Flashcards
endocrine disorders
Cards in this deck (106)
- 1Name the glands of the endocrine systempineal, hypothalamus, pituitary (Master), thyroid, parathyroid, thymus, adrenal, pancreas, ovaries (female) & Testes (Male)
- 2Overview of Endocrine system rolesControls growth and development, processes of reproduction, metabolism, maintenance of fluid and electrolyte balance, mobilisation of immune defences, stress response
- 3Overview of How the Endocrine system manages its rolessecretes hormones or chemical messengers that control the flow of info between tissues and organs & help maintain homeostasis in conjunction with NS
- 4Is the endocrine system fast acting?no - slow, however once initiated it tends to be longer-lasting than NS
- 5What gland is referred to as the "master" and whyPituitary gland - because its hormones control the function of many OTHER endocrine glands - e.g. the pancreas (endocrine glands produce insulin and glucagon whereas exocrine glands produce pancreatic juice for digestion)
- 6Can other body parts secrete hormones?Yes - the liver, kidney, heart, GI tract and adipose tissue
- 7How are hormones classified?- the chemical structure of a hormone determines the hormones water solubility This effects how it's transported in the blood how quickly it is degraded and what receptors it connects upon
They can be classified into two main groups: Amino acid-based & steroid - 8Amino acid-based hormones can be further broken into:Amines & amino acids - e.g. derivatives like adrenaline and thyroxine (both derived from tyrosine)
Peptide & protein hormones - e.g. insulin & glucagon amino acid derivatives - 9How are Amino-acid-based hormones defined?Water-soluble, travel freely in blood and binds to the cell-surface receptor (cannot cross lipid membrane due to polar nature)
- 10How are Steroid Hormones defined?Travel in blood bound to carrier, bind to intracellular receptor, lipid soluble
- 11Expand on steroid hormonessynthesized from cholesterol
incl genital & adrenal cortical hormones such as cortisol, lipid soluble = cannot travel freely in blood so need to be transported attached to a protein carrier, when they are in a bound state, they are inactive they MUST leave the carrier protein to interact with the receptors but as the free or unbound hormone is lipophilic, they can freely cross the lipid cell membrane and these hormones interact with intracellular receptors - 12What is the one exception to the rule of hormone classification?thyroid hormone
Although it is an amino acid-based hormone it acts like a steroid hormone and so needs a carrier to transport it in the blood it can cross the lipid cell membrane and it interacts with cellular receptors - 13How are hormones regulated?they release from source gland into blood to be carried to target organ for response (can be far) - endocrine glands are stimulated to synthesise & release hormones in response to 1 or 3 stimuli
Hormonal, Neural or Humoral - 14What kind of feedback system regulates the production of many hormones?negative feedback - the body likes to maintain physiological variables such as hormones within a fairly narrow range to maintain homeostasis
- 15How do hormones produce their effects?By interacting with high affinity receptors on target cells of the tissue (e.g. thyroid hormone will only bind to thyroid receptors)
- 16Humoral stimuli: explainHormones stimulate other endocrine organs to release their hormones
Hypothalamic hormones stimulate release of most anterior pituitary hormones Anterior pituitary hormones stimulate targets to secrete still more hormones
Hypothalamic–pituitary–target endocrine organ feedback loop
o Hormones from final target organs inhibit release of anterior pituitary hormones - 17Explain Neural stimuliNerve fibres stimulate hormone release Example in image (stress response): Sympathetic nervous system fibres stimulate adrenal medulla to secrete catecholamines – adrenaline and noradrenaline
- 18Explain Humoral stimuliChanging blood levels of ions and nutrients directly stimulate secretion of hormones Example:
Declining blood Ca2+ concentration stimulates parathyroid glands to secrete PTH (parathyroid hormone)
