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Clinical Diagnosis > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the Endocrine system?

A

The endocrine system produces hormones which act as chemical messengers passing into the bloodstream to their target tissues

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2
Q

What can the endocrine system be divided into?

A

The Endocrine Organs:
These produce hormones
Eg. Pituitary, adrenal, thyroid & parathyroid

The Endocrine Components within other organs that also have another function
E.g. Pancreas, Ovary, Testis

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3
Q

What is The Diffuse Endocrine System?

A

Scattered cells within organs or tissues (often these are called paracrine rather then endocrine)
E.g. endocrine cells in the gut and bronchial mucosa

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4
Q

the most important diseases of all endocrine glands are associated with an: ??

A

over or under production of hormones

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5
Q

What the components of The pituitary gland?

A

The Adenohypophysis
(aka Anterior Pituitary)

&
The Neurohypophysis
(aka Posterior Pituitary)

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6
Q

What does The Adenohypophysis
(aka anterior pituitary) do?

A

which secretes & synthesises a number of hormones
most of which then act on other endocrine glands

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7
Q

What hormones are released from anterior pituitary gland?

A

Andrenocorticotropic Hormone (ACTH)
Thyroid stimulating hormone

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8
Q

What is Andrenocorticotropic Hormone (ACTH)?

A

Controlled by 3 communicating centres in the body:
The Hypothalamus, The Pituitary Gland, The Adrenal Glands.
Aka the Hypothalamic- Pituitary- Adrenal (HPA) Axis

When cortisone levels in the blood are low, the hypothalamus releases corticotrophin – releasing hormone (CRH)
stimulates the anterior pituitary to secrete ACTH
High levels of ACTH detected by the adrenal gland receptors which release cortisol
Increasing levels of cortisol inhibits release of CRH from the hypothalamus & ACTH from the pituitary gland.

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9
Q

How is Thyroid stimulating hormone released from anterior pituitary gland?

A

Hypothalamus  releases TRH
stimulates anterior pituitary to release TSH
Triggers thyroid to produce T4 & T3 (alongside a need for iodine to produce T3 & T4)
Once levels increase, negative feedback loop to inhibits release of TRH

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10
Q

What is The Neurohypophysis (the posterior pituitary) ?

A

Is in direct continuity with the hypothalamus
It stores & secretes ADH (anti – diuretic hormone)
Stores Oxytocin which is synthesised in the neurones of the hypothalamus.

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11
Q

Most diseases of the pituitary gland are associated with anterior or posterior?

A

Anterior

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12
Q

What is The most important disease of the pituitary gland are tumours of the adenohypophysis also known as?

A

Pituitary Adenomata

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13
Q

What is Pituitary Adenomata?

A

Benign tumours, but can be life threatening due:
Their position
Their ability to secrete excess hormone.

There are 2 types:

Non- Functioning Adenomata:
Progressively enlarge until they break out of the sella turcica in an upward direction
This produces bitemporal hemianopia

Non- Functioning Adenomas

Progressively enlarging to compress to optic chiasm.

Functioning Adenomata:
In theory can produce any adenohypophyseal hormones
but, the majority produce either prolactin or growth hormone, and a few produce ACTH.

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14
Q

What are the clinical features - Functioning Pituitary Adenomata Presentations: Prolactin Producing?

A

Menstrual Disturbances & infertility in women

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15
Q

What are the clinical features - Functioning Pituitary Adenomata Presentations: Growth Hormone Producing?

A

Before puberty> Giantism
After puberty > Acromegaly

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16
Q

What are the clinical features - Functioning Pituitary Adenomata Presentations: ACTH- Producing?

A

Adrenal Cortical Hyperplasia (Cushing’s Disease)

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17
Q

Reduced output from the pituitary gland is rare due to?

A

surgical removal of the pituitary gland

Metastatic tumour which has obliterated the normal pituitary gland

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18
Q

What is disease of the Neurohypophysis?

A

Most failures of ADH and oxytocin prediction are due to the result of damage to the hypothalamus
usually tumour or infarction

Failure of ADH production causes Diabetes Insipidus
Lack of ADH prevents resorption of water in the renal collecting ducts.
Large quantities of very dilute urine are excreted (polyuria)
Therefore person feels thirsty

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19
Q

What are the 2 cell types of the thyroid gland?

