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Y2 medical pathophysiology > Endocrine and Diabetes > Flashcards

Endocrine and Diabetes Flashcards

1
Q

What are the 5 ways in which cells communicate?

A
  • Neural communication
  • Endocrine communication
  • Paracrine communication
  • Exocrine secretions
  • Autocrine communications
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2
Q

Describe neural communications between cells.

A

Neurotransmitter secreted at a synaptic junction.

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3
Q

Describe endocrine communication between cells.

A

Hormones, secreted into the blood circulation, are carried to target tissues throughout the body.

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4
Q

Describe paracrine communication between cells.

A

Products of secretion enter extracellular fluid to affect neighbouring cells.

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5
Q

Describe exocrine secretions between cells.

A

The products of secretion are released into a body cavity.

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6
Q

Give one example of an exocrine secretion.

A

Saliva into the mouth.

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7
Q

Describe autocrine communication between cells.

A

Cells secrete chemical messengers that in some situations bind to receptors on the original cells.

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8
Q

What discoveries did Arnold A. Berthold make in terms of behavioural endocrinology?

A
  • The testes are transplantable organs.
  • Transplanted tested can function.
  • Nerves are not necessary, but a blood-borne product of the transplanted testes is important.
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9
Q

How do endocrine glands exert control?

A

By releasing chemical hormone into the blood.

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10
Q

Do endocrine glands have ducts?

A

No

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11
Q

What parts of the body do the hormones released by endocrine glands affect?

A

Other endocrine glands or body systems.

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12
Q

What processes do hormones control?

A 
Homeostasis
Reproduction
Growth and development
Metabolism 
Response to stress
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13
Q

Describe how hormones are classified?

A
  • Proteins
  • Polypeptides (amino acid derivatives).
  • Lipids (fatty acid derivatives or steroids).
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14
Q

Describe the different categories of hormones available in the blood

A
  • Constant level hormones
  • Variable level hormones
  • Cyclic level hormones
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15
Q

What are the different classes of hormones?

A
  • Amine hormones
  • Peptide hormones
  • Steroid hormones
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16
Q

What are amine hormones derivatives of ?

A

Derivatives of the amino acid tyrosine.

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17
Q

What is the other possible function of peptide hormones?

A

Used as neurotransmitters.

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18
Q

Where are steroid hormones produced?

A

In the adrenal cortex and gonads.

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19
Q

What are the different ways in which hormones can be transported in the blood?

A
  • Water soluble hormones dissolve in the blood and travel via the plasma.
  • Some hormones circulate in the blood, bound to plasma proteins.
  • Free hormones diffuse across the capillary walls to encounter target cells.
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20
Q

What are the two possible ways that hormones are removed from the blood?

A

They are either excreted by the kidneys or metabolised in the blood or target cells.

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21
Q

Which cells act as targets for someones?

A

Cells that have receptors to bind the hormone.

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22
Q

What can compensate for a low concentration of a hormone and what is this called?

A

An increase in the number of receptors. This is up-regulation.

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23
Q

How does a high concentration of hormones affect receptors and what is this called?

A

The number of receptors for the hormone decreases.

This is down-regulation.

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24
Q

How does the hormone-receptor relationship relate to antagonism?

A

A hormone can reduce the number of receptors available for a second hormone resulting in decreased effectiveness of the second hormone.

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25
Q

How does the hormone-receptoror relationship relate to permissiveness?

A

A hormone can induce an increase in the number of receptors for a second hormone, increasing the latter’s effectiveness.

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26
Q

Where are receptors for the peptide hormones and catecholamines ?

A

Present on the extracellular surface of plasma membranes.

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27
Q

Where are receptors or steroid and thyroid hormones?

A

They are present on the intracellular surface of membranes.

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28
Q

Name some processes and factors that hormone receptor binding can affect.

A
  • Ion channels
  • Enzyme activity in part of a receptor.
  • Activity of kinases.
  • Gene proteins and second messengers
  • Genes could also be activated or inhibited, causing a change in synthesis rate of proteins coded for by these genes.
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29
Q

What types of hormones does the hypothalamus secrete?