PTH causes Ca2+ concentrations to rise, and stimulus is removed - 19Negative feedback regulation: hormones Sensor initiate to trophic releasesensors sense decrease in hormone range (outside normal) & initiate change causing an increase in production
hypothalamus secretes appropriate hormone which initiates release of corresponding trophic hormone from anterior pituitary - 20Negative feedback regulation: hormones Trophic hormone to sensor stopa trophic hormone has other glands at target and they stimulate target gland to release appropriate hormone to enter blood and carryout job
when blood levels rise above set point the sensors cause production to decrease by reduction of trophic hormone - 21Short-term stress response overviewCan be actual or potential threats to homeostasis
response co-ordinated by hypothalamus and vary depending on if long or short term, can be physical (fire) or psychological (exam) - 22Running from a fire - stress response examplehypothalamus activates adrenal medulla to release adrenaline & noradrenaline via NEURAL stimuli initiates APs in response, which activates Sympathetic NS
APs travel along SNS fibers to adrenal medulla and stimulate catecholamine hormone release, adrenaline and noradrenaline reinforce other SNS response (e.g. increased HR, elevated BP, blood directed away from non-essential organs)
usually brief and quick - 23Long term stress responsehypothalamus releases corticotrophin releasing hormone which stimulates the anterior pituitary gland to release adrenocorticotropic hormone or ACTH, this travels in blood and binds to cells on the adrenal cortex causing release of glucocorticoids - Cortisol
as adrenal cortex is activated by HORMONAL stimuli and glucocorticoids are steroids the response is slower but tends to be longer lasting - 24Disorders of the endocrine system can be:Primary (originate in target organ releasing hormone) OR Secondary & tertiary (defect in hypothalamus-pituitary system, gland is essentially normal but altered function because of defective levels of corresponding trophic hormone being released from anterior pituitary
- 25What can disorders of the endocrine system originate from?HYPOfunction (e.g. destruction of a gland) OR HYPERfunction (e.g. excessive hormone production due to overstimulation of gland)
- 26Tests used to examine endocrine functionBLOOD - (info on levels of a hormone at time of sample) analysed using radioimmunoassay, ELISA, autoantibodies, biochemical etc.
STIMULATION - Hypofunction
SUPPRESSION - hyperfunction
IMAGING - isotopic scanning (using radioactive iodine to assess thyroid ability to uptake iodine) & non-isotopic (CT, MRI, PET, ultrasound) - 27What is a suppression test and how does it work (endocrine)tests for HYPERfunction of endocrine organ:
Normal negative feedback of an endocrine organ not working →excessive amount of hormone is being produced
HOW: Give external stimulus for the endocrine organ. If the stimulus does not reduce hormone production, then there is possible hyperfunction of the endocrine organ.
Example: Dexamethasone suppression test (case 2) - 28What is a Stimulation test and how does it work (endocrine)tests for HYPOfunction of endocrine organ: A tropic or stimulating hormone is administered to test ability of endocrine organ to increase hormone production (i.e. it is functioning correctly)
If you get an increase in hormone production then organ working well.
If not then = HYPOfunction
Example: ACTH stimulation test (see case study) - 29What is Addison's disease?relatively rare disorder with autoimmune destruction of the adrenal gland being the most common cause
- 30Why do you get hyperpigmentation of the skin with primary adrenal insufficiency?Hyperpigmentation results from excess ACTH. The blood levels of glucocorticoid hormones such as cortisol are regulated by negative feedback mechanisms. If cortisol levels are low, then then hypothalamus secretes CRH which will stimulate the release of ACTH. In primary adrenal insufficiency this will lead to elevated levels of ACTH. Melanocyte-stimulating hormone (MSH) is produced from the same precursor molecule as ACTH, and both MSH and ACTH can have a stimulatory effect on the melanocytes causing them to produce melanin.
