Week 10 Flashcards
1
Q
What organ monitors blood glucose?
A
Pancreas
2
Q
What happens if blood glucose in low?
A
Glucagon released from α cells & upper GI to stimulate glycogen breakdown & gluconeogenesis in the liver
3
Q
What happens if blood glucose is high?
A
Insulin released from β cells to stimulate liver, adipose & muscle to take up glucose
4
Q
List the symptoms of diabetes?
A
- Always tired
- Wounds don’t heal
- Sudden weight loss
- Frequent urination
- Always hungry & thirsty
- Sexual problems
- Blurry vision
- Numb/tingling hands/feet
- Vaginal infections
5
Q
Describe the difference in diagnosis of type 1 & type 2 diabetes?
A
TYPE 1- often in childhood
TYPE 2- usually over 30yrs old
6
Q
Describe the difference in excess body weight association of type 1 & type 1 diabetes?
A
TYPE 1- NOT associated
TYPE 2- OFTEN associated
7
Q
Describe the different associations of type 1 & type 2 diabetes?
A
TYPE 1- higher ketone levels at diagnosis
TYPE 2- high blood pressure &/or cholesterol levels at diagnosis
8
Q
Describe the differences in treatment of type 1 & type 2 diabetes?
A
TYPE 1- insulin injections or insulin pump (replacement therapy)
TYPE 2- initially without medication or with tablets
9
Q
Describe why there is a natural progression from prediabetes to type 2 diabetes?
A
- Disruption of ability to metabolise glucose
- May have hyperinsulinemia due to lower insulin sensitivity
- Full diabetes progresses when β cell failure surpasses critical threshold ~90%
10
Q
What is the glucose level aim when treating type 1 diabetes with insulin?
A
4-7mM (preprandial/ fasting)
11
Q
What should glucose levels be, in normal people, 2hrs after a meal?
A
<7.8mM
12
Q
What glucose level will overload the renal capacity & be detected in urine?
A
> 10mM
13
Q
How is insulin now made?
A
By recombinant DNA technology, allows an identical pure preparation, limiting allergic reactions
14
Q
How is insulin administered and why?
A
- Parentally because it’s a protein that would be destroyed/ digested by gut if oral
- Routine use subcutaneously
- IV infusion in emergencies
15
Q
Insulin formulations can differ in their _____ of action?
A
Duration
16
Q
What can altering amino acids in the insulin structure do?
A
Usefully alter insulin kinetics (designer insulins)
17
Q
Describe the formulation of Insulin Lispro or Insulin Aspart
A
- Rapid-acting soluble
- Designer insulins that prevent dimer formation allowing more active monomers to be bioavailable & used rapidly
18
Q
Describe the formulation & action of Neutral Protamine Hagedorn (NPH)/Isophane Insulin?
A
Intermediate-acting insulin that precipitates insulin into suspensions which slowly dissolve
19
Q
Describe the formulation & action of Insulin Glargine?
A
Longer acting designer Insulin which has decreased solubility at neutral pH, forms aggregates that slowly dissolve.
20
Q
Describe the formulation & action of Insulin Detemir?
A
Long-acting designer insulin with a fatty acid- this confers albumin binding, which slowly dissociates prolonging circulation
21
Q
For type 1 diabetes describe the formulation of insulin replacement?
A
Intermediate-acting preparation/ long-acting analogue is often combined with short-acting analogue before meals
22
Q
What 3 types of diabetes is insulin used for?
A
- Type 1 diabetes
- 1/3rd of Type 2 diabetes
- Gestational diabetes
23
Q
Describe the pros & cons of FIXED dose insulin regiments?
A
- PROS: Can be on any injection regiments, simplify understanding of blood glucose results
- CONS: not offer flexibility of how much carbs patient choose to consume each meal
24
Q
Describe the pros & cons of FLEXIBLE dose insulin regiments?
A
- PROS: more control of what they eat & how to balance blood glucose, can have different carb quantities in meals
- CONS: patients need to understand glucose metabolism, take time & commitment to learn to adjust insulin dose
25
Describe the once daily insulin regimen & who it's appropriate for?
- 1 injection in morning
- Suitable for Type 2
- Long-acting (Glargine) or Intermediate (NPH)
- Less flexible & required basic patient understanding
26
Describe the twice daily insulin regimen & who its appropriate for?
- 2 injections in morning & evening
- Type 1 & Type 2
- Short-acting mixed with intermediate
- Less flexible & requires basic patient understanding
27
Describe the basal-bolus insulin regimen & who its appropriate for?
- Multiple injections throughout day
- Type 1 & some Type 2
- Intermediate or long-acting with short-acting
- Flexible & requires high patient understanding
28
Describe the insulin pump regimen & who its appropriate for?
- Semi-automated as needed throughout the day
- Type 1
- Short-acting insulin
- Flexible & requires medium/high patient understanding
29
What are Oral Hypoglycemic tablets used for?
To alter glucose metabolism in Type 2 diabetes
30
What is the principle oral Hypoglycemic drug?
Metformin (biguanide drug)
31
What are the effects of Metformin (hypoglycemic drug)?
- Potentiate residual insulin by increasing insulin sensitivity
- Reduce gluconeogenesis in liver & opposes action of glucagon
- Increases glucose uptake & utilisation in skeletal muscle
- Slightly delays carb absorption in gut
- Increases fatty acid oxidation
- Suppress appetite
32
How can Metformin stimulate insulin release?
By combining it with other drugs
33
What does Metformin's effect of increased fatty acid oxidation help with?
Obesity associated diabetes & atherosclerosis development
34
Overall, what does Metformin do?
Alters energy metabolism
35
What is the action of Metformin on the mitochondria & what does this result in?
- Increase AMP:ATP ratios activate AMP-activated protein kinase
- AMPK increases transcription of genes important for glucose transport fatty oxidation
36
What are the 2 classes of insulin secretagogues?
1. Sulphonylureas (old)
| 2. Meglitinides (new)
37
Give 4 examples of Sulphonylurea's?
1. Tolbutamide
2. Chlorpropamide
3. Glibenclamide
4. Glipizide
38
Describe the action of Sulphonylurea's?
- Interfere with β cell ion channels to potentiate insulin secretion
- Well tolerated, can lead to weight gain by stimulating appetite
39
When are Sulphonylurea's used & why?
Early stages of type 2 diabetes as they require functional β cells
40
What 2 drugs can Sulphonylurea's be combined with?
1. Metformin
| 2. Glitazones
41
What can the interaction between Sulphonylurea's & other drugs produce?
Severe hypoglycaemia due to competition for metabolising enzymes, plasma binding proteins & excretory pathways.
42
What is the action of Meglitinides (next generation insulin secretagogues)?
Block K-ATP channels to increase insulin release
43
What does the short duration of Meglitinides lead to?
Lower risk of hypoglycaemia
44
Where are the high affinity receptors for Sulphonylurea drugs present
β cell membranes
45
What are Glitazones also known as?
Thiazolidinediones
46
Describe the effects of Pioglitazone (Thiazolidinediones/ Glitazone)?
