Clinical services Flashcards
1
Q
What is an MUR?
A
Medicines Use Review
Involves pharmacist reviewing a patients use of their medications, ensuring they understand how their medicines should be used and why they have been prescribed.
2
Q
Who can have an MUR?
A
At least 70% of patients must fall within national target groups.
Patients taking high risk medications- NSAIDs, diuretics, anticoagulants, or antiplatelets
OR patients recently discharged from hospital who had changes made to their medicines while they were in hospital
3
Q
What is medicines reconciliation?
A
Process of identifying an accurate list of a patients current medications and carrying out a comparison of these with the current list in use, recognising any discrepancies and documenting any changes.
4
Q
When should medicines reconciliation take place?
A
MR should take place whenever patients are transferred from one care setting to another, when they are admitted to hospital, transferred between wards and on discharge
5
Q
Provide some examples of end of bed tests
A
Temperature Pulse rate Respiratory rate Oxygen saturations Weight Blood pressure
6
Q
Provide some examples of near patient tests
A
Urine dipstick Cholesterol screening Blood sugar level Ketones level Urease breath test for H pylori
7
Q
TSH reference range
A
0.5-5.5 mU/L
8
Q
T4 reference range
A
9-25pmol/L
9
Q
T3 reference range
A
2.5-7.8pmol/l
10
Q
If T3 and T4 are high but TSH is low what condition does a patient have?
A
Hyperthyroidism
11
Q
Name three causes of hyperthyroidism
A
Graves disease, tumour of the thyroid, medications e.g. amiodarone
12
Q
Name common signs and symptoms of hyperthyroidism
A
Sweating, tremor, increased irritability, tachycardia, palpitations, arrhythmias
13
Q
If TSH is high but T3 and T4 low what condition does the patient have?
A
Hypothyroidism
14
Q
Provide examples of drugs that can cause hypothyroidism
A
Lithium, amiodarone, dopamine, glucocorticoids
15
Q
Name commons signs and symptoms of hypothyroidism
A
Lethargy, pale skin, slow speech and mental function, constipation, cold intolerance, weight gain
16
Q
A request for U&Es will test for what?
A
Serum sodium, potassium, urea and creatinine
17
Q
How is urea formed?
A
Urea is produced from the breakdown of amino acids in the liver
18
Q
How is urea removed?
A
Excreted in the kidneys
19
Q
What factors can increase urea levels?
A
Dehydration, GI bleed, increased protein breakdown (?e.g. post-op, trauma, infection, malignancy), drugs, high protein diet, increased catabolism (starvation)
20
Q
What factors can decrease urea levels?
A
Malnutrition, liver disease, pregnancy
21
Q
Urea reference range
A
2.5-8mmol/L
22
Q
Why do urea levels rise in dehydration?
A
Urea is an osmotic diuretic, and is reabsorbed in dehydrated states
23
Q
Define hyperkalemia
A
Plasma potassium level >5.5 mmol/L
24
Q
Potassium normal reference range
A
3.5-5.5 mmol/l
25
Name causes of hyperkalemia
Decreased renal excretion (due to AKI/CKD), potassium sparing diuretics, trimethoprim, NSAIDs, excessive potassium intake. Acidosis causes the release of potassium from cells. Dead tissue (rhabdomyolysis and burns) results in potassium moving into the extracellular fluid. Addisons disease, dietary intake.
26
What might cause pseudohyperkalemia?
May occur due to prolonged tourniquet time or if there is a haemolysis of the blood sample
27
Outline the mode of action of calcium gluconate in hyperkalemia management
Stabilises the myocardial membrane, has no effect on the potassium level
28
How might insulin be prescribed for treatment of hyperkalemia?
Give 10 units of actrapid in 50mL of glucose 50% over 10 minutes. Administered via large vien
29
Outline the mode of action of insulin in hyperkalemia management
Shifts potassium into cells
30
How might salbutamol be prescribed for treatment of hyperkalemia?
Prescribed alongside insulin/calcium (should not be used as monotherapy).
Give 10mg over 10 minutes via nebuliser
Note - off label indication
31
Calcium gluconate is contraindicated in what patients?
If adjusted calcium >3.0mmol/L or if patient has digoxin toxicity
32
Salbutamol nebs should be used with caution in what patients?
Ischemic heart disease, previous hx of arrhythmias or open angle glaucoma ,
33
Define hypokalemia
Potassium concentration<3.5mmol/L
34
Outline the possible causes of hypokalemia
Excessive losses such as vomiting, diarrhoea, urinary output or sweating
Inadequate oral intake
Medications - diuretics, insulin, beta-adrenergic agonists (salbutamol), corticosteroids, laxatives)
Magnesium depletion and medicines causing this e.g. amphotericin, aminoglycosides
35
Why might hypokalemia occur in patients with refeeding syndrome?
re-introduction of carbohydrate in malnourished patients results in increased levels o insulin.
36
What is potassium chloride M/R (slow-K) not recommended?
