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Pathophysiology > Endocrine > Flashcards

Endocrine Flashcards

1
Q

endocrine organs

A
  1. hypothalamus - main regulator. ling between nervous and endocrine system
  2. Pituitary
  3. Pineal
  4. Thyroid
  5. Parathyroid
  6. Thymus
  7. Adrenals
  8. Pancrea
  9. ovary/Testes

*Tropic = hormone works on another endocrine gland

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2
Q

What are hormones?

A
  • produced by endocrine glands
  • released in blood stream and travel to different parts of the body (any part with blood)
  • Different classes: metabolic, sex, and tropic
  • feedback loops exist to regulate the homeostatic balance of the endocrine system: positive, negative
  • we produce a LOT of hormones because a lot end up getting filtered out
  • negative feedback = more negative in body, counteract hormones to calm them down
  • positive feedback = enhances hormone response
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3
Q

cellular signaling

A
  • endocrine: hormones enter the circulatory system to effect distant tissues and glands
  • paracrine: signals that do NOT enter the blood stream but instead regulate the activity of nearby cells within the same tissue (neighbors)
  • autocrine: signals that regulate activity in the actual secreting cell from which they were released
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4
Q

topic hormones

A

target other endocrine glands and stimulate growth and secretion of the gland
- all hypothalamus and most anterior pituitary hormones are tropic hormones

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5
Q

water vs lipid soluble hormones

A
  • water: circulate in free unbound forms: non-steroid, made of proteins, short acting responses. bind to surface receptors on outside of cell
  • lipid: circulating bound to a carrier. made of cholesterol. steroids. rapid and long lasting response. pass through plasma membranes.
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6
Q

steroid vs non-steroid hormones

A

STEROID: lipid-soluable.

  • enter cell and nucleus directly to bind to nuclear receptors and cause a direct change within the cells
  • protein synthesis (transscript and translate)
  • mobile receptor model
  • androgens, estrogens, progestins, glucocorticoids, mineralocorticoids, hormones, vitamin D, retinoid
  • activate DNA transcription and translation (protein synthesis)
  • cholesterol

NON-STEROIDAL: water-soluble

  • do NOT enter cells but bind to cell surface receptors
  • deliver secondary message into the cell to induce a response
  • secondary messenger model
  • provides secondary hormone inside cell
  • amino acids
  • first messenger = signal transduction
  • second messenger = calcium, cyclic adenosine monophosphate, cyclic guanosine monophosphate, tyrosine kinase system
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7
Q

Hypothalamus Hormones

A
  • temperature and osmolarity regulation
  • all tropic hormones: all have affects on anterior pituitary
  • without these hormones target glands will atrophy and too much will hypertrophy
  1. GnRH –> incease FSH, incease LH
  2. GHRH –> increase GH
  3. TRH –> increase TSH
  4. SS –> decrease GH, decrease TSH
  5. PRH –> increase PRL
  6. CRH –> increase ACTH
  7. PIH –> decreases PRL
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8
Q

Anterior Pituitary Hormones

A
  • Adenohypophysis: glandular
  • makes its own hormones but stimulated by hypothalamus
  1. FSH –> gonads
  2. LH –> gonads
  3. TSH –> thyroid
  4. ACTH –> adrenal cortex, increases cortisol
  5. GH –> increases growth, increases metabolism, increases blood sugar
  6. PRL –> milk production
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9
Q

Posterior Pituitary Hormones

A
  • neurohypophysis: neurons
  • doesn’t make its own hormones, hormones produced in hypothalamus and then stored and released in post pit
  1. Oxytocin –> smooth muscle birth delivery, mammary glands, positive feedback, cuddling and social hormones
  2. ADH –> increase h2o reabsorption, increases blood pressure
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10
Q

Pineal Gland Hormones

A
  1. melatonin –> sleep cycle, menstrual cycle
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11
Q

Thyroid Gland Hormones

A
  1. TH –> regulates metabolic rate
    * T4 = thyroixine: more secreted but turned into T3
    * T3 = tri-iodothyronine: activates hormones
  2. Calcitonin –> bone building, decreases calcium in the blood and enters bones, stimulation of osteoblasts
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12
Q

Parathyroid Hormones

A
  1. PTH –> increases calcium in blood, increases osteoclasts and breaks down bone, increases calcitriol release = Vit D, released from kidneys, increases calcium absorption in gut
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13
Q

