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Human Disease and Therapeutics > Endocrine Pathology (Diabetes, Thyroid, Parathyroid, Pituitary, Adrenals, Paget's Disease) > Flashcards

Endocrine Pathology (Diabetes, Thyroid, Parathyroid, Pituitary, Adrenals, Paget's Disease) Flashcards

1
Q

Diabetes (diagnostic criteria)

A

relative or absolute deficiency of insulin that causes glucose intolerance

  • fasting sugar >126 mg/dL
  • 75 gm glucose test yields glucose >200 mg/dL after 2 hours
  • HbA1c > 6.5% (provides a good estimate of the average level of glucose in the blood for the previous 3 months; normal is BELOW 5-7%
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2
Q

Statistics related to diabetes

A
  • 8-9% of the US population
  • 73,000 deaths/year in US
  • nearly 50% undiagnosed
  • 14% of population is pre-diabetic (fasting glucose 100-125 of HbA1c 5.75-6.4%)
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3
Q

Symptoms of diabetes

A
  • polydipsia and polyphagia
  • polyuria
  • unexplained weight loss
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4
Q

Functions of insulin: how does it affect

  • uptake of glucose and amino acids
  • glycogenolysis
  • lipolysis
  • proteolysis
A
  • promotes glucose and amino acid uptake through the membranes of muscle (smooth, skeletal, and cardiac), fibroblasts, fat cells. It is an anabolic hormone that helps to control normal growth patterns and tissue development
  • decreases glycogenolysis, lipolysis, and proteolysis
  • does not affect glucose uptake in neurons, kidney, or RBCs (diabetics can have very high intracellular glucose in these tissues resulting in hyperosmotic conditions –> organ pathology)
  • insulin is secreted from beta cells in pancreas
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5
Q

consequences of diabetes (no insulin)

A
  • increasaed lipolysis –> ketosis and triglycerides in the blood
  • increased glycogenolysis and gluconeogenesis
  • protein catabolism of muscle –> muscle wasting
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6
Q

features of type 1 diabetes

A
  • no natural insuling (insulin-requiring)
  • young, 5% of cases, typically thin
  • loss of beta cells (autoimmune process usually triggered by environment, such as viral infection
  • ketoacidosis and dehydration
  • deep labored breathing from the ketoacidosis
  • nausea, coma, anorexia
  • glucose levels usually up to 500 before diagnosis
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7
Q

features of type 2 diabetes

A
  • adult onset, non insulin dependent
  • insulin levels usually normal, but increased resistance to insulin
  • correlates with excessive visceral fat (diet controls in about 20% of cases)
  • correlates with hypertension, risk of atherosclerosis, and dyslipidemia –> metabolic syndrome
  • some genetics (likely polygenic autosomal)
  • obesity
    minimal ketones or acidosis, but very high glucose
  • some ethnic groups with higher risk (Pima indians, Hispanics, African Americans, etc.)
  • can result from amyloidosis (damage to pancreatic beta cells
  • major metabolic complication is hyperosmolar coma
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8
Q

diabetes insipidus

A

increased urine production not related to glucose metabolism and often related to ADH abnormality. usually rare.

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9
Q

metabolic syndrom definition

A

a group of risk factors that can increase your chance of developing heart disease, diabetes, and stroke.

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10
Q

features/risk factors related to metabolic syndrome

A
  • complex interaction between obesity and insulin resistance (insulin receptors refractory to insulin)
  • abnormal lipid metabolism (high triglycerides and LDLs, low HDLs)
  • excess fat around waist
  • hypertension
  • increased risk for atherosclerosis
  • pro-thrombic tendency
  • pro-inflammatory state (related to elevated visceral fat cells)
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11
Q

Pathogenesis of metabolic syndrome

A
  • increased visceral adiposity
  • decreased glucose metabolism and insulin sensitivity (inhibited by increased levels of free fatty acids)
  • increased hepatic inflammation, cirrhosis, and fatty accumulation
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12
Q

major complications of metabolic syndrome

A
  • very high glucose
  • hyperosmolar consequences, including coma
  • brain swelling due to increased osmolarity –> coma and seizures
  • cardiac disease
  • dehydration
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13
Q

features of gestational diabetes

A
  • due to the stress of pregnancy (3-10% of pregnancies)
  • usually goes away after birth of child, but can develop type II DM later
  • consequences: insufficient placental function, abnormally large babies with excessive insulin secretion, early fetal hypoglycemia causing malformations (because insulin is a growth factor)
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14
Q

