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ENDOCRINE > ENDOCRINE-Pathology > Flashcards

ENDOCRINE-Pathology Flashcards

1
Q

What is Cushing syndrome?

A

↑ cortisol due to a variety of causes

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2
Q

Which are main causes of Cushing syndrome?

A

Exogenous corticosteroids
Primary adrenal adenoma, hyperplasia or carcinoma
ACTH secreting pituitary adenoma; paraneoplastic ACTH secretion

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3
Q

1 cause of Cushing syndrome

A

Exogenous corticoesteroids

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4
Q

What is the result of Exogenous corticosteroids use?

A

↓ ACTH, bilateral adrenal atrophy

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5
Q

In these cases of Chushing syndrome ↓ ACTH, atrophy of uninvolved adrenal gland

A

Primary adrenal adenoma, hyperplasia or carcinoma

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6
Q

1º Aldosteronism

A

Conn syndrome

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7
Q

How else can Primary adrenal adenoma, hyperplasia or carcinoma present?

A

1º Aldosteronism

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8
Q

ACTH secreting pituitary adenoma

A

Cushing disease

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9
Q

What is Cushing disease?

A

ACTH secreting pituitary adenoma

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10
Q

Example of Paraneoplastic ACTH secretion

A

Small cell lung cancer, bronchial carcinoids

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11
Q

Which are the results of Cushing disease and Paraneoplastic ACTH secretion?

A

↑ ACTH, bilateral adrenal hyperplasia

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12
Q

Who is the responsible for the majority of endogenous cases of Cushing syndrome?

A

Cushing disease

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13
Q

Which are the findings in Cushing syndrome?

A

Hypertension, weight gain, moon facies, truncal obesity, buffalo hump, hyperglycemia (insulin resistance), skin changes (thining, striae), osteopororsis, amenorrhea, and immune suppression

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14
Q

Which are the screening test for Cushing syndrome?

A

↑ free cortisol on 24 hr urinalysis
Midnight salivary cortisol
Overnight low dose dexamethasone suppression test: Measure serum ACTH

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15
Q

If Overnight low dose dexamethasone suppression test Measuring serum ACTH is decreases, what is your suspicious?

A

Adrenal Tumor

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16
Q

If Overnight low dose dexamethasone suppression test Measuring serum ACTH is increased, what is your suspicious?

A

Distinguish between Cushing disease and ectopic ACTH secretion

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17
Q

What is needed to Distinguish between Cushing disease and ectopic ACTH secretion?

A

High dose (8 mg) dexamethasone suppression test and CRH stimulation test

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18
Q

What is expected with High dose (8 mg) dexamethasone in Ectopic secretion? Why?

A

Ectopic secretion will not decrease with dexamethasone because the source is resistant to negative feedback

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19
Q

What is expected with CRH stimulation test in Ectopic secretion? Why?

A

Ectopic secretion will not increase with CRH because pituitary ACTH is suppressed

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20
Q

When are ACTH levels consider supressed?

A

< 5 pg/ mL

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21
Q

When are ACTH levels consider elevated?

A

> 20 pg/ mL

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22
Q

What can cause Primary hyperaldosteronism?

A

Adrenal hyperplasia

Adrenal secreting adrenal adenoma

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23
Q

What is the Conn syndrome?

A

Aldosterone secreting adrenal adenoma

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24
Q

Which are the results of primary hyperaldosteronism?

A

Hypertension
Hypokalemia
Low plasma renin

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25
Q

How is the Na+ due to aldosterone escape?

A

Normal

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26
Q

Can edema be present due to Aldosterone escape?

A

No

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27
Q

How can primary Hyperaldosteronism be presented?

A

May be bilateral or unilateral

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28
Q

Which is the treatment for primary Hyperaldosteronism?

A

Surgery to remove the tumor and/or spironolactone

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29
Q

What is spironolactone?

A

a K+ spairing durietic that acts as Aldosterone antagonist

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30
Q

What happens in secondary hyperaldosteronism?

A

Renal perception of low intravascular volume results in an overactive renin angiotensin system

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31
Q

Causes of secondary hyperaldosteronism

A

Renal artery stenosis, CHF, cirrhosis, or nephrotic syndrome

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32
Q

How is renin in secondary Hyperaldosteronism?

A

High plasma renin

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33
Q

Which is the treatment for secondary Hyperaldosteronism?

A

Spironolactone

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34
Q

What is addison disease?

A

Chronic primary adrenal insufficiency due to adrenal atrophy or destruction by disease

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35
Q

Examples of destruction diseases that cause Addison disease

A

Autoimmune, TB, Metastasis

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36
Q

Who are deficient in Addison disease?

A

Deficiency of aldosterone and cortisol

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37
Q

Which are the findings in Addison disease?

