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CEP > Week 4 > Flashcards

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
Q

How to prevent vascular complications

A

Small vessel diseases- control blood glucose levels
Large vessel diseases- lifestyle, reducing smoking, lowering blood pressure, reducing cholesterol

26
Q

What is pharmacokinetics

A

Study of drug absorption, distribution, metabolism and excretion

27
Q

What is the therapeutic window

A

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
Q

Fate of an orally administered drug

A

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
Q

Routes of drug administration

A

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
Q

Absorption depends on:

A

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
Q

What is meant by bioavailability

A

The fraction of the total dose administered that reaches the plasma

32
Q

Chemical properties that affect drug absorption

A

Chemical nature
Molecular weight
Solubility
Partition coefficient- ratio between hydrophilic and lipophilic parts

33
Q

Physiologic variables affecting drug absorption

A

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
Q

Types of parenteral routes

A

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
Q

Factors affecting absorption of drugs from GIT

A

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
Q

What is meant by first pass metabolism

A

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
Q

Pharmaceutical interventions affecting absorption

A

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
Q

What are enteric coated tablets

A

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
Q

Factors affecting transdermal absorption

A

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
Q

Passage through layers of cells

A

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
Q

What is meant by pinocytosis

A

Facilitated diffusion and active transport- of limited importance for drugs

42
Q

What is meant by lipophilicity

A

Ability of a chemical compound to dissolve in fats, oils, lipids and non-polar solvents

43
Q

Distribution depends on

A

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
Q

What is alpha1-acid glycoprotein

A

A plasma protein
A carrier of basic and neutrally charged lipophilic compounds
Increased levels in inflammatory conditions

45
Q

Apparent volume of distribution (AVD)

A

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
Q

Lipid solubility and “ion trapping”

A

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
Q

“Ion trapping”

A

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
Q

Ion trapping definition

A

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
Q

Where does metabolism occur

A

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
Q

The liver portal vein

A

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
Q

First pass metabolism - different bio transformations

A

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
Q

Excretion

A

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
Q

How do you quantitatively detect a drug in urine or blood

A

Liquid chromatography and mass spectrometry

54
Q

Dose interval affects drug concentration

A

Dose interval depends on plasma half life:
Time taken for half of drug to be eliminated from plasma

55
Q

What are the five rights of drug administration

A

Right patient
Right drug
Right route of administration
Right dose
Right time

Personalised medicine

56
Q

How would you best discriminate between type 1 and type 2 diabetes mellitus

A

Examine for urine ketones

57
Q

Ketoacidosis

A

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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