Gen Path - Class 20

Front 1

What is the primary function of the endocrine system?

Back 1

Produce hormones

Front 2

What are three factors that influence hormone responsiveness?

Back 2

(1)Hormone concentration (greater amount = stronger response), (2)Abundance of receptors on target cell (more receptors = greater sensitivity), (3)Influence of other hormones

Front 3

What are six functions of the hypothalamus?

Back 3

(1)Control of ANS (smooth and cardiac mm), (2)Regulation of emotions & behaviour, (3)Regulation of eating & drinking, (4)Control of body temperature, (5)Regulation of circadian rhythms & consciousness, (6)Hormonal production and control

Front 4

What effect does Corticotropin-releasing hormone (CRH) have on the anterior pituitary?

Back 4

ACTH & MSH

Front 5

What effect does Growth hormone-releasing hormone (GHRH) aka somatocrinin have on the anterior pituitary?

Back 5

GH

Front 6

What effect does Growth hormone-inhibiting hormone (GHIH) aka somatostatin have on the anterior pituitary?

Back 6

Inhibits GH

Front 7

What effect does Thyrotropin-releasing hormone (TRH) have on the anterior pituitary?

Back 7

TSH & PL

Front 8

What effect does Gonadrotropin-releasing hormone (GnRH) have on the anterior pituitary?

Back 8

FSH & LH

Front 9

What effect does Prolactin releasing hormone (PRH) have on the anterior pituitary?

Back 9

PRL

Front 10

What effect does Prolactin-inhibiting hormone (PIH) aka Dopamine have on the anterior pituitary?

Back 10

Inhibits PRL

Front 11

How is the anterior pituitary regulated?

Back 11

Regulated by positive stimulation exerted by the cells in the hypothalamic centers and by negative feedback inhibition created by the hormones produced by target endocrine cells in the thyroid, adrenals, and gonads.

Front 12

What type of cells do the hormones of the posterior pituitary act on?

Back 12

These hormones act on non-endocrine cells

Front 13

What are two types of thyroid cells?

Back 13

(1)Follicular cells, (2)C-cells

Front 14

What do follicular cells secrete?

Back 14

Thyroxine (Tetraiodothyronine T4) and Triiodothyronine (T3)

Front 15

What do C-cells secrete?

Back 15

Calcitonin – maintains calcium homeostasis. Calcitonin release is influenced by [calcium] in serum.

Front 16

What are seven functions of thyroid hormones?

Back 16

(1)Regulate oxygen use, (2)Regulate basal metabolic rate, (3)Regulate cellular metabolism, (4)Regulate growth and development, (5)Increase lipolysis, (6)Increase cholesterol secretion, (7)Increase use of glucose and fatty acids for ATP production.

Front 17

What are five functions of parathyroid hormone?

Back 17

(1)regulates calcium and phosphate, (2)Stimulates the release of calcium from bones and resorption of calcium from urine in KDs, (3)Promotes Vit D activation, (4)Promotes diuresis by inhibiting resorption of Na+ and Bicarbonate, (5)Reduces clearance of uric acid

Front 18

What are the three parts of the adrenal cortex?

Back 18

(1)Zona glomerulosa – mineralcorticoids (e.g. Aldosterone), (2)Zona fasiculata – glucocorticoids (e.g. cortisol), (3)Zona reticularis – sex hormones (e.g. estrogens & androgens)

Front 19

What hormones control the parts of the adrenal cortex?

Back 19

ACTH: Zona fasiculata, Zona reticularis

Renin-angiotensin system: Zona glomerulosa

Front 20

What two hormones does the adrenal medulla secrete?

Back 20

(1)Epinephrine, (2)Norepinephrine

Front 21

What are two examples of pituitary hyperfunction?

Back 21

(1)Prolactomas, (2)Somatotropic adenomas

Front 22

What is prolactomas?

Back 22

Most common adenoma of the pituitary. Small, benign tumours. Inhibits secretion of LH – therefore no ovulation

Front 23

What are four sypmtoms of prolactomas?

Back 23

Prolactin secreting cells -- hyperprolactinemia – symptoms are: (1)Amenorrhea, (2)Galactorrhea, (3)Infertility, (4)Men – impotence, loss of libido.