A

Hypotension
Hyperkalemia
Acidosis
Skin and mucosal hyperpigmentation

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38
Q

What causes Hypotension in Addison disease?

A

Hyponatremic volume contraction

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39
Q

Which is the reason of skin and mucosal hyperpigmentation?

A

Due to MSH, a by product of ↑ ACTH production from proopiomelanocortin (POMC)

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40
Q

Which are the characteristics of Addison disease?

A

Adrenal Atrophy and Absence of hormone production

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41
Q

In Addison disease who are affected?

A

Involves all 3 cortical divisions (spares medulla)

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42
Q

Characteristic of Secondary adrenal insufficiency

A

↓ pituitary ACTH production

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43
Q

What distinguish Addison disease with Secondary adrenal insufficiency?

A

Secondary adrenal insufficiency has no skin/ mucosal hyperpigmentation and no hyperkalemia

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44
Q

What is the Waterhouse-Friederichsen syndrome?

A

Acute primary adrenal insufficiency due to adrenal hemorrhage

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45
Q

Which are the associated causes to Waterhouse-Friederichsen syndrome?

A

Neisseria meningitidis septicemia
DIC
Endotoxin shock

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46
Q

Most common tumor of the adrenal medulla in children

A

Neuroblastoma

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47
Q

Normal age of apperance of Neuroblastoma

A

<4 years old

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48
Q

From where does Neuroblastoma is originated?

A

Neural crest cells

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49
Q

Where can Neuroblastoma make an apperance?

A

Anywhere along the sympathetic chain

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50
Q

Which is the most common presentation of Neuroblastoma?

A

Abdominal distention and a firm, irregular mass, that can cross the midline

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51
Q

Which is the differential diagnosis of Neuroblastoma?

A

Wilms tumor, which is smooth and unilateral

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52
Q

What lab helps in Neuroblastoma diagnosis?

A 
Homovanillic acid (HVA), Increased in urine
Bombesin +
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53
Q

What is Homovanillic acid (HVA)?

A

A breakdown product of dopamine

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54
Q

How often can a Neuroblastoma generate hypertension?

A

Less likely to develop hypertension

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55
Q

Which oncogen is associated to Neuroblastoma?

A

Overexpression of N-myc oncogene

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56
Q

Most common tumor of the adrenal medulla in adults

A

Pheochromocytoma

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57
Q

From where does pheochromocytoma derives?

A

From chromaffin cells (arise from neural crest)

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58
Q

How else is pheocrhromocytoma known?

A

Rule of 10’s

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59
Q

What does the rule of 10’s in pheochromocytoma means?

A 
10% malignant
10% bilateral
10% extra-adrenal
10% calcify
10% kids
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60
Q

What does Pheochromocytoma secretes?

A

Epinephrine, norepinephrine and dopamine

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61
Q

What can the secretions of Pheochromocytoma cause?

A

Episodic hypertension

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62
Q

Which diseases are associated to Pheochromocytoma?

A

von Hippel Lindau disease

MEN 2A and 2B

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63
Q

How does symptoms occur in pheochromocytoma?

A

In “spells”- relapse and remit

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64
Q

Which are the characteristics of episodi hyperadrenergic symptoms caused by pheochromocytoma?

A 
5 Ps
Pressure (↑ BP)
Pain (headche)
Perspiration
Palpitations (tachycardia)
Pallor
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65
Q

Which are the findings in Pheochromocytoma?

A 
Urinary VMA (Vanillylmandelic acid )
Plasma catecholamines are ↑
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66
Q

What is VMA (Vanillylmandelic acid )?

A

Breakdown products of norepinephrine and epinephrine

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67
Q

Which is the treatmenf fot pheocrhromocytoma?

A

Irreversible α antagonist and β blockers followed by tumor resection

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68
Q

Example of Irreversible α antagonist

A

Phenoxybenzamine

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69
Q

When giving pharmacologic treatment for pheochromocytoma, wha do you need to be careful?

A

α blockade must be achive before giving β blockers to avoid a hypertensive crisis

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70
Q

Clinical findings in Hypothyrodism

A 
Cold intolerace (↓ heat production)
Weight gain, ↓ appetite
Hypoactivity, lethargy, fatigue, weakness
Constipation 
↓ reflexes
Myxedema (facial/ periorbital)
Dry, cool skin; coarse, brittle hair
Bradycardia, dyspnea on exertion
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71
Q

Which are clinical findings for Hyperthyrodism?

A 
Heat intolerance (↑ heat production)
Weight loss, ↑ appetite
Hyperactive
Diarrhea
↑ reflexes
Pretibial myxedema (Graves disease)
Periorbital edema
Warm, moist skin, fine hair
Chest pain palpitations, arrhytmias
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72
Q

In hyperthyrodism, what causes Chest pain, palpitation, arrhytmia?

