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Path E3 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Hyposecretion of hormones

A

A genesis
Atrophy
Destruction

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2
Q

Hyper-secretion of hormones

A

Tumor

Hyperplasia

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3
Q

Anterior pituitary Hormones

A

FLAT PIG

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4
Q

Somatotroph

A

Growth Hormone

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5
Q

Mammography

A

Prolactin, essential for lactation

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6
Q

Corticotroph

A

Corticotropin (ACTH)

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7
Q

Gonadotroph

A

Gonadotropins (LH, FSH)

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8
Q

Thyrotoph

A

Thyrotpin (TSH)

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9
Q

Posterior pituitary is composed mostly of

A

Glial cells and axonal processes

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10
Q

Posterior pituitary stores

A

Oxytocin

Antidirutetic hormone

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11
Q

Anterior pituitary hyperfunction almost always associated with

A

adenoma

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12
Q

Adenoma: ACTH

A

Cushing syndrome

Nelsons syndrome

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13
Q

Adenoma: GH

A

Gigantism

Acromegaly

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14
Q

Adenoma: Prolactin

A

Galactorrhea and amenorrhea

Sexual dysfunction, infertility

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15
Q

Adenoma: TSH

A

Hyperthyroidism

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16
Q

Adenoma: FSH LH POMC

A

Hypogonadism
Mass effects
Hypopituitarism

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17
Q

Anterior lobe hypofunction causes

A

Nonfunctional pituitary adenoma
Postpartum ischemic necrosis
Ablation/destruction by surgery radiation or adjacent tumor

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18
Q

Hypofunction: GH

A

Pituitary dwarfism

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19
Q

Hypofunction: Gonadotropin

A

Amenorrhea and infertility in women

Decreased libido impotence and lack of pubic auxiliary hair in men

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20
Q

Hypofunction: Prolactin

A

No postpartum lactation

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21
Q

Hypofunction: TSH

A

Hypothyroidism

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22
Q

Hypofunction: ACTH

A

Hypoadrenalism

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23
Q

Gigantism is caused by

A

An edema in the anterior lobe that secretes GH

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24
Q

Gigantism occurs before

A

Closure of the peiphyseal plates in the long bones

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25
Q

Clinical features of gigantism

A

Generalized increase in the size of the body

Arms and legs are disproportionately long

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26
Q

Acromegaly is caused by

A

Increased GH due to an adenoma AFTER epiphyseal plates close

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27
Q

Acromegaly clinical features

A

Enlarged bones of the hands feet and face
Prognathism, development of a diastema
Hypertension and congestive heart failure may be seen

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28
Q

Gigantism or acromegaly have a better prognosis

A

Acromegaly is more guarded- due to complications of hypertension and CHF

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29
Q

Pituitary dwarfism potential causes

A

Failure of the pituitary gland to produce growth hormones

Lack of response to growth hormone by tissues

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30
Q

Clinical features of pituitary dwarfism

A

Short stature

Small jaws and teeth

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31
Q

Pituitary dwarfism treatment

A

Hormone replacement therapy if caused by lack

-prognosis good if replacement works

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32
Q

The thyroid gland produces hormones that regulate

A

The rate at which the body carries out its necessary functions

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33
Q

Thyroid storm

A

Sudden onset of severe hyperthyroidism usually triggered by stress. A medical emergency-patients often die of cardiac arrhythmia if untreated

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34
Q

Hyperthyroidism treatment

A

Depends on cause

Reactive iodine can be used to destroy overactive thyroid tissue

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35
Q

Graves Disease female predominance

A

7:1

Autoimmune disease with a significant genetic component

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36
Q

Graves Disease manifestations

A

Hyperthyroidism
Exophthalamos
Skin lesions

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37
Q

Hypothyroidism caused by

A

Decreased thyroid hormone production

  • iodine deficiency
  • AI destruction of thyroid
  • Ablation surgery or radiation
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38
Q

Cretinism

A

Hypothyroidism developing in infancy or early childhood

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39
Q

Myxedema

A

Hypothyroidism developing in older children and adults

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40
Q

Cretinism signs

A

Impaired development of skeleton and CNS
Short stature
Severe mental retardation
Protruding tongue

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41
Q

Myxedema

A 
Generalized apathy
Mental sluggishness-can mimic depression
Obesity
Cold intolerance
Enlarged tongue
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42
Q

Hypothyroidism: Serum TSH

A

Increased in primary cases due to loss of feedback inhibniotn
Not increased in cases caused by primary hypothalamic or pituitary disease

