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Pathology I > Endocrine Pathology > Flashcards

Endocrine Pathology Flashcards

1
Q

Hormones released from anterior lobe of pituitary gland

A
  • Growth hormone (GH)
  • Prolactin (PRL)
  • Follicle Stimulating hormone (FSH)
  • Luteinizing hormone (LH)
  • Adrenocorticotropic hormone (ACTH)
  • Thyroid Stimulating hormone (TSH)
  • Melanocyte Stimulating hormone (MSH)
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2
Q

Hormones released from posterior lobe of pituitary gland

A
  • Vasopressin (Antidiuretic Hormone, ADH)

- Oxytocin

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3
Q

Key point of hyperpituitarim

A
  • Adenomas are responsible for excess hormone production
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4
Q

Significance of pituitary location

A
  • Optometric considerations
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5
Q

Hyperpituitarism

A
  • Growth hormone overproduction
  • Somatotroph cell adenomas
  • Mutations in the GNAS1 gene
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6
Q

Growth hormone overproduction depends on

A
  • Patient’s Age
  • Gigantism
  • Acromegaly
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7
Q

Gigantism results from

A
  • Excess GH in child

- Before epiphyseal closure

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8
Q

Gigantism

A
  • Elongated arms and legs

- Generalized increase in body size

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9
Q

Acromegaly results from

A
  • Excess GH in adults

- After epiphyseal closure

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10
Q

Acromegaly

A
  • Bone density increase
  • Enlargement of mandible, hands, feet
  • Gonadal disturbances
  • Diabetes
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11
Q

Most frequent type of hyperfunctioning pituitary adenoma

A
  • Prolactinomas (Lactotroph Adenomas)
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12
Q

Role of prolactin

A
  • Maintain lactation
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13
Q

Lactation suppression occurs via

A
  • GnRH Hypothalamus / Pituitary Axis

- Reduction of FSH / LH

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14
Q

Increased serum levels of prolactin (>100ug/L)

A
  • Adenoma
  • Physiologic hyperprolactinemia of pregnancy
  • Interference with normal dopamine inhibition
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15
Q

Physiological causes of hyperprolactinemia

A
  • Sleep

- Stress

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16
Q

Drug induced causes of hyperprolactinemia

A
  • Haloperidol
  • Reserpine
  • H2 antagonist
  • Fluoxetine
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17
Q

Systemic causes of hyperpituitarism

A
  • Hypothyroidism
  • CRF
  • Cirrhosis
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18
Q

Hormonal causes of hyperprolactinemia

A
  • Estrogen
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19
Q

Prolactinoma symptoms

A
  • Amenorrhea
  • Galactorrhea
  • Infertility
  • Loss of libido
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20
Q

Diagnosis of prolactinoma

A
  • Presenting symptoms
    History of systemic Illness, drugs/medications
  • MRI
  • Transsphenoidal resection
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21
Q

Hypopituitarsim

A
  • Decreased secretion of pituitary hormones
  • Diseases of the hypothalamus
  • Disease of the pituitary
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22
Q

Pituitary diseases involved in hypopituitarism

A
  • Nonsecretory pituitary adenomas
  • Surgery or radiation
  • Ischemic necrosis (Sheehan Syndrome)
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23
Q

Sheehan Syndrome

A
  • Sudden infarction of the anterior lobe
  • Hemorrhage or shock during delivery
  • Ischemic necrosis
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24
Q

Sheehan Syndrome symptoms

A
  • Lactation failure
  • ACTH deficiency
  • TSH deficiency
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25
Q

Thyroid hormones

A
  • 3,5,3’,5’-Tetraiodothyronine (T4 thyroxine)
  • 3,5,3’-Triiodothyronine (T3)
  • 3,3;,5’Triiodothyronine (rT3)
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26
Q

Pathology of thyroid disease

A
  • G Protein
  • cAMP
  • Target genes
  • Expression
  • Feedback inhibition
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27
Q