- 31What is Cushing's syndromeCushing’s syndrome = umbrella term for hypersecretion of cortisol from any cause
If cause results from excess ACTH by a tumor in the pituitary gland this is called cushing’s disease other causes can include having an adrenal tumor or a non-pituitary ACTH secreting tumor for example in the lung or it can result from long term oral cortico steroid treatment - 32How to measure cortisol levels (and what for)a salivary cortisol measurement a specimen is collected by patients before bed and sent to the laboratory the following day and normal unstressed patients you would expect to see a marked fall in slavery cortisol in the late evening whereas in patients with Cushing syndrome cortisol levels and salivary cortisol remain elevated
- 33Thyroid Hormone (TH) : What is ita collective name for 2 hormones produced & released by thyroid gland - body's MAJOR metabolic hormone = TH affects essentially every cell in body
- 34How does Thyroid Hormone work?↑ metabolism, protein synthesis, roles in growth & development & neural maturation
Act like steroid hormones (see above notes) TH enters target cell and binds to intracellular receptors within nucleus
o Triggers transcription of various metabolic genes - 35What 2 forms is Thyroid Hormone found in?both iodine-containing amine hormones
T 4 (thyroxine): main form secreted into circulation, longer half life than T3, major form secreted by thyroid follicles (90%); consists of two tyrosine molecules with four bound iodine atoms – why it is important to have iodine in diet! * iodine deficiency can result in decreased production of T3 & T4
T 3 (triiodothyronine): thought to be active form; has two tyrosines with three bound iodine atoms
Most T 3 converted from T 4 at tissue level - 36How is secretion of Thyroid Hormone (TH) regulated?By hypothalamic pituitary thyroid feedback system
- 37How does hypothalamic pituitary thyroid feedback system workThyrotropin-releasing hormone is produced by the hypothalamus
which ↑ release of thyroid stimulating hormone from the anterior pituitary gland
TSH then binds receptors on thyroid epithelial cells stimulating the production & release of thyroid hormones
as the level of thyroid hormone increases this is sensed by receptors in the hypothalamus and the anterior pituitary and negative feedback inhibition causes the reduction in the secretion of further TRH and TSH
this allows blood levels to be regulated within a narrow range
stimuli for increased levels of thyroid hormone include things such as cold and stress which dominate the hypothalamic pituitary thyroid system at the hypothalamic level
leading to increased levels of TRH TSH and ultimately thyroid hormone - 38Thyroid Function testsTSH - gives initial indication of function
following an abnormal result of TSH:
Serum FT4 (& FT3) and/or thyroid antibodies - 39What is the most common cause of TH HYPERsecretion (Hyperthyroidism)Grave's disease (auto immune disease where immune system creates antibodies that bind to TSH receptors on thyroid gland & cause abnormal stimulation resulting in increased production of T3 & T4
- 40What happens in Hyperthyroidism when abnormal antibodies are made against normal cellsthey mimic TSH, stimulating TH release (increased levels of thyroid hormones cause negative feedback inhibition and a decrease in TSH secretion from the anterior pituitary, thus resulting in the low levels of TSH that are seen with this disorder)
- 41What might you see in a blood test of someone with HyperthyroidismHIGH FT4 and LOW TSH levels
- 42What are some symptoms of hyperthyroidismelevated metabolic rate, sweating, rapid and irregular heart beat, nervousness, weightloss DESPITE adequate food
- 43What is exophthalmos?A symptom of Hyperthyroidism where the eyes protrude due to the tissue behind them becoming oedematous (excess interstitial fluid) and fibrous
- 44What 2 main causes result in hyperthyroid symptomsa hypermetabolic state and an increase in SNS activity - An increased sensitivity to catecholamines (similar to acute stress in SNS activity. Several symptoms of hyperthyroidism resemble those of excessive SNS activity. β-blockers can provide immediate relief of any adrenergic symptoms)
- 45What treatments are available for HYPERthyroidismDRUGS - carbimazole tablets (a thioamide) – (Carbimazole decreases thyroid hormone synthesis by interfering with the organification - that's the oxidation in binding of iodine) OR Beta-blockers sometimes to provide immediate relief of adrenergic symptoms