A

↑ Number and sensitivity of β adrenergic receptors

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73
Q

Lab findings in Hypothyroidism

A

↑ TSH
↓ free T3 and T4
Hypercholesterolemia

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74
Q

Which lab test is sensitive for primary hipothyroidism?

A

↑ TSH

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75
Q

Why Hypercholesterolemia is a finding in Hypotyhyroidism?

A

Due to ↓ LDL receptor expression

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76
Q

In Primary hyperthyroidism which are the lab findings?

A

↓ TSH
↑ free T3 and T4
Hypocholesterolemia

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77
Q

Why Hypocholesterolemia is a finding in Hypotyhyroidism?

A

Due to ↑ LDL receptor expression

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78
Q

Most common cause of hypothyroidism in iodine sufficient regions

A

Hashimoto thyroiditis

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79
Q

How is Hashimoto thyroiditis consdier?

A

Autoimmune disorder

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80
Q

Antibodies foun in Hashimoto thyroiditis

A

Antithyroid peroxidase, anthythyroglobulin antibodies

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81
Q

Broad-antigen serotype related to Hashimoto thyroiditis

A

HLA-DR5

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82
Q

Which cancer is associated to Hashimoto thyroiditis?

A

↑ risk for Non Hodgkin lymphoma

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83
Q

How is Hashimoto thyroiditis at the begining?

A

May be thyrotoxicosis during follicular rupture

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84
Q

Histologic findings in Hashimoto thyroiditis

A

Hurthle cells

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85
Q

What are the hurtle cells?

A

Lymphoid aggregate with germinal centers

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86
Q

Findings in Hashimoto thyroiditis

A

Moderately enlarged, nontender thyroid

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87
Q

Causes of Congenital hypothyroidism

A 
Maternal hypothyrodism
Thyroid agenesis
Thyroid dysgenesis
Iodine deficiency
Dyshormonogenic goiter
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88
Q

This is a another name for Congenital hypothyroidism

A

Cretinism

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89
Q

Most common cause of Congenital hypthyroidism in US

A

Thyroid dysgenesis

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90
Q

Clinical findings in Congenital hypothyroidism

A 
6 Ps
Pot bellied
Pale
Puffy faced child
Protruding umbilicus
Protuberant tongue
Poor brain development
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91
Q

Causes of Hypothyroidism

A 
Hashimoto thyroidtis
Congenital hypothyroidism
Subacute thyroiditis
Riedel thyroiditis
Iodine Deficiency
Goitrogens
Woll Chaikoff effect 
Painless thyroiditis
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92
Q

Another name for Subacute Thyroiditis

A

de Quervain

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93
Q

Self limited hypothyroidism often following a flu like illness

A

Subacute Thyroiditis (de Quervain)

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94
Q

How is the evolution of Subacute Thyroiditis?

A

May be hyperthyroid early in cpurse then becomes hypothyroidism

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95
Q

Hystology of Subacute Thyroiditis (de Quervain)

A

Granulomatous inflammation

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96
Q

Findings in Subacute Thyroiditis (de Quervain)

A

↑ ESR (erythrocyte sedimentation rate), jaw pain, early inflammation, very tender thyroid (de Quervain is associated with pain)

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97
Q

What happens in Riedel Thyroiditis?

A

Thyroid replaced by fibrous tissue (hypothyroid)

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98
Q

How much can the Riede thyroiditis can extent?

A

Fibrosis may extend to local structures (eg airway) mimicking anaplastic carcinoma

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99
Q

How is Riedel Thyroiditis consider?

A

A manifestation of IgG4 related systemic disease

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100
Q

Findings of Riedel Thyroiditis

A

Fixed, hard (rock like), and painless

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101
Q

Other causes of hypothyroidism

A

Iodine deficiency, goitrogens, Wolff Chaikoff effect, painless thyroiditis

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102
Q

Disease that curse with Hyperthyroidism

A

Toxic multinodular goiter
Graves disease
Thyroid storm

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103
Q

What happens in Toxic multinodular goiter?

A

Focal patches of hyperfunctioning follicular cells working independently of TSH due to mutations in TSH receptor

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104
Q

Which secretion is affected in Toxic multinodular goiter?

A

↑ release of T3 and T4

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105
Q

Normaly how are hot nodules of Toxic multinodular goiter consider?

A

Rarely malignat

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106
Q

What is the Jod Basedow phenomenom?

A

Thyrotoxicosis if a patient with iodine deficiency goiter is made iodine repleted

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107
Q

Which disease is related to Jod Basedow phenomenom?

A

Toxic multinodular goiter

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108
Q

Most comon cause of Hyperthyroidism

A

Graves disease

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109
Q

Which are the causes of clinical manifestation of Graves disease?

