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Pharmacology > Endocrine System > Flashcards

Endocrine System Flashcards

1
Q

What is the role of glucose in muscle tissue?

A

Cellular respiration, producing ATP + energy. Increases glycolysis to produce energy

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2
Q

What is the role of glucose in fat (adipose) tissue?

A

Production of glycerol, which is used in the production of fatty acids

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3
Q

What is the role of glucagon? And where is it produced?

A

Glucagon is produced by ALPHA cells of the islets of Langerhans in the pancreas.

It increases blood glucose.

When blood glucose levels are low, it stimulates the conversion of glycogen stored in the liver to glucose

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4
Q

Where is insulin produced and what is it’s role?

A

Insulin is produced by the BETA cells of the islets of Langerhans in the pancreas.

Insulin stimulates uptake of glucose. Insulin binds to insulin receptors (tyrosine kinase receptor) = activates glucose transporter. Insulin reduces synthesis + release of glucose in liver.

If there is excess glucose, insulin encourages its storage as glycogen in the liver and muscles and as fat in adipose tissue.
If there is insufficient insulin, the body can utilise its glucose, which will then accumulate in the blood (hyperglycaemia) + spill over into urine.

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5
Q

How is blood glucose regulated?

A
  1. Blood glucose increases e.g. following a meal
  2. More glucose enters beta-cells
  3. Metabolism of glucose causes increase in intracellular ATP, which
    closes Katp channels = depolarisation of beta cell
  4. Depolarisation causes influx of Ca2+ ions through voltage-sensitive
    Ca2+ channels
  5. Triggers insulin release
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6
Q

What levels should blood glucose not exceed in normal people?

A

Not exceed 100mg/dl in blood before meals, and 140mg/dl after meals

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7
Q

What hormones are released from the gut in response to food?

A

Incretins. Glucagon-like insulintropic peptide (GIP) + glucagon-like peptide (GLP-1) are hormones released from the gut in response to food. They increase insulin release by a direct action on pancreatic beta-cells. There action is terminated by dioeotidyl peptidase (DPP-4)

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8
Q

What is the normal levels of blood sugar?

A

= 70-120 mg/dl

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9
Q

What is type 1 diabetes?

A

-autoimmune disease, where beta cells that produce insulin are
destroyed
-used to be called insulin-dependent diabetes mellitus (IDDM)
-without treatment, body utilises fat for energy = produces ketones.
These are acidic + accumulate in the blood, being eliminated in the
urine, causing acidosis (ketoacidosis).

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10
Q

What is type 2 diabetes?

A

-produce some insulin but this is either low in quantity or the cells
are resistant to its action (insulin resistant)

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11
Q

What are the features of diabetes?

A
  • thirsty
  • freq urination
  • sudden weight loss
  • neuropathic manifestations e.g. numbness, tingling
  • poor healing of wounds
  • sexual problems
  • blurry vision
  • always hungry
  • loss of eye sight
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12
Q

What blood tests are you to diagnose diabetes?

A
  • FPG (fasting plasma glucose test)
    • pt must fast for 8h
    • blood sampling to determine amount of glucose
  • OGTT (oral glucose tolerance test)
    • how body reacts to sugar intake
    • tests if pt is resistant to insulin
    • pt must drink beverage with high sugar
    • blood sampling 2h before + after drinking beverage
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13
Q

What are the complications of diabetes?

A

Affects many organs
-skin
-eyes -crystals can form due to high levels of glucose in capillaries-lead
to blindness
-nerves -neuropathic manifestations
-kidneys -renal failure due to accumulation of glucose
-lungs
-CV system =stroke, PVD, hypertension, CAD
-blood vessels (causes high BP + cholesterol = increases risk of more
cardiovascular problems e.g. formation of atherosclerotic plaques,
angina, ischemia)
-respiratory complications =asthma, COPD, pulmonary fibrosis,
pneumonia

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14
Q

Why can’t insulin be given orally?

A

It’s a protein, so is inactivated by enzymes in the gut.

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15
Q

What is HbA1c levels?

A

Measure of % of Hb in the blood that is carrying glucose -glycated Hb.

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16
Q

What are some symptoms of mild hypoglycaemia (<3.3 mmol/L)?

A
  • Sweating
  • trembling
  • palpitations
  • anxiety
  • tingling
  • pallor
  • hunger
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17
Q

What are some symptoms of moderate/severe hypoglycaemia (<2.8 mmol/L)?

A
  • confusion
  • visual disturbance
  • weakness
  • speech disorder
  • behaviour disorder
  • drowsiness
  • coma
  • convulsions
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18
Q

What is short-acting insulin?