- Increases insulin sensitivity
- Reduces exogenous insulin needed by ~30%
- Reduces blood glucose & free fatty acid conc
- Promote transcription of several genes with products important in insulin signalling
47
What do Pioglitazone & Rosiglitazone's (Thiazolidinediones/ Glitazone) act on?
Peroxisome proliferator activated receptor (PPAR-γ) agonists in adipose tissue, muscle & liver
48
What 2 side effects can Pioglitazone cause?
1. Weight gain
| 2. Fluid retention
49
What 3 diseases have been linked to Pioglitazone?
1. Bladder cancer
2. Heart failure
3. Osteoporotic fractures
50
What is the function of PPAR-γ ligand?
Promote transcription of genes important in insulin signalling (lipoprotein lipase, fatty acid transporters, Glut-4 etc)
51
What is Pioglitazone used for clinically?
Additive to other oral hypoglycaemic drugs ie. Metformin & Sulphonylureas
52
What is Acarbose?
Inhibitor of intestinal α-glucosidase
53
What is the effect of Acarbose?
Delays carbohydrate absorption in small intestine reducing the postprandial spike in glucose
54
When is Acarbose used?
Type 2 diabetes often in combination with other hypoglycemics
55
What are the 2 side effects of Acarbose?
1. Flatulence
| 2. Diarrhoea
56
Give 3 examples of selective sodium glucose cotransporter 2 (SGLT2) inhibitors?
1. Canagliflozin
2. Dapagliflozin
3. Empagliflozin
57
When are selective sodium glucose cotransporter 2 (SGLT2) inhibitors used?
Type 2 diabetes as mono therapy when diet & exercise along not adequate for whom metformin is contraindicated or inappropriate
58
What are the actions of selective sodium glucose cotransporter 2 (SGLT2) inhibitors?
- Block glucose reabsorption by proximal tubule leading to therapeutic glucosuria
- Controls glycaemia independently of insulin pathways
59
What do selective sodium glucose cotransporter 2 (SGLT2) inhibitors lead to compared to placebo?
- Reduced HbA1c up to 1.17%
| - Well tolerated, reduce weight & systolic BP
60
What is the side effect of selective sodium glucose cotransporter 2 (SGLT2) inhibitors?
Associated with increased risk of urinary tract infections
61
Where are glucagon-like peptide-1 (GLP-1) secreted?
L-cells in the gut
62
Where are gastric inhibitor peptide (GIP) secreted?
K-cells in gut
63
What are the effects of Incretins?
- Directly stimulate insulin biosynthesis & secretion
- Inhibit glucagon secretion in pancreas, delay gastric emptying, increase cardiac output & satiety signals in brain
- Indirectly increase insulin sensitivity in muscle & decrease gluconeogenesis in liver
64
What are Incretins rapidly degraded by?
Enzyme called dipeptidyl peptidase-4 (DPP-4)
65
Give 3 examples of Incretin mimetics? (analogs of extending-4/GLP-1)
1. Exenatide
2. Exenatide LAR
3. Liraglutide
66
What is the regimen of Exenatide & its side effect?
- Twice daily
| - Nausea
67
What is the regimen of Exenatide LAR & its side effect?
- Long-acting release formulation administered weekly
| - Less nausea
68
What is the action of Liraglutide?
Additional fatty side-chain that confers albumin binding & slows renal clearance
69
What are the actions of Incretin mimetics/analogs?
Lowers blood glucose after meal by increasing insulin secretion & suppressing glucagon secretion
70
When would you use dIncretin mimetics/analogs?
Type 2 diabetes in addition to oral agents to improve control & aid weight loss
71
What is the route of Incretin mimetics/analogs?
Subcutaneously as peptide analogs
72
What are the potential side effects of Incretin mimetics/analogs?
- Hypoglycemia
| - Range of GI effects
73
Give 2 examples of DDP-4 inhibitors/Gliptins?
1. Sitagliptin
| 2. Vildagliptin
74
What are the effects of DDP-4 inhibitors/Gliptins?
- Enhance endogenous incretin effects by blocking DPP-4
| - Lowers blood glucose by increasing 1st phase of insulin response after meals
75
Describe Sitagliptin as a drug?
Well tolerated & weight neutral
76
What are the side effects of Vildagliptin?
- Respiratory tract infections
- Headache
- Serious pancreatitis
77
What does the adrenal cortex arise from?
Intermediate mesoderm
78
Describe the location of the adrenal glands?
Retroperitoneally on upper pole of the kidneys
79
List the 5 layers of the adrenal gland from exterior to interior?
1. Capsule (fibrous)
2. Zona glomerulosa
3. Zona fasciculata
4. Zona reticularis
5. Medulla
80
What hormone is produced in the Zona glomerulosa (adrenal cortex)?
Mineralocorticoid (aldosterone)
81
What hormone is produced in the Zona fasciculata (adrenal cortex)?
Glucocorticoids (cortisol)
82
What hormone is produced in the Zona reticularis (adrenal cortex)?
Androgens (DHEA & androstenedione)
83
What hormone is produced in the adrenal medulla?
Epinephrine/Adrenaline
84
What is the zona glomerulosa controlled by?
Renin-angiotensin
85
What is the function of the aldosterone release from zona glomerulosa?
Electrolyte & fluid homeostasis
86
What is the zona fasciculata controlled by?
ACTH
87
What is the function of the glucocorticoid release from zona fasciculata?
Carbohydrate, lipid & protein metabolism
88
The adrenal cortex produces _____ hormones?
Steroid
89
What is the blood supply of the adrenal cortex?
- Superior, middle & inferior adrenal arteries which anastomose under the capsule
- Cortex receives short cortical arteries run in parallel with cords of cells to medulla
90
What is the blood supply of the adrenal medulla?
- Draining from the cortex
| - Fresh arterial blood in long cortical arteries
91
What does the blood draining from the cortex into the medulla contain?
Adreno-corticosteroids which influence the production of adrenaline by medullary cells
92
What are the 6 short-term stress responses to increased catecholamines from the adrenal medulla?
1. Increased heart rate
2. Increased BP
3. Liver converts glycogen to glucose & releases it to blood
4. Dilation of bronchioles
5. Changes in blood flow patterns leading to decreased digestive system activity & reduced urine output
6. Increased metabolic rate
93
What are the 2 long-term stress responses to increased mineralocorticoids from the adrenal cortex?
1. Retention of sodium & water by kidneys
| 2. Increased BP & blood volume
94
What are the 3 long-term stress responses to increased glucocorticoids from the adrenal cortex?
1. Proteins & fats converted to glucose/ broken down for energy
2. Increased blood glucose
3. Suppression of immune system
95
What is the major role of cortisol?
Ability to cope with physical (trauma, infection, allergies) or neurological (anxiety, restraint) stresses
96
What are the 3 pharmacological actions of cortisol?
1. Anti-inflammatory
2. Anti-allergic
3. Anti-immune
97
What are the 4 possible causes of Cushing's disease/syndrome (glucocorticoid excess)?
1. ACTH-releasing pituitary tumour
2. Ectopic ACTH-releasing tumour (usually in lungs, pancreas or kidney)
3. Tumour of the adrenal cortex = hyper-secretion of cortisol
4. Administration of pharmacological doses of glucocorticoid drugs
98
What are the 7 clinical features of Cushing's disease/syndrome?