A

Hypophyiotropic hormones

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30
Q

What type of hormones does the pituitary secrete?

A

Anterior and posterior pituitary glands.

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31
Q

What type of glands are the hypothalamus and pituitary?

A

Endocrine.

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32
Q

How do secretions from the hypothalamus affect the pituitary?

A

They activate the pituitary to make secretions. The hypothalamus regulates the pituitary.

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33
Q

What is the main purpose of the anterior pituitary?

A

It controls the functions of numerous other endocrine glands.

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34
Q

Where is the anterior pituitary found?

A

In a bone cavity at the base of the skull.

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35
Q

What are the 5 endocrine cell types in the anterior pituitary ?

A 
Gonadotroph
Lactotroph
Somatotroph
Corticotroph
Thyrotroph
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36
Q

Where is the pancreas located?

A

In the retroperitoneal space between the duodenum and spleen

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37
Q

Is the pancreas endocrine or exocrine?

A

Both

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38
Q

What are the exocrine functions of the pancreas?

A

Secrets key digestive enzymes such as amylase and lipase and neutralises the pH of the stomach acid entering the top of the duodenum.

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39
Q

What is the purpose of amylase?

A

Breaks down large sugars.

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40
Q

What is the purpose of lipase?

A

Breaks down fats.

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41
Q

What cells are in the endocrine section of the pancreas?

A

Alpha cells
Beta cells
Delta cells

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42
Q

Describe the purpose of the endocrine cells of the pancreas.

A
  • Alpha cells (glucose production to raise blood glucose levels).
  • Beta cells (insulin production to lower blood glucose levels).
  • Delta cells (somatostatin production to suppress the release of growth hormone).
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43
Q

What are the pancreatic islet hormones?

A

Glucagon
Insulin
Amylin

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44
Q

When is insulin present in the blood?

A

When blood glucose is high.

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45
Q

Describe the functions on insulin.

A
  • Increases glucose uptake in cells.
  • Converts glucose to glycogen by glycogenesis.
  • Increases amino acid uptake and protein synthesis.
  • Promotes lipogenesis.
  • Slows down gluconneogenesis.
  • Causes blood glucose levels to drop.
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46
Q

How does hypoglycemia affect insulin?

A

Inhibits release of insulin.

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47
Q

When is glucagon present in the blood?

A

When blood glucose is low.

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48
Q

What cells does glucagon act on?

A

Acts on hepatocytes.

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49
Q

What are the main functions go glucagon?

A
  • Converts glycogen to glucose by glycogenolysis.

- Forms glucose from lactic acid and amino acids by gluconeogenesis.

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50
Q

How does hyperglycaemia affect glucagon?

A

Inhibits release of glucagon.

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51
Q

What is hypoglycaemia?

A

When blood glucose is too low

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52
Q

What is hyperglycaemia?

A

When blood glucose is too high

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53
Q

In what cells is Amylin stored?

A

Beta cells

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54
Q

Describe the secretion of Amylin.

A

Amylin is co-secreted with insulin when blood glucose is high.

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55
Q

What are the main functions of Amylin?

A
  • Decreases gastric emptying.
  • Supresses glycogen secretion.
  • Supresses glucose production.
  • Promotes satiety.
  • Decreases appetite.
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56
Q

What is satiety?

A

The feeling of fullness

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57
Q

What causes Type 1 (IDDM) diabetes?

A

Pancreas fails to produce insulin due to loss of beta cells. Amylin is also reduced in this scenario.

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58
Q

What causes Type 2 (NIDDM) diabetes?

A

Failure to respond to insulin. Can have lower response to insulin or insufficient insulin produced.

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59
Q

What causes Alzheimers (brief)?

A

Glucose metabolism fails at the CNS level.

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60
Q

What type of diabetes does diabetes of pregnancy resemble?

