A

↑ Serum calcium (not severe or sustained)

↑ Serum phosphorus

↑alkaline phosphatase

hypercalciuria

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9
Q

Percent of hyperthroidism that is radiographically evident?

A

3.5-50%

More likely to see if disease has been occuring >5yrs

More likely if the patient has exopthalmos

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10
Q

Radiographic findings in Hyperthyroidism?

A

Osteoporosis (expected findings)

Focal cystic lesions resembling multiple myeloma

Latice pattern in hands and feet with cortical striations

Possible path fx

Rarely: looser’s zone in femoral neck

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11
Q

Etiology of osseous changes in Hyperthyroidism?

A

Hyperosteoblastosis and Hyperosteoclastosis, although resorption dominates

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12
Q

Findings of hyperthyroidism in children?

A

Accelerated skeletal maturation

Premature craniosynostosis

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13
Q

Thyroid Acropachy occurs?

A

Generally after treatment for hyperthyroidism, although may be an initial finding of the disease.

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14
Q

non-radiographic Thyroid Acropachy findings?

A

exopthalmos, progressive painless soft tissue swelling of the fingers and toes, pretibial myxedema, clubbing of the fingers

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15
Q

Thyroid Acropachy radiographic findings?

A

Periosteal bone formation in diaphyses of metacarpals, metatarsals, & proximal and middle phalanges. May be seen in long bones.

Periostitis that is asymmetric, more on radial aspect, is dense and solid with a feathery contour.

Positive bone scan

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16
Q

Thyroid Acropachy DDX?

A

Other disorders associated with periosteal bone formation:

Hypertrophic osteoarthropathy (not usually in hands and feet)

Pachydermoperiostosis (Periosteal rxn not limited to diaphysis)

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17
Q

Causes of primary hypothyroidism?

A

Atrophy

Radiotherapy or Surgery

Hashimoto’s (autoimmune thyroiditis)

Lymphoma

Cystinosis

amyloidosis

Mets

Iodine deficiency (intake or metabolism)

Some meds

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18
Q

Radiographic appearance of adult-onset hypothyroidism?

A

Occasionally, bone may appear more compact, with increased radiodensity due to decreased bone formation and resorption.

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19
Q

radioghraphic changes in jevenile myxedema and cretinism?

A

Delayed bony maturation

Infant - absence of the distal femoral and proximal tibial epiphyses

Fragmented irregular epiphyseal contours (epiphyseal dysgenesis)

Delayed dental development

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20
Q

Skull findings in Cretinism

A

Brachycephaly

Enlarged sella

Prominent sutures with wormian bones

underdevelopment of the paranasal sinuses and mastoid air cells

prognathous lower jaw

Short bullet-shaped T12 & L1

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21
Q

What neuropathy is commonly associated with hypothyroidism?

A

Carapal tunnel (7%)

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22
Q

What epiphyseal injury may be the presenting feature of adolescent hypothyroidism, or a result of treatment?

A

SCFE

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23
Q

What osseous complication can be seen with hypothyroidism due to weakening of subchondral bone?

A

Collapse of surfacces similar to AVN and HPT.

Observed at tibial plateau.

Osteolytic lesions of the epiphyses has also been noted.

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24
Q

Growth hormone aka?

A

somatotropin

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25
Q

Skull features of acromegally?

A

Large mandible - “Lantern jaw”

Poor dental occlusion

Separation of the teeth

Large frontal sinus’s

Prominent forehead - Calvarial thickening

prominence of the tongue

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26
Q

Extremity features of acromegally?

A

Broad, spade-like hands

Fingers are separated and blunted

enlarged frame

widened joints

osteophytosis

cortical thickening

overtubulation phalanges and tetatarsals

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27
Q

Common presenting sx of an acromegallic?

A

Headaches

visual disturbances

rheumatic complaints/arthropathy

compression neuropathy

fatigue and lethargy

myopathy

28
Q

Findings in acromegallic myopathy?

A

increased serum creatinine phosphokinase

decreased mean action potential duration

29
Q

sesamoids in acromegally?

A

Sesamoid index >30 is indicative

30
Q

Spinal findings in acromegally?

A

Scalloped vertebrae

elongated, wide vertebrae

increased disc height

beaking of the pubic symphysis

increased sternal angle angulation

prominence of costochondral junction

potential cauda equina compression

31
Q

Cause of parathyroid hyperplasia in renal osteodystrophy?

A

Phosphate retention

32
Q

renal osteodystrophy in childhood commonly due to what?

A

Strutural abnormalities of the urinary tract

Rarely due to chronic inflammatory disease

33
Q

renal osteodystrophy and endocrine abnormalities?

A

Osteomalacia and rickets due to lack of vit D coversion

secondary HPT

34
Q

The pathologic and radiologic findings of renal osteodystrophy are divided into what?

A

HPT

Rickets

Osteomalacia

Osteoporosis

Soft tissue clacificatoin

vascular calcification

miscellaneous alterations

35
Q

Causes of primary HPT?

A

Diffuse hyperplasia (10-40%)

Single adenoma (50-80%0

Multiple adenomas (10%)

Rarely: carcinoma

36
Q

Causes of secondary HPT?

A

Chronic renal failure (high serum phosphate)

Malabsorption states: pancreatic insuffiecience, nontropical sprue, gluten enteropathy (low serum phosphate)

37
Q

Tertiary HPT cause?