1. Hyperglycaemia
2. Muscle wasting
3. Increase free fatty acid (FFA) in plasma
4. Increased insulin release
5. Tissue edema, hypokalemia, hypertension
6. GI Tract ulceration
7. Decreases in protein synthesis
99
Why does Cushing's disease/syndrome result in hyperglycaemia?
- Gluconeogenesis in liver
| - Sometimes called adrenal/steroid diabetes
100
Why does Cushing's disease/syndrome result in muscle wasting?
Loss of protein synthesis in muscle & bone (& most tissues)
101
Why does Cushing's disease/syndrome result in increase FFA in plasma?
Reduced lipogenesis & enhanced lipolysis
102
What does increased insulin release in Cushing's disease/syndrome result in?
- Redistribution of fat stores to face, neck, upper trunk
“buffalo hump”
- β-cell exhaustion
103
Why does Cushing's disease/syndrome result in tissue edema, hypokalaemia, hypertension?
Increased glomerular filtration (glucocorticoid effect) & water & Na+ retention (mineralocorticoid effects)
104
Why does Cushing's disease/syndrome result in GI tract ulceration?
Excess H+ secretion & decreased mucous production (alkalosis due to increased H+ loss in GI tract & kidney)
105
What are the 2 possible treatments for Cushing's disease/syndrome?
1. Surgical removal of tumour
| 2. Decreases in drug dosage
106
What 3 pathways stimulate the glomerulosa cells to synthesise aldosterone?
1. Increase renin-angiotensin cascade
2. Increase ACTH from anterior pituitary
3. Increase plasma [K+]
107
What effects does aldosterone have on the kidney?
- Decrease Na+ & H2O excretion
- Increase [K+] excretion
- Increase effective circulating volume, extracellular fluid volume & BP
108
What is the Juxta-glomerular apparatus?
- Specialized structure formed by distal convoluted tubule & glomerular afferent arteriole
- Main function is regulate blood pressure & filtration rate of glomerulus
109
List the structures that form the Juxta-glomerular apparatus?
- Granular cells/ Juxtaglomerular cells on the afferent arteriole (from renal artery)
- Macula densa on the distal tubule
- Extraglomerular mesangial cells
110
What does the Granular cells/ Juxtaglomerular cells allow?
Renin to pass into the afferent arteriole
111
What do the macula dense cells detect?
Sodium concentrations in the distal tubule (osmolality)
112
Describe the suppression of glucocorticoid activity in renal cortical tubular cells?
- 11 beta-HSD metabolises cortisol, making it have little affinity for mineralcortisol receptor (MR)/glucocorticoid receptor (GR). Aldosterone, not metabolised & occupies MR & GR
- Glycyrrhetinic acid inhibits 11 beta-HSD, cortisol is not metabolised & occupies MR & Gr over aldosterone
113
What are the 4 primary causes of Addison's disease (primary adrenal cortical insufficiency)?
1. Tuberculosis/ metastatic tumours
2. Autoimmune adrenalitis --> adrenal failure
3. HIV - decreased immunity & increased viral & bacterial infections
4. Atrophy due to prolonged steroid therapy
114
What are the 6 clinical features of Addison's disease?
1. Loss of weight/appetite, muscle weakness, nausea, vomiting
2. Low plasma glucose esp. after fasting
3. Hyponatriemia & Hyperkalaemia
4. Dehydration & hypotension due to 3
5. Lethargy & dizziness on standing up due to 4
6. Severe present with skin pigmentation
115
Why in severe cases of Addison's disease do patients present with skin pigmentation?
Excess ACTH acting as Melanocyte stimulating hormone (MSH)
116
Describe the 2 possible treatments for Addison's disease?
1. Glucocorticoid replacement therapy- Hydrocortisone administration morning (25mg)/afternoon (12.5 mg)
2. IV saline infusion if severely dehydrated & condition life threatening & administration of Fludrocortisone (mineralocorticoid agonist)
117
What does the adrenal medulla develop from?
Neural crest cells
118
What important cell does the adrenal medulla contain?
Chromaffin cells (postganglionic sympathetic neurons) which produce catecholamines
119
What are chromaffin cells directly controlled by?
Preganglionic sympathetic neurons
120
What 2 catecholamines do the 2 populations of chromaffin cells secrete?
1. Epinephrine (adrenaline) - 90/80%
| 2. Norepinephrine (noradrenaline)
121
What 2 hormones have chromaffin cells also been shown to secrete?
1. Dopamine
| 2. Enkephalins (pain control)
122
What 2 ways can we compare groups in evidence?
1. Comparing results with gold standard
| 2. Comparing one sample with another after an intervention
123
What does the T-test allow for?
Statistically compare means between 2 groups (1 dependent continuous variable ie. height, 1 independent binary categorical variable ie. sex)
124
What does the Chi-square-test allow for?
Statistically compare frequencies (1 dependent categorical variable ie. alternative drug types, 1 independent categorical variable ie. deprivation category)
125
What does the T-test give?
Probability (p-value) that such a difference (or greater difference) would be found by chance, if the null hypothesis is TRUE
126
How do we know when the probability is unlikely?
We chose an arbitrary cut-off p<0.05 (reject the null hypothesis)
127
Describe the 3 slightly different t-tests?
1. Comparison of mean with a single value
2. Comparison of means of independent samples
3. Comparison of means of paired data
128
What 2 things should you report in the t-statistics?
1. Degrees of freedom (df)
| 2. Associated probability (p-value)
129
What does a P<0.05 mean?
Sample means significantly different
130
What does a P>0.05 mean?
Sample means NOT significantly different
131
What does a difference in the Chi-square test imply?
A "relationship" or "association" ie. values of one variable may influence values of the other
132
What is the Chi-square test for independence?
Association between 2 categorical variables (ie. is cholesterol status associated with gender)
133
What is the Ch-square test for goodness of fit?
Tests the difference between frequencies of a single categorical variable and some hypothesised frequency
134
What is Correlation?
Measures the strength of relationship between 2 numerical variables measured by the correlation coefficient (r)
135
What does r= -1 mean?
A perfect negative correlation (as 1 variable increases the other decreases)
136
What does r= +1 mean?
A perfect positive correlation (as 1 variable increases so does the other)
137
What do you use for basic correlation?
Continuous data
138
What is linear regression used to Predict?
Relationship between independent variables & an outcome (dependent) variable
139
What must there be between independent & outcome for regression?
Linear relationship
140
What is the regression coefficient?
Slope of the best-fitting straight line through a scatter plot of data
141
What is linear regression closely related to?
Correlation
142
What is the linear regression equation?
```
y= βx + c (intercept)
(β= slope of the best fitting straight line)
```
143
What does the p-value of the regression coefficient (β) indicate?
- Probability that the "true" slope of the line is= 0 (null hypothesis is NO SLOPE)
- Significant p-value (p<0.05) indicates that there is a significant slope (β NOT equal to 0)
144
In Scotland, how many people & their families each year will require palliative care?
