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Y3R5: Medicine I 🩺 > L8: Pituitary Disorders > Flashcards

L8: Pituitary Disorders Flashcards

1
Q

Anatomy of hypothalamus

A
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2
Q

Anatomy of pituitary gland

A
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3
Q

Lobes of pituitary gland

A
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4
Q

Types of cells in anterior Lobe

A

a. Chromophobe cells “NON functioning”
b. Chromophil cells “functioning i.e. secreting”

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5
Q

Types of Chromophil cells in Pituitary Gland

A
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6
Q

Posterior Lobe of Pituitary Gland

A
  • Act as storage for Oxytocin & Anti- Diuretic Hormone (ADH), which are synthesized in the hypothalamus in the Para-ventricular & Supra-optic nuclei
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7
Q

Control of Pituitary Gland

A
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8
Q

What are Releasing factors for Pituitary Gland?

A
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9
Q

What are Release-inhibiting Factors for Pituitary Gland?

A
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10
Q

Negative Pituitary Feedback (long & Short)

A
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11
Q

What are disorders of Pituitary gland?

A
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12
Q

Def of Hyperprolactenemia

A

S. prolactin > 25 ng /dl.

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13
Q

Causes of Hyperprolactenemia

A
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14
Q

Physiologic Causes of Hyperprolactenemia

A
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15
Q

Pathological Causes of Hyperprolactenemia

A
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16
Q

Pharmacologic Causes of Hyperprolactenemia

A
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17
Q

idiopathic Causes of Hyperprolactenemia

A
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18
Q

CP of Hyperprolactenemia

A
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19
Q

Mass effects of Pituitary Hyperprolactenemia

A
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20
Q

Work up of Patient with Hyperprolactinemia

A
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21
Q

Investigations for Pituitary Hyperprolactinemia

A
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22
Q

TTT of Pituitary Hyperprolactinemia

A
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23
Q

Medical TTT of Pituitary Hyperprolactinemia

A
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24
Q

Duration of Medical TTT of Pituitary Hyperprolactinemia

A
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25
Q

Bromocriptine in Medical TTT of Pituitary Hyperprolactinemia

A
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26
Q

cabergoline in Medical TTT of Pituitary Hyperprolactinemia

A
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27
Q

Surgical TTT of Pituitary Hyperprolactinemia

A
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28
Q

Indications of Surgical TTT of Pituitary Hyperprolactinemia

A
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29
Q

Complications of Surgical TTT of Pituitary Hyperprolactinemia

A

Hypopituitarism, CSF rhinorrhea, Meningitis, Optic nerve damage.

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30
Q

Radiotherapy in Pituitary Hyperprolactinemia

A
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31
Q

Function of GH

A
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32
Q

What stimulates GH?

A
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33
Q

What Inhibits GH?

A
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34
Q

Def of Acromegaly

A

It is the clinical syndrome that results from persistent hypersecretion of growth hormone (GH) & hence IGF-1 in adults

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35
Q

Causes of Acromegaly

A
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36
Q

CP of Acromegaly

A

Refer to Summary

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37
Q

Changes in appearence

  • CP of Acromegaly
A
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38
Q

Acromegalic Facies

  • CP of Acromegaly
A
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39
Q

Hands & feet

  • CP of Acromegaly
A
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40
Q

Bones & Joints

  • CP of Acromegaly
A

Kyphosis & Osteoarthrosis

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41
Q

Organomegaly

  • CP of Acromegaly
A
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42
Q

Metabolism & Electrolytes

  • CP of Acromegaly
A
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43
Q

Neurological Manifestations

  • CP of Acromegaly
A
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44
Q

Endocrinal Manifestations

  • CP of Acromegaly
A
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45
Q

Major causes of death in untreated acromegaly

A
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46
Q

Indicators of disease activity in acromegaly

A
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47
Q

Investigations for Acromegaly

A
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48
Q

Lab Investigations for Acromegaly

A
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49
Q

OGTT for Acromegaly

A
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50
Q

Rad Investigations for Acromegaly

A
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51
Q

X-Ray in Acromegaly

A
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52
Q

CT & MRI in Acromegaly

A
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53
Q

Abdominal & Chest Imaging in Acromegaly

A
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54
Q

Hand & Spine X-Ray in Acromegaly

A
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55
Q

Other Investigations for Acromegaly

A

 Visual field examination
 ECG & ECHO
 Colonoscopy & Investigations of DM & HTN

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56
Q

TTT of Acromegaly

A
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57
Q

Surgical TTT in Acromegaly

A

Trans-sphenoidal (most common) or Tans- frontal

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58
Q

Pituitary Irradiation in Acromegaly

A

If surgery is refused or contraindicated BUT with tumors with NO supra-sellar extension