A

Autonomous glad secondarty to long standing secondary HPT

38
Q

Hypercalcemai DDX?

A

Hyperproteinemia

Malignancy

Endocrine Disorders

Drugs

Granulomatous Disorders

Pediatric disorders

Immobilization

Miscellaneous

39
Q

Definition of PHPT?

A

Hypercalcemia of malignancy in the absence of demonstrable skeletal mets or primary HPT.

40
Q

Lab perameters in HPT?

A

Hypercalcemia

Hypophosphatemia

hyperphosphatasia

hypercalciuria

Occasionally: Hyperchloremic acidosis, hydroxyprolinuria, hyperglycemia, hyperuricemia, and hypomagnesemia

41
Q

Initial complaints with HPT?

A

Urinary tract calculi and nephrolithiasis

peptic ulcer disease

pancreatitis

10-25% have bone aching and tenderness of peripheral joints and spine

42
Q

Types of bone resorption by area of bone reabsorbed?

A

Subperiosteal (*HPT*)

Intracortical

endosteal

subchondral

trabecular

subligamentous

subphyseal

43
Q

Resorption patterin in hands with HPT?

A

Subperiosteal along radial aspect of phalanges, particularly the middle phalanges of the 2nd and 3rd digits.

Ulnar aspect affected less.

44
Q

Sites of subperiosteal resorption in HPT?

A

Phalangeal Tufts (most sensitive finding)

Medial aspect of proximal tibia, humerus and femur

Superior and inferior margins of ribs

Articular (hands/feet, clavicles, SI’s, symphisis pubis)

45
Q

Location of most distincive area of subchondral resorption in HPT?

A

SI joints, may mimic AS

Erosion with reactive new bone formation produces an ill-defined, sclerotic articular margin and “pseudo-widening” of the joint space.

46
Q

Skull findings in HPT?

A

Diffuse sclerosis with loss of the diploic space

Focal areas of thickening

well-defined or poorly defined radiopaque areas

“Salt and pepper” skull

47
Q

When are Brown Tumors observed most often?

A

Primary HPT

48
Q

What are brown tumors?

A

Focal accumulations of fibrous tissue and giant cells.

Can lead to osseous expansion

May undergo necrosis and liquefaction, producting cysts

49
Q

Radiographic features of Brown Tumors

A

Well-defined

Single or multiple

Eccentric or cortical in locatioin

MC locations: Facial bones, pelvis, ribs, femora

50
Q

Bone sclerosis and HPT

A

More common in secondary HPT

Diffuse sclrosis or localized/patchy (rare in primary)

Location: Metaphyseal, skull, vertebral endplates

causes Rugger-jersey appearance in spine

51
Q

% of people with HPT and CPPD?

A

18-40%

52
Q

Connective tissue effects of HPT?

A

Capsular and ligamentous laxity and tendinous degradation secondary to enzymatic degradation and direct effect of PT hormone

53
Q

Infant HPT?

A

Autosomal recessive

or

Transient, secondary to HypoPT in mother

54
Q

Multiple Endocrine Neoplasia

Multiple endocrine adenomatosis

Wermer’s Syndrome

A

95% have primary HPT

Autosomal dominamt

Type IIA is called Sipple’s syndrome

Can resemble Marfan’s

55
Q

Term for periosteal bone formation in ROD?

A

periosteal neostosis

Commonly demonstrates a zone of radiolucency between periosteal and parent bone

56
Q

3 signs of risk for SCFE?

A

Coxa vara

Subperiosteal erosion on medial aspect of femoral neck

increased width of cartilaginous growth plate

(also uremia > 2yrs)

57
Q

Sites of ST calcification in ROD?

A

Corneal and conjunctival tissue

viscera

vasculature

subcutaneous

periarticular

58
Q

Causes of HypoPT?

A

postsurgical/posttraumatic

Absence or atrophy of glands (idiopathic)

Maternal HyperPT

Radiation to gland

59
Q

Features of HypoPT?

A

MC: Osteosclerosis (generalized or localized)

SubQ calcification

DISH/AS like changes

Thickening of cranial vault and facial bones

Increased intracranial pressure w/ sutural diastasis

ventricular dilatation

calcification of basal gangila

GI hypersecretion and spasm

Labs - Low Ca, high P

60
Q

PHPT cause?

A

X-linked dominant

End-organ resistance to PT hormone

61
Q

PHPT somatotype?

A

Short stature, obese, round face, brachydactyly

Other - Abnormal dentition, retardation, strabismus, impared taste and olfaction

62
Q

PHPT characterized by?

A

Renal unresponsiveness to PTH but normal osseous response

63
Q

Radiographic features of PHPT and PPHPT?

A

Can be same as HPT - Suberiosteal resorption, brown tumors, osteosclerosis, periosteal neostosis, and SCFE

______________________________

Short metacarpals (not specific)

perpendicular exostoses (as opposed to pointing away from joint)

calvarial thickening

Bowing of extremitis

basal ganglion calcification

ST calcification

64
Q

Common presentation for child/adolescent with PHPT?

A

Tetany

Convulsions

Hyperexcitability

Cramping

Stridor

65
Q

Acromegally Spine Findings

A

posterior scalloping

increased disc space

Endocrine Disorders (12 decks)

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