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Patho > Endodrine > Flashcards

Endodrine Flashcards

1
Q

Key components of the endocrine system

A

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

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2
Q

Water soluble hormones

A

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

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3
Q

Water soluble hormones examples

A

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 

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4
Q

Lipid soluble hormones

A

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

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5
Q

Examples of lipids soluble hormones

A

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

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6
Q

Positive feedback loop

A

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

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7
Q

Negative feedback loop

A

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

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8
Q

Cyclic variation feedback

A

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

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9
Q

Adrenocoeticotropin ACTH/corticotropin

A

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

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10
Q

Thyroid stimulating hormone (TSH)/thyrotropin

A

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

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11
Q

Growth hormone

A

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

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12
Q

Prolactin PRL

A

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

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13
Q

Thyrotopin releasing hormone (TRT)

A

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

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14
Q

Corticotropin releasing hormone (CRH)

A

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

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15
Q

Growth hormone releasing hormone (GHRH)

A

Produced by Anterior pituitary
Simulates release of growth hormone

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16
Q

Growth, hormone inhibitory hormone (GHIH)/somatostatin

A

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

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17
Q

Gonadotropin releasing hormone (GnRH)

A

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

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18
Q

Prolactin inhibitory hormone (PIH)

A

Produced by hypothalamus
Inhibits synthesis and secretion of prolactin

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19
Q

Antidiuretic hormone (ADH)/vasopressin

A

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

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20
Q

Oxytocin

A

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

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21
Q

Thyroxine T4
Triiodothyronine T3

A

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

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22
Q

Insulin

A

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

23
Q

Glucagon

A

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

24
Q

Aldosterone

A

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

25
Q

Cortisol

A

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)

26
Q

Effects of aging on the thyroid

A

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

27
Q

Effects of aging on the pancreas

A

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

28
Q

Effects of aging on the adrenals

A

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

29
Q

Primary thyroid disease

A

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

30
Q

Secondary thyroid disease

A

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

31
Q

Subclinical, thyroid disorders

A

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

32
Q

Thyrotoxicosis

A

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

33
Q

Graves’ disease

A

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

34
Q

Nodular, thyroid disease

A

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

35
Q

Myxedema coma

A

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

36
Q

Thyrotoxic crisis/thyroid storm

A

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

37
Q

Hyperaldosteronism

A

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

38
Q

Cushing’s disease

A

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

39
Q

Addison’s disease

A

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

40
Q

Obesity and insulin resistance

A

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

41
Q

Hypoglycemia

A

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

42
Q

Diabetic keto acidosis

A

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

43
Q

Hyperosmolar hyperglycemic nonketotic syndrome, HHS

A

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

44
Q

Chronic, diabetes mellitus complications

A

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

45
Q

Microvascular disease

A

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

46
Q

Microvascular disease

A

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

47
Q

Type one diabetes mellitus

A

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

48
Q

Type two diabetes mellitus

A

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

49
Q

Labs for diabetes mellitus

A

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

50
Q

Retinopathy

A

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

51
Q

Nephropathy

A

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

52
Q

Neuropathy

A

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)

53
Q

Cardiovascular

A

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

54
Q

Peripheral artery disease

A

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

Patho (17 decks)

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