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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
Thyroid hormones
- 3,5,3',5'-Tetraiodothyronine (T4 thyroxine) - 3,5,3'-Triiodothyronine (T3) - 3,3;,5'Triiodothyronine (rT3)
26
Pathology of thyroid disease
- G Protein - cAMP - Target genes - Expression - Feedback inhibition
27
Effects of thyroid hormones
- Normal human maturation - Normal brain development - Normal growth - Influence BM - Increase heart rate, contractility and CO - Stimulate lipolysis - CHO absorption
28
Causes of hyperthyroidism
- Pituitary Adenoma - Germ Cell Tumors - Follicular Adenoma - Toxic Multinodular Goiter
29
Grave's Disease (hyperthyroidism)
- Thyrotoxicosis - Infiltrative Ophthalmopathy - Infiltrative Dermopathy
30
Grave's Disease (hyperthyroidism) pathogenesis
- Autoimmune disorder - Thyroid stimulating immunoglobulins (TSI) - Thyroid growth stimulating immunoglobulins (TGI)
31
Thyroid follicular epithelium in Grave's Disease
- Diffuse hypertrophy | - Diffuse hyperplasia
32
Clinical aspects of Grave's Disease
Hypermetabolic state: - Nervousness - Palpitations - Weakness - Weight loss - Heat intolerance
33
Clinical presentation of Grave's Disease
- Exophthalmos - Thyroid Storm - Cardiovascular Insufficiency
34
Diagnosis of Grave's Disease (hyperthyroidism)
- Increased sTSH | - Decreased T3 and T4
35
Etiology of hypothyroidism
- Thyroid tissue deficiency - Iodine deficiency - Hypothalamic lesion - Hypopituitarism - Peripheral resistance
36
Cretinism associated with hypothyroidism
- Associated with iodine deficiency - Offspring of iodine deficient mothers - Iodine is essential for thyroid hormone synthesis
37
Manifestation of cretinism
- Severe mental retardation | - Protruding tongue
38
Clinical presentation of myxedema in hypothyroidism
- Apathy - Cold Intolerance - Mucopolysaccharide - rich edema - Coarsening of facial features
39
Diagnosis of hypothyroidism
- Increased TSH | - Decreased T4
40
Thyroid nodules (neoplasm of the thyroid gland)
- Solitary, Neoplastic - Younger Patient, Neoplastic - Hx of radiation, Thyroid CA - Radioactive iodide uptake, Benign lesion
41
Papillary carcinoma
- Most common CA of thyroid | - Radiation exposure
42
Pathology of papillary carcinoma
- Branching papillae - Fibrovascular cores - Orphan Annie nuclei (cytoplasmic invaginations)
43
Clinical findings of papillary carcinoma
- Non-functional - Painless - Good prognosis
44
Action of Cortisol (Glucocorticoids)
- Stress Hormone - Maintain plasma glucose (increase gluconeogenesis) - Lipolysis - Muscle activity
45
Muscle activity of cortisol (glucocorticoids)
- Decrease glucose uptake and metabolism - Decrease protein synthesis - Increase amino acid release (protein breakdown)
46
Hypercortisolism
- Cushing Disease | - Primary pituitary lesion secreting ACTH
47
Cushing Syndrome (hypercortisolism) may result from
- Adrenal Adenoma - Adrenal CA - Bilateral adrenal hyperplasia
48
Two types of Cushing Syndrome
- Latrogenic | - Paraneoplastic
49
Clinical manifestations of hypercortisolism)
- Striae - Moon facies - Buffalo hump - Osteoporosis
50
Laboratory findings of hypercortisolism (hyperadrenalism)
- Hyperglycemia - Hypokalemia - Increased serum cortisol - ACTH (depends)
51
Pathology of hyperadrenalism (hypercortisolism)
- Adrenal Adenoma - Adrenal CA - Bilateral hyperplasia - Benefit from steroid treatment
52
Endocrine pancreas produces
- Beta insulin - Delta cells - Alpha glucagon
53
Actions of pancreatic hormones in adipose tissue
- Increase glucose uptake - Increase lipogenesis - Decrease lipolysis
54
Actions of pancreatic hormones in striated muscle
- Increase glucose uptake - Increase glycogen synthesis - Increase protein synthesis
55
Actions of pancreatic hormones in the liver
- Decrease gluconeogenesis - Increase glycogen synthesis - Increase lipogenesis
56
Beta cell response to increasing blood sugar
- Glucose enters cell via GLUT-2 channel - Stimulation and release of insulin - Membrane Depolarization - Insulin release
57
Insulin binds to target tissues causing
- Protein synthesis (GLUT-4 channels) - Glucose enters target tissues - Blood concentration of glucose declines
58
Pathology of the endocrine pancreas significantly increases the risk of developing
- Cardiovascular disease and mortality - Decreases life expectancy - Decreases life expectancy in the absence CVD
59
Type I diabetes etiologies can be
- Genetic - Autoimmunity - Environmental
60
Diagnosis of Type II diabetes
- Random glucose > 200 mg/dL - Fasting glucose > 126 mg/dL (on more than one occasion) - Abnormal oral glucose tolerance test
61
Pathogenesis of Type II diabetes
