Endocrine system Flashcards

1
Q

What is the endocrine system? function

A

This is a network of glands that produce and release hormones
They help control important body functions

Along with the bodies ability to change calories into energy it also influences other things such as:
Bone growth
Heart beat
Tissue growth
Fertility
Development of disease and a host of hormone-related disorders

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2
Q

The endocrine feedback system

A

This helps to control the balance of hormones within the bloodstream

The feedback system will detect when there is too much or too little of a certain hormone and signal to the correct gland to solve the problem

If the feedback system has difficulty correcting the hormone balance this is known as a hormone imbalance

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3
Q

Whats exocrine gland?

A

Secretes substances
Released through ducts
Secreted outside of the body or into the GI tract

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4
Q

Whats endocrine gland?

A

Releases hormones
Ductless glands
Directly released into the bloodstream

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5
Q

A hormone imbalance can be caused by what?

A

A hormone imbalance can be caused by a number of reasons:
A problem with the feedback system
Disease
Genetic disorder
Infection
Injury
Tumor
Failure of a gland to stimulate another gland

Most tumors or nodules are noncancerous, usually do not spread,
A tumor or nodule may interfere with the gland’s hormone production.

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6
Q

What is a hormone?

A

-Chemical signals released into the bloodstream
-Transported to target tissues
-Coordinate the activity of the cell
-Effective in small amounts

this will vary depending on the physiological change that has been detected, which hormone it is and which organ will be activated to respond to this change.

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7
Q

Hormone classification water soluble (hydrophilic) - peptides/amines overview

A

Polypeptide or protein chains, or amines
Manufactured on rough endoplasmic reticulum before packaging into golgi bodies prior to release – BULK TRANSPORT
Often secreted as pro-hormones
Examples EPO, ACTH, FSH
Water-soluble hormones (all amino acid-based hormones except thyroid hormone) exert their effects through an intracellular second messenger that is activated when a hormone binds to a membrane receptor.

Hormone-Target Interaction - Individual hormones only affect certain target cells, receptor molecules are present on specific organs

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8
Q

Hormone classification lipid soluble (lipophilic) - steroids overview

A

Principally derived from steroids
Could be cholesterol based
Penetrate through the cell membrane
Examples testosterone, oestrogen, cortisone
Passive transport

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9
Q

Chemical Classification Of Hormones:
Peptide and Protein:
Peptide and protein hormones are short and long chains of amino acids respectively
Majority of peptide hormones are secreted by: Hypothalamus, Anterior and posterior pituitary, Pancreas

Amines:
Derived from tyrosine, Hormones secreted by: Thyroid gland, Adrenal medulla (catecholamines- adrenalin & noradrenalin)

Steroids Natural lipids derived from cholesterol, Hormones of adrenal cortex, gonads and most placental hormones

Synthesis, Storage, Secretion
Peptide Hormones
Synthesized using the classical protein synthesis pathways, Synthesized as inactive prohormones which are finally activated to the active hormone
Golgi complex concentrates final product into vesicles stored in the cytoplasm, Upon the correct stimulus, vesicle fuse with the plasma membrane and release their contents by exocytosis

Steroid Hormones
Most material derived from LDL, Requires series of enzymatic reactions. Steroid hormones are “NOT STORED” after formation. Once synthesized, they diffuse through plasma membrane and enter blood. Only cholesterol (steroid hormone precursor) is stored within cells Therefore, rate of secretion of steroid hormones is controlled by rate of steroid hormone synthesis. Steroid hormones can be modified once released into the blood into a more potent form

Transport
Peptide hormones are simply dissolved in the blood, Steroid hormones reversibly bound to plasma proteins e.g. Albumin binds any hormone, However, some plasma proteins only bind specific hormones (e.g. testosterone binding protein), Only unbound version of steroid hormone is biologically active, Once the hormone has interacted with its target, it is rapidly inactivated, Chemical properties of a hormone dictate method of artificial administration, e.g. Steroid hormones cannot be destroyed by digestive enzymes, therefore administered orally
Intracellular Actions of Hormones
See Pre slides for Endocrine for this information.