A

Pure endocrine gland composed of 2 cell types:
Thyroid Follicle Cells  produce Thyroxine (T4) & Tri-iodthyronine (T3)
T3 & T4 involved in:
metabolic processes, almost always by increasing their activity and therefore increasing basal metabolic rate.

The parafollicular cells or “C” cells  produce calcitonin
Calcitonin involved in :
calcium homeostasis, inhibition of osteoclastic bone reabsorption.

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20
Q

What is a goitre?

A

The term “goitre” is used to describe any swelling of the thyroid gland

Thyroid enlargement can have many causes
it can be associated with both a decreased and increased thyroid hormone output.

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21
Q

What is the difference between hypo and hyperthyroidism?

A

Excessive Secretion of thyroid hormones (TH) > Hyperthyroidism

Reduced Secretion of thyroid hormones (TH) > Hypothyroidism

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22
Q

What is Hyperthyroidism?

A

Excessive secretion of TH
Clinical Presentation is related to an increased metabolic rate

Clinical Features of Hyperthyroidism:
Feeling Hot
Increased Sweating
Weight loss – loss of subcutaneous fat
Proximal Muscle Weakness
Rapid heart Rate, palpitation
Atrial Fibrillation
Diarrhoea
Anxiety and Restless Hyperactivity
Goitre

23
Q

What are the common causes of hyperthyroidism?

A

Autoimmune  known as Grave’s Disease
Thyroiditis  due to viral infection
Post Pregnancy
Taking too much thyroid hormone to treat hypothyroidism.

24
Q

What is graves disease?

A

is an autoimmune form of hyperthyroidism
Associated with a specific clinical presentation:

Clinical Presentation:
Exophthalmos
protuberant, staring eyes due to expansion of retro- orbital soft tissue due to expansion of adipose tissue.
Goitre & other findings associated with hyperthyroidism

25
Q

What is hypothyroidism?

A

In infants, hypothyroidism produces the clinical syndrome known as cretinism or congenital hypothyroidism, which presents as:
Puffy face
Enlarged tongue
coarse features
Protuberant abdomen
Delayed physical & mental milestones

It is usually due to untreated maternal hypothyroidism
rarely seen any more in the developed world
It is still a problem in parts of the world due to dietary iodine deficiency

In Adults, hypothyroidism, when manifests as a syndrome called myxedema which is due to a reduced metabolic rate.

Symptoms include:
Progressive slowing of physical & mental activity
increasing lethargy
Sensitivity to cold
Puffy face
Coarse dry skin
thinning of the hair (particularly the lateral eyebrows)
Hoarseness and deepening of the voice
Increased predisposition to hyperlipidaemia

26
Q

Most common causes of Hypothyroidism include?

A

Autoimmune
called Hashimoto’s Disease

Secondary
due to total or partial removal of the thyroid gland due to either cancer or an aggressive form of Grave’s disease.
Or due to certain types of drug therapy.

27
Q

What is hashimoto’s disease?

A

Most common in middle ages women
Autoimmune destruction of thyroid
Antibodies produced against thyroglobulin

Clinical Presentation
Same as for any form of hypothyroidism
Goitre
Patients likely to have other autoimmune diseases such as vitiligo or SLE.

28
Q

What is thyroid malignancy?

A

3 main types:
Papillary carcinoma
usually in young adults
is slow growing and usually has good prognosis

Follicular Carcinoma
middle aged people
commonly metastasises via the bloodstream to the bone.
Diagnosis is usually made following a spontaneous fracture.

Anaplastic Carcinoma
Rapidly, aggressive tumour. Poor prognosis.
Can cause tracheal compression.

29
Q

What are parathyroids?

A

Small endocrine glands whose sole function is to secrete parathormone (PTH)

30
Q

What is Parathyorome (PTH)?

A

Important in calcium balance, acting at two sites:

The bone surface
where is stimulates the resorption of mineralised bone by osteoclasts with the release of calcium into the blood stream.

2) The renal tubules
Stimulates reabsorption of calcium ions from urine.

Generally,

increased PTH secretion increases serum calcium levels
Reduced PTH secretion, reduces serum calcium levels.

Inappropriate secretion leads to either:
pathological increase  Hypercalcemia
pathological decrease  Hypocalcemia

31
Q

What is Hyperparathyroidism?

A

PTH stimulates osteoclastic reabsorption of bone, and causes increase released of calcium from bone into the blood plasma  Hypercalcemia.
Normally regulated by a feedback mechanism

Two types of hyperparathyroidism
Primary Hyperparathyroidism
usually due to a parathyroid adenoma which secretes excess PTH  leads to increased osteoclastic activity.
2. Secondary Hyperparathyroidism
Persistently low serum calcium levels seen in chronic renal disease causes continuous stimulation of the parathyroids.