Front 24

What is somatotropic adenomas?

Back 24

Growth Hormone secreting cells. Hypersecretion of GH.

Front 25

What are four results of hypersecretion of GH?

Back 25

(1)Pre-puberty -- Gigantism, (2)Adults -- Acromegaly, (3)Hyperglycemia, (4)Hypercalcemia

Front 26

What is gigantism?

Back 26

Before epiphyseal growth plates close. 7-9 feet tall.

Front 27

What are four symptoms of acromegaly?

Back 27

(1)Enlargement of acral parts of the extremities (fingers, hands& toes), tongue, jaws, and nose, (2)Cardiomegaly, (3)Hyperglycemia, (4)hypercalcemia

Front 28

What are two other adenomas?

Back 28

(1)ACTH – over secreted d/t pituitary tumour; results in Cushing’s disease (xs cortisol; hyperpigmentation), (2)TSH – leads to hyperthyroidism – VERY rare

Front 29

What are five causes of pituitary hypofucntion?

Back 29

(1)Congenital developmental defects – dwarfism, hypogonadism, (2)Tumours, (3)Circulatory disturbances such as ischemia (Post-partum necrosis – Sheehan’s syndrome), (4)Trauma, (5)Empty sella syndrome

Front 30

What is empty sella syndrome?

Back 30

A condition in which the pituitary gland shrinks or becomes flattened. CSF has leaked into the sella turcica, putting pressure on the pituitary gland. This causes the gland to shrink or flatten.

Front 31

What is primary empty sella syndrome?

Back 31

Occurs when one of the layers (arachnoid) covering the outside of the brain bulges down into the sella and presses on the pituitary.

Front 32

What is secondary empty sella syndrome?

Back 32

Occurs when the sella is empty because the pituitary gland has been damaged by: A tumour, Radiation therapy, Surgery

Front 33

What is Panhypopituitarism/Dwarfism?

Back 33

Partial or total failure of all anterior pituitary hormones: [ACTH, TSH, LH, FSH, hGH, PRL]. Less than 4’ 10” tall. Caused by over 200 medical conditions. Pituitary dwarfism: Lack of growth hormone.

Front 34

What are seven symptoms of Panhypopituitarism/Dwarfism?

Back 34

(1)Weakness, (2)Cold intolerance, (3)Poor appetite, (4)Weight loss, (5)Hypotension, (6)Lack of menstruation, (7)Dwarfism – in children

Front 35

What is Diabetes Insipidus?

Back 35

Posterior lobe disorder. Lack of ADH (ADH – prevents resorption of water, Urinate 5-6L a day). Kidney tubules fail to re-absorb water – therefore incr’d excretion of dilute urine. No glucose in the urine. Consequent: poor turgor, dry membranes, fatigue, weakness, dizziness, constipation, dcr’d BP

Front 36

What are three causes of diabetes insipidus?

Back 36

(1)Loss of hypothalamic function, (2)Problem with the neurohypophyseal tract, (3)Tumours

Front 37

What are four symptoms of diabetes insipidus?

Back 37

(1)Polydipsia (XS thirst), (2)Nocturia, (3)Polyuria (5-6L of hypotonic urine/day), (4)Dehydration

Front 38

What is Nephrogenic Diabetes Insipidus?

Back 38

KD don’t respond to ADH

Front 39

What is pituitary disease?

Back 39

Nonfunctioning Pituitary Tumours. “silent adenomas”. 25% of pituitary tumours. Cells do not secrete hormones. Can compress the pituitary causing hypopituitarism and partial blindness(compressing of the optic chiasm)

Front 40

What is thyroid disease?

Back 40

Common. Increases with age. T3/T4 affect almost all body tissues: Skin, nails, hair, heart, GI tract, eyes, respiratory tract, blood vessels, nerves, bone, muscle. Great results when detected. Diseases: Hyperfunction, Hypofunction, Goiter, Tumours

Front 41

What is hyperthyroidism?

Back 41

Results in excess of thyroid hormones in the blood

Front 42

What are four causes of hyperthyroidism?

