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endocrine system Flashcards

1
Q

what is the endocrine system

A

complex network of glands and organs that produce and release hormones into the bloodstream to regulate various bodily functions.
they act as chemical messengers to travel around the body ad target cells and organs.

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2
Q

what are the main glands and organs involved in the endocrine system

A

-hypothalamus
-pituitary gland
-thyroid gland
-parathyroid gland
-adrenal gland
-pancreas
-gonads (ovaries and testes)

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3
Q

nocioception (for pain/stimulus response)
proprioception (movement)

A
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4
Q

what does the hypothalamus do and where is it situated

A

located in the rain, links the nervous system to the endocrine system via pituitary gland.
produces, releases and inhibits hormones that control the secretion of hormones from the pituitary gland.

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5
Q

what does the pituitary gland do and where is it situated

A

back of the brain, often known as the master gland.
regulates other endocrine glands.
divided into:
-anterior pituitary gland- produces hormones.
-posterior pituitary- stores and releases hormone produced by hypothalamus.

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6
Q

what does the thyroid gland do and where is it situated

A

located in the neck.
produces thyroid hormones that regulate metabolism, growth, and development.
also produces calcitonin, which helps regulate calcium levels.

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7
Q

what does the adrenal glands do and where is it situated

A

situated on top of the kidneys
-adrenal cortex- produces corticosteroids (cortisol, aldosterone, and adrenal androgens)
-adrenal medulla produces catecholamines (adrenaline and noradrenaline)

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8
Q

what does the pancreas do and where is it situated

A

has both endocrine and exocrine functions.
endocrine function involves producing insulin (lowers blood sugar), glucagon (raises blood sugar) and somatostatin (regulates other pancreatic hormones)
exocrine function involves production and secretion of digestive enzymes into gastrointestinal tract.

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9
Q

what does the gonads do and where is it situated

A

-ovaries- produce oestrogen and progesterone, regulate female reproductive function.
-testes- produces testosterone, which regulates male reproductive functions.

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10
Q

what are the three main types of hormones

A

-peptid hormones
-steroid hormones
-amine hormones

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11
Q

what are peptide hormones

A

-made up of amino acids
-e.g: insulin, glucagon, growth hormone and more
-they act on cell membrane receptors.

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12
Q

what are steroid hormones

A

-derived from cholesterol
-e.g: cortisol, aldosterone, oestrogen, progesterone and testosterone
-act on intracellular receptors and affect gene transcription.

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13
Q

what are amine hormones

A

-derived from amino acids
-include thyroid hormones and catecholamines (adrenaline and noradrenaline)
-act on both cell membrane and intracellular receptors.

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14
Q

explain the lock and key model

A

enzyme –> enzyme-substrate complex –> enzyme- products complex –> enzyme + products.

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15
Q

how do hormones work

A

-Hormones bind to specific receptors on target cells.
-A target cell responds to a hormone because it bears receptors for the hormone
-trigger intracellular signally cascades that regulate: gene expression, protein synthesis, or other cellular activities.

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16
Q

what do feedback mechanisms do

A

maintain homeostasis by regulating hormone production

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17
Q

what does negative feedback do

A

inhibit further hormone release when levels are adequate

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18
Q

what does positive feedback do

A

amplify hormone secretion in response to specific stimuli

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19
Q

what is endocrine shock

A

A broad category of shock caused by hormonal imbalances, leading to metabolic disturbances.

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20
Q

what is hypoglycaemia

A

A specific type of metabolic shock caused by an excessively low blood glucose level, often due to an overdose (excess) of insulin or inadequate food intake.

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21
Q

what is hyperglycaemia

A

A specific type of metabolic shock caused by excessive high blood sugar levels, commonly caused by missed medications , medications or illness

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22
Q

what is diabetic ketoacidosis

A

DKA is a condition in which high blood sugar and acid buildup in the blood occur because the body lacks enough insulin, producing ketones. High levels of ketones make your blood acidic.