A

Type 2

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61
Q

What is diabetes of pregnancy?

A

Onset during pregnancy, resolves postpartum.

62
Q

What are the possible transplants used to treat type 1 diabetes?

A
  • Islet cell transplants
  • Partial pancreas transplant
  • Full pancreas transplant
63
Q

What are the positives and negatives of islet cell transplants to solve type 1 diabetes?

A

N- 90% of people require insulin treatment after 5 years.

P -May delay insulin treatment requirement.

64
Q

What are the positives and negatives of partial pancreas transplants to solve type 1 diabetes?

A

P - prevents kidney from damage.

N - Kidneys from relatives are preferred.

65
Q

What are the positives and negatives of full pancreas transplants to solve type 1 diabetes?

A

N - 50% rejected, limited by the effects of immunosuppressive medications.

66
Q

How do the treatments for Type 1 diabetes work?

A

Treatments mimic physiology - insulin dosage is taken when you eat and a basal dose given once per day.

67
Q

Why must insulin be given as an injection to people with Type 1 diabetes?

A

Insulin is a peptide hormone and won’t survive in the stomach.

68
Q

What are the dangers of having too much Amylin in the blood?

A

Cell death caused by amylin fibres.

69
Q

What is parmlintide and what is it used for?

A

An analog of amylin that improves postprandial blood glucose.

70
Q

Why is pramilintide beneficial rather than amylin?

A

It overcomes the tendency of human amylin to;

  • Aggregate and form insoluble particles.
  • Adhere to surfaces
71
Q

What are the positive effects of Parmlintide in the body?

A
  • Reduces HBA1c
  • Reduces insulin requirement
  • Reduces body weight
72
Q

How is Type 2 (NIDDM) diabetes characterised?

A
  • Relentless deterioration of pancreatic beta cell function leading to an initial over production of insulin.
  • Insulin resistance
73
Q

What is step 1 in the treatment of Type 2 (NIDDM) diabetes? And what are the positives and negatives of this treatment

A

Lifestyle changes to decrease weight and increase activity.

P- low cost
N- fails for most in 1st year

74
Q

What is step 1 in the treatment of Type 2 (NIDDM) diabetes?

A

Additional medical therapies

75
Q

What are the sites of action of drugs used for treating type 2 (NIDDM) diabetes and what is the general cause at each of these sites?

A
  • Liver (to change glucose production).
  • Pancreas (to stimulate insulin secretion)
  • Adipose tissue (to alter the glucose uptake).
  • Muscle (to alter glucose uptake)
  • Intestine (to modify glucose absorption)
76
Q

What are the possible issues with monitoring glucose?

A
  • Exercise alters glucose levels.
  • Food intake variable
  • Illness uses glucose
  • Stress uses glucose
  • Alcohol can cause hypoglycaemia
77
Q

What are the microvascular complications associated with diabetes?

A
  • Retinopathy (changes in vision)
  • Nephropathy (changes in kidney function with may lead to renal failure).
  • Neuropathy
78
Q

What are the microvascular complications associated with diabetes?

A

CHD
Cerebrovascular disease
PAD

79
Q

Describe the histological changes seen in people suffering with retinopathy.

A

Potential aneurysms caused by blood vessels bursting and causing tissue damage.

80
Q

How is micro albumin used in terms of nephropathy ?

A

Microalbumin is a measure of albumin in the urine. If this increases, this suggests kidney function isn’t normal.

81
Q

How is hypertension define in terms of systolic and diastolic blood pressure?

A

SBP > 130mmHg

DBP > 80mmHg

82
Q

How is severe hypertension define in terms of systolic and diastolic blood pressure?

A

SBP >140mmHg

DBP > 90mmHg

83
Q

Describe the pharmacotherapy required to treat hypertension and blood pressure in terms of controlling diabetes.

A

ACE inhibitors and angiotensin receptor blockers required.

84
Q

How is dyslipidaemia treated in diabetic patients?