A

Chemical Classification Of Hormones:
Peptide and Protein:
Peptide and protein hormones are short and long chains of amino acids respectively
Majority of peptide hormones are secreted by: Hypothalamus, Anterior and posterior pituitary, Pancreas

Amines:
Derived from tyrosine, Hormones secreted by: Thyroid gland, Adrenal medulla (catecholamines- adrenalin & noradrenalin)

Steroids Natural lipids derived from cholesterol, Hormones of adrenal cortex, gonads and most placental hormones

Synthesis, Storage, Secretion
Peptide Hormones
Synthesized using the classical protein synthesis pathways, Synthesized as inactive prohormones which are finally activated to the active hormone
Golgi complex concentrates final product into vesicles stored in the cytoplasm, Upon the correct stimulus, vesicle fuse with the plasma membrane and release their contents by exocytosis

Steroid Hormones
Most material derived from LDL, Requires series of enzymatic reactions. Steroid hormones are “NOT STORED” after formation. Once synthesized, they diffuse through plasma membrane and enter blood. Only cholesterol (steroid hormone precursor) is stored within cells Therefore, rate of secretion of steroid hormones is controlled by rate of steroid hormone synthesis. Steroid hormones can be modified once released into the blood into a more potent form

Transport
Peptide hormones are simply dissolved in the blood, Steroid hormones reversibly bound to plasma proteins e.g. Albumin binds any hormone, However, some plasma proteins only bind specific hormones (e.g. testosterone binding protein), Only unbound version of steroid hormone is biologically active, Once the hormone has interacted with its target, it is rapidly inactivated, Chemical properties of a hormone dictate method of artificial administration, e.g. Steroid hormones cannot be destroyed by digestive enzymes, therefore administered orally
Intracellular Actions of Hormones
See Pre slides for Endocrine for this information.

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10
Q

Examples of Endo? and structure

A

Thymus thyroid pancreas adrenals

Ductless
Vascularity
intracellular vacuoles or granules that store their hormones.

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11
Q

Examples of exo? and structure

A

salivary glands, sweat glands and glands within the gastrointestinal tract.

Exocrine Glands
less vascular and
have ducts or a hollow lumen
Pituitary gland is the control centre – controls several other glands
Hypothalamus collects information and secretes hormones – hypothalamus + pituitary gland work together = hypothalamic-pituitary axis
Back to the abdomen!

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12
Q

Hypothalamus overview

A

Situated in the brain
A collecting centre for information
Regulation of hormone secretion
Forms part of the hypothalamic-pituitary axis

The hypothalamus is the master of the endocrine system.

It is situated in the brain at the base of the optic chiasm (posterior to the orbits, where the optic nerves partially cross)

It acts as a collecting centre for information about with the internal environment of the body and uses much of this information to regulate the secretion of the hormones produced by the pituitary gland.

And you can see the hypothalamus is actually attached to the pituitary gland via a stalk-like structure.

With the pituitary gland it forms part of the hypothalamic-pituitary axis – which we will briefly look at in a minute

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13
Q

Pituitary gland overview

A

‘Master’ gland
Also known as the hypophysis
Pea-sized structure made up of 2 lobes
Situated in a bony hollow beneath the base of the brain

It releases hormones produced by the hypothalamus which either inhibit or stimulate other organs to release their hormones.

The gland consists of two parts (often called lobes), each of which has different functions which you can look into if you wish.

It is usually about the size of a pea and is situated in a bony hollow beneath the base of the brain. This bony hollow is called the sella turcica or the pituitary fossa.

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14
Q

Pituitary fossa & Sella turcica, what is it on x-rays

A

This is an important feature for radiographers – we check there is no rotation of this on lateral skull x-rays and on a lateral cervical spine x-ray also. This can be enlarged or eroded which may indicate certain pathologies.