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23
Q

what is adrenal crisis

A

lack of cortisol
(it can also occur if existing cortisol replacement does not meet body’s needs)

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24
Q

what does insulin do

A

plays a crucial role in maintaining blood glucose levels by helping cells to absorb glucose.
-helps store glucose (as glycogen)
-promotes fat storage
-prevents fat breakdown
-regulates protein synthesis

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25
cellular effects of DKA.
26
what is homeostasis
process by which living organisms maintain a stable internal environment despite changes in external conditions. -balance and stability -feedback mechanisms -negative feedback -positive feedback -dynamic equilibrium
27
how does homeostasis maintain balance and stability
regulating temperature, pH levels, glucose concentration and other vital conditions.
28
what are feedback mechanisms
detect changes and respond accordingly. -sensors -control centre -effectors
29
what is negative feedback
When a change is detected, negative feedback works to counteract the change and bring conditions back to their normal range. e.g: if body temp rises, sweating and increased blood flow to akin are activated to cool the body.
30
what is positive feedback
used to amplify a response e.g: blood clotting
31
what is the normal pH range of blood
7.35-7.45
32
what is acidosis
when blood become too acidic (pH falls below 7.35) -respiratory acidosis- lungs cant get rid of enough CO2, causing it to build up. -metabolic acidosis- too much acid in the blood or nit enough bicarbonate.
33
what is alkalosis
when blood become too alkaline (pH rises above 7.45) -respiratory alkalosis- loosing too much CO2 due to rapid breathing. -metabolic alkalosis- too much bicarbonate or losing too much and, such as promoted vomiting or overuse of antacids.
34
what are some critical endocrine conditions
-endocrine shock: broad category of shock caused by hormonal imbalances, leading to metabolic disturbances. -hypoglycaemia: metabolic shock caused by excessively low blood glucose levels, often due to an overdose of insulin or inadequate food intake. -hyperglycaemia: metabolic shock caused by excessive high blood sugar levels, commonly caused by missed medications or illness. -diabetic ketoacidosis: high blood sugar and acid build up in the blood because the body lacks enough insulin, producing ketones, causing your blood to become acidic.
35
what is adrenal insufficiency
condition characterized by inadequate production of steroid hormones, primarily cortisol, and sometimes aldosterone, from the adrenal glands. The condition can be classified as primary, secondary, or tertiary adrenal insufficiency, each with distinct pathophysiological mechanisms.
36
what is primary adrenal insufficiency (Addisons)
it is caused by an autoimmune destruction (main cause), but can also be caused by infections, metastatic cancer, adrenal haemorrhage and genetic disorders. it is caused by direct damage to or dysfunction of the adrenal cortex.
37
what is secondary adrenal insufficiency
often due to: -pituitary disorders -chronic steroid use -pituitary infarction. cause: -inadequate production of adrenocorticotropic hormone (ACTH) by the pituitary gland
38
what is tertiary adrenal insufficiency
often results from chronic exogenous glucocorticoid use which suppresses the HPA axis, or hypothalamic disease it is caused by impaired hypothalamic function leading to decreased corticotropin-releasing hormone (CRH) production.
39
what is cortisol and what are some of its uses
cortisol is the bodys main stress hormone. -metabolism: crucial for glucose metabolism, protein catabolism, and fat mobilisation. deficiency leads to hypoglycaemia, decreased gluconeogenesis and weight loss. -stress response: can cause hypotension and sock in severe cases if cortisol is in deficiency.
40
what is aldosterone and what what does it deficiency lead to
regulates sodium and potassium levels by promoting sodium reabsorption and potassium excretion in the kidneys. deficiency leads to hyponatremia, hyperkalaemia and volume depletion, it can also contribute to shock. it is used rot maintain blood pressure by influencing fluid balance