A

Autoantibodies (IgG) stimulate TSH receptors on thyroid
Retroorbital fibroblasts
Dermal fibroblasts

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110
Q

Clinical manifestations of Graves disease

A

Hyperthyrodism, diffuse goiter (Autoantibodies (IgG) stimulate TSH receptors on thyroid)
Exophthalmos: proptosis, extraocular muscle swelling (Retroorbital fibroblasts)
Pretibial Mixedema (Dermal fibroblasts)

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111
Q

When is Graves disease often presented?

A

During Stress (eg. Childbirth)

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112
Q

What is the Thyroid storm?

A

Stress induced catecholamine surge seen as a serious complication of Graves disease and other hyperthyroid disorders

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113
Q

Which is a cause of death in Thyroid storm?

A

Tachyarrhytmia

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114
Q

How is Thyroid storm presented?

A

Agitation, delirium, fever, diarrhea, coma, and tachyarrhytmia

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115
Q

How is Alkaline Phosphatase in Thyroid storm? Why?

A

↑ ALP due to bone turnover

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116
Q

How do you treat a Thyroid storm?

A

3 Ps
β blockers ( Propanolol)
Propylthiouracil
Corticoesteroids (Prednisone)

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117
Q

When is Thyroidectomy indicated?

A

Treatment option fot Thyroid cancers and hyperthyrodism

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118
Q

These could be complications of Thyroidectomy

A

Hoarseness (Due to recurrent laryngeal nerve damage)
Hypocalcemia (due to removal of parathyroid glands)
transection of inferiori thyroid artery

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119
Q

Most common thyroid cancer

A

Papillary carcinoma

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120
Q

Which is the prognosis of Thyroid papillary carcinoma?

A

Excelent prognosis

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121
Q

Histologic findings in Thyroid papillary carcinoma

A

Empty appearing nuclei (“Orphan Annie” eyes)
Psamoma eyes
Nuclear grooves

122
Q

When is increased the risk for Thyroid papillary carcinoma?

A

With RET ad BRAF mutations

Childhood irradiation

123
Q

What are the Orphan Annie eyes histologic findings?

A

Empty appearing nuclei in Thyroid papillary carcinoma

124
Q

Most common thyroid cancers

A 
Papillary carcinoma
Follicular carcinoma
Medullary carcinoma
Undifferentiated/ Anaplastic carcinoma
Lymphoma
125
Q

How is the prognosis of Thyroid follicular carcinoma?

A

Good prognosis

126
Q

Which are differential characteristics of Thyroid follicular carcinoma and Thyroid follicular adenoma?

A

Invades thyroid capsule, uniform follicles

127
Q

From which cells does Thyroid Medullary carcinoma comes from?

A

From parafollicular “C cells”

128
Q

What does Thyroid Medullary carcinoma produce?

A

Produces calcitonin

129
Q

Hystologic findings for Thyroid Medullary carcinoma

A

Sheets of cells in an amyloid stroma

130
Q

Which gen mutations are associated to Medullary carcinoma?

A

MEN 2A and 2B (RET mutations)

131
Q

Who are at higher risk for Thyroid Anaplastic Carcinoma?

A

Older patients

132
Q

How else is Anaplastic carcinoma known?

A

Undifferentiated

133
Q

Hystoligic characteristics of Thyroid Anaplastic carcinoma

A

Invades local structures

134
Q

Prognosis of Thyroid Anaplastic carcinoma

A

Very poor prognosis

135
Q

Thyroid Lymphoma is associated to this disease

A

Hashimoto Thyroiditis

136
Q

How is Hyperparathyroidism classified?

A

Primary
Secondary
Tertiary

137
Q

Which is the common cause of primary hyperparathyroidism?

A

Ussually an adenoma

138
Q

Labs found in primary hyperparathyroidism

A 
Hypercalcemia
Hypercalciuria
Hypophosphatemia
↑ PTH
↑ ALP
↑ cAMP in urine
139
Q

Which are the symptoms of primary hyperparathyroidism?

A

Most often asymptomatic
May present with weakness and constipation (“groans”), abdominal/flank pain (kidney stones, acute pancreatitis), depression

140
Q

Which disease is associated with primary hyperparathyroidism?

A

Osteitis fibrosa cystica

141
Q

What is Osteitis fibrosa cystica?

A

Cystic bone spaces filled with brown fibrous tissue

142
Q

What happens in secondary hyperparathyroidism?

A

Secondary hyperplasia due to ↓ gut Ca2+ absorption and ↑ PO4 3-

143
Q

When is more often to see secondary hyperparathyroidism?

A

In chronic renal disease

144
Q

What does chronic renal disease causes in secondary hyperparathyroidism?