Pancreas

A
  • Pancreatic Islet Cells
  • alpha cells: secrete glucagon, secreted when low blood glucose, stimulates glycogeneolysis (glycogen breaks apart into glucse)
  • beta cells: secrete insulin: secreted when high blood glucose, facilitated transport of glucose into muscles and liver cells
  • delta cells: regulators
  1. insulin –> decreases blood sugar, increases glucose in liver (storage), after a meal it is secreted, anabolic hormones (leads to synthesis of proteins, lipids, and nucleaic acids)
  2. glucagon –> increases blood sugar, breaks down glycogen into glucose for energy, secreted between meals to keep blood sugar stable,
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14
Q

Adrenal Cortex Hormones

A
  • adrenal glands release hormones that aid in dealing with daily stressors
  • all hormones derived from cholesterol
  • growth and secretion stimulated by adrenocorticotropic hormone

*ACTH (stimulates cortisol production)

  1. aldosterone –> increases na+ uptake in epithelial cells, decreases blood volume
  2. cortisol –> released during times of stress, increases blood sugar by gluconeogensis, anti-inflammatory, immune and growth supresion, influences awareness and sleep habits, inhibits bone-protein matrix
  3. weak androgens and estrogens –> estrogen, DHEA

Layers:

  1. glomerulosa –> mineralcorticoids, aldosterone (increaess sodium reabsorption), salt, sodium
  2. Fasiculata –> glucocorticoids, cortisol, stress, sugar
  3. Reticularis –> weak androgens, DHEA, sex
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15
Q

Adrenal Medulla Hormones

A
  • chromaffin cells: pheochromocytes
  • fight or flight responses to hypoglycemia hypoxia, hypercapnia, acidosis, hemorrhage, glucagon, nicotine, histamine, and angiotensin II, increaes inflammation
  • epi is 10X morepotent than norepi
  1. catecholemines –> increaess epinephine and norepinephrine
    - epinephrine: adrenalin
    - norepinephrine: noradrenalin
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16
Q

Thymus hormones

A
  1. thymosin –> matures and recruits T cells (in kids)
17
Q

Gonad Hormones

A
  1. Testosterone
  2. Estrogen
  3. Progesterone
18
Q

Hypothalmic Disorders

A
  1. infundibulum disruption –> anterior pituitary secretions decrease (mnostly caused by trauma)
  2. hypopituitarism –> infarction, loss of blood between hypothalamus and anterior pituitary
  3. hyperpituitarism –> benign tumor and increases secretion or hormones with a disrupted infundibulum
  • only thing that would increase is prolactin release becayse PIH is inhibited
19
Q

Anterior Pituitary Disorders

A
  1. panhypopituitarism: affects all hormones secreted by ant. pit. blood and nercous system issues (infundibulum breaks)
  2. hypopituitarism: pituitary infarction/necrosis = sheehan syndrome (blood loss post partum females, reversable), hemorrhage, shock
  3. hyperpituitarism: typically caused by benign slow-growth pituitary adenoma, headache and fatigue, visual changes
  4. hypersecretion of prolactin: most common from adenoma/prolactinoma, amenorrhea, galactorrhea, hirsutism, osteopenia, hypogonadism, erectile hysfunction, impaired libido
20
Q

Growth Hormones Pathologies

A
  • open = before puberty
  • closed = after puberty
  • decreased GH and open epiphysieal plates = dworfism
  • decreased GH and closed epiphyseal plates = metabolic syndrome
  • increased GH and open epiphyseal plates = gigantism
  • increased GH and closed epiphyseal plates = acromegaly (organs grow)
21
Q

Posterior Pituitary Disorders

A
  1. syndrome of inappropriate anti-diuretic hormone secretion SIADH, hypersecretion of ADH, water intoxication, too much water in blood and diluted electrolytes, brain injury or infarction, pumonary disease, psychiatric drugs
  2. Diabetes Insipidus
22
Q

Diabetes Insipidus

A
  • insufficiency of ADH: not absorbing enough water and peeing it all out
  • increase in thirst
  • polyuria, polydipsia
  • inability to concentrate urine
  1. neurogenic: insufficient amounts of ADH
    - dehydration, give ADH to fix (easy fix)
  2. Nephrogenic: kidneys (DCT)
    - receptor problem
    - lots of increaes in ADH but receptor problem
    - not easy to fix - hormones may not help to fix it
  3. Psychogenic: excessive consumption
    - mental instability
    - > 10ml fluid a day
    - therapy treatment
23
Q

