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Week 4 Flashcards

1
Q

What is diabetes

A

A disease of high glucose but also blood pressure and lipids
Common and expensive
Associated with significant morbidity
It’s training and support can be managed well

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2
Q

Symptoms of diabetes

A

Weight loss
Tiredness
Infection- candidiasis (thrush), urine
Osmotic symptoms- polyuria, thirst, blurred vision, tiredness
Coma
Some have no symptoms

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3
Q

Diagnosing diabetes mellitus

A

Urine testing
Measuring blood insulin
Blood glucose values (repeat if they have no symptoms)
Oral glucose tolerance test- gold standard
Glycated haemoglobin- HbA1c : 48mmol/mol reflects previous 10 weeks of ambient circulating glucose

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4
Q

What blood glucose levels indicate diabetes

A

Random glucose >_ 11.1mmol/l
Fasting glucose >_ 7.0mmol/l

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5
Q

What is an oral glucose tolerance test

A

Fasting state
Measure glucose- time 0
75g glucose drink over 5 mins
Wait 2 hours
Measure glucose - time 2 hrs

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6
Q

What causes diabetes

A

Insulin deficiency
Insulin resistance
Or a combination

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7
Q

What is insulin

A

Moves glucose out of blood stream for storage/ building
Major anabolic hormone
Maintains supply of glucose to tissues
Regulates metabolism in muscle
Promotes protein synthesis
Inhibits breakdown of fat

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8
Q

What do pancreatic beta cells do

A

Secrete insulin
Found in islet of Langerhans in pancreas

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9
Q

What is proinsulin

A

A substance produced by pancreas which is converted to insulin
It’s a prohormone precursor to insulin made in beta cells of the islets of Langerhans in pancreas

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10
Q

What’s a prohormone

A

A committed precursor of a hormone consisting of peptide hormones synthesised together that has a minimal hormonal effect by itself

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11
Q

What is a precursor

A

A substance from which another- usually more active or mature substance is formed

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12
Q

Classification of diabetes

A

Two main types:
Type 1 diabetes
Type 2 diabetes

Gestational diabetes- during pregnancy some women have such high levels of blood glucose that their body is unable to produce enough insulin to absorb it all

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13
Q

Type 1 diabetes

A

Where the body’s immune system attacks and destroys the cells that produce insulin
Absolute insulin deficiency
Can present any age usually <40
Usually normal weight or slim
Dramatic onset
Family history less common
Presence of ketones in urine and breath
Insulin required to sustain life

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14
Q

Type 2 diabetes

A

Where the body doesn’t produce enough insulin or the body’s cells don’t react to insulin
Insulin resistance
Relative insulin deficiency
8% population -more common
Onset typically >40 but getting younger
Genetic predisposition
Associated with obesity
Insidious onset of symptoms, insulin not required to sustain life
No ketones as insulin is present

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15
Q

Cause of type 1 diabetes

A

Autoimmune (Insulitis)- an inflammation of the islets of Langerhans- the body’s T lymphocytes attack and destroy the beta cells that produce insulin

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16
Q

Cause of type 2 diabetes

A

Insulin resistance (mainly in skeletal muscle and liver)
Beta cell dysfunction leading to a relative reduced insulin secretion
High glucose levels

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17
Q

“The 3 steeds of a diabetics chariot” Elliott Joslin

A

Diet, exercise, insulin —— glucose control

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18
Q

Glucose control in diabetes

A

Type 1- lifestyle, insulin
Type 2- lifestyle, reduce insulin resistance, increase glucose excretion, increase insulin

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19
Q

Types of insulins

A

Meal time insulins- soluble (Actrapid, Humulin S), Rapid acting insulin (Aspart (Novorapid), Lispro (humalog), glulisine (Apidra))
Longer acting insulins- Zinc insulins ( Insulatard, Humulin I), Long acting (Determir (levermir), glargine (Lantus), Glargine U300 (toujeo), Degludec (tresiba))

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20
Q

Other medication to lower glucose

A

Tablets- Insulin sensitisers, insulin secretogogues, gut absorption, glucose excretion, incretin breakdown inhibitors
Injection- incretin mimetic