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15
Q

Adrenal glands: where are they what hormone do they release

A

Adrenal glands: two glands that are positioned on top of the kidneys and release the hormone cortisol, also adrenalin and noradrenalin

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16
Q

Ovaries: what hormones, function

A

Ovaries: release eggs and produce sex hormones

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17
Q

Islet cells in the pancreas: function

A

Islet cells in the pancreas: control the release of insulin and glucagon

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18
Q

Parathyroid gland: where are they and their role

A

Parathyroid gland: 4 glands in the neck that play a role in the development of bone

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19
Q

Pineal gland: where is it and hormone

A

Pineal gland: near the center of the brain linked to sleep patterns releases Melatonin during low light

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20
Q

Testes, what hormones and function

A

Testes: produce sperm and sex hormones

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21
Q

Thymus gland: where is it and function

A

Thymus gland: in the upper chest and develops the immune system early in life releases thymosin

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22
Q

Thyroid gland: where is it and function

A

Thyroid gland: the butterfly shaped gland found in the front of the neck and this controls metabolism, releases two hormones Tri-iodothyronine (T3) and Thyroxin (T4)

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23
Q

What does insulin do?

A

What does insulin do?

cells of the pancreas secrete insulin when blood glucose levels rise above 6 mmol/litre

Promotes entry of glucose into target cells (liver cells, adipose cells, muscle cells)

Promotes conversion of glucose to glycogen in the liver

Promotes fat storage

Glycogen is a stored form of glucose. It is a large multi-branched polymer of glucose which is accumulated in response to insulin and broken down into glucose in response to glucagon.

Glycogen is mainly stored in the liver and the muscles and provides the body with a readily available source of energy if blood glucose levels decrease.

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24
Q

Islets of Langerhans contain 3 types of cells, what are they?

A

Located below and behind the stomach
Islets of Langerhans contain 3 types of cells
α cells – produce glucagon
β cells – produce insulin
δ cells (Delta cells)– produce somatostatin

25
Q

Adrenal glands: consist of two parts, what secretes what?

A

Adrenal medulla releases
- Adrenaline
- Noradrenaline

Adrenal cortex secretes
- Mineralocorticoids (aldosterone)
- Glucocorticoids (cortisol)
- Sex hormones (testosterone

26
Q

Adrenal medulla overview?

A

Part of autonomic nervous system
Spherical chromaffin cells are modified postganglionic sympathetic neurons
Amine hormones
Fight and flight response

Vesicles store the hormones

27
Q

Adrenal Insufficiency overview

A

Primary- Intrinsic failure of the adrenal gland resulting in inability to produce cortisol and/or aldosterone (Addison’s Disease); Surgical removal of adrenal gland
ACTH may be high

Secondary – Due to disease of the hypothalamus and/or pituitary gland; prolonged steroid use;
ACTH may be low
Secondary cause of adrenal insufficiency- TB, AIDS, bleeding in adrenal gland, amyloidosis, surgical removal of adrenal gland, certain treatment used for Cushing’s syndrome.

28
Q

slide 29
Acute Pancreatitis,
Chronic Pancreatitis,
Hereditary Pancreatitis
Pancreatic Cancer.
necrotising pancreatitis.
Pancreas adenocarcinoma

A
29
Q

2 cases of pancreatic tumours with tumour-vessel contiguity These patients generally will be given the benefit of the doubt and will be scheduled for operation.

Tumour ingrowth into stomach, colon, mesocolon, inferior vena cava or aorta constitute definite criteria for unresectability.

Also the presence of hepatic metastases, peritoneal metastases or para-aortic lymphnode metastases is an absolute sign of unresectability.

Mesenteric lymph node metastases, not immediately adjacent to the pancreas usually also indicate unresectability.

On the left a pancreatic tumour in direct contiguity with the confluence of the portal and superior mesenteric vein.

The tumour surrounds the confluence for more than half the cirumference (>180?).

This tumour was regarded as unresectable.

A
30
Q

The CT shows an acute necrotising pancreatitis.

Necrosis of the pancreatic parenchyma can be
diagnosed on a contrast-enhanced CT ⩾ 72 hours.
Necrosis of peripancreatic tissue can be very difficult to diagnose, but is suspected when the collection is inhomogeneous, i.e. various densities on CT..