32
Q

What are the clinical presentations of Hyperparathyroidism?

A

Nausea & Vomiting
Drowsiness, chronic fatigue.
Dehydration
Confusion and / or Depression
Muscle Spasms
Bone pain / tenderness
Joint Pain
Irregular heart beat
Fractures

33
Q

What are the adrenal glands?

A

The adrenal glands have 2 distinct endocrine components:

The Cortex
Synthesizes, stores and secretes 3 main types of hormones (steroid hormones synthesized from cholesterol):
Glucocorticoid, Mineralocorticoid (aldosterone) and sex hormones- Androgens & oestrogen

The Medulla
Part of the sympathetic nervous system (derived embryologically from the neural crest)
Synthesizes Adrenaline & Noradrenaline (aka epinephrine & norepinephrine)

34
Q

What is secreted at the adrenal cortex?

A

Glucocorticoid & Sex Hormone Secretion
is under the control of ACTH, which is secreted by the pituitary gland.
therefore excessive secretion of these hormones may be secondary to an ACTH – secreting adenoma of the pituitary.

Aldosterone secretion
is controlled by renin production by the juxtaglomerular apparatus in the kidney
(refer back to previous lectures on cardiovascular system / hypertension / renal)

35
Q

What is cushing’s disease?

A

A condition caused by uncontrolled, excessive production of adrenal cortical hormones.
In particular, Cortisol (glucocorticoid)

Cause:
Excessive therapeutic administration of corticosteroids
most common cause
Pituitary Adenoma
Adrenal Adenoma

36
Q

What are the clinical presentations of cushing’s disease?

A

Moon Face
Acne
Hirsutism
Severe Osteoporosis - high risk of vertebral compression fractures
Skin Fragility
Poor Wound healing
Trunk obesity with stria
Peptic ulcers
Hypertension & Diabetes
Hypokalaemia & psychiatric disturbances

37
Q

What is addisons disease?

A

Caused by chronic adrenal cortical insufficiency due to lack of glucocorticoids & mineralocorticoids

Caused by:
Destruction of the adrenal cortex by autoimmune disease
usually autoimmune thyroiditis, autoimmune gastritis or any other endocrine autoimmune disease.

Clinical Presentation
Chronic Dehydration & loss of appetite.
Brownish pigmentation of skin & buccal mucosa
Lethargy & weakness

38
Q

What is Addisonian Crisis?

A

Occurs if prolonged high dose therapeutic corticosteroid therapy is abruptly stopped.
Prolonged corticosteroid therapy leads to suppression of normal endogenous steroid production by the adrenal cortex

Addisonian crisis presents as:
Hypotensive shock
Hypoglycaemia
risk of sudden death

39
Q

The Islets of Langerhans are the endocrine cells which secrete?

A

Insulin, Glucagon & Somatostatin

40
Q

What is insulin?

A

Secreted by the B- cells
Permits transfer of blood glucose into cells
Stimulates synthesis of glycogen in the liver and skeletal cells
Lowers blood sugar levels ( in the absence of insulin, blood glucose levels rise and cells become depleted of glucose).

41
Q

What does glucagon do?

A

Opposes the function of insulin

42
Q

What does Somastostatin do?

A

has many functions & found widely throughout the body
In the pancreas  inhibits release of insulin & glucagon from the Islets.
in other organs, has other functions.

43
Q

What is Pancreatic Polypeptide & Amylin ?

A

function is unknown

44
Q

What is diabetes mellitus?

A

The most common and important disease associated with the endocrine pancreas.
It is a chronic disease of carbohydrate, fat and protein metabolism resulting from an inadequate action of the hormone INSULIN .
It is a multisystem disease.

45
Q

What is the Normal Regulation of Blood Glucose?

A

Cells in our body use glucose as a source of immediate energy.
If we exercise, we require a higher concentration because muscles require glucose for energy.
Glucose is a preferred source of energy as it provides both energy and water through the Krebs Cycle and aerobic metabolism.
Your body can use protein & fat, but their breakdown creates ketoacidosis which is not its optimal state. Excess of ketoacids produces metabolic acidosis.