Back 42

(1)Autoimmune – Grave’s disease (85% of all cases), (2)Idiopathic Goiter, (3)Tumour – hyperfunctioning thyroid adenoma, (4)Temporary hyperfunctioning in Hashimoto’s – see hypothyroid

Front 43

What is Grave's disease?

Back 43

Autoimmune. Antibodies to TSH receptor on follicular cells -- stimulation of production of T3/T4. Thyroid-stimulating immunoglobulins. Women 10x more affected than men. May be associated with other autoimmune disorders.

Front 44

What are nine clinical features of Grave's disease?

Back 44

(1)Exophthalmos – bulging eyes, (2)Diffusely enlarged thyroid, (3)Restlessness, Nervousness, Anxiety, (4)Sweating, (5)Tachycardia, (6)Cardiac palpitation, (7)Weight loss with INCREASED appetite, (8)Muscular tremor, (9)Diarrhea

Front 45

What is a thyroid storm?

Back 45

Potentially fatal. Acute episode of thyroid overactivity: high fever, severe tachycardia, delirium, dehydration, extreme irritability. Untreated Grave’s dz. Triggers: surgery, infection, ketoacidosis, MI, difficult labour/delivery, overdose of thyroid medication

Front 46

What is hypothryroidism?

Back 46

Decreased function and inability to meet the body’s demands for Thyroid hormones

Front 47

What are five causes of hypothryroidism?

Back 47

(1)Developmental defects – congenital thyroid aplasia, (2)Thyroiditis – inflammation of the thyroid, (3)Hashimoto’s disease, (4)Thyroidectomy – removal of thyroid, (5)Iodine deficiency - rare

Front 48

What are 10 clinical features of hypothyroidism?

Back 48

(1)Children – decreased growth and development of CNS (Thyroid dwarfism, Cretinism – retarded mental development, (2)Adults – Myxedema – skin appears puffy and dough-like, (3)Slows function of all organs, (4)Sleepy, (5)Tires easily, (6)Lack of endurance, (7)Constipation, (8)Bradycardia, (9)Weak and achy muscles, (10)Lowered body temperature

Front 49

What is Hashimoto's disease?

Back 49

Autoimmune disease. Most common cause of Hypothyroidism over age 6. Thyroid gland is attacked by various autoantibodies. 10x more common in women.

Front 50

What is a goiter?

Back 50

Enlargement of the thyroid. Consists of nodules that deforms the thyroid. Abnormal amount of macrophages and lymphocytes. Most do not cause endocrine symptoms. May cause compression of surrounding structures (Coughing, Hoarseness)

Front 51

What four structures is the thyroid closely related to?

Back 51

(1)Trachea, (2)Esophagus, (3)Jugular vein, (4)Rec. laryngeal nerve

Front 52

What are four potential results of a goiter?

Back 52

(1)Dyspnea, (2)Dysphagea, (3)Facial Edema, (4)Hoarseness

Front 53

What is a thyroid tumour?

Back 53

Benign are very common (10:1 - benign:malignant). Malignant are rare.

Front 54

What is hyperparathyroidism?

Back 54

Over secretion of parathyroid hormone. Results in increased levels of PTH circulating in the blood.

Front 55

What are three causes of hyperparathyroidism?

Back 55

(1)Primary – tumour or hyperplasia, (2)Secondary – chronic renal failure (chronic hypocalcemia) & Hypovitaminosis D, (3)Hereditary

Front 56

What is primary hyperparathyroidism?

Back 56

The most common cause of hyperparathyroidism is the development of a benign tumor in one of the parathyroid glands. 80% caused by benign parathyroid adenoma (Enlargement of one of the parathyroid glands). Hyperplasia (18%) (All four glands are enlarged). Parathyroid carcinoma (2%)

Front 57

What is the pathology of primary hyperparathyroidism?

Back 57

Excess PTH in circulation. Bones – stimulates osteoclasts. Kidneys – resorption of calcium, promotes the formation of active Vit D (helps absorb calcium from intestine).

Front 58

What are nine clinical features of hyperparathyroidism?

Back 58

(1)"moans, groans, stones, and bones...with psychic overtones", (2)Decalcification of bones -- fractures (osteopenia/osteoporosis), (3)Hypercalcemia, (4)Nephrocalcinosis – deposition of calcium salts in the kidney, (5)Urolithiasis – formation of urinary stones, (6)Hypophosphatemia, (7)Muscle weakness, (8)Lethargic, (9)Depression, Irritability

Front 59

What is hypoparathyroidism?

