Week 6, Endocrine Control, Study Guide For Pathophysiology Final

Front 1

What are the functions of the endocrine system

Back 1

1.growth and development 2.sex differentiation 3.metabolism 4.adaptation with homeostasis as a goal

Front 2

How does the endocrine adapt (with homeostasis as a goal)

Back 2

1.regulation of digestion 2.use and storage of nutrients 3. electrolyte and water metabolism 4.reproductive functions

Front 3

What are the 3 hormonal mechanisms in the endocrine system

Back 3

1. endocrine 2. paracrine 3. autocrine

Front 4

Hormones function as chemical messengers, what are 3 charactistics of this functionality

Back 4

-move through the blood to distant target sites of action -can act locally as paracrine or autocrine messengers that incite more local effects - they are present in body fluids at all times in greater or lesser amounts as needed

Front 5

What are 2 specific characteristics of hormones

Back 5

-single hormone can exert various effects in different tissues -a single function can be regulated by several hormones

Front 6

What 2 things need to be noted with dealing with cellular response and hormones

Back 6

-number of receptor present (through up or down-regulation) -Affinity of these receptors for hormones (affected by many things)

Front 7

What are the 3 types of endocrine disorders can we have

Back 7

Primary disorders, secondary disorders and Tertiary disorders

Front 8

What does primary disorders mean (endocrine disorders)

Back 8

Primary disorders originate in the gland responsible for producing the hormone

Front 9

What does secondary disorders represent (endocrine disorders)

Back 9

Pituitary function is disrupted

Front 10

What do tertiary disorders represent (endocrine disorders)

Back 10

hypothalamic function is disrupted

Front 11

What are the 4 hormones ESSENTIAL for normal body growth and maturation

Back 11

1.Growth Hormone (GH) 2.Insulin 3.Thyroid hormone 4.Androgens

Front 12

What is acini, what organ does it belong to, and what is its function within that organ

Back 12

acini is a tissue found in the pancreas and it secretes digestive juices into the duodenum (it is exocrine)

Front 13

What are the Islets of Langerhans, organ location and function

Back 13

tissue found in the pancreas - secretes hormones into the blood - composed of beta cells that secrete insulin, alpha cells that secrete glucagon, and delta cells that secrete somatostatin

Front 14

What is the normal action of insulin on glucose

Back 14

-increases glucose transportation into skeletal muscle and adipose tissue - increases glycogen synthesis - decreases gluconeogenesis

Front 15

what is the normal action of glucagon on glucose

Back 15

- promotes glycogen breakdown - increases gluconeogenesis

Front 16

Besides insulin and glucagon what are 3 other hormones (or category of hormone) that affect blood glucose

Back 16

1. catecholamines (epinephrine & norepinephrine by helping maintain levels during stress) 2. Growth hormone (by increasing protein synthesis in all cells of the body, mobilizes fatty acids from adipose tissue, and antagonizes the effects of insulin) 3. glucocorticoids (critical to survival during periods of fasting and starvation & stimulate gluconeogenesis by the liver)

Front 17

What is the definition of prediabetes

Back 17

impaired fasting plasma glucose and impaired glucose tolerance

Front 18

Diabetes 1 results from what 2 things

Back 18

loss of beta cell function and considered an absolute insulin deficiency

Front 19

What are the 2 subdivisions (and definition) of Type 1 Diabetes

Back 19

Type 1A: immune-mediated diabetes and Type 1B: idiopathic diabetes

Front 20

What 3 factors are involved in the development of Type 1A diabetes

Back 20

1.genetic predisposition (diabetogenic genes) 2. A hypothetical triggering event involving an environmental agent that incites an immune response 3. Immunologically mediated beta cell destruction

Front 21

What are 4 charastistics (factors in) Type 1B diabetes

Back 21

1. cases where beta cell destruction in which no evidence of autoimmunity is present 2. only a small number of people have this type and of those most are African or Asian decent 3. it is strongly inherited 4. people who have it have episodic ketoacidosis due to varying degrees of insulin deficiency with periods of absolute insulin deficiency that may come and go

Front 22

Diabetes 2 results from what 2 causes

Back 22

impaired ability of the tissues to use insulin and/or a relative lack of insulin or impaired release of insulin in relation to blood glucose levels

Front 23

What are the 3 metabolic abnormalities that contribute to hyperglycemia in Type 2 Diabetic patients

Back 23

1. impaired beta cell function and insulin secretion 2. peripheral insulin resistance 3. increased hepatic glucose production

Front 24

What are the 3 polys of diabetes (and definition)