Thyroid Disorders

A
  1. Hyperthyroidism: increased T3/T4, decreased TSH, decreased TRH
    - graves disease = autoimmune disorder antibodies to TSH receptors on thyroid, overstimulation of t3/t4, decreased TSH and TRH, goiter
    - thyrotoxicosis = producing too much t3/t4, inflammatory disorder
    - thyrotoxic crisis = increased t3/t4, increased metabolism, skinny, increased dry skin, increased sleep issues
  2. hypothyroidism: decreased T3/T4, increased TSH, increased TRH most common
    - autoimmune thyroiditis/Hashimoto Disease = developed countries, iodine deficiency, antibodies to T3, T4, or thyroid
    - thryroiditis = inflamm of thyroid causes decrease in T3
    - postpartum thyroiditis (hypo or hyper)
    - Thyroid carcinoma = sign/symptoms: fatigue, weight gain, hair loss, myexedema
24
Q

Parathyroid Disorders

A
  1. hyperparathyroidism: increased blood calcium, hypercalcemia
    - excess secretion of PTH increases threshold and decreases excitability
    - skeletal and muscle weakness
    - areflexia
  2. hypoparathyroidism: decreased blood claclium
    - low PTH levels
    - usually caused by parathyroid damage during surgery
25
Q

Endocrine Pancreas Disorders

A
  1. diabetes mellitus

2. microvascular and macrovascular disease

26
Q

Diabetes Mellitus

A
  • glucose intollerance
  • polyuria, polydipsia, polyphagia (increased hunger becayuse peeing out glucose)
  • hyperglycemia = increased glucose

TYPE 1: no insulin is produced, insulin dependent

  • damages pancreas
  • pancratic atrophy and specific loss/damage to beta cells and loss - immune disorder or non-immune (trauma)
  • give exogenous insulin to treat
  • increased blood glucose but decrease of glucose in cells
  • genetic susceptibility, automimmune
  • viral infection, destruction of beta cells
  • immune destruction of beta cells = autoantibodies, antibodies to insulin
  • ketoacidosis: fruity breath
  • inability to breakdown sugar leads to break down of proteins and fats

TYPE 2: insulin produced but resisted, non-insulin dependent

  • increased insulin blood levels
  • some insulin receptors still work
  • diet and exercise decreases sugar load in blood
  • years of increased blood sugar breaks down insulin receptors (resistence)
  • more common (90% of people)
  • risk factors: obesity, family history, ethnicity, puberty, female and metabolic syndrome (decreased GH in adulthood)
  • decreased beta cell response to plasma glucose, abnormal glucagon secretion
  • Glycated Hemoglobin (HBA1c) = can show history of high blood sugar for 3-4 months in the past
  • glyucated = protein gets sugar stuck on it
27
Q

Acute Conditions of Diabetes Mellitus

A
  1. Hypoglycemia: 90% type 1, don’t eat enough before exercise, overdosing on insulin
  2. Diabetic Ketoacidosis: serious, rely on fat and protein to create glucose, fats and proteins break down and cause ketoacidosis, increase in catecholamines, cortisol, glucagon, GH
28
Q

Microvascular and Macrovascular Disease

A

Endocine Pancreas Disorders

  1. microvascular:
    - retinophaty - blind, both type 1 and 2
    - nephropathy - damage to glomerulues, bad urine
    - neuropathy - damage to nerve endings
  2. macrovascular: Type 2 only
    - coronary artery disease
    - stroke
    - peripheral artery disease
    - atherosclerosis, increased clotting, bad diet and exercise
  3. Infection: decreased immune function
29
Q

Adrenal Cortex Disorders

A
  1. cushing disease: increased ACTH leads to increased cortisol
    - excessive ant pit secretion of ACTH
    - excessive cortisol
    leads to..
  2. Cushing syndrome: excessive levels of cortisol regardless of cause
    - stress, tumor, adrenal cortex issues
    - weight gain, fatigue
  3. addison disease: decreased BP, dwecreased na+, decreased cortisol
    - hyposecretion of adrenocorical hormones
    - decreaed cortisol with possible decreased aldosterone
    - fatigue, orthostatic hypotension, syncope, hypoglycemia, decreased na+, uincreased k+ and Ca
  4. Hyperaldosteronism: Conn disease
    - hypertension, myalgias, wekaness, chronic headaches, increased na+, decreased K+
    - increased HP
  5. hypersecretion of adrenal androgens and estrogens: feminizatino of males and virilization of females
30
Q

Adrenal Medulla Disorders

A

catecholamine Hypersecretion (norepi, epi)

  • chromaffin cell tumor
  • pheochromocytoma (benign tumor secretes too much epi/norepi)
  • secretions on a continuous or episodic basis
  • hypertension, headaches, sweating, tachycardia, tachypnea, anxiety, chest pain

Pathophysiology (13 decks)

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