The body and tail of the pancreas do not enhance.
There is normal enhancement of the pancreatic head (arrow)

Often fluid can accumulate in this region also.

A
31
Q

Pancreas adenocarcinoma overview

A

About 95% of cancers of the exocrine pancreas are adenocarcinomas.

These cancers usually start in the ducts of the pancreas.

About 10%, if caught early, are disease free after treatment

The most aggressive of all cancers, 53% of patients at diagnosis also have metastatic spread

The early-portal phase is also called the pancreatic phase. It has a scan-delay of 40-50 sec. Water as contrast.
This is the most important phase for detecting and staging a pancreatic tumour.
At that moment the normal pancreatic parenchyma will enhance optimally, because it gets all of its bloodsupply through the arterial and capillary system.
In this phase there is optimal attenuation difference between the hypoattenuating tumour and the normal enhancing pancreatic parenchyma.

32
Q

Disorders of the Endocrine System

A

Acromegaly —
Addison’s disease —
Cretinism
Cushing’s syndrome —
Diabetes insipidus
Diabetes mellitus —
Pheochromocytoma –
Dwarfism
Gigantism
Graves’ disease —
Hyperparathyroidism —
Hypoglycemia –
Syndrome of inappropriate antidiuretic hormone (SIAD)
Virilism

33
Q

Diabetes mellitus, types overview

A

Type 1
This is where the pancreas fails to produce insulin due to the loss of beta cells
Glucose levels remain high in the blood

Diabetes Type I: Insulin Dependent Diabetes Mellitus (IDDM)
- Results from destruction of the insulin producing β cells in the pancreas.
- Peak onset in ages 11 and 13 (Juvenile onset diabetes); very rare occur after the age of 30.
- Aetiology: may be viral, environmental, and/or genetic.
- Symptom onset abrupt
- Prone to Ketoacidosis

Type 2
This is when the cells fail to respond to insulin properly
Glucose is not able to be utilised by cells despite hyperglycaemia

Diabetes type II:
- May have normal insulin levels and/or β cells.
- Characterised by poor utilisation of insulin
- Generally occurs over 40 years of age and accounts for majority of cases (Obesity may change the age of disease onset).

34
Q

Complication of Diabetes

A

Accelerated atherosclerosis with medial calcification

Microvascular disease; abnormal function of capillary basement membrane leading to:
Nephropathy
Retinopathy

Diabetic neuropathy; autonomic dysfunction; demyelination abnormalities of Schwann’s cells

35
Q

What is nephropathy?

A

Nephropathy is the deterioration of kidney function. The final stage of nephropathy is called kidney failure, end-stage renal disease (ESRD).

36
Q

What is Retinopathy?

A

Retinopathy means disease of the retina. There are several types of retinopathy but all involve disease of the small retinal blood vessels.
Signs of retinopathy can be seen when the retina is viewed through the pupil with an ophthalmoscope.

37
Q

Diabetic foot overview

A

Due to nerve damage and poor circulation

Nerve damage – loss of feeling in feet so may not feel shoes rubbing, may not feel hot and cold… Cause sores on the feet that can become infected. When blood glucose is high, the extra glucose feeds the infection and so it worsens.

Poor blood flow means not enough blood flow can get to an area to aid healing of a sore. If the infection doesn’t heal it can become gangrenous. Skin and tissue around the sore dies and becomes black and smelly. If bone becomes infected also, get osteomyelitis.

38
Q

Signs and symptoms of daibetes

A

Classic symptoms
Weight loss
Polyuria (increased urination)
Polydipsia (increased thirst)
Polyhagia (increased hunger)

Other symptoms
Blurred vision
Headache
Fatigue
Slow healing of cuts
Itchy skin
Skin rashes

39
Q

Hypoglycemia , what is it and what are the causes?