A

E.g. soluble insulin

  • onset 30-60 min
  • peak 4h
  • effects only lasts 30min

Insulin analogues e.g. insulin lispro have a FASTER onset + shorter action

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19
Q

What are intermediate-acting insulin’s?

A

E.g. isophane insulin

  • onset 1.5h
  • peak 7h
20
Q

What are long-acting insulin’s?

A

E.g. insulin zinc suspension

  • onset 2-4h
  • peak 6-20h
  • duration 36h

Long acting analogue insulin
E.g. insulin glargine

21
Q

What is the basal-bolus regimen?

A
  • injection of long-active analogue at breakfast

- injections of short-acting analogue at meal times

22
Q

What are the drug interactions with insulin?

A

-beta blockers -can increase the hypoglycaemic effect of insulin
-ACEi -can increase sensitivity to insulin
-alcohol -enhanced hypoglycaemic effect
-some antidepressants e.g. MAOIs enhances hypoglycaemic effect
-anabolic steroids e.g. testosterone can enhance blood glucose lowering
effects of insulin
-aspirin -in large doses can lower blood sugar levels

23
Q

What drugs antagonise the action of insulin or impair glucose tolerance?

A

-corticosteroids e.g. prednisolone can raise blood sugar + induce
diabetes
-levothyroxine
-furosemide & thiazide diuretics can raise blood sugar levels
-CCB e.g. nifedipine
-lithium
-antipsychotics e.g. clozapine associated with increased risk of glucose
intolerance
-smoking - requires more insulin -may be due to reduced absorbtion of
insulin due to peripheral vascoconstriction + rise in hormones that
oppose action of insulin.

24
Q

What are the different types of oral antidiabetic drugs?

A
  • biguanides e.g. metformin
  • sulphonylureas e.g. gliclazide
  • glitazones e.g. rosiglitazone
  • prandial glucose regulators e.g. nateglinide
  • enzyme inhibitors e.g. acarbose
25
Q

How do biguanides work?

A

Metformin

  • doesn’t alter insulin production or release -increases insulin sensitivity
  • reduces blood glucose by increasing the body’s ability to use it

Side effects;

  • lactic acidosis
  • N+V
  • diarrhoea
26
Q

How do giltazones work?

A

(Thiazolidinediones)

  • improve sensitivity to insulin
  • used in combination with metformin or sulphonylureas
27
Q

How do sulphonylureas work?

A

-stimulate insulin secretion by binding to a receptor on beta cell -
lowers blood glucose concentration
-e.g. glibenclamide

Side effects;

  • hypoglycaemia
  • weight gain
  • GI disturbances

Interactions;
-drugs which may urine acidic = reduces excretion of sulphonylureas
-drugs which can increase hypoglycaemia e.g. warfarin, NSAIDs, MAOi,
some antibiotics + alcohol

28
Q

How do prandial regulators work?

A

-stimulate insulin release

29
Q

How do glycosides inhibitors work?

A

-delay glucose absorbed from GI following meal - inhibit enzyme
alpha-glycosidase of intestine = delays splitting down of sugars
to monosaccharides
-e.g. acarbose + miglitol

30
Q

What’s the difference between haemodialysis + peritoneal dialysis?

A

Haemodialysis needs an external membrane to filter the blood.

31
Q

What hormones do the thyroid gland produce?

A

-T3: tri-iodothyronine
-T4: tetra-iodothyronine (thyroxine/levothyroxine)
Both responsible for optimal growth, development, function +
maintenance of body tissues. Difference is the number of iodine
numbers
-somatostatin -growth hormone
-calcitonin -regulates calcium in blood - contributes to bone formation +
metabolism

Main function - regulates metabolism + temp + affects secretion of hormones + NT

32
Q

How is T3 + T4 synthesised?

A

When circulating levels of T3 + T4 fall, thyrotrophin (TSH) is released from the anterior pituitary gland.
|
This stimulates transport of colloid (by endocytosis) onto the follicular cells
|
Colloid droplets fuse with lysosomes - protease enzymes degrade the thyroglobulin, releasing T3 + T4 into circulation
|
Both thyroid hormones act on receptors in plasma membrane + on intracellular receptors to produce number of actions

33
Q

What are the actions of T3 + T4?

A
  • increase oxygen utilisation
  • increase heat production
  • increase glucose + amino acid uptake
  • increase mitochondria size, number + activity
  • increase RNA polymerase activity
  • increase mRNA
  • increase enzyme activity
  • increase protein synthesis
  • increase sympathetic effects
34
Q

How are thyroid hormones regulated?

