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Year 2 > Endocrine Week 1 > Flashcards

Endocrine Week 1 Flashcards

1
Q

What are the 5 main classes of drugs used to treat T2DM?

A 
Biguanides
Sulphonylureas
Thiazoladinediones
Incretins (GLP1 agonists and DPP4 inhibitors)
SGLT2 inhibitors
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2
Q

How do biguanides work and give an example?

A

Metformin
They increase the sensitivity of body cells to insulin, they inhibit glycerophosphatase in the liver and decrease gluconeogenesis (production of glucose from lactate and other sources).

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3
Q

What is the difference between an endocrine and exocrine gland?

A

Endocrine - secrete hormone directly into the blood

Exocrine - secrete hormone via duct

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4
Q

What are the three main hormone groups?

A

Amine, peptide and steroid

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5
Q

How are steroid hormones produced and give an example?

A

Derived from cholesterol e.g. mineralocorticoids, glucocorticoids, progesterone

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6
Q

How are amine hormones produced and give an example?

A

Derived from a single amino acid e.g. adrenaline, noradrenaline and dopamine

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7
Q

How are peptide hormones produced and give an example?

A

Derived from multiple amino acids (3-200) e.g. insulin, leptin

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8
Q

How do peptide hormones act?

A

G-protein coupled receptors/tyrosine kinase receptors, go on to activate secondary messengers

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9
Q

How do steroid hormones act?

A

Intracellular receptors, bind to DNA affecting gene transcription

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10
Q

What are the differences between the endocrine and exocrine pancreas?

A

Endocrine: Islets of Langerhans

  • alpha cells: glucagon
  • beta cells: insulin
  • delta cells: somatostatin
  • PP cells: pancreatic polypeptide

Exocrine: Acini cells - produce digestive enzymes e.g. lipases, proteases, amylase and bicarbonate

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11
Q

What is the embryological origin of the pancreas?

A

Endoderm, 2 buds extend from the primitive duodenum at the junction of foregut and midgut and fuse.

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12
Q

How does immunohistochemistry work?

A

A solution of antibodies is used where the antibodies are tagged with a marker, and the antibodies bind to specific antigens (proteins) in a tissue proving that there are cells present that produce those proteins.

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13
Q

What does paracrine mean?

A

A cell which secretes chemical messengers which act nearby.

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14
Q

What does autocrine mean?

A

A cells which secretes chemical messengers that act upon the same cell.

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15
Q

What are the different embryological origins of the parts of the adrenal glands?

A

Cortex: from mesoderm - the urogenital ridge
Medulla: from ectoderm - neural crest cells

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16
Q

What are the three layers of the adrenal cortex (outer to inner)?

A

Zona glomerulosa
Zona fasiculata
Zona reticularis

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17
Q

What does the zona glomerulosa produce?

A

Aldosterone

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18
Q

What does the zona fasiculata produce?

A

Glucocorticoids and androgens

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19
Q

What does the zona reticularis produce?

A

Glucocorticoids and androgens

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20
Q

What does the adrenal medulla produce?

A

Catecholamines: adrenaline and noradrenaline (is thought of as part of the sympathetic NS)

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21
Q

What is pheochromocytoma?

A

Rare tumour of the adrenal medulla, XS catecholamine production

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22
Q

How does being overweight increase your risk of developing T2DM?

A

Adipose tissue releases various cytokines called adipokines: leptin, adiponectin and resistin.

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23
Q

What is the function of the adipokine lectin?

A

Tells hypothalamus about stored levels of fat

24
Q

What is the function of the adipokine resistin?

A

Lowers the levels of FFA’s

25
Q

What is the function of the adipokine adiponectin?

A

Enhances hypothalamic stimulation of glucose production -> leading to hyperglylcaemia

26
Q

What diseases can lead to the development of secondary diabetes?

A

Cystic fibrosis
Hereditary haemochromatsis
Chronic pancreatitis

  • these all affect who the pancreas functions and disrupt normal endocrine function and insulin production.
27
Q

What is the pathogenesis of diabetic retinopathy?

A

Early stages: non-proliferative

  • hyperglycaemia damages small vessel walls causing microaneurysms
  • more bleeding from vessels causes dot haemorrhages
  • microinfarcts cause cotton wool spots
  • protein leaks out forming hard exudates

Later stages:

  • damage to veins and vessels blocks blood supply = ischaemia
  • VEGF released causing angiogenesis
  • can cause vitreous haemorrhage
  • can cause macular oedema
28
Q

What is the pathogenesis of diabetic nephropathy?