A

Lifestyle modifications are recommended to improve the lipid profile of patients;

  • Reduction of saturated trans fats in the diet
  • Weight loss
  • Increased physical activity
85
Q

In what diabetic patients may statin therapy be used?

A
  • Patients with overt cardiovascular disease.

- Patients older than 40 years without CVD but with one or more risk factors.

86
Q

What are the risk factors for cardiovascular disease (CVD)?

A
  • Dyslipidaemia
  • Hypertension
  • Smoking
  • Positive family history of premature CAD
  • The presence of micro or macroalubimna.
87
Q

What is the main purpose of nephropathy screening?

A

To reduce the risk or slow progression of nephropathy and to optimise glucose and blood pressure control.

88
Q

Describe the Hypothalamus-Pituitary adrenal axis in terms of Cortisol.

A
  • The hypothalamus releases corticotrophin releasing hormone (CRH) - this is passed down via the hypophyseal portal blood supply to the anterior pituitary.
  • ACTH is released and acts on the adrenal glands.
  • Cortisol is produced by the adrenal glands.
  • Cortisol produces a range of metabolic effects which aid the stress response.
  • Cortisol also feedback to the pituitary to stop producing ACTH and to the hypothalamus to stop producing CRH.
89
Q

What type of hormone is ACTH and what gene is it produced from?

A

A peptide hormone produced from the POMC gene

90
Q

What transcription factor regulates the expression of the POMC gene?

91
Q

How is ACTH produced ?

A

Specific PC1 and PC2 enzymes produce ACTH and other peptides by cleaving POMC.

92
Q

What causes Cushing’s disease?

A

Corticotrophinomas cause Cushing’s disease which is caused by excessive glucocorticoid production.

93
Q

What effect does Tpit mutations have?

A

Lead to ACTH deficiency and therefore low glucocorticoids.

94
Q

What are the actions of POMC peptides?

A
  • Produce ACTH
  • Produce alpha-MSH and beta-endorphins
  • Alpha-MSH exerts its effects through various G-protein coupled receptors
  • Beta-endorphins have pain killing actions and act through opioid receptors in the same way as morphine.
95
Q

What controls ACTH?

A

Hypothalamic CRH and adrenal steroids.

96
Q

How does ACTH affect adrenal steroid production ?

A

Increases it

97
Q

What diseases is excess ACTH seen in ?

A

Cushing’s and Addison’s

98
Q

What does deficiency of ACTH cause?

A

Adrenal failure in the pituitary gland

99
Q

What are the different ACTH tests?

A
  • Circadian rhythmn
  • Plasma ACTH
  • Short synacthen test
  • Long synacthen test
  • Dexamethasone suprpression test
100
Q

How does the plasma ACTH test indicate issues and diseases?

A

Levels may be very high if ACTH is being produced ectopically for example if a tumour which has the POMC gene over expressed.

101
Q

What is produced by the cortex of the adrenal glands?

A
  • Glucocorticoids
  • Mineralcorticoids
  • Androgens
102
Q

What is produced by the medulla of the adrenal glands?

A

Catecholamines such as adrenaline.

103
Q

Name the functions of glucocorticoids using the example of Cortisol.

A
  • Increases protein catabolism.
  • Increases hepatic glycogenolysis (breakdown of glycogen stores to release glucose from the liver into the blood supply).
  • Increases hepatic gluconeogenesis ( increases the liver production of glucose from lactate, amino acids and pyruvate).
104
Q

What is the effect of glucocorticoids on ACTH secretion?

A

Inhibits ACTH secretion by a negative feedback mechanism.

105
Q

What is the effect of glucocorticoids on water excretion?

A

Permissive effect which is required for initiation of diuresis in response to water loading.

106
Q

Where is aldosterone produced?

A

The cortex of the adrenal glands.

107
Q

Describe the functions of mineralcorticoids using the example of aldosterone ?

A
  • Increase the reabsorption of sodium from the distal tubes of the kidney.
  • Have separate action promoting the excretion of potassium
  • Alter distribution of sodium and potassium ions across cell membranes throughout the body.
108
Q

What are the 2 classes of adrenal sex steroids.