Effects of thyroid hormones

A
  • Normal human maturation
  • Normal brain development
  • Normal growth
  • Influence BM
  • Increase heart rate, contractility and CO
  • Stimulate lipolysis
  • CHO absorption
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28
Q

Causes of hyperthyroidism

A
  • Pituitary Adenoma
  • Germ Cell Tumors
  • Follicular Adenoma
  • Toxic Multinodular Goiter
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29
Q

Grave’s Disease (hyperthyroidism)

A
  • Thyrotoxicosis
  • Infiltrative Ophthalmopathy
  • Infiltrative Dermopathy
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30
Q

Grave’s Disease (hyperthyroidism) pathogenesis

A
  • Autoimmune disorder
  • Thyroid stimulating immunoglobulins (TSI)
  • Thyroid growth stimulating immunoglobulins (TGI)
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31
Q

Thyroid follicular epithelium in Grave’s Disease

A
  • Diffuse hypertrophy

- Diffuse hyperplasia

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32
Q

Clinical aspects of Grave’s Disease

A

Hypermetabolic state:

  • Nervousness
  • Palpitations
  • Weakness
  • Weight loss
  • Heat intolerance
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33
Q

Clinical presentation of Grave’s Disease

A
  • Exophthalmos
  • Thyroid Storm
  • Cardiovascular Insufficiency
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34
Q

Diagnosis of Grave’s Disease (hyperthyroidism)

A
  • Increased sTSH

- Decreased T3 and T4

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35
Q

Etiology of hypothyroidism

A
  • Thyroid tissue deficiency
  • Iodine deficiency
  • Hypothalamic lesion
  • Hypopituitarism
  • Peripheral resistance
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36
Q

Cretinism associated with hypothyroidism

A
  • Associated with iodine deficiency
  • Offspring of iodine deficient mothers
  • Iodine is essential for thyroid hormone synthesis
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37
Q

Manifestation of cretinism

A
  • Severe mental retardation

- Protruding tongue

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38
Q

Clinical presentation of myxedema in hypothyroidism

A
  • Apathy
  • Cold Intolerance
  • Mucopolysaccharide - rich edema
  • Coarsening of facial features
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39
Q

Diagnosis of hypothyroidism

A
  • Increased TSH

- Decreased T4

40
Q

Thyroid nodules (neoplasm of the thyroid gland)

A
  • Solitary, Neoplastic
  • Younger Patient, Neoplastic
  • Hx of radiation, Thyroid CA
  • Radioactive iodide uptake, Benign lesion
41
Q

Papillary carcinoma

A
  • Most common CA of thyroid

- Radiation exposure

42
Q

Pathology of papillary carcinoma

A
  • Branching papillae
  • Fibrovascular cores
  • Orphan Annie nuclei (cytoplasmic invaginations)
43
Q

Clinical findings of papillary carcinoma

A
  • Non-functional
  • Painless
  • Good prognosis
44
Q

Action of Cortisol (Glucocorticoids)

A
  • Stress Hormone
  • Maintain plasma glucose (increase gluconeogenesis)
  • Lipolysis
  • Muscle activity
45
Q

Muscle activity of cortisol (glucocorticoids)

A
  • Decrease glucose uptake and metabolism
  • Decrease protein synthesis
  • Increase amino acid release (protein breakdown)
46
Q

Hypercortisolism

A
  • Cushing Disease

- Primary pituitary lesion secreting ACTH

47
Q

Cushing Syndrome (hypercortisolism) may result from

A
  • Adrenal Adenoma
  • Adrenal CA
  • Bilateral adrenal hyperplasia
48
Q

Two types of Cushing Syndrome

A
  • Latrogenic

- Paraneoplastic

49
Q

Clinical manifestations of hypercortisolism)

A
  • Striae
  • Moon facies
  • Buffalo hump
  • Osteoporosis
50
Q

Laboratory findings of hypercortisolism (hyperadrenalism)