A

Causes hypovitaminosis D → ↓ Ca2+ absorption

145
Q

Effects of secondary hyperparathyroidism

A

Hypocalcemia
Hyperphosphatemia in chronic renal failure (vs hypophosphatemia with most other causes)
↑ ALP, ↑ PTH

146
Q

Refractory (autonomous) hyperparathyroidism

A

Tertiary hyperparathyroidism

147
Q

Which is the cause of Tertiary hyperparathyroidism?

A

Resulting from chronic renal disease

148
Q

Findings on Tertiary hyperparathyroidism

A

↑↑ PTH, ↑ Ca2+

149
Q

What is and who causes Renal osteodystrophy?

A

Bone lesions due to 2º or 3º hyperparathyroidism due in turn to renal disease

150
Q

Causes of Hypoparathyroidism

A

Accidental surgical excision of parathyroid glands
Autoimmune destruction
DiGeorge syndrome

151
Q

Findings in Hypoparathyroidism

A

Hypocalcemia

Tetany

152
Q

Which signs could be found in Hypoparathyroidism?

A

Chvosek sign

Trousseau sign

153
Q

What is the Chvosteck sign?

A

Tapping of facial nerve (tap the Cheek) → contraction of facial muscles

154
Q

What is the Trousseau sign?

A

Occlusion of brachial artery with BP cuff → carpal spasm

155
Q

Alternative name for Pseudohypoparathyroidism

A

Albright hereditary osteodystrophy

156
Q

Genetic adquiring pattern of Albright hereditary osteodystrophy

A

Autosomal dominant

157
Q

What happens in Pseudohypoparathyroidism?

A

Autosomal dominant unresponsiveness of kidney to PTH

158
Q

What happens in Albright hereditary osteodystrophy?

A

Autosomal dominant unresponsiveness of kidney to PTH

159
Q

Findings of Albright hereditary osteodystrophy

A

Hypocalcemia
Shortened 4th/5th digits
Short stature

160
Q

Pathology that curses with Low serum calcium and high PTH levels

A

Secondary hyperparathyroidism

161
Q

Causes of Secondary hyperparathyroidism

A

Vitamin D deficiciency

Chronic renal failure

162
Q

Low levels of PTH and Low levels of calcium

A

Hypoparathyroidism

163
Q

Which levels of PTH are consider low?

A

<10 pg/ mL

164
Q

High levels of both PTH and calcium

A

Primary hyperparathyroidism

165
Q

Causes of primary hyperparathyroidism

A

Hyperplasia
Adenoma
Carcinoma

166
Q

Low levels of PTH but high levels of Calcium

A

PTH independent hypercalcemia

167
Q

Causes of PTH independent hypercalcemia

A

Excess Ca2+ ingestion

Cancer

168
Q

Which is the most common pituitary adenoma?

A

Prolactinoma (benign)

169
Q

How are pituitary adenoma classified?

A 
Functional (hormone producing)
Non functional (silent)
170
Q

How are nonfunctional Adenomas presented?

A

With mass effect (bitemporal hemianopia, hypopituitarism, headache)

171
Q

How is prolactinoma presented?

A

Amenorrhea
Galactorrhea
Low libido
Infertility

172
Q

How is somatotropic adenoma presented?

A

Acromegaly

173
Q

Treatment for prolactinoma

A

Dopamine agonist

174
Q

Dopamine agonists

A

Bromocriptine or Cabergoline

175
Q

What is acromegaly?

A

Excess GH in adults

176
Q

Which is the typical cause of Acromegaly?

A

Pituitary adenoma

177
Q

Findings in Acromegaly

A

Large tongue with deep furrows, deeps voice, large hands and feet, coarse facial features, impaired glucose tolerance (insulin resistance)

178
Q

Which is the most common cause of death in gigantism patients?

A

Cardiac failure

179
Q

Characteristics of GH increased in children

A

Gigantism (↑ linear bone growth)

180
Q

Characteristics of Diabetes insipidus

A

Characterized by intense thrist and polyuria inability to concentrate urine due to lack of ADH

181
Q

Which are the possible causes of Diabetes insipidus?

A

Central or nephrogenic

182
Q

Etiology of central Diabetes Insipidus

A

Pituitary Tumor, autoimmune, trauma, surgery, ischemic encephalopaty, idiopathic

183
Q

How is ADH in Central Diabetes Insipidus?

A

↓ ADH

184
Q

Findings in Central Diabetes insipidus

A

Urine specific gravity 290 mOsm/L

Hyperosmotic volume contraction

185
Q

How is Central Diabetes insipidus diagnose?

A

Water restriction test> 50% ↑ in urine osmolarity

186
Q

Treatment for Central Diabetes Insipidus

A 
Intranasal DDAVP (Desmopressin)
Hydration
187
Q

How is the water restriction test made?