~40,000
145
What is palliative care according to WHO?
Improves quality of life of patients & families facing life-threatening illness
through prevention & relief of suffering by
means of early identification & impeccable assessment & treatment of pain & other problems, physical, psychosocial & spiritual
146
Whats the GMC definition of "Approaching the end of life"?
Likely to die within the next 12 months
147
End of life, according to GMC guidance, is those facing imminent death & those with what 4 factors?
1. Advanced, progressive, incurable conditions
2. General frailty (likely to die in 12 months)
3. At risk of dying from sudden crisis of condition
4. Life threatening conditions caused by sudden catastrophic events
148
Give 4 examples of non-cancer disease which require palliation of symptoms?
1. Motor Neurone disease
2. End-stage Cardiac failure
3. End- stage COPD
4. Advanced renal disease
149
What are the 4 key themes for palliative care development?
1. Early identification of patients who may need palliative care
2. Advance/ anticipatory care planning (decisions with cardiopulmonary resuscitation (DNACPR))
3. Care in last days/ hours of life
4. Delivery of effective & timely care
150
What are the Liverpool Care pathway (LCP) report findings?
- Where used properly, many people died peaceful, dignified deaths
- But... in many cases it was associated with poor experiences of care
151
What is the response from the Liverpool Care pathway (LCP) report?
- 'One chance to get it right’: 5 priorities
for care of dying people
- ‘Care for people in the last days & hours of life’
152
What are the 3 Palliative care aims?
1. Whole person approach
2. Focus on quality of life, including good symptom control
3. Care encompassing the person with the life- threatening illness & those that matter to them
153
List the 6 principles of good end of life care?
1. Open communication
2. Anticipating care needs & encouraging discussion
3. Effective input from multidisciplinary team
4. Symptom control (physical & psycho-spiritual)
5. Preparing for death- patient & family
6. Providing support for relatives both before & after death
154
What is Generalist palliative care?
Integral part of routine care delivered by all health & social care professionals to those with progressive & incurable disease, whether at home/ care home/ hospital
155
What is Specialist Palliative care?
Same principles of palliative care, but can help people with more complex palliative care needs
156
List the physical symptoms of end of life?
- Pain
- Dyspnoea
- Nausea/vomiting
- Anorexia / weight loss
- Constipation
- Fatigue
- Cough
157
What are the 4 different physical causes of pain at end of life?
1. Cancer related (85%)
2. Treatment related
3. Associated factors- cancer & debility
4. Unrelated to cancer
158
Describe bone pain?
Worse on pressure or stressing bone / weight
| bearing
159
Describe nerve pain (neuropathic)?
Burning/ shooting/ tingling/ jagging/ altered sensation
160
Describe liver pain?
Hepatomegaly/ right upper quadrant tenderness
161
Describe raised intracranial pressure pain?
Headache (&/or nausea) worse with lying down, often present in the morning
162
Describe colic pain?
Intermittent cramping pain
163
How effective is the 3-step approach WHO pain ladder?
70-90%
164
What is the regimen for painkillers in cancer?
- Oral
| - Analgesics should be given at regular intervals, not on demand
165
What are the functions of Adjuvants in the WHO analgesic ladder for cancer pain?
To help calm fears & anxiety, adjuvant drugs may be added at any step of the ladder
166
Give 3 examples of non-opioids in the 1st step of the WHO analgesic ladder for cancer pain?
1. Aspirin
2. Paracetamol
3. NSAID
167
Give 3 examples of weak opioids in the 2nd step of the WHO analgesic ladder for cancer pain?
1. Codeine
2. Dihydrocodeine
3. Tramadol
168
Give 4 examples of strong opioids in the 3rd step of the WHO analgesic ladder for cancer pain?
1. Morphine
2. Diamorphine
3. Fentanyl
4. Oxycodone
169
What are the indications for morphine use (1st line strong opioid)?
- Moderate-severe pain
| - Dyspnoea
170
What are the actions of morphine (1st line strong opioid)?
- Opioid receptor agonist (μ-receptors)
| - Centrally acting
171
What are the cautions of morphine (1st line strong opioid)?
- Longlist in BNF, including renal impairment & elderly
| - Avoid in acute respiratory depression
172
What are the most common side effects of morphine (1st line strong opioid)?
- N&V, constipation, dry mouth, biliary spasm
| - Watch for signs of opioid toxicity
173
How do you administer Morphine (1st line strong opioid)?
- Enterally- oral/ rectal
- Parenterally- IM / SC injections
- Delivery via syringe driver over 24 hours
174
List the signs & symptoms of opioid toxicity?
- Shadows edge of visual field
- Increasing drowsiness
- Vivid dreams / hallucinations
- Muscle twitching / myoclonus
- Confusion
- Pin point pupils
- Rarely, respiratory depression
175
Describe the prescription of modified release of morphine?
- ‘Background’ pain relief
- Either twice daily preparation at 12 hourly intervals
- Or once daily preparation at 24 hourly intervals
176
Describe the prescription of immediate release of morphine?
- ‘Breakthrough’ pain
- As required (PRN)
- Oramorph liquid/ Sevredol tabs
177
What can you prescribe for the opioid side effect- Constipation?
- Stimulant & softening laxative
- Senna / Bisacodyl + Docusate
- Magrogol e.g. laxido / movicol
- OR Co-Danthramer alone
178
What can you prescribe for the opioid side effect- Nausea?
- Antiemetic
- Metoclopramide
- Haloperidol (consider QT interval)
179
What are the 4 principles to go by when moving on to step 3 opioids?
1. Stop any ‘Step 2’ weak opioids
2. Titrate immediate release strong opioid
3. Convert to modified release form
4. Monitor response & side effects
180
What adjunct medication can you give for liver capsule pain/ raised intracranial pressure?
- Steroids (e.g. Dexamethasone)
| - Remember to consider gastroprotection
181
What adjunct medication can you give for neuropathic pain?
- Amitriptyline
- Gabapentin
- Carbamazepine
182
What adjunct medication can you give for bowel/bladder spasm?
Buscopan (Hyoscine Butylbromide)
183
What adjunct medication can you give for bony pain/ soft-tissue infiltration?
- NSAIDs
| - Radiotherapy for bony metastases
184
Describe Diamorphone & its uses (other opioid)?
- Semi-synthetic morphine derivative
- More soluble than Morphine → smaller volumes needed
- Used for parenteral administration (injection /syringe driver)
185
Describe Oxycodone & its use (oxynorm/oxycontin)?
- 2nd line opioid
| - Less hallucinations, itch, drowsiness, confusion
186
Describe Fentanyl patch & its uses?
- Second line opioid
- Lasts 72 hours
- Only use in stable pain
- Useful if oral & SC routes not available
- Useful if persistent side-effects with morphine / diamorphine
187
Describe the use of syringe drivers for opioids?
- Delivery over 24 hours- usually sub-cutaneous
- Useful when oral route inappropriate
- Often useful for rapid symptom control
- Multiple medications can be added
188
What does psychospiritual distress exacerbate?
Physical symptoms
189
What 3 things should you remember to consider regarding psychospiritual distress?