A

Hypothalamus sensitive to number of stimuli (e.g. severe stress)
|
Hypothalamus produces hormone TRH (thyrotropin-releasing hormone)
|
TRH stimulates anterior pituitary gland (hypophysis)
|
Hypophysis produces TSH
|
TSH activates receptors on follicular cells + increases cAMP
|
This stimulates thyroid to produce more T3 + T4, taking iodine from blood
|
Thyroid can be stimulated/blocked depending on level of iodine in blood
|
T3 + T4 can inhibit AP + hypothalamus

35
Q

Why does T4 take longer to act?

A

T3 is the only active one, T4 needs to be converted to T3.

T3 is 3-5 times more potent than T4

36
Q

What is hypothyroidism?

A

Deficiency of thyroidal hormones
-primary hypothyroidism (myxosdema) normally results from a
cell-mediated immune response directed against the thyroid follicular
cells.
-abnormally high levels of TSH result in enlargement of thyroid gland
(goitre)

Effects;

  • bradycardia
  • slow metabolic rate
  • weight gain
  • slow speech, deep voice
  • sensitivity to cold
  • slow thinking
  • infertility
37
Q

What causes hypothyroidism?

A

-drugs (can lower amount of T3 + T4)
-autoimmune destruction of thyroid glands
-blocked hormone formation
Impaired synthesis of T4
-destruction or removal of gland
-iodine deficiency
-receptor blocking antibodies
-pituitary Disease

38
Q

What treatment is available for hypothyroidism?

A

Replacement therapy

  • levothyroxine (T4)
    • stable + long half-life 7day
    • daily dose
    • assessed by monitoring plasma TSH levels
  • liothyronine (analogue of T3)
    • more potent (3-4x) + more rapid acting
    • short half life
    • main I use = hypothyroid coma

Side effects = too high levels of T3 + T4 = symptoms of hyperthyroidism

39
Q

What is hyperthyroidism?

A

Increased thyroidal hormones (Thyrotoxicosis)
-In Graves’ disease, hyperthyroidism is produced by an IgE
antibody that causes prolonged activation of TSH receptors = excessive
excretion of T3 + T4
-increased thyroidal hormones secretion results in hyper activation of
SNS;
-sweating, tachycardia, palpitations, tremor, anxiety, increased basal
metabolic rate

40
Q

What treatment is available for hyperthyroidism?

A

-block sympathetic effects by beta blockers e.g. propranolol
-thionamides - prevent the synthesis of thyroid hormones by
inhibiting peroxidase-catalysed reactions necessary for iodine
organification
-carbimazole
-propylthiouracil
-iodides - inhibit organification + hormone release

41
Q

What are glucocorticoids?

A

-Secreted from the adrenal cortex
-synthesised from cholesterol, follows circadian rhythm (circulation highest in morning, and low point in evening/night)
-have an anti-inflammatory + immunosuppressive action
-facilitate production of glucose in body (gluconeogenesis) - can lead to
hyperglycaemia
-protect glucose-dependent tissues such as brain + heart from
starvation
-decrease sensitivity to insulin
-decrease protein synthesis + increase protein breakdown - can lead to
muscle wastage
-activate lipolysis (fat breakdown)
-decrease calcium absorbing GI tract + increase calcium excretion in
kidney = osteoporosis
-fat redisposition from extremities to trunk, neck + face
-suppresses inflammatory responses - dangerous in infection as body no
longer responds to bacteria
-decreases production of cytokines, prostaglandins + leukotrienes
-decreases production of WBCs + antibodies
-suppresses allergic response
-growth body hair
-resistance to stomach acid decreased = ulcers
-atrophy of skin + thinning due to decreased collagen production

42
Q

What can excessive GCS lead too;

A

Cushing’s syndrome

  • euphoria
  • hypertension
  • tachycardia
  • muscle wasting
  • buffalo hump
  • cataracts
  • moon face
  • increased abdominal fat
  • poor wound healing
  • osteoporosis
43
Q

What drug treatment is available for too much GCS?

A

Steroids

  • prednisolone
  • dexamethasone
  • hydrocortisone in acute adrenocortical insufficiency
44
Q

What is Addison’s disease?

A

Life threatening deficiency of GCS + MCS (mineralocorticoids- hormones that regulate electrolyte balance) both produced by adrenal cortex.

Symptoms;

  • weakness
  • hyperkalemia
  • hyperpigmentation of skin
  • hypoglycaemia
  • hypotension
  • weight loss
45
Q

What are the withdrawal symptoms of GCS if stopped suddenly and why?

A

After chronic drug use, receptors become less sensitive (downregulated). If the drug is suddenly stopped, internal hormones aren’t sufficient enough to stimulate receptors = withdraw symptoms

  • anorexia
  • N+V
  • lethargy
  • postural hypotension
  • fever
  • depression

Pharmacology (11 decks)

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