A

No water intake for 2-3 hr followed by hourly measurements of urine volume and osmolarity and plasma Na+ concentration and osmolarity

188
Q

What is DDAVP?

A

Desmopressin- ADH analog is administered of normal values are not clearly reached

189
Q

Etiology of Nephrogenic Diabetes Insipidus

A

Hereditary (ADH receptor mutation), secondary to hypercalcemia, lithium, demeclocycline

190
Q

What is demeclocycline?

A

ADH antagonist

191
Q

How is ADH in Nephrogenic Diabetes Insipidus?

A

Normal ADH levels

192
Q

Findings in Nephrogenic Diabetes Insipidus

A

Urine specific gravity 290 mOsm/L

Hyperosmotic volume contraction

193
Q

What is the result of water restriction test in Nephrogenic Diabetes Insipidus?

A

No change in urine osmolarity

194
Q

Which is the treatment for Nephrogenic Diabetes Insipidus?

A

Hydrochlorothiazide, indomethacin, amiloride

Hydration

195
Q

Characteristics of Syndrome of innapropiate Antidiuretic hormone secretion (SIADH)

A

Excessive water retention
Hyponatremia with continued urinary Na+ excretion
Urine osmolarity> serum osmolarity

196
Q

How does the body responds to water retention?

A

↓ aldosterone (hyponatremia) to maintain near normal volume status

197
Q

Which is the risk for very low serum sodium levels?

A

Can lead to cerebral edema, seizures

198
Q

When Serum sodium levels are corrected what you need to be careful?

A

Correct slowly to prevent central pontine myelinosis

199
Q

Causes of Syndrome of innapropiate Antidiuretic hormone secretion (SIADH)

A

Ectopic ADH
CNS disorder/ head trauma
Pulmonary disease
Drugs

200
Q

Which drug can cause Syndrome of innapropiate Antidiuretic hormone secretion (SIADH)?

A

Cyclophosphamide

201
Q

What produces ectopic ADH?

A

Small cell lung cancer

202
Q

Treatment for Syndrome of innapropiate Antidiuretic hormone secretion (SIADH)

A

Fluid restriction, IV hypertonic saline, conivaptanm tolvatan, demeclocycline

203
Q

Causes of undersecretion of pituitary hormones

A 
Nonsecreting pituitary adenoma, craneopharyngioma
Sheehan syndrome
Empty sella syndrome
Brain injury, hemorrhage
Radiation
204
Q

What happens in Sheehan syndrome?

A

Ischemic infarct of pituitary following postpartum bleeding

205
Q

Usually how is Sheehan syndrome presented?

A

Failure to lactate

206
Q

What is the empty sella syndrome?

A

Atrophy or compression of pituitary, often idiopathic

207
Q

In which patients is empty sella syndrome more common?

A

Obese women

208
Q

Treatment for Hypopituitarism

A

Hormone replacement therapy (corticosteroids, thyroxine, sex steroids, human growth hormone)

209
Q

What is pituitary apoplexy?

A

Hypopituitarism due to brain injury, hemorrhage

210
Q

Main effects of Insulin deficiency (and glucagon excess)

A

Decreased Glucose uptake
Increased protein catabolism
Increased lipolysis

211
Q

Effect of decreased glucose uptake

A

Hyperglycemia
Glycosuria
Osmotic diuresis
Electrolitic depletion

212
Q

Result of increased protein catabolism

A

Increased plasma amino acids, nitrogen loss in urine

213
Q

Once Increased plasma amino acids, nitrogen loss in urine what could be the result

A

Hyperglycemia
Glycosuria
Osmotic diuresis
Electrolitic depletion

214
Q

In insulin deficiency, what is the result of Increased lipolysis

A

Increased plasma FFAs, ketogenesis, ketonuria, ketonemia

215
Q

Final result of insulin deficiency

A

Dehydration, acidosis → Comma, death

216
Q

Acute manifestations of Diabetes

A

Polydipsia, polyuria, polyphagia, weight loss

217
Q

Acute manifestion of Type 1 Diabetes

A

Diabetic Ketoacidosis

218
Q

Acute manifestation of Type 2 Diabetes

A

Hyperosmolar comma

219
Q

Rare causes of Diabetes Mellitus

A

Unopposed secretion of GH and epinephrine

220
Q

Chronic manifestations of Diabetes

A

Nonenzymatic glycosylation

Osmotic damage

221
Q

What happens in small vessel disease in diabetes?

A

Diffuse thickening of basement membrane

222
Q

Who are affected by Nonenzymatic glycosylation?