A

This is a fall in blood glucose concentrations
It has an affect on the function of the central nervous system

There are two causes,
Spontaneous: alimentary, early diabetes, idiopathic hypoglycaemia, fasting, islet-cell tumor, extrapancreatic neoplasms or hepatic disease

Induced: insulin induced, oral hypoglycemic agents or alcohol

40
Q

Hypoglycemia signs and symptoms

A

Sudden symptoms
Excessive sweating (Diaphoresis), Pallor
Tremor
Tachycardia, palpitations
Visual disturbances
Mental confusion, weakness

Gradual symptoms
Fatigue
Confusion
Headache
Memory loss
Seizures, coma

41
Q

What is Pheochromocytoma?

A

A rare tumor of the adrenal gland tissue which results in the release of to much epinephrine and norepinephrine the hormones that control heart rate, metabolism and blood pressure.

Can occur as a single tumor or multiple
Very few are cancerous
Can occur at any age, most common in early to mid adulthood.
Can be hereditary

Phaochromocytomas secrete adrenaline in an uncontrolled fashion and can cause problems including stroke, heart attack, and even death.

Orthostatic hypotension – Postural….drop in blood pressure when moving from sitting/lying to standing.

Catecholamine release – tumour causes adrenals to release excess hormones – adrenaline (epinephrine) etc

42
Q

What is orthostatic hypotension

A

Orthostatic hypotension – Postural….drop in blood pressure when moving from sitting/lying to standing.

43
Q

Signs and symptoms of Pheochromocytoma

A

Classic symptoms
Headaches
Heart palpitations
Sweating
High blood pressure

Other symptoms
Abdominal or chest pain
Irritability, nervousness
Pallor
Weight loss
Nausea and vomiting
Shortness of breath
Seizures
Problems sleeping.

44
Q

Tests, imaging and treatment for pheochromocytoma?

A

Tests done may include: Abdominal CT scan, Adrenal biopsy, Catecholamines blood test (serum catecholamines), Glucose test, Metanephrine blood test (serum metanephrine)
An imaging test called an MIBG scintiscan, MRI of abdomen, Urine catecholamines, Urine metanephrines, PET scan of abdomen

Treatment involves removing the tumor with surgery however it is important to stabilize the blood pressure and pulse with medication before surgery.

45
Q

What is Addison’s disease?

A

With Addison’s disease the adrenal glands are underactive
This results in a deficiency of adrenal hormones, cortisol and/or aldosterone

Can be caused by an autoimmune reaction causing the bodies immune system to attack and destroy the adrenal cortex, cancer or infection such as TB along with other reasons
It also affects the balance of water, sodium and potassium, as well as the ability to control blood pressure.

As there is a low level of cortisol, a feedback loop increases levels of ACTH being released, this excess ACTH stimulates melanocyte production in the skin which then causes hyperpigmentation

46
Q

Signs and symptoms of Addison’s disease?

A

Loss of appetite
Unintentional weight loss
Hypoglycaemia
Hypotension
Lack of tolerance to stress
Dizzy when standing
Dark skin patches
Weakness

Hyperpigmentation of hands

Chest x-ray may show surprise changes due to increased potassium levels and low blood pressure/high heart rate – so we may see unusual fluid collections like pulmonary oedema.

47
Q

What is Cushing’s syndrome?

A

A condition caused by having to much (hypersecretion) cortisol
It is uncommon, mostly affecting those that take prolonged steroids as these are a man made version of cortisol

Can also be caused by:
Increased secretion of ACTH
Pituitary tumor
Lung tumor
Adrenal cancer

CT or MRI of the pituitary gland and adrenal glands is usually requested to see if there is an adenoma which is causing an excess production of ACTH and therefore cortisol… That may be the cause of Cushing’s.

48
Q

Signs and symptoms of Cushing’s syndrome?

A

Moon shaped face
Weight gain around the trunk
Buffalo hump
Water retention
Spindly legs (due to muscle wasting)
Red stretch marks on the abdomen
Increase in blood pressure
Increase in blood sugar level

Osteoporosis
Causes Insulin resistance and diabetes Mellitus
Reduce the ability of wound healing
Swollen ankle
Hirsutism
Purple Strias on the abdomen

49
Q

Hypoparathyroidism, what is it?

