Endodrine

Question 1

Key components of the endocrine system

Answer 1

Hypothalamus, pituitary, adrenal, pancreas, pineal, parathyroid, ovaries, testes, thymus, thyroid
Endocrine is ductless and goes directly into the blood
Exocrine goes through a duct
Regulation of hormones, released via feedback loop, positive and negative feedback and cyclic variations

Question 2

Water soluble hormones

Answer 2

Are made from amino acids
Act on and interact with plasma, membrane, receptors, and cause cascade of events inside the cell
Duration of action, they are available in storage and transient affect
Receptor locations are on plasma membranes. They are second messengers, and mediate the effects of the hormone on the target cell

Question 3

Water soluble hormones examples

Answer 3

Peptides include growth hormones, insulin, leptin, prolactin
Glycoproteins include follicular, stimulating, hormone, luteinizing, hormones, thyroid stimulating hormone
Polypeptides include endorphins, calcitonin, glucagon, hypothalamic, hormone, Lipo proteins
Amines include epinephrine and norepinephrine, which are also neural transmitters
These are the second messengers cAMP, cGMP, IP3/DAG, calcium 

Question 4

Lipid soluble hormones

Answer 4

Made from cholesterol
Ask across the membrane and interact with genes inside the cell
Duration of action is made on demand, and has a persistent effect
Receptors are inside the cell
They are the first messenger usually do not need a second, but may bind to steroid hormone, receptors and activate second messengers, i.e. water soluble hormones

Question 5

Examples of lipids soluble hormones

Answer 5

Thyroxine amine type T3 and T4
Steroids, including cholesterol, which is a precursor, estrogen, cortisol, aldosterone, progesterone, testosterone
Derivatives of Archiodonic acid (autocrine or paracrine) Leukotrienes,  prostaglandins, thromboxane

Question 6

Positive feedback loop

Answer 6

Surgeons of hormones, increase levels of hormones and stimulate release of more hormones

Question 7

Negative feedback loop

Answer 7

Most common, increased levels of hormones, inhibit release of hormones

Question 8

Cyclic variation feedback

Answer 8

Periodic variations in hormone release, such as menstruation, cortisol for circadian rhythm

Question 9

Adrenocoeticotropin ACTH/corticotropin

Answer 9

Produced in the anterior pituitary
Purpose is to control secretion of adrenal cortex hormones
Stimulated by cortiotropin releasing hormone from the hypothalamus-> stimulates cortisol secretion-> activate adrenal to synthesize steroids
Negative feedback loop

Question 10

Thyroid stimulating hormone (TSH)/thyrotropin

Answer 10

Produce in the anterior pituitary
Purpose is to control secretions of thyroxine, and triiodothyronine by the thyroid gland
Stimulated by the hypothalamus releases TRH

Question 11

Growth hormone

Answer 11

Most important in children
Produce in the anterior pituitary
Purpose is metabolic affects, including fat and glucose, utilization, bone and cartilage growth

Question 12

Prolactin PRL

Answer 12

Produce in the anterior pituitary
Promotes mammary gland, development, and lactation
Stimulated by TRH which stimulates lactotrophic cells in anterior pituitary to produce hormone

Question 13

Thyrotopin releasing hormone (TRT)

Answer 13

Produced by the hypothalamus
Purpose is to stimulate release of thyroid stimulating hormone from post pituitary, modulates prolactin secretion

Question 14

Corticotropin releasing hormone (CRH)

Answer 14

Produced by the hypothalamus
Stimulates release of Adrenocorticotropic hormone (ACTH) and beta endorphin

Question 15

Growth hormone releasing hormone (GHRH)

Answer 15

Produced by Anterior pituitary
Simulates release of growth hormone

Question 16

Growth, hormone inhibitory hormone (GHIH)/somatostatin

Answer 16

Produced by the hypothalamus
Purpose is neuroendocrine, inhibitory effects across multiple systems, inhibits, the growth, hormones, thyroid stimulating hormones, endocrine, exocrine, pancreatic and pituitary secretions, modifies neural transmission and memory function in central nervous system
Stimulated by increase in serum glucose, fatty acids, and amino acids and presence of G.I. hormones in response to food intake