Back 59

Loss of function or hypofunction. Usually iatrogenic (accidental removal with thyroid surgery). Rare – congenital malformation, autoimmune.

Front 60

What are four clinical features of hypoparathyroidism?

Back 60

(1)Hypocalcemia, (2)Skeletal muscles become spastic (hypocalcemic tetany), (3)Heart beat – irregular, (4)Irregular function of nerves

Front 61

What is adrenal cortex disease?

Back 61

Reflect an excess or deficiency of adrenal steroids. All three zones may be affected.

Front 62

What is a way to remember the zones of the adrenal gland?

Back 62

Zona glomerulsoa - SALT

Zona fasciculata - SUGAR

Zona reticularis - SEX

Front 63

What are the three diseases of the hyperfucntioning of adrenal cortex disese?

Back 63

Three overlapping syndromes: (1)Hyperaldosteronism = Conn’s syndrome, (2)Hypercortisolism = Cushing’s Syndrome, (3)Hypersecretion of androgens= Adrenogenital syndrome

Front 64

What is Conn's syndrome?

Back 64

Hyperaldosteronism

Front 65

What are two causes of Conn's syndrome?

Back 65

(1)Adenoma, (2)Hyperplasia

Front 66

What is the pathology and four clinical features of Conn's syndrome?

Back 66

Aldosterone – resorption of sodium/loss of potassium -- water follows

(1)Hypertension, (2)Hypocalcemia, (3)Hypernatremia, (4)Muscle cramps, headaches, muscle weakness

Front 67

What is Cushing's syndrome?

Back 67

Most common Adrenal Cortex disease

Front 68

What are two causes of Cushing's syndrome?

Back 68

(1)Hyperplasia/Neoplasia (Hypersecretion of ACTH from pituitary adenomas (70%) – Cushing’s Disease, Adrenocortical tumours (20%) – Cushing’s Syndrome, ACTH secreted from non-pituitary cancers (ex. Small cell carcinoma of the lung) (10%), (2)Latrogenic – systemic steroids – Exogenous Cushing’s Syndrome

Front 69

What are eight clinical features of Cushing's syndrome?

Back 69

(1)Central obesity – face, trunk (Moon face, buffalo hump), (2)Red face, (3)Thinning hair, (4)Purple striations on the skin of the abdomen, thighs, and breasts, (5)Extremity muscle wasting, (6)Fatigue, weakness, (7)Glucose intolerance/Diabetes, (8)Mentally unstable

Front 70

What is adrenogenital syndrome?

Back 70

Congenital error of steroid metabolism. Excess of androgens: Virilization of external female genitalia (Virilization = the development of male physical characteristics (such as muscle bulk, body hair, and deep voice)) in a female. Clitoromegaly. Early pubic hair. Infertility.

Front 71

What are three causes of adrenal hypofunction?

Back 71

Usually caused by adrenal destruction. (1)Septicemia (25%), (2)Autoimmune disease (70%), (3)Metastasis from breast or lung cancers - RARE

Front 72

What is Addison's disease?

Back 72

Clinical syndrome. Adrenal cortex is infiltrated by lymphocytes and plasma cells. Destruction of cortex -- replaced with fibrous tissue and fat cells.

Front 73

What is the pathogenesis of Addison's disease?

Back 73

Symptoms result from deficient aldosterone and cortisol

Front 74

What occurs when the body is deficient in cortisol?

Back 74

Decreased gluconeogenesis = hypoglycemia, and deficient glycogen in the liver. Weakness, exhaustion, low BP, anorexia, weight loss, nausea, vomiting, low mood or depression.

Front 75

What occurs when the body is deficient in aldosterone?

Back 75

Fluid & electrolyte imbalances. Increased Na excretion; dehydration; low BP, decreased CO. Weakened CV activity -- circulatory collapse, shock, arrhythmias and possible cardiac arrest(potassium retention).

Front 76

What are 10 clinical symptoms of Addison's disease?