1. Uncontrolled physical symptoms
2. Depression
3. Other medical causes ie. hyperthyroidism
190
What are the possible management techniques for psychospiritual distress?
- Counselling/ psychology/ cognitive behavioural therapy
| - Medication if clinically indicated
191
What is the common property of antipsychotics/ neuroleptics/ anti schizophrenic drugs/ major tranquillisers?
Antagonising actions of dopamine in the brain
192
What are the 3 positive symptoms of schizophrenia?
1. Delusions
2. Hallucinations
3. Thought disorders
193
What are the 2 negative symptoms of schizophrenia?
1. Withdrawal from social contact
| 2. Flattening of emotional responses
194
What does the clinical potency of antipsychotics correlate with?
D2 blocking action
195
Describe the dopamine theory?
- ↑ dopamine content in restricted area of temporal lobe of schizophrenics (amygdala)
- ↑ dopamine synthesis & release in striatum of schizophrenics
196
Describe the Glutamate theory?
- ↓ glutamate & receptor density in post-mortem schizophrenic brains
- Mice with ↓ NMDA receptor expression show stereotypic schizophrenic behaviours & ↓ social interactions. Also respond to antipsychotics
197
What do glutamate & dopamine do to GABAergic striatal neurones?
Excitatory & inhibitory effects on GABAergic striatal neurones which project to thalamus & constitute a sensory ‘gate’
198
Too _____ glutamate or too _____ dopamine disables the "gate"?
1. Little
| 2. Much
199
What does a disabled "gate" do?
Allowing uninhibited sensory input to reach the cortex
200
What is excess dopamine responsible for?
Positive symptoms of schizophrenia
201
What is reduced glutamate responsible for?
Negative symptoms of Schizophrenia
202
List the 3 types of 1st generation or "Classical" Antipsychotics?
1. Phenothiazines
2. Butyrophenones
3. Thioxanthines
203
What are 3 examples of Phenothiazines (1st generation antipsychotics)?
1. Chlorpromazine
2. Fluphenazine
3. Pipotiazine
204
What is an example of Butyrophenones (1st generation antipsychotics)?
Haloperidol
205
What are 2 examples of Thioxanthines (1st generation antipsychotics)?
1. Flupentixol
| 2. Clopenthixol
206
List the 3 types of 2nd generation or "Atypical" Antipsychotics?
1. Benzamides
2. Dibenzodiazepines
3. Others
207
What is an example of a Benzamides (2nd generation antipsychotic)?
Amisulpride (selective D2 & D3 receptor antagonist)
208
What are 2 examples of Dibenzodiazepines (2nd generation antipsychotic)?
1. Clozapine
2. Olanzapine
(unselective receptor blocking profile)
209
What are 4 examples of Others types of 2nd generation antipsychotic drugs?
1. Risperidone, paliperidone (mixture of receptor types blocked)
2. Quetiapine (α adrenoceptor blocker)
3. Aripiprazole (Dopamine & 5-HT antagonist)
210
What are the PROS of ‘Atypical’ or 2nd generation antipsychotics?
- Overcome some of the problems of the classical antipsychotics
- Efficacy in treatment-resistant patients
- Improve negative & positive symptoms
211
Is there evidence that 2nd generation antipsychotics are more effective than 1st generation in controlling symptoms?
NO
212
What 4 factors does the distinction between typical & atypical antipsychotics rest on?
1. Receptor profile
2. Incidence of extrapyramidal side-effects
3. Efficacy in treatment-resistant group of patients
4. Efficacy against negative symptoms
213
What group of antipsychotics shows less extrapyramidal side effects?
Atypical 2nd generation antipsychotics
214
What 6 receptors do antipsychotic drugs act on?1
1. Dopamine 1 (D1)
2. Dopamine 2 (D2)
3. α1
4. H1
5. mACh (muscarinic ACh receptor)
6. 5-HT2A (histamine receptor)
215
What are the behavioural effects of antipsychotics?
- Apathy & reduced initiative
- Few emotions, drowsy (can be easily stirred from this)
- Aggressive tendencies inhibited
216
What 2 main types of disturbances to antipsychotics cause?
1. Acute, reversible Parkinson-like symptoms due to block of nigro-striatal dopamine receptors
2. Slowly developing Tardive dyskinesia (serious problem)
217
Describe Tardive Dyskinesia?
- Involuntary movements of face & limbs
- After months/years of treatment
- Associated with proliferation of dopamine receptors in corpus striatum
- Treatment generally unsuccessful
- Less common with newer antipsychotics
218
What are the endocrine unwanted effects of antipsychotics?
Increased prolactin secretion (male/female) by blocking D2 receptors in the pituitary
219
What are the anti-muscarinic unwanted effects of antipsychotics?
- Blurring of vision, dry mouth & eyes, constipation
| - Can help attenuate extrapyramidal actions
220
What is the α-adrenoreceptor blocking unwanted effect of antipyschotics?
Orthostatic hypotension
221
What are the H1-receptor blocking unwanted effects of antipsychotics?
Sedative & anti-emetic actions
222
List the Unwanted effects of antipsychotics?
- Postural hypotension
- Sedation
- Weight gain
- Endocrine actions
- Diabetes
- Autonomic actions (atropine-like)
- Extrapyramidal actions
- Jaundice
- Leucopoenia & agranulocytosis
- Skin reactions (itchy rash)
- Neuroleptic malignant syndrome
223
How would you go about prescribing an antipsychotic for 1st episode schizophrenia?
- Choice should consider side-effect profile
- Titrate to minimum effective dose
- Adjust dose according to response & tolerability within BNF limits
- Evaluate over 6-8 weeks
224
What should you do if the antipsychotic drug prescribed is effective?
Continue at established dose, don't change the brand of drug!
225
What should you prescribe if both 1st & 2nd generation antipsychotic drug's are not effective?
Clozapine
226
What should you do if the schizophrenic patient is not tolerating or has poor compliant for antipsychotic drug?
Prescribe a depot or compliance aid
227
What antipsychotics can be used for acute behavioural emergencies & mania?
- Chlorpromazine
| - Haloperidol
228
What antipsychotic can be used for treatment of emesis?
Prochlorperazine
229
What antipsychotics can be used for treatment of Huntington's disease?
- Olanzapine
- Risperidone
- Quetiapine
230
What antipsychotic can occasionally be used to treat depression?
Flupentixol
231
What is the definition of Complementary Alternative Medicine (CAM)?
Group of diverse medical & health care systems, practices & products that are not generally considered part of conventional medicine
232
What is Complementary or Integrative medicine?
Refers to use of CAM together with conventional medicine
233
What is Alternative medicine?
Referes to use of CAM in place of conventional medicine
234
List the different Alternative medical systems?
- Traditional Chinese Medicine (TCM)
- Ayurvedic Medicine
- Homeopathy
- Naturopathy
- Indigenous healing systems
235
List the different mind-body interventions?
- Meditation
- Yoga
- Deep-breathing exercises
- Qi gong
- Tai chi
- Guided imagery
- Biofeedback
- Dream therapy
236
List the different biological based therapies?