SURGERY - to remove thyroid or radioactive iodine to destroy active thyroid cells (both treatments risk the development of hypothyroidism) - 46What are the most common causes of Primary HYPOthyroidismAutoimmune disease (e.g., hashimotos thyroiditis), Thyroidectomy, ablation, iodine deficiency
- 47What are some common symptoms of HYPOthyroidismDecreased metabolic rate (weight gain), lethargy, bradycardia, cold intolerance, constipation, myxedema (mucus type edema where built up of material around body which can result in puffy face, swollen tongue, swollen hands and feet)
- 48What would you expect to see in a blood test of someone with HYPOthyroidismLOW FT4 and HIGH TSH
- 49What treatment is available for HYPOthyroidismReplacement therapy with synthetic preparations e.g. levothyroxine
- 50regulation of blood glucosemaintained in a VERY narrow range
healthy individuals maintain within 4-6 mmol/L
a number of hormones contribute to regulation, BUT insulin ONLY hormone that LOWERS it - 51What do Insulin, glucagon and adrenaline do to blood glucoseInsulin LOWERS
Glucagon RAISES
Stress hormones (e.g. adrenaline) RAISES - 52How is glucose transported?It's large and polar meaning it cannot cross lipid membrane by simple diffusion
bridges MUST be formed
called - glucose transporters
in case of skeletal muscle and adipose tissue type of transporter used requires insulin or chemical instruction to allow the formation of these glucose bridges so that glucose can enter the cells and be used for energy - 53Relationship between insulin and glucose: What are GLUTSGlucose transports, (GLUTS) are a family of membrane proteins that facilitate the transport of glucose into cells
- 54How many types of GLUTS are there (glucose transports)14 have been identified with each having a SPECIFIC role (although role of some not fully understood)
- 55Describe the role of GLUTs 1 - 4 overviewhave key roles in blood glucose homeostasis at the cellular and whole-body level
- 56What does GLUT 4 do?it is the main transporter for skeletal & cardiac muscles & adipose tissue
insulin binds to the receptors on the cell membrane which causes GLUT 4 molecules to move from inactive space inside cell towards cell membrane
once there, GLUT 4 molecules permit diffusion of circulating glucose into cells - 57What body parts do not use insulin for glucose transport?the brain, RBCs, Kidney and lense of they eye utilise other transporter groups. glucose can enter these cells on a continual basis from the bloodstream
the transport of amino acids and minerals such as potassium is also facilitated whereas lipids can enter by diffusion through the membrane
in the cell, insulin promotes the synthesis of proteins carbohydrates and lipids - 58Where is Insulin producedBy beta cells of islets of Langerhans in the pancreas
- 59What are the actions of insulin?Has several - not only carb metabolism but has effects on fat & protein metabolism too
- 60When is insulin releasedafter a meal blood glucose rises, triggering insulin release, then stimulates uptake use & storage of glucose
- 61Insulin stimulates (what?)Uptake, use & storage of glucose
Glucose → glycogen (glycogenesis)
Glucose → fat (lipogenesis)
protein synthesis - 62Insulin inhibits (What?)Glycogen breakdown (glycogenesis)
Fat breakdown (lipolysis)
Protein breakdown → glucose (Glucogenoenesis) - 63Where is glucagon producedby alpha cells of islets of Langerhans in pancreas
- 64what is glucagons roleworks with insulin as antagonistic pair - in a healthy individual, when blood glucose falls, glucagon levels increase & insulin levels fall
- 65What organ does Glucagon act on primarily?The liver - initiates glycogenolysis which increases bloog glucose level back to 4-6 mmol/L in minutes
it also increases transport of amino acids to liver and stimulates their conversion to glucose (Gluconeogenesis) - 66What does a high concentration of glucagon initiatelipolysis in adipose tissue = increased free fatty acids for energy
- 67What is the main stimulus for glucagon release?HYPOglycaemia - others include high concentration of amino acids, stress and increase exercise
- 68Incretin hormones - Glucagon-like peptide 1 (GLP-1) & Incretin effectthese peptide hormones are secreted from endocrine cells located in the epithelium of the small intestine
Secreted in response to nutrient (Carb, protein, and fat) ingestion
Main 2: glucagon-like peptide 1 (GLP-1) & glucose-dependent insulinotropic peptide (GIP) stimulate insulin secretion from pancreatic beta cells
this amplification of insulin secretion is known as the incretin effect - 69Additional actions of GLP-1↓ glucagon secretion
Delay gastric emptying
↓ appetite
↑ satiety
↓ body weight
Protective effects on beta cells - 70What is faulty in diabetes?The bridges!!