A

A rare condition where the parathyroid glands produce too little parathyroid hormone

Causing the blood calcium levels fall (hypocalcaemia)
Causing the phosphorus levels to rise (hyperphosphataemia)

Caused by, autoimmune conditions such as Addison’s disease, born without parathyroid glands, radiotherapy and low blood magnesium levels because of alcohol misuse

50
Q

Both glands play a role in regulation of serum calcium level
Thyroid Gland, and parathyroid, where are they located?

A

Thyroid gland
Two lobes in the anterior neck on either side of the trachea below the thyroid cartilage

Parathyroid
2 pairs located behind the thyroid gland and releases PTH hormone

51
Q

What can cause an enlarged thyroid?

A

A number of factors can cause an enlarge gland aka goitre to occur. Among the most common are:

Iodine deficiency – Iodine is essential for the production of thyroid hormones. A goitre can occur when the thyroid enlarges in an effort to obtain more iodine. The initial iodine deficiency may be made even worse by a diet high in hormone-inhibiting foods, such as cabbage, broccoli and cauliflower.

Graves’ disease – Goitre can sometimes occur when your thyroid gland produces too much thyroid hormone (hyperthyroidism). In Graves’ disease, antibodies produced by your immune system mistakenly attack your thyroid gland, causing it to produce excess thyroxine T4. This overstimulation causes the thyroid to swell.

Hashimoto’s disease – Goitre can result from an underactive thyroid (hypothyroidism). Also an autoimmune disorder but instead of causing the thyroid to produce too much hormone, Hashimoto’s damages your thyroid so that it produces too little.
Sensing a low hormone level, your pituitary gland produces more TSH to stimulate the thyroid, which then causes the gland to enlarge.

52
Q

What hormones does the thyroid produce, what does it do, and what is it called when it is enlarged?

A

Thyroid gland produces two main hormones — thyroxine (T4) and triiodothyronine (T3)

Help regulate metabolism – the rate at which your body uses fats and carbohydrates, controls your body temperature, heart rate, and production of proteins. Produces calcitonin — a hormone that helps regulate the amount of calcium in your blood.

Your pituitary gland and hypothalamus control the rate at which these hormones are produced and released.

When it’s enlarged, i.e. goitre, the thyroid may produce normal amounts of hormones. It might also, however, produce too much or too little T4 and T3.

53
Q

Signs and symptoms of Hypoparathyroidism

A

Tingling sensation in fingers, toes and lips
Twitching facial muscles
Muscle pains or cramps in legs, feet or abdomen
Tiredness
Mood changes, irritability

Anxious or depression
Dry, rough skin
Course hair that breaks easily
Weak fingernails

54
Q

What is a goitre?

A

A goitre is an abnormal swelling of the thyroid gland that causes a lump to form in the neck.

55
Q

What is graves’ disease?

A

Graves’ disease is a leading cause of hyperthyroidism. This causes the immune system to send antibodies to thyroid gland. The antibodies stimulate the thyroid gland, causing an increased amount of thyroid hormones to be released.

56
Q

What is Acromegaly?

A

Acromegaly
Hormonal disorder which develops when the pituitary gland produces too much growth hormone during adulthood.

The bones increase in size particularly the hands, feet and facial bones.
Usually diagnosed in adults aged 30 – 50
If develops before puberty it is then known as gigantism

57
Q

Signs and symptoms of acromegaly?

A

Large spade-like fleshy hands in acromegaly compared to normal hands on left

Swollen hands and feet
Tiredness
Difficulty sleeping
Gradual changes in your facial features
Numbness and weakness in your hands
Teenagers will be abnormally tall

Other common symptoms as time goes on:
Skin changes – thick course oily skin
Skin tags or sweating
Deepening of the voice due to enlarged sinuses and vocal cords
Joint pain
Headaches
Blurred or reduced vision

58
Q

Dwarfism
Gigantism
Syndrome of inappropriate antidiuretic hormone (SIAD)
Virilism
Cretinism
Diabetes insipidus

A

make cards about these
what they are
signs and symps
imaging/tests