41
what are the mechanisms of autoimmune disease (Addisons disease)
Autoantibodies target adrenal cortex cells, leading to gradual destruction and fibrosis. This reduces the production of cortisol, aldosterone, and adrenal androgens. signs: -hyperpigmentation -electrolyte imbalances -adrenal crisis
42
what are the mechanisms of pituitary dysfunction
Reduced ACTH production leads to decreased stimulation of the adrenal cortex, primarily affecting cortisol production, while aldosterone production remains relatively normal due to regulation by the renin-angiotensin-aldosterone system (RAAS) signs: -mild electrolyte imbalances -adrenal crisis
43
what are the mechanisms of hypothalamic dysfunction
Decreased CRH production leads to reduced ACTH secretion and subsequent cortisol deficiency. Often seen in the context of chronic glucocorticoid therapy, which suppresses the HPA axis. signs/symptoms: -adrenal crisis -mild electrolyte imbalances
44
adrenal crisis
Regardless of type those with adrenal insufficiency are at risk of adrenal crisis which can be life threatening due to lack of cortisol can occur if existing cortisol replacement does not meet the body's need -in particular with illness: fever, vomitting, diarrhoea and trauma.
45
changes during adrenal crisis
RR: increases HR: increases SPO2: increases or decreases BP: decreases CRT: decreases or increases Temp: possible decrease mental status: decrease DEFG: possible decrease
46
what is insulin and what is its role
hormone produced by pancreas that plays a crucial role in regulating blood sugar (glucose) levels. -lowers blood sugar -helps store glucose as glycogen -promotes fat storage -prevents fat breakdown -regulates protein synthesis
47
what are some metabolic responses to hypoglycaemia
-glucose transport and utilisation -glycogenolysis -gluconegenesis -hormonal regulation -ketogenesis -metabolic adaptation
48
what do glucose transporters do (GLUTs)
Cells, especially in the brain, skeletal muscles, and liver, utilize GLUT transporters to take up glucose from the bloodstream into the cytoplasm.
49
what happens to insulin levels
insulin normally facilitates glucose uptake in peripheral tissues, during hypoglycaemia, insulin levels decrease or become less effective, allowing glucose to enter these tissues more freely.
50
what happens during glycogenolysis
in response to low blood glucose levels, glycogen stored in the lover is broken down into glucose-1-phosphate by the enzyme glycogen phosphorylase. glucose-1-phosphate is converted to glucose-6-phosphate, which can be converted to glucose and released into the bloodstream.
51
what is gluconeogenesis
Gluconeogenesis is the synthesis of glucose from non-carbohydrate sources such as amino acids (from muscle protein breakdown), lactate (from anaerobic glycolysis), and glycerol (from adipose tissue lipolysis). These substrates are converted to glucose-6-phosphate, then glucose, and released into the bloodstream to maintain blood glucose levels.
52
how is glucagon regulated
Secreted by the pancreas in response to low blood glucose levels, glucagon stimulates glycogenolysis and gluconeogenesis in the liver.
53
how is adrenaline regulated
Released by the adrenal glands, adrenaline enhances glycogenolysis and gluconeogenesis in the liver and inhibits insulin secretion.
54
what is ketogenesis and what causes it to increase
ketogenesis: production of ketone bodies in prolonged hypoglycaemia, when glycogen stores are depleted, the liver increases ketogenesis (production of ketone bodies) from fatty acids. Ketones can be used as an alternative fuel source by tissues such as the brain and heart.
55
what happens to ATP production in hypoglycaemia
Despite reduced glucose availability, cells maintain ATP production through alternative metabolic pathways (e.g., fatty acid oxidation, ketone body utilisation). Cells adapt to use available substrates for energy production to sustain cellular functions, especially in tissues with high energy demands like the brain.
56
what are the neurological effects of hypoglycaemia
the brain is vulnerable to hypoglycaemia as it has high energy demands and dependance on glucose. Severe hypoglycaemia can lead to neuronal dysfunction, impaired neurotransmitter release, and even neuronal death in extreme cases.