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43
Q

Hypothyroidism: treatment

A

Thyroid hormone replacement therapy

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44
Q

Hypothyroidism: prognosis

A

Good unless treatment delayed

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45
Q

Hashimoto thyroiditis mostly seen in

A

Older women significant genetic component

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46
Q

Hashimoto thyroiditis is a common cause of

A

Hypothyroidism

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47
Q

Hashimoto thyroiditis is a ____ Disease

A

Autoimmune

Progressive destruction of gland
-initially euthyroid progress ot hypothyroidism

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48
Q

Hashimoto thyroiditis patients are usually at risk for

A

Other autoimmune disease dn B cell Non Hodgkin

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49
Q

Goiters most common manifestation

A

Of thyroid disease

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50
Q

Goiters reflect

A

Impaired synthesis of thyroid hormone

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51
Q

Papillary Thyroid Carcinoma pathology

A

Microscopically character by papillae projections

Nuclear clearing

Nuclear grooves

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52
Q

Papillary Thyroid Carcinoma ______ mutation

A

RET proto-oncogene

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53
Q

Follicular thyroid carcinoma May resemble

A

A follicular adenoma

54
Q

Follicular thyroid carcinoma must see

A

Invasion through the capsule or into the blood vessels

55
Q

Medullary Thyroid Carcinoma derived from

A

Parafolluclar cells

56
Q

Medullary Thyroid Carcinoma all have mutations in

A

RET proto-oncogene

57
Q

Medullary Thyroid Carcinoma increased

A

Serum calcium

58
Q

Parathyroid glans mostly composed of

A

Chief cells

59
Q

Parathyroid chief cells secrete

A

PTH

-important regulator of blood calcium levels

60
Q

2 cells of parathyroid glands

A

Chief cells

Oxyphil cells-unknown Function

61
Q

Does the parathyroid need stimulation from pituitary or hypothalamus

A

No just needs to detect a decreased level of blood calcium

62
Q

Actions of PTH

A

Increase tubular reabsorption of calcium
Increase urinary phosphate excretion
Increase renal conversion of vitamin D into its active from
Increase osteoclast is activity

63
Q

Net affect of PTH

A

Increase the level of free calcium which inhibits further PTH secretion

64
Q

PTH converters Vitamin D

A

Into its active form which increases the GI calcium absorption

65
Q

Primary Hyperparathyrodism

A

An autonomous spontaneous overproduction of PTH

66
Q

Secondary Hyperparathyroidism

A

A secondary phenomenon in pts with chronic renal failure

67
Q

Primary HP is usually a result of

A

Parathyroid hyperplasia or adenoma

68
Q

Primary hyperparathyrodism clinical features

A

Painful bones

Stones

Abdominal Browns

Psychic moans

69
Q

Painful bones

A

Fractures associated with osteoporosis

70
Q

Stones

A

Kidney stones are frequent in primary hyperpara

71
Q

Abdominal groans

A

Constipation peptic ulcers and gallstones are frequent

72
Q

Psychic Mona’s

A

Depression lethargy and seizures

73
Q

Renal insufficiency leads to

A

Hyperphosphatemia

74
Q

Hyperphosphatemia

A

Increased amounts of phosphate in the blood because of decreased excretion

75
Q

Hyperphosphatemia decreases _______ thereby stimulating_______

A

Serum calcium

Production of parathyroid hormone—>glands become hyper plastic

76
Q

Damaged kidneys are unable to produce

A

Vitamin D

Which leads to reduced absorption of calcium in the intestines

77
Q

Secondary hyperparathyoirdims calcium blood levels

A

Are usually near normal

78
Q

Which hyperparathyroidism is less severe

A

Secondary

79
Q

Renal osteodystrophy

A

Defective bone growth due to renal failure

80
Q

Causes of hypoparathyroidism

A

Surgically induced
Congenital absence
AI

Rare

81
Q

Hypoparathyroidism clinical manifestation

A

Hypocalcemia
Increased neuromuscular excitability
Cardiac arrhythmias
Increased intracranial pressure and seizures

82
Q

The endocrine pancreases is composed of

A

Islets of langerhans

83
Q

Islet of langerhans cells

A

Beta cells
Alpha cells
Delta cells
PP cells

84
Q

Beta cells

A

Produce insulin

85
Q

Alpha cells

A

Produce glucagon

86
Q

Delta cells produce

A

Somatostatin

87
Q

PP cells produce

A

VIP- a pancreatic polypeptide

88
Q

Glucagon

A

Mobilizes carbohydrates stored in the liver into circulation when the body needs them. Promotes glycogenolysis and gluconeogensis in fasting states

89
Q

Insulin

A

Major anabolic hormone many synthetic and growth promoting effects-allows glucose to be transported and stored in cells within the body after meals

90
Q

Somatostatin

A

Suppresses both insulting and glucagon

91
Q

VIP

A

Exerts several GI effects

92
Q

Normal glucose levels

A

70-120mg/dL

93
Q

Diabetic if any one of these criteria

A

Random glycemic of > 200mg/dL with classical S&S

Fasting glucose levels of >126mg/dL on more than one occasion

Abnormal glucose tolerance test

94
Q

Insulin and Glucose homeostasis depends on 3 processes:

A

Gluconeogenesis

Glucose uptake by tissues

Actions of insulin and glucagon

95
Q

Insulin increases the rebate of

A

Glucose transport into certain cells of the body

96
Q

Diabetes Type I

A

A chronic AI

-beta cells of the pancreas get destroyed by self reactive T cells and autoAbs

97
Q

Type I diabetes results in

A

Absolute deficiency in insulin production

98
Q

Clinical Type I

A

Before 20 in normal weight

Character by decreased blood insulin

AutoAbs are detectable in the blood

AKA: Juvenile diabetes

99
Q

Diabetes Type I symptoms

A

Polydipsia
Polyuria
Polyphagia
Ketoacidosis

100
Q

Polydipsia

A

Increased intake of fluids

101
Q

Polyuria

A

Increase in the frequency and amount of urination

102
Q

Polyphagia

A

Increased food intake excessive hunger

103
Q

Ketoacidosis

A

Accumulation of ketoacidosis in the blood resulting from excessive breakdown of fats

104
Q

Diabetes II result of

A

Insulin resistance

Decreased insulin secretion

Adult onset

105
Q

Type 2 diabetes clinical features

A

> 40
Obesity
Insulin levels in blood may be normal or increased
Same symptoms as type I

106
Q

Who is most likely to die from diabetes

A

Type I

107
Q

Type I The pancreas

Where as in type 2

A

the pancreas fails to produce insulin

The pancreas makes insulin but the receptors fail to respond

108
Q

Diffuse glomerulosclerosis

A

90% of diabetics
Microangiopathy around glomerular capillaries and deposition of matrix

Proteinuria, total renal failure

109
Q

Nodular glomeruloscerlosis

A

15-30% of person with long term diabetes; specific to diabetes
Ball like deposition of matrix at the periphery of the glomerulus

Total renal failure

110
Q

Zollinger-Ellison Syndrome

A

Pancreatic islet cell tumor, hypersecretion of gastric acid, peptic ulcers

111
Q

Hormones produced by the adrenal cortex

A

Cortisol
Aldosterone
Estrogen
Progesterone

112
Q

Catecholamines produced by the adrenal medulla

A

Epinephrine
Norepinephrine
Dopamine

113
Q

2 Types of Hyperadrenalism

A

Hypercortisolism

Hyperaldosteronism

114
Q

Cushing’s syndrome (hypercortisolism) causes

A

Excess administration of exogenous glucocorticoids

Primary adrenal hyperplasia or neoplasm

Pituitary source

Ectopic ACTH secretion by neoplasm

115
Q

Primary pituitary source known as cushings

A

ACTH oversecretion by pituitary microadenoma

116
Q

Cushing short term clinical features

A

Weight gain and hypertension

Moon faces

Buffalo hump

117
Q

Long term cushings clinical features

A

Decreased muscle mass, weakness

Diabetes

Osteoporosis

Cutaneous striae hirsutism

Mental disturbances: mood swings, depression, psychosis

Menstrual irregularities

118
Q

Hyperaldosteronism characterized by chronic excess aldosterone secretion results in

A

Sodium retention, potassium excretion

Hypertension and hypokalemia

119
Q

Primary hyperaldosteronism

A

Very rare
Hyperplasia neoplasm idiopathic
Decreased levels of plasma renin

120
Q

Secondary hyperaldosteronism

A

Aldosterone released in response to activation of renin angiotensin system

Increased levels of plasma renin

121
Q

Hypoadrenalism

A

Primary or secondary

Secondary decreased stimulation of adrenals from deficiency of ACTH

122
Q

Hypoadrenalism symptoms

A

Weakness
Fatigue
GI disturbances

123
Q

Acute Adrenocortical insufficiency

A

In patients on exogenous steroids
—>rapid withdrawal ——>adrenal crisis

Vomiting
Abdominal pain
Hypotension
Coma
Death
124
Q

Primary Chronic Adrenocortical insufficiency (Addison’s Disease)

A

Progressive destruction of the adrenal cortex

  • ACTH serum elevated
  • Destruction of cortex prevents response to ACTH
125
Q

Primary Chronic Adrenocortical insufficiency (Addison’s Disease) destruction is caused by

A

AI process
Infection (TB AIDs)
Metastatic Disease

126
Q

Primary Chronic Adrenocortical insufficiency (Addison’s Disease) Symptoms

A

Easily fatigued
GI disturbances
Hyperpigmentation
Craving salt

127
Q

Secondary Adrenocortical insufficiency is any disorder of

A

Of the hypothalamus or pituitary that reduces output of ACTH

128
Q

Secondary Adrenocortical insufficiency is similar to Addisons (primary) except t

A

No skin/mucosa pigmentation

129
Q

Pheochromocytoma a neoplasm of

A

Chromaffin cells

130
Q

chromaffin cells make

A

Epinephrine

131
Q

Pheochromocytoma

A

F>M 30-60

Hypertension
Tachycardia
Tremor
Headache

132
Q

Pheochryomcytoma rules of 10s

A

10%

Bilateral
Extra adrenal
Malignant
Familial syndromes

Path E3 (8 decks)

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