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21
Q

Medication other than insulin

A

Blood pressure: ACE inhibitors, beta blockers, calcium channel blockers, diuretics
Lipids: statins, fibrates

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22
Q

Complications of diabetes

A

Platelet dependent thrombosis
Microvascular- retinopathy, cataracts, glaucoma, nephropathy, neuropathy
Macrovascular- stroke, cerebrovascular disease, transient ischemic attack, cognitive impairment, coronary heart disease, peripheral vascular disease, feet wounds likely to heal slow contributing to gangrene
Hyperglycaemia and hypoglycaemia
Hearing impairments

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23
Q

Diabetic neuropathy

A

Sensory, motor and autonomic nerves can all be damaged due to blockage of blood vessels that supply them
Longest nerves often get damaged first

24
Q

Symptoms of autonomic neuropathy

A

Digestive problems
Vomiting, diarrhoea, constipation
Problems with how well bladder works
Problems having sex
Dizziness or faintness
Loss of typical warning signs of a heart attack
Loss of warning signs of low blood glucose
Increased or decreased sweating
Changes in how eyes react to light and dark

25
How to prevent vascular complications
Small vessel diseases- control blood glucose levels Large vessel diseases- lifestyle, reducing smoking, lowering blood pressure, reducing cholesterol
26
What is pharmacokinetics
Study of drug absorption, distribution, metabolism and excretion
27
What is the therapeutic window
The gap between effective dose and toxic concentration The dose range of a drug that provides safe and effective therapy with minimal adverse effects Want to be as large as possible
28
Fate of an orally administered drug
Total oral dose (not dissolved)—> dissolved in GIT (broken down in stomach or intestine, not absorbed, secreted into bile)—> absorbed—> in liver (secreted into bile, metabolised) —> general circulation (bound to plasma proteins)—> in tissues (metabolised/excreted, tissue bound) —> at site of action
29
Routes of drug administration
Enteral routes- oral,rectal Parenteral routes- given by route other than digestive tract e.g. injecting Percutaneous- by way of skin, e.g. inhalation, sublingual, topical/transdermal, through mucous membranes (intranasal)
30
Absorption depends on:
Route of administration Blood flow at the site of administration Dose of drug Active vs passive diffusion through membrane Drug solubility in aqueous body fluids and in lipids
31
What is meant by bioavailability
The fraction of the total dose administered that reaches the plasma
32
Chemical properties that affect drug absorption
Chemical nature Molecular weight Solubility Partition coefficient- ratio between hydrophilic and lipophilic parts
33
Physiologic variables affecting drug absorption
Gastric motility- movement of substance from mouth through GIT out body The pH at absorption site Area of absorbing substance Blood flow Presystemic elimination Ingestion with or without food
34
Types of parenteral routes
Subcutaneous Intra-muscular Intra-venous Intra-arterial Intra-thecal ( injection into spinal canal or into subarachnoid space so it reaches CSF) Intra-peritoneal (within peritoneal cavity, area that contains abdominal organs)
35
Factors affecting absorption of drugs from GIT
Dispersal/solubility of drug in gut contents (influenced by formulation of drug) Stability of drug- acid/alkali and digestive enzymes Lipid solubility of drug Time available for absorption Concentration of drug Blood flow Interaction with food Effect of drug on GIT, effect of meals First pass metabolism
36
What is meant by first pass metabolism
Where a drug gets metabolised at a specific location in body that results in a reduced concentration of the active drug upon reaching site of action
37
Pharmaceutical interventions affecting absorption
Particle size (low is better) Dry-power inhaler Enteric coated tablets (slow release) Slow/delayed release preparations Don’t change drug but change formulation
38
What are enteric coated tablets
Enteric coating is a polymer applied to oral medication that acts as a barrier to prevent gastric acids in stomach from dissolving or degrading drugs after you swallow them Also protects stomach from harmful effects of the drug
39
Factors affecting transdermal absorption
Lipid solubility Formulation Skin thickness- area, age, damage Hydration- occlusive dressings (non permeable dressing no air or moisture can penetrate in or out) Blood flow
40