Decreased ability to form glucose bridges into cells
Less glucose enters cells
Cells don’t work as well (are starved of an energy source) High levels of glucose remain in the blood → macrovascular and microvascular complications - 71Diabetes Mellitusbody's ability to produce or respond to insulin is impaired - leading to hyperglycaemia and changes in nutrient metabolism & storage (carbs, pro, fat)
3 types, 1, 2 & gestational - 72What results in Type 1 diabetesLoss of the pancreatic islet β cells – resulting in insulin deficiency
- it usually presents in childhood
- in most patients (70 to 90%) the loss of beta cells is associated with the formation of autoantibodies - 73Type 1 Diabetes: Autoimmune overview70-90% patients Type 1A
o Genetic susceptibility and interactions with environmental factors are thought to trigger cell-mediated destruction of pancreatic β cells
(thought that when individuals who are genetically predisposed are exposed to interactions with one or more environmental factors such as a viral infection cell-mediated destruction of the pancreatic beta cells can be triggered) - 74Type 1 diabetes: autoimmune (what happens in the body)Formation of T1D autoantibodies, activation of Immune system - T cells, B cells, dendritic cells & macrophages - results in inflammation and islet B cell destruction
- 75How to determine between Type 1 and Type 2 diabetes?Islet autoantibody test
If present, then confirm Type 1 - 76Type 1 diabetes: NonimmuneIdiopathic diabetes (Type 1B) cause of Beta cell destruction unknown, NO immune response or autoantibodies detected
- 77Type 2 Diabetes Mellitus: OverviewInvolves genetic, epigenetic & environmental interactions
usually presents in adulthood
Insulin resistance & Beta-cell dysfunction - lead to hyperglycaemia - 78Insulin resistanceType 2 diabetes
reduced biological response to insulin, esp in liver, muscle, adipose tissue - 79Risk Factors for Type 2 DiabetesAge, obesity, hypertension, physical inactivity, family history, gestational diabetes, metabolic syndrome; 'prediabetes'
approx. 90% are overweight with visceral obesity as high risk - 80Insulin deficiency Page 14!!
- 81Blood glucose & HbA1c levels normal, hyper & diabetesNORMAL fasting plasma 4-6 mmol/L, HbA1c < 40 mmol/mol
INTERMEDIATE HYPERGLYCAEMIA fasting plasma 6.1-6.9 mmol/L
HbA1c 41-49 mmol/mol
DIABETES fasting plasma >7 mmol/L
HbA1c >50 mmol/mol - 82What does intermediate hyperglycaemia indicateprediabetes
- 83What is glycated haemoglobin test for (HbA1c)blood glucose measures
someone displaying symptoms may only require 1 test, 2nd may confirm - 84Oral Glucose tolerance test-Patient given a quantity of concentrated glucose solution and plasma levels are monitored at regular intervals people with normal blood glucose tolerance blood levels rise and then return to normal within 2-3 hours people with impaired glucose tolerance or diabetes glucose levels rise more and take much longer to return to normal
- 85HbA1c test - what does it measure & key advantagesQuantity of haemoglobin that has become glycated
provides a measure of chronic glycemic exposure (reflects average level of last 3 months with average rbc life span 120 days) - 86What can alter RBC lifecycle and interfere with HbA1c test?illness or blood transfusion
- 87Why is measuring HbA1c levels the test of choice to screen, diagnose and monitor people with T2DM?provides measure of chronic glycaemic exposure, reflecting the average previous 3 months, rather than a measure at a single time point NO fasting is required
it is less affected by day to variation in plasma (e.g. due to changes in diet, exercise, smoking, etc)