Question 17

Gonadotropin releasing hormone (GnRH)

Answer 17

Produced by hypothalamus
Simulates release of follicular, stimulating hormone, and luteinizing hormone, targets, anterior pituitary, G.I. tract, pancreas, hypothalamus, and central nervous system
Two forms 14 and 28 amino acids

Question 18

Prolactin inhibitory hormone (PIH)

Answer 18

Produced by hypothalamus
Inhibits synthesis and secretion of prolactin

Question 19

Antidiuretic hormone (ADH)/vasopressin

Answer 19

Produced by hypothalamus and posterior pituitary
Regulates water excretion as urine by the kidneys -> plasma osmolality, increased permeability of distal tubule’s, and collecting ducts
Regulated by Osmo receptors of the hypothalamus, including osmolality receptors if stimulated signal thirst

Question 20

Oxytocin

Answer 20

Produced by the hypothalamus and posterior pituitary
Facilitates milk expression during breast-feeding and uterine contractions, causing labor, initiation, and progression
Suckling

Question 21

Thyroxine T4
Triiodothyronine T3

Answer 21

Produced by the thyroid, regulate protein, fat, carbohydrate catabolism, metabolic rate, body heat, insulin antagonist, maintains growth hormone secretion, skeletal maturation, central nervous system development, muscle tone, and vigor, G.I. secretions, cardiac rate, force and output, respiratory rate, oxygen, utilization, calcium mobilization, red blood cell production, lipid turnover, free fatty acid, release, cholesterol synthesis
Released in response to metabolic demands such as gender, pregnancy, gonodal and adenocoetical, increased their levels, nutrition, and chemicals

Question 22

Insulin

Answer 22

Released by the pancreas
Increase glucose uptake, it cells except neurons
Increase cell membrane, permeability for amino acid, potassium, and phosphate
Protein, fat, and glucose synthesis
Storage of glucose and Glycogen and liver and muscle
Growth and gene expression, Targets liver, muscle and Adipose cell
Hyper glycemia can cause hyperkalemia
Similar by increase glucose serum
Inhibited by decrease glucose concentration

Question 23

Glucagon

Answer 23

Released by the pancreas
Opposite effects of insulin, increases serum glucose concentrate
Stimulates glycogenolysis
Increases gluconeogenesis from amino acids
Activate adipose cell lipase to liberalize fatty acid or conversion of glucose (increase myocardial contractility, increase renal blood flow, enhance, bile, secretions, increase, gastric secretion)
Simulated by decrease your glucose concentration, increased serum, amino acid, concentrations, and exercise
Inhibited by high glucose levels

Question 24

Aldosterone

Answer 24

Produced by the zona golumerulosa (adrenal)
Electrolyte regulation, increase absorption of sodium and secretes potassium
Increases intravascular fluid volume
Stimulate sodium and potassium transport in sweat, glands, salivary, gland, intestinal, epithelial cells
RAAS

Question 25

Cortisol

Answer 25

Produced by the zona fasciculata (adrenal cortex) Carbohydrate, protein, and fat metabolism (stress response inflammation and immune response, membrane stability, intravascular, volume and blood vessel tone) elevate serum glucose, gluconeogenesis, and decrease glucose utilization by cells, reduce proteins, stores, increases liver, and plasma, amino acids for glucose production promotes mobilization of fatty acids from adipose tissue increases your own fatty acid levels, conserves carbohydrates, if chronically elevated causes, weight gain, fat deposition, face, chest and torso Catecholamines dependent on Corazon in the internal (receptor sensitivity is dependent on circulating cortisol can be up or down, regulated by catecholamine receptors) Adrenocorticotropic hormone (ACTH) increase during times of stress, anti-inflammatory properties, stabilize lysosomal, membranes, decreases capillary membrane, permeability, prevents migration of white blood cells, and phagocytosis of damage cells reduces IL 1 to lower a fever, suppress T lymphocytes production, and block allergic response (cancel press immune response)

Question 26

Effects of aging on the thyroid

Answer 26

Causes atrophy and hypertrophy Decreased thyroid stimulating hormone decreases response to TRH which results in hypothyroid