A

Small vessel disease

Large vessel disease

223
Q

Small vessel disease in Diabetics

A

Retinopathy
Glaucoma
Nephropathy

224
Q

Findings in Retinopathy in Diabetic patients

A

Hemorrhage, exudates, microaneurysms, vessel proliferation

225
Q

Findings in Nephropathy in Diabetic patiens

A

Nodular sclerosis, progressive proteinuria, chronic renal failurem arteriosclerosis leading to hypertension, Kimmelstiel Wilson nodules

226
Q

Consequences of Large vessel atherosclerosis in Diabetes

A 
Coronary Artery disease
Peripheral Vascular oclussive disease
Gangrene
Limb loss
Cerebrovascular disease
227
Q

Which is the most common cause of death in MI?

A

Large vessel atherosclerosis

228
Q

What happens in Osmotic damage in Diabetes Mellitus?

A

Sorbitol accumulation in organs with aldosereductase and ↓ or absent sorbitol dehydrogenase

229
Q

Clinical effects of Osmotic damage

A

Neuropathy

Cataracts

230
Q

Manifestations of Neuropathy

A

Motor, sensory, and autonomic degeneration

231
Q

Test for Diabetes Mellitus diagnosis

A

Fasting serum glucose
Oral glucose tolerance test
HbA1c

232
Q

What is the purpose of HbA1c?

A

Reflects average blood glucose over prior 3 months

233
Q

Primary defect in Type 1 Diabetes

A

Autoimmune destruction of β cells

234
Q

Is insulin necessary for treating Type 1 Diabetes?

A

Always

235
Q

Often Age of Type 1 Diabetes onset

A
236
Q

Is Type 1 Diabes associated to Obesity?

A

No

237
Q

Which is the Genetic predisposition of Type 1 Diabetes?

A

Relatively weak (50% concordance in identical twins), polygenic

238
Q

What is associated to Type 1 Diabetes?

A

HLA-DR3 and 4

239
Q

How is the glucose intolerance in Type 1 Diabetes?

A

Severe

240
Q

How is insulin sensitivity in type 1 Diabetes?

A

High

241
Q

Which Diabetes type presents with more Ketoacidosis?

A

Type 1

242
Q

How are β cell numbers in the islets?

A

Decreased

243
Q

How are serum insulin levels in Type 1 Diabetes?

A

Decreased

244
Q

In which Diabetes type is more common to see classic symptoms of polyuria, polydipsia, poliphagia and weight loss?

A

Diabetes Type 1 more common

Sometimes Diabetes Type 2

245
Q

Classic symptoms in Diabetics

A

Polyuria, polydipsia, poliphagia and weight loss

246
Q

Histology findings in Type 1 Diabetes

A

Islet Leukocyte infiltrate

247
Q

Histology findings for Type 2 Diabetes

A

Islet amyloid polypeptide (IAPP) deposits

248
Q

Primary defect in Type 2 diabetes

A

↑ resistance to insulin, progressive pancreatic β cell failure

249
Q

Is insulin necesary for treating Type 2 diabetes?

A

Sometimes

250
Q

Age of onset for Type 2 diabetes

A

> 40 yr

251
Q

Which Diabetes Type is associated to Obesity?

A

Type 2

252
Q

How is the genetic predisposition of type 2 Diabetes?

A

Relatively strong (90% concordance in identical twins), polygenic

253
Q

Is type 2 diabetes associated to HLA system?

A

No

254
Q

How is glucose intolerance in Type 2 Diabetes?

A

Mild to moderate

255
Q

How is insulin sensitivity in Type 2 diabetes?

A

Low

256
Q

β cells numbers in the islet in Type 2 diabetes

A

Variable (with amyloid)

257
Q

Histology of Type 2 Diabetes

A

Islet amyloid polypeptide

258
Q

One of the most important complications of diabetes (usually type 1)

A

Diabetic ketoacidosis

259
Q

Which is the usual reason to develop Diabetic ketoacidosis?

A

Due to ↑ insulin requirements from stress (eg, infection)

260
Q

Which is the pathophysiology of Diabetic Ketoacidosis?

A

Excess fat breakdown and ↑ Ketogenesis from ↑ free fatty acids, which are then made into ketone bodies (β hydroxybutyrate> acetoacetate)

261
Q

Signs/symptoms in Diabetic ketoacidosis

A 
Kusmaul respirations
Nausea/ vomiting
Abdominal pain
Psychosis/ delirium
Dehydration
Fruity breath odor
262
Q

Reason of fruity breath odor in Diabetic Ketoacidosis

A

Exchaled acetone

263
Q

What are the Kusmaul respirations?

A

Rapid/ deep breathing

264
Q

Labs found in Diabetic Ketoacidosis

A 
Hyperglycemia
↑ H+ 
↓ HCO3- (anion gap metabolic acidosis)
↑ blood ketones levels
Leukocytosis
Hyperkalemia
265
Q

What happens to K+ in Diabetic Ketoacidosis?