Long-term complications of diabetes

A
  1. (early) ketoacidosis, hyperosmolar coma, urinary tract infections
  2. issues in the eyes: ophthalmic swelling, cataracts, retinopathy, neuropathy, glaucoma, and blindness
  3. accelerated atherosclerosis (damaged microcirculation with high unhealthy lipid levels and consequences seen in the heart (MI), kidneys (glomerulosclerosis, pyelonephritis), and brain (stroke)
  4. peripheral neuropathies (loss of touch and pain sensation in extremities; gangrene)
  5. autonomic nerve dysfunction (abnormal GI motility, hypotonic bladder, increased UTIs)
  6. more prone to infections/slower healing
  7. symptoms worsen with stress
  8. renal damage (elevated sclerosis) due to inflammation and infection –> ESRD
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15
Q

most common cause of death in diabetics

A

coronary atherosclerosis that leads to myocardial infarction

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16
Q

oral problems seen in diabetic patients

A
  • increased periodontal disease
  • poor wound healing (issues with surgery and implants)
  • infections (candidiasis)
  • xerostromia –> caries
  • patients should be care to avoid hypoglycemia in the dental office –> emergency situation
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17
Q

goal of insulin-replacement therapy

A
  • replicate natural insulin patterns (basal background levels with burst release in response to rising glucose levels during eating)
  • insulins are categorized by their onset of action, how quickly they are absorbed, and half life.
  • insulin in the US is prepared in a lab (not from animals)
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18
Q

Release and management of thyroid hormone

A
  • controlled by hypothalamic release of TRH, which stimulates the pituitary to release TSH
  • excessive activation of the thyroid leads to a hypermetabolic state causing protein catabolism and enhanced sympathetic nervous system activity
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19
Q

T/F thyroid disease affects men more than women

A

False- it affects women more than men.

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20
Q

Clinical findings in hyperthyroidism

A
  • nervousness
  • hot and sweating (heat intolerant)
  • weight loss
  • muscle weakness
  • tremors
  • palpitations/tachycardia
  • thyroid storm (fever, tachycardia, sweating, shaking, agitation, and unconsciousness)
  • lab test show: elevated T4/T5, low TSH
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21
Q

Graves disease (definition and cause)

A
  • 90% of cases of hyperthyroidism, found in 2% of females
  • cause: autoimmune (antibodies function as agonists to thyroid-related receptors causing excessive activation
  • possible cause is increased TSI
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22
Q

Symptoms of graves disease

A
  • hyperthyroidism
  • exophthalamos
  • englarged thyroid gland (hyperplasia)
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23
Q

Plummer’s disease

A
  • multinodular goiter

- 5-10% of hyperthyroidism cases

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24
Q

clinical findings of hypothyroidism

A
  • hypo-metabolic state
  • in children = “cretinism” with reduced mental and physical development
  • enlarged thyroid
  • low temperature
  • dry coarse skin and hair
  • sluggish
  • cold intolerance
  • modest weight gain
  • myxedema (severe cases)
  • high TSH (good screen for the condition)
  • can be caused by iodine deficiency
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25
Q

Hashimoto’s disease

A
  • type of hypothyroidism (9-10% incidence in US - most common form of thyroid deficiency)
  • autoimmune, usually females
  • may start as hyperthyroidism followed by permanent hypothyroidism
  • hypopituitarism
  • can be caused by radiation (either accidental or therapeutic)
  • TSH high, but T4 low
  • typically not painful
  • thyroid enlarges and then atrophies
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26
Q

Goiter

A
  • most common lesion of the thyroid (usually a thyroid enlargement)
  • rarely associated with hypothyroidism; usually associated with iodine deficiency
  • not a cancer
  • diagnosed with fine needle aspiration (versus biopsy) to determine if the thyroid has large follicle filled with colloid and relatively few cells.
27
Q

Thyroid adenomas

A
  • most common thyroid neoplasm

- not malignant

28
Q

Thyroid carcinomas

A
  • typically low risk and low metastasis

- papillary carcinoma most common with good prognosis especially in young women

29
Q

thyroid nodules

A
  • most are benign, common, and found in 6% of women and 2% of males
  • use fine needle aspiration to diagnose
30
Q

T/F The parathyroid gland is NOT regulated by the pituitary gland

A

True

31
Q

What are the functions of the parathyroid glands and parathyroid hormone (PTH)?