Question 27

Effects of aging on the pancreas

Answer 27

Cells replaced by fat, decline and beta cell function, pancreatic cell regeneration, declines, fibrosis, and shrinkage of ECM, fat accumulation in the endocrine tissue Decrease insulin, decrease insulin, receptors results in resistance

Question 28

Effects of aging on the adrenals

Answer 28

Cortex loses, weight, more fibrous, cortisol, negative feedback, diminishes due to impaired sensitivity of HPA glucocorticoid clearance. Decrease in kidney and liver chronic elevation and cortisol impairs recovery from stressful stimuli, and contribute still awesome muscle bone mass hypertension visceral, Bestie, diabetes, suppressed immunity, decrease in cognitive function, plasma levels of androgens decrease Disrupt circadian rhythm

Question 29

Primary thyroid disease

Answer 29

Most common in the United States outside the United States related to iodine deficiency Autoimmune thyroiditis (Hashimoto, lymphocytic thyroiditis) -inflammatory destruction of thyroid gland Circulating auto antibodies and T lymphocytes can be due to genetics , manifestations with goiter, post partum thyroiditis related to Hashimoto happens 6 to 12 months postpartum, congenital, hypothyroidism, tissue absent, absent thyroxine impairs neuro development screamed at birth Thyroid cancer, high risk, if history of ionizing radiation Idiopathic

Question 30

Secondary thyroid disease

Answer 30

Pituitary failure to synthesize, thyroid, stimulating hormone and TRH May be due to pituitary tumor, traumatic brain, injury, or subarachnoid hemorrhage

Question 31

Subclinical, thyroid disorders

Answer 31

Typically post, viral ideology that results in autoimmune injury to the thyroid

Question 32

Thyrotoxicosis

Answer 32

Enlarged thyroid hormone Increase T3 and T4, decrease thyroid, stimulating hormone, and both thyroid toxicosis, and Graves’ disease may have exophthalmus, pretibial myxedema, often not seen an nodular disease thyroid may increase in size goiter Any condition, resulting an increase in thyroid, hormone levels, pituitary, thyroid, ectopic, thyroid issue, ingestion of excess in thyroid hormone meds

Question 33

Graves’ disease

Answer 33

Autoimmune type two hypersensitivity may be genetic environmental Increase in T3 and T4, decreasing thyroid, stimulating hormone may have exophthalmus , pretibial myxedema, thyroid may increase in size goiter Exact cause unknown Autumn an override normal regulatory mechanism TSI stimulation of thyroid, stimulating hormone receptor in gland results in hyperplasia, causing goiter and increase in thyroid hormone and T3

Question 34

Nodular, thyroid disease

Answer 34

Thyroid gland increases in size and response to increase thyroid, stimulating hormone May not have exophthalmus, and pretibial myxedema that is associated with graves and thyrotoxicosis can be benign or cancerous Follicular cells form nodules that function autonomously and produce excess thyroid hormone

Question 35

Myxedema coma

Answer 35

Caused by infection or illness such as UTI, CHF,CVA, abrupt stop of thyroid meds overuse of narcotics or sedatives Hypothermia, hypoventilation, hypotension, hypoglycemia, lactic, acidosis, and decreased level of consciousness Severe depletion of thyroid hormone

Question 36

Thyrotoxic crisis/thyroid storm

Answer 36

Caused by Hyperthyroid undiagnosed, then exposed a stressor Hyperthermia, tachycardia, increase output, heart failure, agitation, delirium, nausea, vomiting Sudden release of T4 and T3, that exceed metabolic demand

Question 37

Hyperaldosteronism

Answer 37

Caused by adrenal, carcinoma, or secondary causes dysfunction of RAAS DECREASE, POTASSIUM, INSULIN RESISTANCE, LEFT VENTRICULAR REMODELING, HYPERTENSION, increase volume Excess secretion of aldosterone from adrenal cortex

Question 38

Cushing’s disease

Answer 38

Can be caused by pituitary adenoma or increased ACTH Lots of circadian rhythm of ACGTH AND CORTISOL IN ABILITY TO INCREASE ACTH in response to stress, steroid induced Weight gain increase in adipose tissue , truncal striae, insulin resistance, protein wasting, moon, face, bruises, easily, diabetes, muscle weakness, proximal, thinning of hair, emotional liability, acne, buffalo hump, osteoporosis, hypertension, cardiac hypertrophy Due to increased cortisol