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59
Q

Medical TTT of Acromegaly

A
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60
Q

Approach for Dx of Acromegaly

A
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61
Q

Def of Gigantism

A

Growth hormone ( GH and IGF-1 ) excess that occurs before fusion of the epiphyseal growth plates —> rapid, excessive linear growth & extremely tall
stature

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62
Q

Causes of Gigantism

A
  • Pituitary GH-secreting Hyperplasia (Commonest) OR adenoma
  • Hypothalamic GH-releasing hormone excess
  • Ectopic GH or GHRH secretion [rare].
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63
Q

CP of Gigantism

A
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64
Q

DDx of Rapid Linear Growth

A
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65
Q

Investigations & TTT of Gigantism

A
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66
Q

Hormones of posterior pituitary

A
  • ADH
  • Oxytocin
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67
Q

what is another name of ADH?

A

Vasopressin

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68
Q

Function of ADH

A
  • Stimulate water reabsorption by renal tubules water retention
  • Vasoconstriction
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69
Q

Functions of Oxytoxin

A
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70
Q

Hypothalamic posterior pituitary control

A
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71
Q

Control of ADH

A
72
Q

Def of Diabetes Insipidus

A
73
Q

Classification of Diabetes Insipidus

A
74
Q

Causes of Pituitary “Cranial – Central” diabetes insipidus

A
75
Q

Causes of Nephrogenic “Peripheral” DI

A
76
Q

CP of Diabetes Insipidus

A
77
Q

DDx of Diabetes Insipidus

A

Other Causes of Polyuria

78
Q

Dx of Diabetes Insipidus

A

Lab & Rad

79
Q

Lab Dx of Diabetes Insipidus

A
80
Q

Urine Osmolarity

Dx of Diabetes Insipidus

A
81
Q

Plasma Osmolarity

Lab Dx of DI

A
81
Q

Significance of Fluid Deprivation Test

A

Test differentiates patients with DI from patients with primary polydipsia.

81
Q

Physiologic Principle of Fluid Deprivation Test

A
82
Q

Dose in Desmopressin challenge [DDAVP]

A

The patient is then given 4 µg IV or SC desmopressin or 10 µg nasal with urine volume and urine & serum osmolality measured over the next 4h (/30 min).

83
Q

Significance of Desmopressin challenge [DDAVP]

A

Test differentiates central DI from nephrogenic DI.

84
Q

Physiologic Principle of Desmopressin challenge [DDAVP]

A

Physiologic principle: DDAVP causes urine concentration.

  • Patients with central DI will concentrate urine after receiving DDAVP; patients with nephrogenic DI will not.
85
Q

Rad Dx of DI

A

CT, MRI of Sella tursica to exclude pituitary tumor.

86
Q

TTT of DI

A
87
Q

TTT of Central DI

A
88
Q

Drug of Choice in Central DI

A
89
Q

SE of Pitressin tannate in oil

A

pallor, angina, bronchospasm, uterine contraction.

90
Q

TTT of Nephrogenic DI

A
91
Q

Drugs used in Nephrogenic DI

A
92
Q

Def of SIADH

A
93
Q

When should SIADH be suspected?

A
  • SIADH should be suspected in any patient with euvolemeic hyponatremia, hyposmolality & urine osmolality > 100 mosmol/kg
94
Q

Pathophysiology of SIADH

A
95
Q

Etiology of SIADH

A
96
Q

what are CNS Problems that cause SIADH?

A

Stroke, Hge, infection, trauma & psychosis —-> enhance ADH release.

97
Q

Pulmonary Causes of SIADH

A

pneumonia (legionella), T.B.

98
Q

Tumors causing SIADH

A
  • Ectopic production of ADH by small cell carcinoma of the lung (most common).
  • Less common H & N cancer, olfactory neuroblastoma, lymphoma, leukemia.
99
Q

Drugs Causing SIADH

A

( Increase ADH release or effect)

  • Chlorpropamide, Carbamazepine, high-dose IV Cyclophosphamide & SSRIs.
100
Q

Surgery & SIADH

A

Hyponatremia is a common late complication of trans-sphenoidal pituitary surgery.