A
  • secrete parathyroid hormone (in response to low blood calcium)
  • parathyroid hormone (PTH) will activate receptors on bone, GI tract, and kidneys to regulate calcium levels
  • PTH activates osteoclasts –> bone resorption, can cause osteoporosis if excessive
  • PTH increases tubular reabsorption of clacium, activates vitamin D, and increases GI absorption
32
Q

Features of primary hypercalcemia/hyperparathyroidism

A
  • one of the most common endocrine disorders
  • usually an adenoma of the parathyroid gland
  • results in hypercalcemia
  • treatment is surgical
  • metastasis and carcinomas are rare
33
Q

symptoms of primary hyperparathyroidism

A
  • osteoporosis (due to increased osteoclast function)
  • increased systemic levels of calcium –> constipation, weakness, anorexia, stones, peptic ulcers, depression, or coma
  • bones, stones, moans, and groans
  • also causes cystic bone lesions and hypercalcification
  • arrhythmias
  • lab results: high serum calcium, hypophosphatemia
34
Q

features of secondary hypercalcemia

A
  • intestinal malabsorption of vitamin D or calcium –> excessive secretion of PTH
  • drugs (ex. thiazides)
  • renal failure
35
Q

How do glucocorticoid affect bones?

A
  • promote osteoporosis
  • antagonize Vit. D-stimulated intestinal Ca2+ transport and stimulates renal secretion –> blocks osteoblast function
  • chronic use of glucocorticoids leads to osteoporosis
36
Q

Features/causes of hypoparathyroidism

A
  • rare

- most common cause = accidental removal of parathyroid glands during thyroid surgery

37
Q

symptoms of hypoparathyroidism

A
  • hypocalcemia, decreased PTH, tetany, dental changes in children (poor enamel, brittle/missing teeth)
38
Q

Hoe does calcitonin regulate bone mineral homeostasis?

A
  • action oppose PTH
  • inhibits osteoclast activity to decrease blood calcium levels
  • useful for treatment of Paget’s disease of bone
39
Q

What is the pathology of Paget’s Disease?

A
  • normal osteoclastic and osteoblastic remodeling activity is DISRUPTED
  • considered a disorder of bone remodeling
  • results in excessive bone removal followed by excessive bone formation
  • irregular and weakened bone pattern and increased likelihood of fractures
  • cause unknown, but may be triggered by viral infection
40
Q

Features/symptoms of Paget’s Disease

A
  • common in caucasians (3-4%); second most common bone disease following osteoporosis; it is a chronic disease
  • usually people are > 40 yrs
  • often asymptomatic but can result in bone pain and fractures, also arthritis if disease is near joints
  • high serum alkaline phophates
41
Q

Common sites for Paget’s Disease

A
  • vertebrae, skull, and long bones
42
Q

Where are the anterior and posterior pituitary glands derived from?

A
  • anterior - derived from Rathke’s pouch/roof of mouth

- posterior - derived from the hypothalamus

43
Q

Method of secretion for anterior and posterior pituitary glands

A
  • anterior = portal circulation from the hypothalamus (“releasing factors/hormones”
  • posterior = neurons release neurotransmitters in systemic circulation
44
Q

hormones of the anterior pituitary, with their corresponding releasing hormones and their targets

A
  • TSH (TRH from hypothalamus, target: thyroid/secretion of T4)
  • ACTH (CRH from hypothalamus, target: adrenal cortex/secretion of cortisol and other adrenal hormones)
  • FSH, LH (GNRH from hypothalamus, target: reproductive tissues, regulates ovulation and gamete production)
  • GH (GHRH from hypothalamus, target: liver, IGF-1, whole body to promote anabolism)
  • Prolactin (inhibited by dopamine from hypothalamus, target: lactation)

hypothalamus will also secrete GIH (aka somatostatin) which will inhibit growth hormone release.

45
Q

How is growth hormone related to insulin?

A
  • GH is an insulin antagonist

- it is released in response to hypoglycemia and blocked by hyperglycemia

46
Q

features of Klinefelter’s syndrome

A
  • XXY
  • hypogonadism
  • 0.5% incidence
47
Q

most common age for a pituitary adenoma

A

40-70 yrs

48
Q

4 types of pituitary adenomas and related symptoms

A
  1. prolactin (affects reproductive functions)
  2. growth hormone (results in gigantism if before puberty, primarily linear bone growth; results in acromegaly if after puberty, non-linear bone growth/thickening with elevated levels of IGF-1)
  3. corticotropin (increased ACTH –> Cushing’s disease)
  4. unclassified (doesn’t make much of anything)

pituitary adenomas will often put pressure on the optic chiasm resulting in loss of lateral visual fields.