Question 39

Addison’s disease

Answer 39

Adrenal insufficiency cause by primary/autoimmune infection, or tumor or genetic X-linked adrenoleukodystrophy Secondary -prolong suppression of Cortisol secretion secondary to glucocorticoids Adrenal insufficiency -decrease cortisol, and aldosterone synthesis increased ACTH Fatigue, malaise personality, changes, anorexia, nausea, vomiting, diarrhea, hypotension, abdominal pain, weakness, hyper pigmentation, cardiac insufficiency, weight loss Decrease cortisol

Question 40

Obesity and insulin resistance

Answer 40

Adipokines (leptin and adioponectin) are produced by white adipose tissue and obesity changes levels. Decrease insulin synthesis and increase insulin resistance. Elevated free fatty acid increases, triglycerides and cholesterol . Induce, insulin resistance and contribute to fatty liver, Hyper lipidemia, atherosclerosis. Altar oxidative phosphorylation in cellular mitochondria, insulin resistance, and changes in energy metabolism Obesity is associated with hyper insulinemia and decrease insulin receptors

Question 41

Hypoglycemia

Answer 41

Acute complication of diabetes mellitus Cold and clammy need some candy Rapid onset Symptoms include altered, mental status, tachycardia, palpitations, diaphoresis, tremors, restlessness, agitation An adult glucose less than 70 In peds 30 to 47 in the first 48 hours a life Due to excess insulin

Question 42

Diabetic keto acidosis

Answer 42

Acute complication of diabetes mellitus Onset slow Symptoms include dry, mouth, malaise, headache, polyuria, key tones, Kuszmaul’s, polydipsia, weight loss, nausea, vomiting, itching, abdominal pain, lethargy shortness of breath, fruity breath Glucose greater than 250 low bicarbonate, high ion gap, high plasma, protein levels of beta hydroxybutyrate’, acetoacetane, and acetone Relative insulin insufficiency mild to moderate results in hyperglycemia, causes solute diuresis causes polyuria, which causes dehydration and thirst polydipsia, if not reversed leads to hyper osmolality and CNS depression, if profound follow, same pathway, but can get worse leading to Lipo lysis formation of beta hydroxybutyric acid acetoacetic acid accumulation of ketones, DKA and Kuszmaul’s

Question 43

Hyperosmolar hyperglycemic nonketotic syndrome, HHS

Answer 43

Acute complication of diabetes mellitus Slow onset Polyuria, polydipsia, volume depletion, dehydration, hypotension, tachycardia, hypo, perfusion, weight loss, nausea, vomiting, abdominal pain, hypothermia, stupor, coma, seizures Glucose greater than 600 with no ketosis , serum osmolality, greater than 320 increase in bun and creatinine If increase in stress, hormones are involved, such as glucagon, catecholamines, cortisol growth, hormone leads to insulin resistance, high glucose, pro-inflammatory cytokines, such as TNF alpha IL 6 and 13, again results in insulin resistance, decrease proteins synthesis, and cream proteolysis increase GlucaGen lysis increase gluconeogenesis again results in insulin resistance

Question 44

Chronic, diabetes mellitus complications

Answer 44

Production of reactive, oxidative, stress, oxidative, stress, and cellular death Polypol pathway- Aldose reductase (AR) catalyzes to metabolism of glucose to sorbitol dehydrogenase catalyzes the metabolism of sorbitol to fructose. Excessive glucose results in depletion of NADPH a cofactor in the production of glutathione Glucose induced activation of PKC, has been shown to increase production of ECM and cytokines enhance contractility, permeability and vascular proliferation induce the activation of cytosolic phospholipase A2, inhibit, potassium, sodium , ATPase Glycation process (glucose fixation) affect, circulating proteins, such a serum, albumin, lipoprotein insulin, hemoglobin the formation of advance deglycation end products (AGE) implicate, reactive, intermediate, such as methylglyoxal. AGE form cross link on long live EXC metric, proteins are react within their specific receptor RAGE resulting in oxidative stress and pro-inflammatory, signaling implicated in endothelium dysfunction arterial stiffening and microvascular complications