A
  • renal enlargement and hyperfiltration
  • GFR increases
  • afferent arteriole vasodilates increasing glomerular pressure
  • GBM thickens
  • capillary damage occurs due to increased pressure and sheer stress on vessel walls
  • microalbuminuria
  • macroalbuminuria
  • end stage renal failure
29
Q

What is the pathogenesis of diabetic neuropathy?

A
  • Damage that occurs to small blood vessels in the body causes reduced blood supply to neural tissue and nerves and impaired nerve signalling
  • High glucose impairs ability of nerves to send signals
  • Mainly affects the PNS causing numbness and paralysis/loss of sensation of limbs
  • Can also affect the ANS in various ways:
    1. CVS: postural hypotension
    2. Genitourinary issues: erectile dysfunction
    3. GI: gustatory sweating, gastroparesis
    4. Diabetic amyotrophy: nerve disorder causing muscle wasting
30
Q

Describe the polyol metabolism pathway that is active in diabetes and is involved in the breakdown of glucose:

A
  • Most cells in the body need insulin for glucose uptake, but retina kidneys and nervous tissue are insulin independant
  • They will take up any glucose available and any XS will enter this polyol pathway
  • Glucose normally broken down by hexokinase
  • If there is XS glucose it is broken down by polyol pathway
  • Polyol pathway breaks down glucose into sorbitol using the enzyme ALDOSE REDUCTASE
  • Use of polyol pathway reduces availability of NADPH and NAD which are needed for important metabolic reactions in the body
  • XS polyol pathway action -> XS sorbitol -> lack of NADPH/NAD -> reactive oxygen species build -> cellular damage
  • The sorbitol produced glycates nitrogens on proteins like collagen forming advanced glycation end products (AGE’s) which cause inflammation and further small vessel damage
31
Q

How does haemotoxylin and eosin staining work?

A 
Haemotoxylin = basic dye that stains acidic structures blue e.g. nuclei, ribosomes
Eosin = acidic dye that stains basic structures red/pink e.g. cytoplasmic proteins
32
Q

How does sudan black staining work?

A

Stain lipid containing structures a brown/black colour e.g. like myeline
- Zona fasiculata cells stained brown/black as they have a high cholesterol and lipid content

33
Q

What is a carcinoma?

A

Malignant epithelial cell tumour

34
Q

What is a sarcoma?

A

Malignant tumour of connective (non-epithelial) tissue

35
Q

What is a melanoma?

A

Malignant skin cancer

36
Q

What are the hormones produced by each of the 4 cell types in the pancreas and what are the cell proportions?

A 
Alpha cells (70%) make glucagon
Beta cells (15%) make insulin
Delta cells (~10%) make somatostatin
PP cells (~10%) make pancreatic polypeptide
37
Q

What is the function of somatostatin produced by delta cells?

A

Inhibits insulin and glucagon secretion

38
Q

What is the function of pancreatic polypeptide produced by PP cells?

A

Inhibits pancreatic exocrine secretions and gallbladder contraction

39
Q

What is the process by which insulin is secreted?

A
  • Insulin is synthesised in the endoplasmic reticulum and packaged into secretory vesicles in the golgi apparatus
  • Plasma glucose levels are the initiating signal for release
  • The ATP:ADP ratio in the cell increases as [glucose] increases
  • ATP sensitive K channels close on the membrane of beta cells
  • This causes the cell to depolarise
    -Voltage gated Ca channels open and there is an influx of Ca triggering insulin secretion
  • The secretion is biphasic
    = first 10 mins the preformed insulin is secreted
    = next 2 hours newly synthesised insulin is secreted
40
Q

What is the relationship between oral glucose and insulin?

A

Endogenous insulin release is better in response to oral glucose rather than IV glucose, as GI hormones like CCK and vasoactive intestinal peptide (VIP) enhance the insulin release and ‘prepare/warn’ the beta cells about the glucose that has just been consumed.

41
Q

How does insulin signal to cells to uptake glucose?

A
  • Binds to tyrosine kinase receptor which autophosphorylates
  • The TK receptor has docking sites which other proteins can bind to and become phosphorylated
  • Various other proteins are phosphorylated and a chain of secondary messengers (PDK-1) result in the activation of protein kinase B (Akt)
  • PK-B causes translocation of GLUT4 receptors for the uptake of glucose
42
Q

What are the metabolic effects of insulin on the organs of the body?

A

LIVER: stimulates glycolysis, glycogen synthesis, lipogenesis, VLDL formation and secretion

ADIPOSE: stimulates triglyceride synthesis

MUSCLE: stimulates glycogen synthesis

PERIPHERAL TISSUE: activates LDL to convert VLDL -> glycerol + FA and increases cellular uptake of amino acids to stimulate protein synthesis

43
Q

What is the aetiology of T2DM?