A

Hyperkalemia, but depleted intracellular K+ due to transcellular shift from ↓ insulin

266
Q

Complications of Diabetic Ketoacidosis

A

Life threatening mucormycosis
Cerebral edema
Cardiac arrythmias
Heart failure

267
Q

Who causes life threatening mucormycosis?

A

Rhizopus infection

268
Q

Treatment for Diabetic Ketoacidosis

A

IV fluids, IV insulin, and K+ (to replete intracellular stores)

269
Q

Is glucose necessary for treating Diabetic Ketoacidosis?

A

Glucose if necessary to prevent hypoglicemia

270
Q

Tumor of β cells of the pancreas

A

Insulinoma

271
Q

Which is the effect of Insulinoma?

A

Overproduction of insulin→ Hypoglicemia

272
Q

What is found in patients with insulinoma?

A

Whipple triad

273
Q

What is the Whipple triad?

A

Episodic CNS symptoms:
Lethargy
Syncope
Diplopia

274
Q

Findings on symptomatic patients with insulinoma

A

↓ blood glucose and ↑ C peptide levels (vs exogenous insulin use)

275
Q

Treatment for Insulinoma

A

Surgical Resection

276
Q

Which tumors cause Carcinoid syndrome?

A

Carcinoid Tumors (neuroendocrine cells), especially metastatic small bowel tumors

277
Q

What do Metastatic small bowal tumor secrete?

A

High levels of Serotonin (5HT)

278
Q

In these cases the carcinoid syndrome is not seen…

A

If tumor is limited to GI tract (5HT undergoes first pass metabolism in the liver)

279
Q

Findings of Carcinoid syndrome

A

Recurrent diarrhea
Cutaneous flushing
Asthmatic wheezing
Right sided valvular disease

280
Q

What is increased in urine in Carcinoid syndrome?

A

↑ 5- hydroxyindoleacetic acid (5-HIAA) in urine

281
Q

Which vitamin deficiency is found in carcinoid syndrome?

A

Niacin deficiency (pellagra)

282
Q

Which is the treatment for Carcinoid syndrome?

A

Resection, somatostatin analog (ocreotide)

283
Q

What is the rule of 1/3s in Carcinoid syndrome?

A

1/3 metastasize
1/3 [resent with 2 nd malignancy
1/3 are multiple

284
Q

Most common malignancy in the small intestine

A

Carcinoid syndrome

285
Q

Gastrin secreting tumor of pancreas or duodenum

A

Zollinger Ellison syndrome

286
Q

Where is commonly found the Zollinger Ellison syndrome?

A

Pancreas or duodenum

287
Q

What is the final result of Zollinger Ellison syndrome?

A

Acid hypersecretion causes recurrent ulcers in distal duodenum and jejunum

288
Q

Clinical presentation of Zollinger Ellison syndrome

A 
Abdominal pain (peptic ulcer disease, distal ulcers)
Diarrhea (malabsorption)
289
Q

What is associated to Zollinger Ellison syndrome?

A

May be associated with MEN 1

290
Q

What does MEN means?

A

Multiple Endocrine Neoplasis

291
Q

What syndrome is MEN-1?

A

Wermer syndrome

292
Q

Which Tumors are related to MEN-1?

A 
Parathyroid tumors
Pituitary tumors (prolactin or GH)
Pancreatic endocrine tumors- Zollinger Ellison syndrome, insulinomas, VIPomas, glucagonomas (rare)
293
Q

How is MEN-1 commonly presented?

A

Kidney stones and stomach ulcers

294
Q

Which syndrome is MEN-2A?

A

Sipple syndrome

295
Q

Tumors related to MEN 2A

A

Medullary thyroid carcinoma (secretes calcitonin)
Pheocromocytoma
Parathyroid hyperplasia

296
Q

MEN 2B Tumors realted

A

Medullary thyroid carcinoma
Pheocromocytoma
Oral/ intestinal ganglioneuromatosis (mucosal neuromas)

297
Q

What characteristics are associated to MEN 2B?

A

Marfanoid habitus

298
Q

Mnemonic for MEN 1

A

3 P’s (from cephalad to caudad: Pituitary, Parathyroid, and Pancreas; remember by drawing a diamond)

299
Q

Mnemonic for MEN 2A

A

2 P’s (Parathyroids and Pheochromocytoma: remember by drawing a square)

300
Q

Mnemonic for MEN 2B

A

1P (Pheocromocytoma remeber by drawing a Triangle)

301
Q

Mode of inheritance of all MEN syndromes

A

Autosomal dominant

“All MEN are dominant”

302
Q

Which mutliple endocrine neoplasias have ret gene mutations?

A

MEN 2A and 2B

ENDOCRINE (4 decks)

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