- Derangement in Beta cell secretion of insulin - Beta cell damage - Beta cell exhaustion - Amyloid Deposition
62
Type II diabetes effects
- Decreased response of peripheral tissues to respond to insulin - Post receptor signaling is decrease in insulin receptors
63
Pathways qssociated with pathogenesis of long-term diabetic complications
- Formation of advanced glycation end products (AGEs) - Activation of protein kinase C (PKC) - Intracellular hyperglycemia with disturbances in polyol pathways
64
AGEs bind to a specific receptor
- RAGE receptor Located in - Inflammatory Cells - Endothelium - Vascular smooth muscle
65
Detrimental properties of AGEs in the vascular compartment
- 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
Release of cytokines from inflammatory cells as a result of AGEs
- TGF – β ; deposition of excess basement membrane material | - VEGF ; responsible for changes in diabetic retinopathy
67
Extracellular matrix (ECM) alterations by AGEs
- ECM - Proteins hold cells and tissues together | - AGE accumulation in ECM
68
AGE accumulation in the ECM
- Cross-linking of polypeptides of same protein (e.g., collagen type I and IV, Elastin)
69
Effects of cross-linking of polypeptides of same protein (e.g., collagen type I and IV, Elastin) when AGEs accumulate in the ECM
- Decreases vascular compliance (stiffens blood vessels) | - Causes leakage of vessels in systemic circulation and retinal blood vessels
70
ECM alterations as a result of AGE accumulation causes
- Trapping of nonglycated proteins (e.g., LDL, albumin, plasma proteins) which... - Accelerates atherosclerosis - Basement membrane thickens
71
Tissues that do not require insulin for glucose transport
- Nerves - Lenses - Kidneys - Blood vessels
72
In the tissues that do not require insulin for glucose transport, glucose is metabolized to
- Sorbitol (oxidative stress)
73
Glucose metabolism to Sorbitol depletes
- NADPH
74
NADPH is needed for
- Gluthathione Regeneration
75
Depletion of NADPH due to metabolism of glucose to sorbitol causes
- Less NADPH availability - Less glutathione regeneration - Oxidative damage
76
Diabetic complications associated with
- Cataracts - Oxidative injury to lens - Gangrene secondary to atherosclerosis - Diabetic neuropathy leading to ulcers - Proliferative retinopathy - Nephrosclerosis
77
Basic anatomy/histology of the parathyroid gland
- Chief cells with CaSR (calcium sensing receptor)
78
Parathyroid gland function
- Synthesis and secretion of parathyroid hormone | - Maintains Ca+2 in circulation
79
Hyperparathyroidism causes
- Vitamin D deficiency | - Bone homeostasis
80
Primary hyperparathyroidism may arise from
- Hyperplasia - Adenoma - Carcinoma
81
Secondary hyperparathyroidism may arise from
- Prolonged hypocalcemia
82
Prolonged hypocalcemia causes
- Increased PTH secretion | - Osteoclast stimulation
83
Osteoclast stimulation in secondary hyperparathyroidism can cause
- Chronic renal failure - Impaired vitamin D synthesis - Malabsorption syndromes
84
Chronic renal failure results in
- Hyperphosphatemia
85
Hyperphosphatemia (from chronic renal failure) results in
- Secondary hyperparathyroidism - Hypocalcemia develops (damaged kidneys) - PTH secretion increases at all levels of serum Ca2+ - Increases osteoclast activity - Metabolic acidosis
86
Morphology of hyperparathyroidism
- Cancellous bone shows dissecting osteitis
87
Pathology of hyperparathyroidism
- Microfractures and secondary hemorrhages - Brown Tumor - Cystic degeneration
88
Brown tumor
- Vascularity, hemorrhage, and hemosiderin deposition
89
Cystic degeneration causes severe hyperparathyroidism, resulting in
- Increased bone cell activity - Peritrabecular fibrosis - Cystic Brown tumors
90
Morphology of severe hyperparathyroidism
- Generalized Osteiti Fibrosa Cystica -von Recklinghausen Disease of Bone
91
Pathological findings of hyperparathyroidism in bone
- Osteoporosis - Osteitis fibrosa cystica - Fractures
92
Pathological findings of hyperparathyroidism in the thyroid gland
- Parathyroid adenoma
93
Pathological findings of hyperparathyroidism in the kidney
- Nephrolithiasis - Polyuria - Nephrocalcinosis
94
Pathological findings of hyperparathyroidism in the brain
- Depression | - Seizures
95
Pathological findings of hyperparathyroidism in the GI/abdominal region
- Gallstones - Peptic ulcers - Acute pancreatitis
96
Metabolic Syndrome of the endocrine pancreas
- Central obesity - Atherogenic dyslipidemia - Insulin resistance or glucose intolerance - Prothrombotic state - Raised blood pressure - Proinflammatory state

Pathology I (9 decks)

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