A
  • progressive condition
  • insulin resistance and may be impaired secretion
  • ENVIRONMENTAL FACTORS: your age, physical inactivity, being overweight (BMI 25-30) or obese (BMI 30+) increase your chances of development
  • GENETIC FACTORS: at least 40% people have one affected parent
44
Q

What is the pathophysiology of T2DM?

A
  • Target cells become resistant and hyporesponsive to insulin
  • Various theories about adipose tissue and its effects:
  • IN OBESITY THE FATTY TISSUE INCREASES INSULIN RESISTANCE
  • BETA CELLS COMPENSATE FOR INSULIN RESISTANCE BY PRODUCING MORE INSULIN
  • EVENTUALLY CELLS TIRE OUT AND BETA CELL FUNCTION DECLINES AND BLOOD GLUCOSE RISES
  • > XS adipose reduced the sensitivity of insulin-responsive glucose transporters
  • > large amounts of FFA compete with glucose as an energy source so cells don’t want to use glucose
  • > adipose releases adipokines that reduce the sensitivity of insulin receptors
  • physical inactivity causes down-regulation of insulin-sensitive kinases
45
Q

What are normal fasting and fed blood glucose levels?

A

Normally tightly regulated between 4-5mM fasting, and 8-12mM fed

46
Q

What is pre-diabetes and what is its diagnostic markers?

A

Condition of impaired glucose tolerance that is a marker that diabetes is developing.
Fasting = 5.6-6.9mM, HbA1C = 39-48mmol/l

47
Q

What are the diagnostic levels of blood glucose and HbA1C for diabetes?

A

Fasting blood glucose = >6.9mM

HbA1C = 48mmol/l +

48
Q

What are symptoms of T2DM?

A
  • dry mouth
  • Thirst
  • polynocturia
  • polyuria (Toilet)
  • Tired
  • weight loss (Thin)
49
Q

What are the complications of T2DM?

A

Microvascular complications can occur (retinopathy, nephropathy and neuropathy) although are more commonly associated with T1DM.

Macrovascular complications: atherosclerosis, 2x greater risk of stroke and 3x greater risk of MI.

50
Q

What is the pathophysiology of the atherosclerosis that can cause macrovascular complications in T2DM?

A
  • endothelial damage
  • inflammation and damaged endothelium releases ICAM
  • endothelial wall becomes permeable to LDL’s which accumulate
  • ICAM attracts monocytes
  • Monocytes invade and become macrophages
  • Macrophages release PDGF causing smooth muscle migration from media to intima
  • Macrophages engulf LDL’s forming foam cells
  • Plaque formation
51
Q

How is T2DM tested for?

A
  • Urine testing using dipstick for glucose, ketones and protein
  • Blood testing for glucose, ketones and haemoglobin
52
Q

What is HbA1C and why is it a good marker in T2DM?

A

Hb joins with glucose in the blood forming glycated Hb (HbA1C).
The higher your HbA1C the greater your risk of developing diabetic complications.
As RBC’s have a lifespan of ~120 days HbA1C can be used as an indicator of blood glucose control over a long time period.

53
Q

What is the management and drug plan for someone with T2DM?

A
  1. Set glycaemic target
  2. Establish and maintain lifestyle adjustments (smoking cessation, weight loss, low fat diet)
  3. Lipid control and anti-platelet therapy
  4. Metformin/sulphonylurea
  5. Add one of sulphonylurea, thiazolidinedione or DPP4-inhibitor
  6. Add/substitute oral thiazolidinedione or DPP4 inhibitor
  7. Add/substitute injectable insulin/GLP1 agonist
54
Q

How do sulphonylureas work and give an example?

A

Gliclazide
Increase insulin release by binding to K-ATP channels and keeping them closed, therefore constant Ca influx and insulin release.

55
Q

How do thiazolidinediones work and give an example?

A

Pioglitazone
Are PPAR-gamma agonists and increase transcription of insulin sensitive genes, increase the sensitivity of body cells to insulin.

56
Q

How do SGLT2 inhibitors work and give an example?

A

Dapagliflozin

Inhibit glucose reabsorption so more is lost in the urine.

57
Q

How do incretins work and give an example?

A

a) GLP1 agonists - exanatide -> cause greater insulin release in response to oral glucose (increase the sensitivity of cells in the body to insulin)
b) DPP4 inhibitors - linagliptin -> prevent GLP1 breakdown by DPP4 and increase insulin release

Year 2 (22 decks)

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