Back 76

(1)Fatigue, (2)Weight loss, (3)Nausea / Vomiting / Anorexia, (4)Weakness, (5)Low mood or depression, (6)Hypotension -- Frequent syncope (fainting), (7)Susceptible to infections, (8)Cannot tolerate stress, (9)Hyper-pigmentation of mucous membranes and skin – ‘tanned’ appearance, (10)ACTH cannot stimulate the secretion of corticosteroids (used to diagnose)

Front 77

What is pheochromocytoma?

Back 77

Vascular tumour of chromaffin cells in the medulla. Increased production of nor-epi and epi. Main CM: HTN. Also: tachycardia, diaphoresis, postural hypotension, tachypnea, HA, N/V

Front 78

What is diabetes mellitus?

Back 78

Chronic systemic disorder characterized by hyperglycemia, and disruption of metabolism ofCHO’s, fats, and protein. It is the consequence of absolute or relative insulin deficiency or an abnormal response of target tissues to insulin

Front 79

What is Type I diabetes mellitus?

Back 79

Insulin dependent; Juvenile onset. Absolute deficiency of insulin production & secretion. Autoimmune against beta-cells -- fibrosis and hyalinization. Prone to ketoacidosis and metabolic derangements

Front 80

What is Type II diabetes mellitus?

Back 80

Non-insulin dependent; Adult-onset. Cellular resistance to insulin + loss of compensatory insulin secretion as a response. Normal Beta cells – m/b increased number. Not normally prone to ketoacidosis or metabolic problems

Front 81

What is the pathogenesis of diabetes mellitus?

Back 81

Insulin deficiency/inhibition of it’s action (antibodies to insulin or insulin receptors)/lack of response to insulin -- results is hyperglycemia

Front 82

Does type I or type II have a stronger genetic predisposition?

Back 82

Type II

Front 83

What are the environmental factors that influence type I and II diabetes?

Back 83

Type 1 – viral infections – measles/cocksackievirus B

Type 2 – obesity

Front 84

What are six cardinal signs of type I diabetes mellitus?

Back 84

(1)Polydipsia, (2)Polyuria/glucosuria, (3)Polyphagia, (4)Weight loss, (5)Ketonuria, (6)Weakness, fatigue, dizziness

Front 85

What are six cardinal signs of type II diabetes mellitus?

Back 85

(1)Polydipsia, (2)Polyuria/Glucosuria, (3)Polyphagia, (4)Recurrent blurred vision, (5)Weakness, fatigue, dizziness, (6)Often asymptomatic

Front 86

What four organs suffer complications from diabetes mellitus?

Back 86

(1)CV system, (2)Kidneys, (3)Eyes, (4)Nervous System

Front 87

How is the cardiovascular system complicated by diabetes mellitus?

Back 87

Cardiovascular complications account for most morbidity and mortality. Atherosclerosis -- CHD, Cerebrovascular Dz, Aortic aneurysms , gangrene

Front 88

How are the kidneys complicated by diabetes mellitus?

Back 88

Diabetic nephropathy - glomerulosclerosis

Front 89

How are the eyes complicated by diabetes mellitus?

Back 89

Diabetic retinopathy – (microangiopathy of retinal vessels) is the leading cause of blindness in the US. Also causes glaucoma and cataracts (deposition of sorbitol and fructose in the lens matrix).

Front 90

How is the nervous system complicated by diabetes mellitus?

Back 90

Peripheral neuropathy – sensory, motor and autonomic

Front 91

What is diabetic ketoacidosis?

Back 91

Type 1. Hyperglycemia b/c insufficient insulin. Creates ‘starvation’ -- triggers secretion of counter-regulatory hormones –glucagon – an attempt to incr glucose into the cells & tissues. Result is incr’d catecholamines, cortisol, & GH. Body can’t use glucose for fuel, has to use fat and protein, incr’d release of ketones. Diabetic emergency. Usually triggered by: Acute infection or Failure to use insulin properly

Front 92

What are three clinical manifestations of diabetic ketoacidosis?

Back 92

(1)Thirst, polyuria, weakness, nausea, (2)Dry mouth, hot/dry skin, fruity breath (acetone), confusion, lethargy, deep &rapid respiration, (3)Coma