57
what are the cellular effects of hypoglycaemia
cellular stress: -cellular stress responses -oxidative stress -mitochondrial dysfunction
58
what are the cellular effects of hypoglycaemia on homeostasis
Cellular metabolism can be disrupted, leading to alterations in ion concentrations (e.g., calcium, potassium), which affect cellular signalling and function.
59
what are the cellular effects of hypoglycaemia on lipolysis and ketogenesis
Increased breakdown of fats (lipolysis) and production of ketone bodies can occur, especially in prolonged hypoglycaemia, providing alternative energy sources but also potentially leading to metabolic acidosis if ketone levels become too high.
60
effects of hypoglycaemia
RR: increases HR: increases SPO2: decreases or increases BP: stable or decrease CRT: stable or decrease Temp: stable mental status: decrease DEFG: decrease
61
hypoglycaemic risk factors (medical and lifestyle)
medical: -insulin treatment -renal dialysis -sepsis -endocrine illness lifestyle: -drug ingestion -inadequate carbohydrates -increased exercise -pregnancy -breastfeeding -inadequate glucose monitoring.
62
what are metabolic responses of hypoglycaemia
-glucose transport and utilisation -metabolic pathways -oxidative stress -advanced glycation end-products (AGEs) -inflammation -endothelial dysfunction
63
what is mitochondrial dysfunction
Too much glucose causes the mitochondria (cell's energy producers) to generate harmful molecules called reactive oxygen species (ROS), which damage proteins, fats, and DNA.
64
what is antioxidant system overload
The body’s defence systems (like glutathione and superoxide dismutase) become overwhelmed by the excess ROS, leading to more oxidative stress and cell damage.
65
how are Advanced Glycation end-products (AGEs)
 formed and how do they work
High blood sugar causes proteins, fats, and DNA to become "sticky" through a process called glycation, forming harmful molecules called AGEs (Advanced Glycation End Products). AGEs bind to receptors (RAGE), triggering inflammation, increasing oxidative stress, and disrupting normal cell functions
66
what are the cellular effects of severe hyperglycaemia
Diabetic Retinopathy: Damage to the retinal blood vessels leads to vision problems and blindness. Diabetic Nephropathy: Damage to the kidneys' filtering system causes proteinuria and eventual renal failure. Diabetic Neuropathy: Nerve damage results in sensory loss, pain, and autonomic dysfunction. Cardiovascular Complications: Increased risk of atherosclerosis, hypertension, and coronary artery disease. Poor Wound Healing: Hyperglycaemia impairs immune function and reduces collagen synthesis, leading to chronic wounds and infections
67
what changes occur due to hyperglycaemia
RR:increases HR:increases SPO2:stable BP:increases CRT:stable Temp:stable mental status:decrease DEFG: increase
68
what is diabetic ketoacidosis
Diabetic ketoacidosis (DKA) is a serious complication of diabetes, characterized by hyperglycaemia, ketonemia, and metabolic acidosis
69
what are cellular mechanisms in DKA
-insulin deficiency -lipolysis and ketogenesis -ketone bodies -electrolyte imbalance -osmotic diuresis -metabolic acidosis
70
what can ketone bodies supply and how do they aid acidosis
Ketone bodies provide an alternative fuel for tissues, including the brain, when glucose is scarce. Too many ketone bodies can make the blood acidic, lowering its pH and causing ketoacidosis.
71
what are the cellular effects of diabetic ketoacidosis (DKA)
Hyperglycaemia: Blood glucose levels are typically elevated above 7.8 mmol/L. Ketosis: Presence of ketones in blood (3.0 mmol/L) and urine (2+). Metabolic Acidosis: Low blood pH (<7.3) and low bicarbonate levels (<18 mmol/L). Dehydration: Signs include dry mucous membranes, tachycardia, and hypotension. Electrolyte Imbalance: Hyperkalaemia initially, followed by hypokalaemia due to urinary losses. Altered Mental Status: Ranges from alertness to confusion and coma, depending on severity.
72
what are the effects of diabetic ketoacidosis
RR:increase HR: increase SPO2:stable BP:decrease CRT:stable Temp:decrease or stable metal status:decrease DEFG:increase
73

PARA400 (12 decks)

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