A

Androgens

Oestrogens

109
Q

What is the purpose of androgens as adrenal sex steroids?

A

Promote formation of secondary sexual hair.

110
Q

What are adrenal steroids produced from?

A

Cholesterol

111
Q

How is Aldosterone controlled by the Renin angiotensin system?

A

Renin is produced by the kidney and acts to convert Angiotensinogen to Angiotensin I. This activates the angiotensin converting enzymes which converts Angiotensin I to Angiotensin II then acts on the adrenal glands to regulate aldosterone production.

112
Q

In general, what is Addison’s disease?

A

Hyperfunction of the adrenal glands

113
Q

Name some causes of Addison’s disease.

A
  • Autoimmune adrenalitis (autoimmune inflammation of the adrenal glands).
  • Tuberculosis
  • Adrenalectomy (removal of the adrenal glands)
  • Secondary tumour deposits
  • Haemochromatosis
  • Histoplasmosis
  • Adrenal Haemorrhage
114
Q

Name some clinical features of Addison’s disease.

A
  • Tiredness
  • General weakness and lethargy
  • Anorexia
  • Nausea and vomitting
  • Weight loss
  • Dizziness and postural hypotension
  • Pigmentation
  • Loss of body hair in women
  • Hypoglycaemia
  • Depression
115
Q

What disease does excess Cortisol lead to?

A

Cushing’s syndrome

116
Q

What disease does excess androgens lead to?

A

Androgenital syndrome

117
Q

What disease does excess aldosterone lead to?

A

Conn’s syndrome

118
Q

What disease does excess Oestrogens lead to ?

A

Feminisation

119
Q

What are the causes of Cushing’s syndrome?

A
  • Corticosteroids or ACTh treatment.
  • Pituitary hyper secretion of ACTH.
  • Adrenal adenoma
  • Adrenal carcinoma
  • Ectopic ACTH secretions by tumours
120
Q

What is adrenal carcinoma?

A

A tumour in the adrenal glands that affects cortisol production.

121
Q

What are the clinical features of Cushing’s syndrome ?

A
  • Truncal obesity
  • Thinning of skin
  • Puple striae
  • Excessive bruising
  • Hirsutism
  • Excess hair
  • Skin pigmentation
  • Hypertension
  • Glucose intolerance
  • Muscle weakness
  • Back pain
  • Psychiatric disturbances
122
Q

Describe normal cortisol production.

A

Production of cortisol by adrenal cortex stimulated by ACTH.

Cortisol exert negative feedback on the release of ACTH.

123
Q

Describe Cortisol production in Cushing’s disease.

A
  • Increased ACTH secretion.
  • Pituitary insensitive to feedback by normal levels to Cortisol.
  • Higher levels of Cortisol required to produce negative feedback o ACTH secretions.
124
Q

Describe cortisol production when adrenal tumours are present.

A
  • Autonomous cortisol production.

- High circulating levels of cortisol inhibits ACTH secretion.

125
Q

Describe cortisol production when there is Ectopic ACTH secretion.

A
  • High levels of ACTH secreted by tumours stimulate excessive production
  • Secretion of ACTH by pituitary inhibited
126
Q

What are the possible tests for adrenal hyper function ?

A

Screening tests:

  • 24 hour urinary free cortisol excretion.
  • Overnight/ 48 hours low dose dexamethasone suppression test.
  • Insulin tolerance test.
127
Q

What is adrenogenital syndrome?

A

Inherited defects in the enzymes necessary for cortisol production.

128
Q

What factors lead to suspicions of adrenogenital syndrome ?

A
  • Ambiguois genitalia in female neonate.
  • Salt-losin crisis in neonate.
  • Family history of CAH
  • Hypertension in a neonate or infant
  • Precocious puberty in boys
  • Early appearance of pubic hair in girls.
  • Secondar amenorrhoae virilizzato in adult women.
129
Q

What are the causes of Conn’s syndrome?