101
Q

Diagnostic Criteria of SIADH

A
102
Q

Investigations for SIADH

A
103
Q

TTT of SIADH

A
104
Q

Vasopressin antagonist in TTT of SIADH

A

Tolvaptan

  • Competitive vasopressin receptor 2 antagonist
  • Used for resistant hyponatremia
104
Q

Hypertonic saline in TTT of SIADH

A

In emergency (slowly I.V. infusion)

  • Rapid normalization (> 0.5mmol/h) of Na+ may be ass. With Central Pontine Mylenosis & other CNS damage.
104
Q

Def of Polyuria

A

Urine volume > 2000 cc/day

104
Q

Causes of Polyuria

A
  • Physiological (functional)
  • Psychological (hysterical)
  • Pathological
105
Q

Physiological Causes of Polyuria

A
  • High water intake : ↓ ADH secretion
  • Winter time : ↓ sweating
  • Alcoholic beverages, coffee, tea, beer
106
Q

Psychological Causes of Polyuria

A

Compulsive water drinking

  • Low plasma osmolality < 290 mosmol/kg
  • Water deprivation: ↓ urine volume & ↑ urine osmolality
  • No improvement after ADH
  • Treatment is by sedative & hypnotic
107
Q

Pathological Causes of Polyuria

A
  • Renal
  • Endocrinal
  • Drugs
  • Miscellaneous
108
Q

Renal causes of Polyuria

A
109
Q

Endocrinal Causes of Polyuria

A
110
Q

Drugs Causing Polyuria

A

Drugs causing nephrogenic DI : lithium, Demeclocycline

111
Q

Miscellenoues Causes of Transient Polyuria

A

Migraine, Epilepsy, Paroxysmal tachycardia, Bronchial asthma

112
Q

Def of Pituitary Dwarfism

A

1ry deficiency of GH in childhood.

113
Q

Causes of Pituitary Dwarfism

A

 Deficiency of GH-RH from hypothalamus

 Deficiency of GH from pituitary

 End organ unresponsiveness (Levi-Laron syndrome)

114
Q

CP of Pituitary Dwarfism

A

 Proportionate dwarfism.
 Pseudo-super-intelligence.
 Protein induced hypoglycemia

115
Q

Investigations for Pituitary Dwarfism

A

1) Fasting level of GH: low (+ low IGF-1)

2) Growth hormone stimulation test: negative

3) Insulin induced hypoglycemia: normally ↓ blood sugar to 50 mg →↑ GH level.

116
Q

TTT of Pituitary Dwarfism

A

Recombinant GH.

117
Q

Causes of Froehlich’s Syndrome

A

Hypothalamo-pituitary tumor (as craniopharyngioma).

118
Q

CP of Froehlich’s Syndrome

A
119
Q

Characters of Samboxa shape obesity

A

fat is deposited in the face, shoulder, trunk,
hips but sparing the extremities

120
Q

Def of Laurence-Moon-Biedel Syndrome

A

Rare congenital AR disease

121
Q

CP of Laurence-Moon-Biedel Syndrome

A
  • Features of Froehlich’s syndrome
  • Polydactyly
  • Skull deformations, mental retardation
  • Retinitis pigmentosa
122
Q

TTT of Laurence-Moon-Biedel Syndrome

A

Recombinant GH.

123
Q

DDx of hypopituitarism in children

A
  • Dwarfism.
  • Infantilism = Short stature & hypogonadism
124
Q

Def of Short Stature

A
  • Child whose height is 2 standard deviations (SD) or more below the mean for children of that sex and chronologic age (and ideally of the same racial-ethnic
    group).
  • This corresponds to a height that is below the 3rd percentile of normal people for their own sex & age.
125
Q

Causes of Short Stature

A
  • Endocrinal causes
  • Chronic severe-illness during childhood
  • Skeletal causes
  • Genetic disordes
126
Q

endocrinal causes of Short Stature

A
127
Q

Chronic Severe Illness & Short Stature

A
128
Q

Skeletal causes of Short Stature

A
  • Congenital
  • Acquired
129
Q

Congenital Skletal Causes of Short Stature

A
  • Achondroplasia
  • Osteochondrodystrophy
  • Osteogenesis imperfecta
130
Q

Achondroplasia

A

disproportionate dwarfism

  • Height > Span & Upper segment > Lower segment
  • Big skull & depressed nose
131
Q