- Herbal medicine
- Bach flower remedies
- Bee venom therapy
- Chelation therapy
- Vegetable juice therapy
237
List the different manipulative & body-based methods?
- Osteopathy
- Chiropractic
- Craniosacral therapy
- Alexander technique
- Acupuncture
- Rolfing
- Kinesiology
238
List the different energy therapies?
- Therapeutic touch
- Healing touch
- Reiki
- Magnet therapy
- Light therapy
- Crystal therapy
- Qi gong
239
How do you make a homeopathic preparation?
- Principle of similars
| - Preparations must undergo potentiation: serial dilutions of mother tincture, succession
240
What is the common homeopathic dilution?
30C = 1 in 100*30
241
What is the annual public spend on homeopathy?
~£45m
242
What are the direct & indirect risks associated with homeopathy?
- DIRECT harm: no risk of interactions with "high potency" medicines
- INDIRECT harm: delay in receiving appropriate treatment, attitudes of practitioner
243
What are the regulations for homeopathy?
- No legal regulation of homeopaths in the UK: Society of Homeopaths, Faculty of Homeopathy, British Homeopathic Association
- Homeopathic products regulated by EU directive
244
What is the difference between herbal & homeopathic medicines?
- Both are natural
- Homeopathic is unlikely to have an active ingredient
- Herbal medicine is likely to have an active ingredient that can interact with other medications
245
List other drugs that St John's Wort (Hypericum for depression) interacts with?
- Hormonal contraceptives
- Anti-depressives
- Anti-coagulants
- Anti-epilepsy agents
- Heart medications
- Anti-cancer agents
- Anti-virals for HIV
etc. ..
246
What are the direct & indirect risks associated with herbal medicine?
- DIRECT harm: Adverse drug reactions, Drug interactions, Quality control
- INDIRECT harm: Delay in receiving appropriate treatment
247
What regulates herbal medicines in the UK market?
MHRA regulations
248
What 3 things does the MHRA monitor to regulate herbal medicines?
1. Safety, quality, efficacy as per any regular medicine- Marketing Authorisation (MA)
2. Safety & quality (not efficacy) based on traditional usage- Traditional Herbal Medicines Registration (THR)
3. The “herbalist exemption”- Regulation 3 of The Human Medicines Regulations 2012
249
What does DD Palmer (straight Chiropractor) state about disease?
95% of all diseases are caused by displaced vertebrae
250
Describe Chiropractic?
- Straight vs Mixer
- Detect "subluxations" & block flow of "innate intelligence", use of X-rays or gadgets
- Spinal manipulations including high velocity, low-amplitude thrusts, audible "crack"
251
What gadgets are used in Chiropractic?
- BJ Palmer & Neurocalometers
| - E meters & the Church of Scientology
252
What are the direct & indirect risks of Chiropractic & Osteopathy?
- DIRECT harm: 50% of chiropractic patients suffer an adverse reaction, tearing of artery wall leading to stroke, injury to the spinal cord, Chiropractic X rays
- INDIRECT harm: Delay in receiving appropriate treatment, Attitudes of practitioner, Anti-vaccination
253
What are the only 2 CAM modalities under statutory regulation?
1. General Chiropractic council (GCC)
| 2. General Osteopathic Council (GOsC)
254
Describe Acupuncture?
- Ch’i (Qi, “ch-ee”) as a ‘vital energy’: Flows through ‘meridians’ associated with major organs, illness due to disrupted flow of Ch’i
- Insertion of needles along meridians: restores flow of Ch’i, 1-10cm in depth, with/without rotation, left in place for sec/hrs
255
Describe the diagnosis process during Acupuncture?
- Inspection
- Auscultation
- Olfaction
- Palpitation
- Inquiring
256
What are the direct & indirect risks of acupuncture?
- DIRECT harm: Infections, Pneumothorax
| - INDIRECT harm: Delay in receiving appropriate treatment, Attitudes of practitioner
257
How can you become a registered acupuncture?
Premises & practitioners must be licensed via local authority (same as tattooing/body piercing)
258
What are the regulations for Acupuncture?
Voluntary regulation via several organisations ie. British Acupuncture council
259
What 2 things are tightly controlled in the body's fluid compartments?
1. Volumes
| 2. Composition
260
What are the 2 major divisions of the body's fluid compartments?
1. Intracellular
| 2. Extracellular
261
What can the extracellular be divided further into?
1. Plasma
2. Interstitial
(synovial, intra-ocular, CSF etc)
262
What is composition determined by?
Movement across the plasma membrane
263
Describe the volume in the major compartments for a 70kg man?
- Total body fluid: 42L
- Intracellular fluid: 28L (incl. ~2L blood cells)
- Interstitial fluid: 11L
- Plasma: 3L
264
What is the barrier between plasma & interstitial fluid?
Capillary wall
265
What is the barrier between extracellular fluid & intracellular fluid?
Plasma membrane
266
How does the body get a gain in fluid?
- Food & water intake
| - Oxidation of food
267
How does the body get losses in fluid?
- Urine (1500ml)
- Faeces (100ml)
- Sweat (50mls)
- Insensible losses (900ml)
268
What is the average total losses of body fluid's?
2550ml
269
What is insensible water loss?
- Transepidermal diffusion: water that passes through the skin & is lost by evaporation
- Evaporative loss from respiratory tract
- Insensible losses are solute free
270
What are the types of sensor's which regulate body fluid?
- Osmoreceptors in hypothalamus
- Low pressure baroreceptors in right atria & great veins
- High pressure sensors in carotid sinus/aorta
271
What happens if the total sodium drops & osmolality start the same?
Total volume falls (including plasma volume)
272
What happens if the total sodium rises & osmolality stays the same?
Total volume will rise
273
What are compensatory mechanisms really linked to?
Low volume (low GFR, stimulation of JGA) or high volume (increased GRF & release of ANP)
274
If you eat too much/too little salt, where is the only controllable route of loss?
Via urine (hormonal control)
275
What's the possible non-hormonally controlled increased losses of NaCl?
- Exercise/heat causing increased sweating
| - Diarrhoea causing increased loss via faeces
276
Describe the intake of NaCl?
Normally in excess of need (hedonistic)
277
Describe the control of plasma Na+?
- Hormones must act on the kidney
- DCT is the area of control in nephron
- No receptors detecting Na+
- Controlled indirectly via volume sensors
- Changes in Na+ lead to changes in blood volume
278
What is the equation for working out Net sodium excretion?
Na+ filtered (changed via GFR) - Na+ reabsorbed (changed via rate of flow, aldosterone, ANP etc)
279
What 4 things occur if osmolality rises?
1. Increase in thirst
2. Increase in release of ADH
3. Increase in water intake/retention
4. Increase in volume
280
What 5 things occur if increase in volume leads to an increase in stretch of vascular system?
1. Baroreceptors
2. Decrease in renin release
3. Decrease in aldosterone release
4. Increased release of ANP (cardiac myocytes)
5. Decreased sodium & water retention
281
What 7 things occur if decrease in volume leads to a decrease in stretch of vascular system?
1. Baroreceptors
2. If pressure falls (decreased vol.), influences ADH release & thirst centres
3. Increase renin release
4. Increased angiotensin II
5. Increase aldosterone release
6. Decreased release of ANP
7. Increased sodium & water retention
282
What should you remember about K+?