there is less biological variability compared to 2 fasting blood glucose tests in the same person - it has simpler sampling and analysis requirements - 883 structural classifications of adipose tissue1. lean with normal metabolic function
2. obese with mild metabolic dysfunction
3. obese with full metabolic dysfunction
with ↑weigh, you get ↑info with a corresponding loss of metabolic control - 89Development of Type 2 diabetesIR associated with obesity induced by proinflammatory adipokines, free fatty acids and the chronic inflammation that is associated with adiposity particularly visceral adiposity - initially normal glucose tolerance is maintained by compensatory increase in insulin secretion, however, reaches point where failure to ↑ insulin secretion sufficiently leads to impaired glucose tolerance
at some point beta cell compensation is followed by beta cell failure and a ↓ in insulin secretion which leads to overt diabetes - 90Why is screening for early diabetes so important?blood glucose can be elevated for MANY years before diagnosis - vascular complications are likely to have already started
catch it early! - 91Hypoglycaemia overviewlowered BGL (<4 mmol/L)
- 92hypoglycaemia common causestoo much insulin, not enough food (carbs) or increased exercise
- 93Hypoglycaemia: clinical manifestationso Tachycardia, palpitations, diaphoresis (excessive sweating), tremors, Pallor, anxiety, confusion
- 94Hypoglycaemia: treatmentGlucose (tablets, jellybeans, whatever available) and/or glucagon injection
Glucagon raises blood glucose levels by encouraging liver to release glucose into blood stream
Regular testing of blood glucose levels KEY to understanding & oreventing hypos. - 95Diabetic ketoacidosis (DKA) what is ithyperglycaemia, ketosis & metabolic acidosis resulting from a deficiency in insulin and increase in counter regulatory hormones (e.g. adrenaline) - more common in Type 1
- 96Diabetic ketoacidosis: factorsPoor adherence to insulin treatment
- 97Diabetic ketoacidosis: clinical manifestationsPolyuria & dehydration; kussmaul respirations (fast deep breath) sweat or fruity breath odour
- 98Diabetic ketoacidosis: Whats happening in the body hyperglycaemiaHyperglycemia = osmotic diuresis, dehydration and a critical loss of electrolytes
- 99Diabetic ketoacidosis: whats happening in the body: insufficient insulininsufficient insulin = immobilization of fat stores for energy and the released free fatty acids are taken to the liver for conversion to ketones which are acidic
- 100Diabetic ketoacidosis: whats happening in the body: Increased ketonesincreased levels of ketones require buffering by bicarbonate ions hence you also get a decrease in serum bicarbonate levels
- 101DIabetic ketoacidosis: Whats happening in the body: Kassumal respirationsKussmaul respirations = compensatory prevent a further decrease in pH by reducing the amount of CO2 which is also acidic in the blood
- 102DIabetic ketoacidosis: Treatmento Administration of insulin to decrease glucose levels, fluids and replacement of electrolytes
- 103Hyperosmolar hyperglycaemic state (HHS)similar to DKA but without ketosis. Occurs more frequently T2DM patients
- 104Chronic complications of DM: Microvascular diseaseo Diabetic retinopathy
o Diabetic nephropathy
o Diabetic neuropathies - 105Chronic complications of DM: Macrovascular diseaseo Coronary artery disease
o Stroke
o Peripheral arterial disease - 106Chronic complications of DM: OtherInfection & Impaired wound healing
The level & duration of glycemia influences the development of diabetes-related complications -
good close limit control through pharmacological and lifestyle management is important to reduce the risk of these
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- Flashcards on endocrine disorders, created by Ella Glynn on 14/06/2022.
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