Functioning body tissues continuously absorb glucose from the blood stream.
People without diabetes are able to eat a meal of carbohydrates and can replenish circulating blood glucose in approximately 10 minutes after eating.
As BG levels rise, pancreas activates insulin- sensitive cells to produce insulin.
Glucose enters in the liver activated enzymes which convert glucose to glycogen
 glycogen is stored in muscle, liver & fat.
When BG levels drop after a meal has been digested, insulin secretion stops and glycogen synthesis stops.
When there is a requirement for energy, the liver breaks down stored glycogen & converts it back into glucose

If we eat beyond what our energy requirements are, we continue to have elevated blood glucose levels and excess glycogen continues to be stored.

Sedentary, overweight or obese people will accumulate triglycerides in their muscle cells. This causes the cells to use fat rather than glucose to produce muscular energy

Blood glucose levels are normally being monitored continuously and normally throughout every minute of the day.

A delicate balance between the pancreas, intestine, brain and adrenals is vital to maintain normal BG levels.

Too little  Hypoglycaemia (not enough energy for cells)
Too much  Hyperglycaemia (too much, can have a paralyzing effect on cells)

46
Q

What are the different types of diabetes?

A

There are 2 main forms:
Type 1 Diabetes
aka Insulin Dependant Diabetes Mellitus or Juvenile Onset Diabetes.

Type 2 Diabetes
aka Non – Insulin Dependant Diabetes.

But there are also 2 further classifications:
Type 3 Diabetes (very rare!)
specific type of diabetes causes by rare genetic defects to the Islets.

Type 4
Gestational Diabetes

47
Q

What is type 1 - insulin dependant diabetes?

A

Usually presents in childhood or adolescence.
Autoimmune
Majority of patients have circulating antibodies to the endocrine cells of the Islets which produce insulin.
There is lymphocytic infiltration and destruction of the insulin producing cells of the Islets.
This destruction leads to insulin deficiency
which in turn leads to hyperglycaemia and other secondary metabolic complications.

48
Q

What is Type 2 Diabetes (Non Insulin Dependant)?

A

1 in 10 people over the age of 40 have Diabetes in the UK (approx. 4.9million people)
with an estimated 13.6 million being at risk or pre-diabetic in the UK.
It is the leading cause of preventable sight loss.
Type 2 Diabetes leads to almost 9600 leg, toe or foot amputations every year (that’s 185 a week).
Over 700 people with diabetes die prematurely every week.
1 in 6 people in the UK hospitals, have diabetes.
10% of total NHS funding is spent on type 2 diabetes

More common than type 1
Unlike Type 1 where there is an absolute absence of insulin, in Type 2 the insulin blood levels are initially normal, and may even initially rise in the early stages.
eventually insulin levels fall below normal.
this is due to INSULIN RESISTANCE

49
Q

What are risk factors for type 2 diabetes?

A

Obesity, Low levels of physical activity, unhealthy diet, genetics

50
Q

What is the link between insulin resistance and type 2 diabetes?

A

Appears to be mediated by abdominal obesity
Studies have shown a strong link between excess upper body fat and Type 2 Diabetes.
Combination of excess risk factors associated with increased abdominal fat which lead to continuous increased inflammation in the body, and abdominal fat causing further increased inflammation in the body.
Abdominal fat also has an effect on mediation of hormones.
Prolonged Inflammation plays a key role in insulin resistance and the
Exact pathogenesis is unclear.

51
Q

What are complications of Diabetes Mellitus?

A

Significantly increased mortality risk due to the complications of diabetes mellitus.

Complications of DM include:
Increased risk of infections
Increased severity of atherosclerosis & its complications
Extensive small vessel disease (arteriosclerosis)
Renal Glomerular Disease
Retinal Vascular Disease
Peripheral Nerve Damage

As a result of these complication, diabetes has a predisposition to develop:

Ischemic Heart Disease
Cerebrovascular Disease
Peripheral Gangrene of lower limbs
Chronic Renal Disease
Reduced Visual Acuity due to Diabetic Retinopathy – leading to blindness
Peripheral Neuropath

52
Q

True or false? Peripheral Neuropathy is an important cause of diabetic ulcers

A

True

53
Q

What causes ulcers?

A

Most commonly presents as a glove & stocking distribution
Leads to loss of sensation, including the loss of pain sensation
normal pain withdrawal reflex is lost
Therefore areas of skin become repeatedly damaged from friction e.g. ill fitting footwear.
This can lead to formation of an ulcer.

Clinical Diagnosis (22 decks)

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