A
  • Adrenal adenoma
  • Bilateral hypertrophy of zone glomerulosa cells.
  • Adrenal carcinoma
130
Q

What are the clinical features of Conn’s syndrome?

A
  • Hypertension
  • Muscle weakness and occasional paralysis
  • Latent tetany and paraesthesiae
  • Polydipsia and polyuria
131
Q

What are the common causes of secondary hyperaldosteronism ?

A
  • Congestive cardiac failure
  • Cirrhosis of liver with ascites
  • Nephrotic syndrome
  • Renal artery stenosis
  • Sodium losing nephritis
  • Batter’s syndrome
  • Renin-secreting tumours
132
Q

Where is the thyroid located?

A

Just below the Larynx in the neck.

133
Q

What does the Thyroid produce? and what is the purpose of this?

A

T4 (Thyroxine) and T3 (Triiodothyronine) which stimulate metabolism of all our cells.

Calcitonin which decreases blood calcium concentration by inhibiting breakdown of bone.

134
Q

Where is glycoprotein hormone produced?

A

Hypotrophy cells

135
Q

What is TSH secreted in response to and what is it’s main purpose.

A

TRH stimulation and acts at the Thyroid gland to regulate production of T4/T3.

136
Q

What is TSH-R and what is its purpose?

A

A G protein couple receptor, activating the cAMP pathway to increase T4/T3 production which in turn regulates growth and metabolism.

137
Q

What regulates TSH production?

A

T4/T3 negative feedback inhibition at TRH neurones and at Thyrotroph at the level of the pituitary.

138
Q

What are the signs and symptoms of disorders of the thyroid gland?

A
  • Weight gain
  • Moon face
  • Fat accumulation on the upper back
  • Skin changes and delayed healing of wounds
  • Mood swings
  • Impaired memory or concentration
139
Q

What is hypothyroidism?

A

underachieve thyroid gland

140
Q

What is hyperthyroidism?

A

Overactive thyroid gland

141
Q

What is associated with an increase in the size of the thyroid and why?

A

The thyroid goitre is associated with an increase in the size of the thyroid. This would be expected to be seen in hyperthyroidism when there is excessive thyroid production.

142
Q

What is a Goiter?

A

A swollen thyroid gland

143
Q

How is a goitre treated?

A

Radioactive iodine is used and will enter the thyroid and kill off the thyroid which produces too much hormone.

144
Q

How is goitre treated for patients who can’t undergo radiotherapy and how do each of these work?

A

Propythiouracil - blocks thyroid hormone synthesis.

Propranolol - blocks hormone effects and inhibits the conversion of T3 to T4

145
Q

What usually causes Thyroiditis?

A

A viral infection

146
Q

What generally indicates thyroids?

A

Tender thyroid with fever and malaise

147
Q

How is thyroiditis managed?

A

If mild it can be managed with beta blockers but it usually managed based on specific symptoms.

148
Q

What is Hasimoto Thyroiditis?

A

Inflammation of the thyroid which triggers symptoms and can produce a goitre. The inflammation could also reduce the thyroid function for a period of time

149
Q

How is hypothyroidism treated?

A

25-50mcg daily of synthetic thyroxine.

150
Q

What are the symptoms of hypothyroidism?

A
  • Patients can be asymptomatic
  • Weakness, fatigue, lethargy, decreased energy
  • Cold intolerance
  • Dry skin, decreased sweating, hair loss
  • Constipation
  • Inability to concentrate, memory loss
  • Weight gain
    o Food is not being metabolised for energy so is stored
  • Dyspnea
  • Peripheral paresthesias
  • Depression
  • Anorexia – become this way due to weight gain
  • Muscle cramps, musculoskeletal pain
  • Infertility
  • Impaired glucose tolerance
    o Glucose levels will rise given that the glucose will not be metabolised
  • Decreased hearing
  • Carpal tunnel syndrome

Y2 medical pathophysiology (12 decks)

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