Its an intracellular ion
283
How is K+ lost?
Predominantly via urine, little lost in sweat/faeces in normal conditions
284
Describe the control of K+?
- Control at the kidney
- K+ is freely filtered
- Predominantly reabsorbed again in PCT with controlled secretion at the DCT
- Secretion linked to Na+ reabsorption (sodium pump)
285
What % of K+ is inside cells?
98%
286
What do we get a significant & variable intake of K+?
From diet
287
What does intracellular K+ act as?
Reservoir (attenuates change)
288
What does an increased K+ in plasma do?
- Increases activity of basolateral sodium pump
- More K+ enters
- Increased secretion across simple diffusion channels on apical membrane
- Increased secretion of aldosterone
289
What are the effects of K+ plasma driven by?
Direct detection of raised K+ levels by the aldosterone-secreting cells of the adrenal cortex
290
What is the effects of aldosterone on the DCT?
- Increases activity of sodium pump (basolateral)
- Increases no. of Na+ pumps (basolateral)
- Increases no. of Na+ & K+ channels in apical membrane
291
What is the result of aldosterone on the DCT?
Increased reabsorption of sodium & increased secretion of potassium
292
Describe Conn's syndrome?
Hyperaldosteronism leading to 1. hypertension from increased
| fluid volume & 2. hypokalaemia
293
List the 4 types of IV crystalloids fluids?
1. 5% Dextrose (glucose)
2. 0.18% NaCl 4% Dextrose
3. 0.9% NaCl (isotonic saline)
4. Plasmalyte
294
Describe the distribution of IV 5% Dextrose?
- Initially through ISF & plasma, glucose
metabolised so effectively adding just water
- Further distributes into cells, ISF & plasma
295
Describe the distribution of IV Plasmalyte?
Through ISF & plasma, does not enter cells
296
List the 3 types of IV colloid fluids?
1. 4.5% Albumin
2. Hydrolysed Gelatin
3. Blood
297
Describe IV 4.5% albumin fluid?
- Supplied in 0.9% NaCl
- Tends to stay in plasma, does not enter cells
- Blood product
298
Describe IV hydrolysed gelatin fluid?
- Supplied in 0.9% NaCl
- Initially tends to stay in plasma, does not enter cells
- Protein metabolised over time, so equivalent to 0.9% NaCl
299
Describe the distribution of IV blood fluids?
Stays in vasculature & increases blood volume
300
What are the 4 questions to ask before prescribing fluids?
1. In terms of volume where is my patient starting from?
2. Does my patient need IV fluid?
3. Am I prescribing
maintenance/ Replacement/ Resuscitation fluid?
4. Want volume & what type of fluid?
301
What are the clinical features of Diabetes ketoacidosis?
- Hyperglycaemia: dehydration, tachycardia, hypotension, clouding of vision
- Acidosis: air hunger (Kussmaul's respiration) acetone breath, abdominal pain, vomiting
302
What are 4 reasons why a patient may be dehydrated?
1. Hyperglycaemia
2. Vomiting
3. Kaussmaul respiration
4. Altered conscious level (reduced intake)
303
What 3 treatments would you give for a dehydrated adult patient?
1. Start: 1000mls 0.9% saline over 1st hr
2. IV insulin infusion 6 units/hr
3. K+ IV (slowly)
304
What happens to the K+ during dehydration?
- Potassium has shifted out of cells (serum K+ may be normal)
- Excreted by kidneys (total loss)
- May be additional losses if vomiting
305
Where does audit come from?
- Department of Health, 1989, ‘Working for Patients’
- Quality improvement in delivery of health care
- Part of the clinical governance agenda
306
What is your role as a newly qualified doctor in regards to an audit?
- More than tick box exercise
- Audits can improve practice / quality / patient experience
- Audits can be published
307
What 3 things does the audit do for clinical governance agenda?
1. Personal responsibility
2. Organisational culture
3. Reduce variation between providers
308
Define the purpose of a clinical audit?
Quality improvement process that seeks to improve patient care & outcomes through systematic review of care against explicit criteria & implementation of change
309
Define the purpose of research?
Attempt to derive generalisable new knowledge by addressing clearly defined questions with systematic & rigorous methods
310
Describe how clinical audits & research can interconnect?
- Audit can be the final stage of research project
- Research findings identify areas for audit
- Audit helps with dissemination of research findings
- Audit identify's gaps in research evidence
311
What are the questions you ask when performing research or an audit?
- RESEARCH: what should we be doing?
| - AUDIT: are we doing it right (does it reach a predetermined standard)?
312
List the 7 common elements of clinical audit's & research?
1. Professionally led
2. Influence on clinical practice
3. Formal data collection
4. Methodological rigour
5. Data analysis / interpretation
6. Publishable?
7. Ethics
313
Is there ethics involved in research & clinical audits?
- RESEARCH: YES!
| - AUDIT: NO, may be needed if it's judged to put patients at risk, if uncertain, seek advice from ethics committee
314
What are the 2 key factors in distinguishing research & audit according to National Research Ethics service?
- INTENT: to generate new knowledge (research) to measure performance against a standard of care (audit)
- ALLOCATION OF TREATMENT SERVICE if by protocol (research)
315
What question do we ask in qualitative research?
What is the patient experience of receiving this service?
316
What is the quantitative research hypothesis test?
How do patient outcomes compare between this service (or treatment) & an alternative?
317
What does PICO (parts to a quantitative research question) stand for?
- Patient/ Precipitants
- Intervention
- Comparison
- Outcome
318
Define Service Evaluation?
Review process undertaken solely to define/judge current service with the intention of benefiting those who use it, used to inform local practice
319
What are the 3 components of Service Evaluation?
1. Structure (what you need- infrastructure, staff)
2. Process (what to do)
3. Outcome (what you expect)
320
What are the 3 service evaluation questions?
1. Does the service achieve its objectives?
2. Does the service (still) meet pt’s needs?
3. Is the service equitable?
321
What are the 2 main parts of an audit?
1. Retrospective- notes review (beware missing data)
| 2. Prospective- ongoing data collection (beware the “Hawthorne effect”)
322
List the 8 steps to doing an audit?
1. Identify a topic/ problem
2. Identify local resources (local audit dept)
3. Choose standard, create the audit proforma
4. Define the sample
5. Collect data
6. Compare data with the standard
7. Develop & implement change
8. Re-audit
323
What does the "Johnston et al Quality in Health Care 2000" state are the 5 main barriers?
1. Lack of resources
2. Lack of expertise/ advice in project design & analysis
3. Problems between group members
4. Lack of an overall plan for audit
5. Organisational impediments
324
What does the "Johnston et al Quality in Health Care 2000" state are the 6 key facilitators?
1. Modern medical records systems
2. Effective training
3. Dedicated staff
4. Protected time
5. Structured programmes
6. Shared dialogue between purchasers & providers
325
List the different criteria for choosing a topic?
- High cost, volume, or risk to staff or users?
- Evidence of a serious quality problem?