A
  • Hyperglycemia
  • Hypokalemia
  • Increased serum cortisol
  • ACTH (depends)
51
Q

Pathology of hyperadrenalism (hypercortisolism)

A
  • Adrenal Adenoma
  • Adrenal CA
  • Bilateral hyperplasia
  • Benefit from steroid treatment
52
Q

Endocrine pancreas produces

A
  • Beta insulin
  • Delta cells
  • Alpha glucagon
53
Q

Actions of pancreatic hormones in adipose tissue

A
  • Increase glucose uptake
  • Increase lipogenesis
  • Decrease lipolysis
54
Q

Actions of pancreatic hormones in striated muscle

A
  • Increase glucose uptake
  • Increase glycogen synthesis
  • Increase protein synthesis
55
Q

Actions of pancreatic hormones in the liver

A
  • Decrease gluconeogenesis
  • Increase glycogen synthesis
  • Increase lipogenesis
56
Q

Beta cell response to increasing blood sugar

A
  • Glucose enters cell via GLUT-2 channel
  • Stimulation and release of insulin
  • Membrane Depolarization
  • Insulin release
57
Q

Insulin binds to target tissues causing

A
  • Protein synthesis (GLUT-4 channels)
  • Glucose enters target tissues
  • Blood concentration of glucose declines
58
Q

Pathology of the endocrine pancreas significantly increases the risk of developing

A
  • Cardiovascular disease and mortality
  • Decreases life expectancy
  • Decreases life expectancy in the absence CVD
59
Q

Type I diabetes etiologies can be

A
  • Genetic
  • Autoimmunity
  • Environmental
60
Q

Diagnosis of Type II diabetes

A
  • Random glucose > 200 mg/dL
  • Fasting glucose > 126 mg/dL (on more than one occasion)
  • Abnormal oral glucose tolerance test
61
Q

Pathogenesis of Type II diabetes

A
  • Derangement in Beta cell secretion of insulin
  • Beta cell damage
  • Beta cell exhaustion
  • Amyloid Deposition
62
Q

Type II diabetes effects

A
  • Decreased response of peripheral tissues to respond to insulin
  • Post receptor signaling is decrease in insulin receptors
63
Q

Pathways qssociated with pathogenesis of long-term diabetic complications

A
  • Formation of advanced glycation end products (AGEs)
  • Activation of protein kinase C (PKC)
  • Intracellular hyperglycemia with disturbances in polyol pathways
64
Q

AGEs bind to a specific receptor

A
  • RAGE receptor

Located in

  • Inflammatory Cells
  • Endothelium
  • Vascular smooth muscle
65
Q

Detrimental properties of AGEs in the vascular compartment

A
  • Release cytokines from inflammatory cells
  • Generate ROS in endothelial cells
  • Increases procoagulant activity in endothelium
  • Enhanced proliferation of vascular smooth muscle
  • Increased synthesis of ECM
66
Q

Release of cytokines from inflammatory cells as a result of AGEs

A
  • TGF – β ; deposition of excess basement membrane material

- VEGF ; responsible for changes in diabetic retinopathy

67
Q

Extracellular matrix (ECM) alterations by AGEs

A
  • ECM - Proteins hold cells and tissues together

- AGE accumulation in ECM

68
Q

AGE accumulation in the ECM

A
  • Cross-linking of polypeptides of same protein (e.g., collagen type I and IV, Elastin)
69
Q

Effects of cross-linking of polypeptides of same protein (e.g., collagen type I and IV, Elastin) when AGEs accumulate in the ECM

A
  • Decreases vascular compliance (stiffens blood vessels)

- Causes leakage of vessels in systemic circulation and retinal blood vessels

70
Q

ECM alterations as a result of AGE accumulation causes

A
  • Trapping of nonglycated proteins (e.g., LDL, albumin, plasma proteins) which…
  • Accelerates atherosclerosis
  • Basement membrane thickens
71
Q