Question 45

Microvascular disease

Answer 45

Chronic complication of diabetes, mellitus Small vessel, disease, angiopathy, small artery, arterials, and microvascular disease, patchy or small areas of gangrene results in minor amputations such as with diabetic toe ulcers

Question 46

Microvascular disease

Answer 46

Chronic complication of diabetes, mellitus Large vessel, disease, angiopathy thrombosis with large vessel, occlusion and arterial venous shunting, causing ischemia, gangrene and amputations Examples include diabetic foot ulcer that results in progressive loss of limb

Question 47

Type one diabetes mellitus

Answer 47

Not typical before six months of age pick a diagnosis 12 years old Type 1A is autoimmune, genetic or environmental Type 1B not auto immune, but secondary causes Alpha and beta cells (Insulin and Amylin) function abnormal to varying degrees excess glucagon causes hyperglycemia hyper ketonemia immune mediated, T cell destruction of beta cells, lymphocyte and macrophage infiltrates islet cells possibility in response to a viral ideology Loss of beta cells means no insulin production

Question 48

Type two diabetes mellitus

Answer 48

Due to genetics, environmental risk factors include obesity, age, hypertension, and activity, family history Metabolic syndrome, increase, weight, increase waist, circumference, increase, triglycerides, decrease HDL, hypertension, and fasting glucose greater than 100 Decrease insulin, secretion, insulin resistance, insulin sensitivity issues. Fails to respond to circulating insulin related to insulin molecule abnormalities, insulin antagonist down, regulator, receptors, altered glucose, transport proteins, decrease activation, post, receptor, kinase. Beta cell dysfunction decrease in number and weight Glucagon increases, pancreatic alpha cells, or less responsive to glucose inhibition causes increase in gluconeogenesis glucosgenolysis Amylin decreased loss of Sadie, and increase glucagon production G.I. hormones ghelin and incretins are decreased causes decrease in insulin response to meals and increase insulin resistance

Question 49

Labs for diabetes mellitus

Answer 49

Hemoglobin A1c measure his hemoglobin A1c molecule greater than 6.5 as a diagnosis for diabetes plus hi fasting glucose. Fasting glucose greater than 126 is diagnostic Random glucose two hours post eating greater than 200 is diagnostic

Question 50

Retinopathy

Answer 50

Diabetes mellitus chronic complication Damage to vessels, vasoconstriction, aggregation, hypoxemia Three types Nonproliferative causes thickening of red retinal, capillary membrane increase membrane permeability with van, dilation, microaneurysm formation Pre-proliferative causes renal ischemia with areas a poor perfusion and infarcts Proliferative causes angiogenesis and fibrous, tissue formation, and retina or optic disc Increases risk for Cataracs, glaucoma, macular edema

Question 51

Nephropathy

Answer 51

Chronic complication of diabetes, mellitus Hyperglycemia causes polypol pathway, protein, kinase see an inflammation, causes advanced glycation end products Renal Glomerular changes glomerular enlargement, glomerular basement membrane thickening Diffuse nodular glomerulosclerosis loss of pedocytes decrease in GFR

Question 52

Neuropathy

Answer 52

Most common complication of diabetes mellitus Inflammation, ischemia, oxidative, stress, advanced glycation end products, increased polyols Causes demyelination nerve degeneration delayed conduction starts with one cell degeneration, and peripheral sensory nerves can involve spinal cord nerves and posterior root ganglia degeneration ( ideology, metabolic and vascular changes related to hyperglycemia may have infectious ideology, causing impaired tissue oxygenation hyperglycemia impaired immune response, decreased sensation, delayed healing)

Question 53

Cardiovascular

Answer 53

Chronic complication of diabetes, mellitus Hypertension, diabetes, associated with microalbuminuria metabolic syndrome hypertension increases risk of coronary artery disease and stroke, heart attacks more fatal in those with diabetes mellitus

Question 54

Peripheral artery disease

Answer 54

chronic complication of diabetes, mellitus Atherosclerosis of lower extremities with increase risk of ulcers gangrene’s and amputation