Passage through layers of cells
Passive diffusion- through cells, involves diffusion through membrane lipids Through intercellular pores, found in some blood vessels, for diffusion of small water-soluble molecules
41
What is meant by pinocytosis
Facilitated diffusion and active transport- of limited importance for drugs
42
What is meant by lipophilicity
Ability of a chemical compound to dissolve in fats, oils, lipids and non-polar solvents
43
Distribution depends on
Blood flow Lipid solubility and diffusion barriers- blood brain barrier, placenta Tissue binding- plasma protein binding (albumin most common, has hydrophobic binding sites for molecules) Albumin- family of globular proteins all water soluble, decreased levels in liver and kidney disease
44
What is alpha1-acid glycoprotein
A plasma protein A carrier of basic and neutrally charged lipophilic compounds Increased levels in inflammatory conditions
45
Apparent volume of distribution (AVD)
The notional volume of fluid required to dilute the absorbed dose to the concentration found in plasma AVD [volume] = dose [unit of mass]/ plasma concentration [mass/vol] If drug is heavily plasma-protein bound AVD~6 litres If heavily tissue bound (little in circulation, plasma conc. is low) AVD>70 litres
46
Lipid solubility and “ion trapping”
Many drugs exist in equilibrium between ionised and unionised forms Only unionised form is sufficiently lipid-soluble to diffuse through membranes Many drugs are weak acids or bases- so their pKa values are in physiological pH range (7.35-7.45), the degree of ionisation depends on local pH Drugs will tend to accumulate in areas where ionisation is favoured
47
“Ion trapping”
Ion trapping doesn’t require any enzyme or energy its similar to osmosis in that they both involve semi-permeable cell membranes Weak acids will tend to be well absorbed from acid environments and accumulate in basic environments. Weak bases tend to be well absorbed from basic environments and accumulate in acidic environments Ion trapping is reason why basic drugs secreted into stomach where pH is acidic and acidic drugs are excreted in urine when it’s alkaline
48
Ion trapping definition
Build up of a higher concentration of a chemical across a cell membrane due to the pKa value of the chemical and the difference of pH across cell membrane
49
Where does metabolism occur
Liver-first pass metabolism mainly oxidation (making more soluble) and conjugation (attach things to drugs to make them more soluble). Bio transformation phase I and II Kidney Skin, lungs Microbiome
50
The liver portal vein
Liver portal vein-> system of veins Originates in unpaired abdominal organs Mixes with liver artery Branches again into capillaries Carries blood from GIT, gallbladder, pancreas and spleen to liver
51
First pass metabolism - different bio transformations
Phase I- oxidation via cytochrome p450 enzymes, introduction of hydroxyl groups, compounds get more hydrophilic Phase II- conjugation reactions, charged groups are conjugated to compounds, compounds get even more hydrophilic . Groups that can be linked: sulphate, glucuronidate and others Phase I and II occur simultaneously in liver
52
Excretion
Kidney- into urine Liver- into bile, enterohepatic circulation (secreted into bile, stored in gall bladder and released in small intestine where drug can be re absorbed back into circulation and returned to liver then excreted by kidneys) or can be excreted by defecation Lungs- exhalation Saliva, sweat etc
53
How do you quantitatively detect a drug in urine or blood
Liquid chromatography and mass spectrometry
54
Dose interval affects drug concentration
Dose interval depends on plasma half life: Time taken for half of drug to be eliminated from plasma
55
What are the five rights of drug administration
Right patient Right drug Right route of administration Right dose Right time Personalised medicine
56
How would you best discriminate between type 1 and type 2 diabetes mellitus
Examine for urine ketones
57
Ketoacidosis
Lack of insulin causes triglycerides (fat) to be broken down This causes excess of fatty acids which (after the maximum can be placed in the TCA cycle to produce energy) are converted to acetoacetate This is why people with type I diabetes lose weight if not treated with insulin- bodies fat broken down Acetoacetate are converted into ketone bodies: Acetoacetate is found in urine- urine ketones Acetone is breathed out (pear drop smell) Beta-hydroxybutyrate- blood ketone

CEP (10 decks)

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