Tissues that do not require insulin for glucose transport

A
  • Nerves
  • Lenses
  • Kidneys
  • Blood vessels
72
Q

In the tissues that do not require insulin for glucose transport, glucose is metabolized to

A
  • Sorbitol (oxidative stress)
73
Q

Glucose metabolism to Sorbitol depletes

A
  • NADPH
74
Q

NADPH is needed for

A
  • Gluthathione Regeneration
75
Q

Depletion of NADPH due to metabolism of glucose to sorbitol causes

A
  • Less NADPH availability
  • Less glutathione regeneration
  • Oxidative damage
76
Q

Diabetic complications associated with

A
  • Cataracts
  • Oxidative injury to lens
  • Gangrene secondary to atherosclerosis
  • Diabetic neuropathy leading to ulcers
  • Proliferative retinopathy
  • Nephrosclerosis
77
Q

Basic anatomy/histology of the parathyroid gland

A
  • Chief cells with CaSR (calcium sensing receptor)
78
Q

Parathyroid gland function

A
  • Synthesis and secretion of parathyroid hormone

- Maintains Ca+2 in circulation

79
Q

Hyperparathyroidism causes

A
  • Vitamin D deficiency

- Bone homeostasis

80
Q

Primary hyperparathyroidism may arise from

A
  • Hyperplasia
  • Adenoma
  • Carcinoma
81
Q

Secondary hyperparathyroidism may arise from

A
  • Prolonged hypocalcemia
82
Q

Prolonged hypocalcemia causes

A
  • Increased PTH secretion

- Osteoclast stimulation

83
Q

Osteoclast stimulation in secondary hyperparathyroidism can cause

A
  • Chronic renal failure
  • Impaired vitamin D synthesis
  • Malabsorption syndromes
84
Q

Chronic renal failure results in

A
  • Hyperphosphatemia
85
Q

Hyperphosphatemia (from chronic renal failure) results in

A
  • Secondary hyperparathyroidism
  • Hypocalcemia develops (damaged kidneys)
  • PTH secretion increases at all levels of serum Ca2+
  • Increases osteoclast activity
  • Metabolic acidosis
86
Q

Morphology of hyperparathyroidism

A
  • Cancellous bone shows dissecting osteitis
87
Q

Pathology of hyperparathyroidism

A
  • Microfractures and secondary hemorrhages
  • Brown Tumor
  • Cystic degeneration
88
Q

Brown tumor

A
  • Vascularity, hemorrhage, and hemosiderin deposition
89
Q

Cystic degeneration causes severe hyperparathyroidism, resulting in

A
  • Increased bone cell activity
  • Peritrabecular fibrosis
  • Cystic Brown tumors
90
Q

Morphology of severe hyperparathyroidism

A
  • Generalized Osteiti Fibrosa Cystica -von Recklinghausen Disease of Bone
91
Q

Pathological findings of hyperparathyroidism in bone

A
  • Osteoporosis
  • Osteitis fibrosa cystica
  • Fractures
92
Q

Pathological findings of hyperparathyroidism in the thyroid gland

A
  • Parathyroid adenoma
93
Q

Pathological findings of hyperparathyroidism in the kidney

A
  • Nephrolithiasis
  • Polyuria
  • Nephrocalcinosis
94
Q

Pathological findings of hyperparathyroidism in the brain

A
  • Depression

- Seizures

95
Q

Pathological findings of hyperparathyroidism in the GI/abdominal region

A
  • Gallstones
  • Peptic ulcers
  • Acute pancreatitis
96
Q

Metabolic Syndrome of the endocrine pancreas

A
  • Central obesity
  • Atherogenic dyslipidemia
  • Insulin resistance or glucose intolerance
  • Prothrombotic state
  • Raised blood pressure
  • Proinflammatory state

Pathology I (9 decks)

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