- Evidence available to inform standards ie. systematic reviews/ national clinical guidelines?
- Is problem amenable to change?
- Is the topic a priority?
- Potential for involvement in national audit project?
326
List the different criteria for choosing a standard?
- Agree the standard (minimal, ideal or optimal)
| - Is it evidence based & related to aspects of care?
327
Describe the minimal, ideal & optimal standards?
- MINIMAL: lowest acceptable level of performance
- IDEAL: care possible under ideal conditions
- OPTIMAL: realistic under normal conditions of practice
328
List the 4 perceived benefits of an audit?
1. Improved communication among colleagues
2. Improved pt care
3. Increased professional satisfaction
4. Better admin & data recording
329
List the 4 disadvantages of an audit?
1. Diminished clinical ownership
2. Fear of litigation
3. Hierarchical & territorial suspicions
4. Professional isolation
330
Who do you contact in the NHS regarding Audit or Service Evaluation?
Clinical Effectiveness Department- Clinical Effectiveness Manager / Coordinator
331
Who do you contact in the NHS regarding research?
Research & Development Office:
- R&D Manager
- Research Governance Officer
- Research Advisor (academic support)
332
Can a study have components of audit, research & service evaluation?
YES
333
Describe what is involved/what isn't involved in an audit?
- Never involves a new treatment
- Never involves allocation of pts to groups
- Should not involve anything being done to pts beyond their normal care
- Simple stats
- Results of local relevance
- Influence on clinical practice locally
- Some aspects may require review by an ethics committee
334
Describe what is involved/what isn't involved in research?
- May involve pts getting new treatment
- May involve pts being allocated to different groups
- May involve pts receiving experimental interventions
- Can involve complex stats
- Results generalisable
- Influence on clinical practice everywhere
- Always requires ethics review
335
What level of glycated haemoglobin gives a diagnosis of diabetes mellitus?
≥48mmol/mol
336
What level of fasting blood glucose gives a diagnosis of diabetes mellitus?
≥7.0mmol/L
337
What level of 2hr blood glucose gives a diagnosis of diabetes mellitus?
≥11.1mmol/L following OGTT
338
What level of random blood glucose gives a diagnosis of diabetes mellitus?
≥11.1mmol/L in presence of symptoms
339
What are the 4 different classifications of diabetes mellitus & how common are they (%)?
1. Type 1 diabetes (ß cell destruction) - 10%
2. Type 2 diabetes (insulin resistance & deficiency, secretory defect) - 85%
3. Other types (genetic, pancreatic/endocrine disease, drugs) - 5%
4. Gestational diabetes
340
When do type 1 diabetes symptoms occur?
When 80% ß cell mass lost
341
Give an example of an environmental factor with leads to ß cell destruction in type 1 diabetes?
Viral infection
342
List the 4 areas that autoantibodies act on in Type 1 diabetes (autoimmune)?
1. Islet cells
2. Insulin
3. GAD (GAD65)
4. Tyrosine phosphatase
343
What are the 2 strong HLA associations in Type 1 diabetes?
1. Linkage to DQA & DQB genes
| 2. Influences by DRB genes
344
What are the 3 environmental factors for Type 2 diabetes?
1. Obesity
2. Stress
3. Reduced physical activity
345
Describe the classical presentation of Type 1 Diabetes Mellitus?
- Thirst, polyuria
- Malaise, fatigue
- Infections ie. candidiasis
- Blurred vision
- Complications
- Incidental finding
- More visceral fat distribution
346
Describe Monitoring for diabetes mellitus
- Monitor blood glucose
| - Test for ketones
347
What is Diasend?
Web-based diabetes management system that allows you to store, review & print insulin pump, CGM & blood glucose meter data on the diasend website for monitoring patterns
348
Describe glycated haemoglobin (HbA1c)?
Form of hemoglobin that is measured primarily to identify the 3-month average plasma glucose concentration
349
What is CS11?
Continuous subcutaneous insulin infusion
350
What are the acute complications of diabetes mellitus?
- Diabetic Ketoacidosis
- Hypoglycaemia
- Other emergencies
351
What are the chronic complications of diabetes mellitus?
- Microvascular: keys, kidneys, nerves (feet)
| - Macrovascular: heart, brain, (feet)
352
What combination of things in the liver make Ketone bodies?
1. Amino acids Leucine, Lysine
| 2. Free fatty acids
353
In diabetic ketoacidotic patients what electrolyte loss should you monitor and be most concerned about?
The huge Potassium loss/shift, this often kills patients!
354
Describe the treatment of diabetic ketoacidosis?
- Insulin IV 6U/hr then by sliding scale
- N/Saline initially (4-6L)
- Dextrose 5% subsequently to replace water losses
- Careful monitoring of K+ & replace as required
355
Describe the symptoms of hypoglycaemia?
- Adrenergic: tachycardia, palpitations, sweating, tremor, hunger
- Neuroglycopaenic: dizziness, confusion, sleepiness, coma, seizures
356
What is the formal definition of hypoglycaemia?
Blood glucose <= 2.2mmoll-1
357
What are the 3 possible causes of hypoglycaemia?
1. Too much insulin
2. Too little food
3. Unusual exercise
358
What is the human counter-regulatory mechanism for fall in blood glucose?
Vagal stimulation --> parasympathetic --> glucagon release --> glycogen release by liver
359
What is the human counter-regulatory mechanism for neuroglycopaenia?
Adrenal medulla stimulation --> sympathetic --> Adrenaline release --> glycogen release by liver
360
What is the treatment for hypoglycaemia?
IV 50% dextrose
361
Describe the emergency- HyperOsmolar Non-Ketotic coma (HONK)?
- Elderly patients
- Often undiagnosed
- Intercurrent stress (MI, chest infection etc)
362
Describe why Metformin Associated Lactic Acidosis (MALA) is an emergency?
Causes Renal impairment
363
Describe the process of glycation?
Protein --> Glucose Schiff base --> Ketoamine --> 5-Hydroxymethylfurfural ---> Increased cross linking & browning of proteins
364
What are the 5 stages of nephropathy?
1. Hyperfiltration
2. Normal
3. Microalbuminuria
4. Overt nephropathy
5. Chronic renal failure
365
What screening would you do for nephropathy?
- Albustix
- Microalbuminuria
- Creatinine
366
How would you manage nephropathy?
- Blood pressure: aggressive treatment ACEI/AIIRA, 130/80 or lower
- Hyperlipidaemia: statin
- Good glycaemic control
- Diet
367
Describe diabetic microangiopathy?
Debris in lumen causes blockage of normal blood supply --> ischaemia --> pain & lack of function
368
What would you look at on examination of the foot?
- General appearance
- "Architecture"
- Pulses
- Sensation (neurosthesiometer, monofilament)
- Education (patient)
369
List the 4 stages of diabetic retinopathy?
Background --> Preproliferative --> Proliferative --> Advanced eye disease
370
What are the 3 types of maculopathy?
1. Exudative
2. Oedematous
3. Ischaemic
371
Describe the management of diabetic retinopathy?
- Screening: annual if no previous DR
- Methods: ophthalmoscope, retinal camera
- "System"
- Blindness audit