49
Q

most common cause/symptoms of hypopituitarism

A
  • non-secretory pituitary adenomas

- consequences: loss of sex characteristics/sterility, retards growth in children, hypothyroidism

50
Q

cause/consequences of hypersecretion of ADH from pituitary (SIADH - syndrome of inappropriate ADH)

A
  • main cause - metastasized carcinoma, CNS infection

- alters kidney function (increased volume/water, hyponatremia, and hemodilation)

51
Q

results of hyposecretion of ADH

A
  • diabetes insipidus
  • polyuria
  • polydipsia
  • no effect on glucose
52
Q

Adrenal gland anatomy/where the various hormones are made

A
  • medulla - makes catecholamines (NE and Epi)
  • cortex - makes steroid hormones
  • mineralcorticoids (aldosterone for salt/water retention)
  • glucocorticoids (cortisol, made from cholesterol, used to increase blood glucose, stress, regulate immune response)
  • adrogens (sex steroids, DHEA can be made into estrogens)
53
Q

features of primary acute adrenal cortex insufficiency

A
  • weakness
  • nausea
  • hyponatremia
  • hypotension
  • depression
  • skin pigmentation (increased MSH with increased release of ACTH from pituitary)
54
Q

Addison disease

A
  • results in adrenal insufficiency
  • primary disease caused by damage to the adrenal cortex (no longer responds to ACTH)
  • secondary disease caused by damage to the pituitary gland (decreased levels of ACTH; cortex still responsive to administered ACTH)
  • cause is autoimmune and more common in white women
  • increased infection
55
Q

features of secondary adrenocortical insufficiency

A
  • due to hypothalamic or pituitary problem
  • no hyperpigmentation with exogenous steroids
  • hypoglycemia**
  • aldosterone is usually normal
  • often caused by rapid withdrawal of exogenous steroids (most common cause of cortical insufficiency)
56
Q

Adrenal crisis

A
  • possible consequence related to primary acute adrenocortical insufficiency
  • sudden need for increased steroid output
  • can be cause by massive adrenal hemorrhage
57
Q

Cushing’s disease - causes/pathology

A
  • leading cause of hypercortisolism (W>M, 5:1)
  • bilateral adrenal hyperplasia
  • adrenals will ultimately shrink due to feedback from hypercortisolism (esp. in the case of an adrenal tumor)
  • in the case of a tumor in the anterior pituitary: ACTH is high and cortisol is high
  • the adrenals may also be acting autonomously
58
Q

symptoms of Cushing’s disease

A
  • moon face
  • osteoporosis
  • buffalo hump
  • obesity (cortisol will increase blood glucose –> increase insulin –> stimulate lipogenesis
  • mood changes
  • think skin with purple stretch marks
  • amenorrhea
  • muscle weakness
  • poor wound healing
  • hypertension
  • patients look similar to those on chronic corticosteroid treatment for arthritis or other inflammatory diseases
59
Q

Cushing’s disease vs. Cushing’s syndrome

A
  • syndrome: consequence of excess ACTH regardless of cause

- disease: form of Cushing’s syndrome caused by a pituitary tumor

60
Q

Cause/consequences of secondary adrenocortical insufficiency

A
  • cause - extended use of exogenous steroids (ex. prednisone), which suppress the normal adrenal glands
  • if treatment is abruptly stopped, there is a transient hypocortisolic reaction
61
Q

Conn syndrome

A
  • hyperaldosteronism
  • usually due to an adenoma (primary hyperaldosteronism)
  • Na+ retention and K+ excretion
  • suppression of renin-angiotensin system
  • secondary hypertension
62
Q

causes of secondary hyperadlosteronism

A
  • renal disease, cirrhosis, or congestive heart failure
63
Q

Adrenal tumors (features/examples)

A
  • adenomas most common (1% prevalence); usually nonfunctional
  • carcinomas rares
  • pheochromocytoma = tumor of the adrenal medulla
64
Q

pheochromocytoma

A
  • tumor of the adrenal medulla
  • usually benign
  • excessive secretion of catecholamines
  • symptoms: hypertension, flushing, increased catecholamines in urine
  • often associated with Neurofibromatosis and Van Hoppel-Lindau disease

Human Disease and Therapeutics (11 decks)

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