Back 24

1. Polyuria (excessive urination) 2. Polydipsia (excessive thirst) 3. Polyphagia (excessive hunger)

Front 25

Diabetes 1 & 2 Clinical Manifestations

Back 25

polyuria, polydipsia, polyphagia, weight loss (type 1), recurrent blurred vision, fatigue, paresthesias (pins and needles feeling in limbs), skin infections

Front 26

What are the chronic complications of diabetes (1 and 2) (DISORDERS)

Back 26

Disorders of the microvasculature (neuropathies, nephropathies, retinopathies, distal symmetric neuropathy, & foot ulceration) and Macrovascular complications

Front 27

What is the mechanism of peripheral neuropathies

Back 27

There is a thickening of the wall of the nutrient vessels that supply the nerve which leads to the assumption that vessel ischemia plays a major role in the development of neural changes. This is a segmental demyelinization process that affects the Schwann cell and is accompanied by a slowing of nerve conduction (SUGAR IS A TOXIN)

Front 28

What is the mechanism of macrovascular damage

Back 28

Chronic inflammation and injury to vascular walls, there is a creation of a "patch" that contains LDL cholesterol, and finally activation of more inflammatory cells and smooth muscle cell proliferation as the body tries to repair the area (SUGAR MAKES FAT STICKY)

Front 29

What are 3 diabetic complications we must educate our patients about

Back 29

1. ketoacidosis (mostly seen in type 1) 2. Hyperosmolar Hyperglycemic state 3. Hypoglycemia (caused by medication)

Front 30

What are the clinical signs and symptoms of ketoacidosis

Back 30

-"Fruity" breath -Kussmaul respiration (deep, labored breathing) -EKG changes -Weight loss from hypovolemia and muscle wasting -hypovolemic shock - coma *****Illness often precipitates this condition*****

Front 31

What leads to ketoacidosis (pathway or road)

Back 31

insulin deficiency + increased catecholamines, cortisol, glucagon lead to= Lipolysis in the body tissues, which leads to= increased fatty acids (which are metabolized by the liver to keto acids).

Front 32

What happens from the pathway of ketoacidosis (pathway leads to ...)

Back 32

The body becomes saturated with keto acids, the blood pH falls, ketones are present in the urine - water follows the ketones. Potassium then moves out of cells as sodium moves in, and is then lost in the urine

Front 33

What is Hyperthyroidism

Back 33

It is a dysfunction of the pituitary, thyroid, or hypothalamus which results in not enough T4

Front 34

What s/sx would you look for with a patient that you suspect has hypothyroidism

Back 34

pale, puffy face, lower heart rate, lethargy, cold intolerance, impaired mental, weight gain

Front 35

What intervention would be provided to a patient with hypothyroidism

Back 35

Health Literacy: lifelong, taking medications w/o food, same time AM, armour is pig, S/S Hyperthyroid (tachycardia, angina, heat intolerance)

Front 36

What needs to be brought to a patient's attention if they are diagnosed with hypothyroidism

Back 36

Caution: intensifies warfarin, CA and FE slows absorption, must take during pregnancy

Front 37

What is Graves Disease

Back 37

It is an autoimmune disorder that leads to hyperactivity of the thyroid gland (hyperthyroidism)

Front 38

What s/sx would you see with graves disease

Back 38

Anxiety, Breast enlargement in men (possible), Difficulty concentrating, Double vision, Eyeballs that stick out, Eye irritation and tearing, Fatigue, Frequent bowel movements, Goiter (possible), Heat intolerance, Increased appetite, Increased sweating, Insomnia, Irregular menstrual, Muscle weakness, Nervousness, Rapid or irregular heartbeat, Shortness of breath with activity, Tremor, Weight loss (rarely, weight gain)

Front 39

What intervention would be provided to a patient with graves disease

Back 39

Health literacy: treatment to destroy thyroid,replace t-4 life long on medications, help with symptoms,

Front 40

What needs to be brought to a patient's attention if they are diagnosed with graves disease

Back 40

Caution: medications liver toxic fetal toxic, avoid pets and children during radioactive iodine, beta blockers used to suppress tachycardia

Front 41

What is Addison's

Back 41

is a rare, chronic endocrine disorder in which the adrenal glands do not produce sufficient steroid hormones (glucocorticoids and often mineralocorticoids).

Front 42

What are the s/sx of Addison's disease

Back 42

"*Fatigue, *weakness, *loss of appetite, *Muscle and joint pain, *Gastrointestinal problems (nausea, vomiting, Darkening
of the skin on the face, neck, and back of hands, Low blood pressure, A craving for salt, inability to respond to stress-fatal if not diagnosed/treated"