Osteochondrodystrophy

A

limbs & trunk are short and deformed

132
Q

Osteogenesis imperfecta

A
  • Fragile bone leading to pathological fracture + malfusion + dwarfism + joint dislocation.
  • Blue sclera.
  • Deafness due to otosclerosis.
133
Q

Acquired Skeletal Causes of Short Stature

A
  • Rickets
  • Pott’s disease of spine
  • Paget’s disease of bone
134
Q

Genetic Disordres & Short Stature

A
135
Q

Algorithm of Short Stature

A
136
Q

what is the most common cause of disproportionate Short Stature?

A

Achondroplasia

137
Q

Algorithm to short stature

A
138
Q

Familial Vs Constitutional short stature

A
139
Q

Approach to short stature

Notes

A
140
Q

How to do Comparison with Child’s Own Genetic Potential?

A
141
Q

Bone Age

A
  • Bone age assessment should be done in all children with short stature.
  • Bone age is delayed compared to CA in almost all causes of pathological short stature.
142
Q

Investigations for short stature

A
143
Q

Managment of short stature

A
144
Q

Types of hypopituitrism in adults

A
  • Isolated & Pan
145
Q

Causes of Isolated Hypopituitrism

A

 ↓ TSH: 2ry hypothyroidism
 ↓ ACTH: 2ry hypocorticism
 ↓ Gonadotrophins: (2ry hypogonadism)

146
Q

Def of Kallman’s Syndrome

A

Kallmann syndrome (anosmia - midline fascial deformities - renal abnormalities & color blindness)

147
Q

Causes of Panhypopituitrism (Simmon’s Disease)

A
148
Q

CP of Panhypopituitrism (Simmon’s Disease)

A
149
Q

Manifestations of hormones deficiency in pamhypopituitrism

A
150
Q

Difference between 1ry & 2ry Decreases in ACTH

A
150
Q

First presentatation in Panhypopiyuitrism

A

2ry hypogonadism

151
Q

GH in Panhypopiyuitrism

A

late & minimal

  • Atrophy of viscera & skin wrinkling & weakness & wasting.
  • Hypoglycemia, premature CVS disease, reduce muscular mass.
152
Q

What Causes Coma in Panhypopiyuitrism?

A

due to :
 Hypoglycemia
 Hypothermia
 Pressure by tumor on brain stem reticular formation

153
Q

DDx of Panhypopiyuitrism

A
154
Q

Investigations for Panhypopiyuitrism

A
155
Q

TTT of Panhypopiyuitrism

A

A. TTT of cause if possible.

B. Replacement therapy

156
Q

Replacment of Panhypopiyuitrism

A
157
Q

Gonadal hormones replacment in Panhypopiyuitrism

A
158
Q

Thyroxin replacment in Panhypopiyuitrism

A
159
Q

Drugs for pituitary Crisis

A

 Hydrocortisone.
 Volume expansion
 Hypertonic saline

160
Q

Classification of pituitary tumors

A
161
Q

Benign pituitary tumors

A
162
Q

Malignant pituitary tumors

A

Primary (germ cell tumors and lymphoma) or secondary to breast cancer and lung cancer.

162
Q

CP of pituitary tumors

A
163
Q

Dx of pituitary tumors

A
164
Q

Lab Dx of Malignant pituitary tumors

A
165
Q

Rad Dx of Malignant pituitary tumors

A

MRI brain (better than CT scan in evaluating pituitary tumors): lesions < 1 cm in diameter (microadenoma) while lesions > 1 cm (macroadenoma).

166
Q

DDx in Malignant pituitary tumors

A

from other causes of sellar masses:

  • Pituitary hyperplasia: Lactotroph hyperplasia during pregnancy.
  • Cysts: Rathke’s cleft.
  • Hypophysitis: lymphocytic hypophysitis.
  • Infiltration: sarcoidosis, and Langerhans cell histiocytosis.
167
Q

Managment of Malignant pituitary tumors

A

according to type, size of the tumor & pituitary hormonal status.

  1. Surgery: trans-sphenoidal or sub frontal approach.
  2. Radiotherapy: conventional or gamma knife technique.
  3. Medical: somatostatin analogues and/or dopamine agonists.
168
Q

Done

A

.

Y3R5: Medicine I 🩺 (47 decks)

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