Associated with oesophageal erosions, GI ulceration, and delayed response for replacement therapy
37
Why is sodium chloride the preferred diluent when administering IV potassium?
Initial replacement with glucose infusions stimulates insulin secretion which may further reduce plasma potassium concentrations
38
What is the maximum concentration that IV potassium can be administered peripherally?
40mmol/L
39
What is the maximum rate that IV potassium can be administered?
20mmol per hour
40
When is high potassium concentrations (40mmol in 500ml) indicated?
Only for use in patients with fluid restrictions, not for rapid
replacement in hypokalemia. Should be given centrally wherever possible
41
How is sodium processed in the kidneys?
Filtered by the glomerulus and 95% is reabsorbed in the renal tubules
42
Define hypernatremia
Serum Na>146mmol/
43
Symptoms of hypernatremia
Extreme thirst, headache, confusion, nausea and vomiting, lethargy, seizures ,nystagmus, myoclonic jerks, loss of consciousness
44
What are the causes of hypernatremia?
```
Water depletion - either inadequate intake or excessive losses
Diabetes insipidus (inability to concentrate urine due to a deficiency of ADH)
Excessive intake of Na is an uncommon cause
Essential hypernatremia (impaired thirst mechanism, can be due to inappropriate vasopressin release as a result of brain damage)
```
45
How do you treat hypernatremia due to diabetes insipidus?
Desmopressin
46
How do you treat hypernatremia due to dehydrated?
Treat with fluids
47
Define hyponatremia
Serum na <130mmol/L
48
Causes of hyponatremia
Renal losses such as diuretics, hypoarenialism,
Diarrhoea, vomiting, burns, peritonitis, pancreatitis
Syndrome of inappropriate antidiuretic hormone (SIADH)
Oedematous states causing the dilution of sodium within the body e.g. severe renal impairment, congestive heart failure, cirrhosis
Hypothyroidism
Over drinking
49
Symptoms of moderate-severe hyponatremia
nausea with/without vomiting, confusion, headache, cardiorespiratory distress, abnormal and deep somnolence, seizures, coma/altered GCS
50
Difference between chronic and acute hyponatremia
```
acute = onset less than 48 hours
chronic = >48 hours
```
51
Management of acute symptomatic hyponatremia with symptoms
hypertonic saline 2.7% via central line (contains 225mmol of Na in 500ml)
ensure that the sodium level does not rise by more than 6mmol/L in the first 6 hours
52
What is the risk of rapid overcorrection of hyponatremia?
Rapid overcorrection leads to risk of demyelination syndrome
53
Provide examples of drugs causing hyponatremia
```
Anticancer agents
Antidepressants
Antieplileptics
ACEi, amlodipine
Diuretics, thiazides, indapamide, amiloride, loop diuretics and potassium sparing diuretics
PPIs
```
54
Where is Mg primarily stored?
The majority of Mg is stored in the bone, muscle and the liver.
It is primarily intracellular – the small amount that is extracellular is protein bound or ionized therefore hypoalbuminemia states may cause levels to appear falsely low.
55
Define hypomagnasaemia
Mg<0.75mmol/L
56
Causes of hypomagnasemia
```
GI losses,
renal losses
Hypercalcemia and hypokalemia
Alcohol use
Uncontrolled diabetes
Re-feeding syndrome
Medications: thiazide and loop diuretics, PPIs, amphotericin B, aminoglycosides, foscarnet, cisplatin, tacrolimus
```
57
MHRA advice regarding PPIs and Mg
MHRA recommends that patients newly started on PPIs should have a baseline Mg level taken at the start of treatment and then periodically
58
Signs and symptoms of hypomagnasemia
Cramps, tetany (intermittent muscle cramps), paraesthesia (pins and needles), convulsions, neuromuscular excitability, arrhythmias and ECG changes
59
When should treatment of hypomagnasemia be commenced?
Treatment of mild hypomagnesaemia should only commence after two measurements 24 hours apart indicating low levels
unless there is high clinical suspicion and the patient is symptomatic
60
First line treatment for mild/asymptomatic hypomagnasmia
Magnesium aspartate 10mmol sachets BD
61
Treatment for severe hypomagnesaemia (<0.5mmol/L)
20mmol Magnesium sulphate in 100-1000mL of saline/glucose over 6-12 hours
62
Treatment of hypermagnesemia
saline
diuretics
may need dialysis - while awaiting dialysis prescribe calcium to reduce neuromuscular and cardiac effects
63
Normal adjusted calcium level
2.12-2.62 mmol/L
64
Why is adjusted calcium used?
50% of serum calcium is bound/complexed, largely to albumin. Only the free calcium is physiologically active therefore the reported 'adjusted' or 'corrected' calcium value should be used
65
Define hypercalcemia
>2.62
Below 3mmol/L is often asymptomatic and does not usually require urgent correction
Over 3.5 mmol/L requires urgent correction due to the risk of dysrhythmia and coma
66
Symptoms of hypercalcemia
Polyuria and thirst, anorexia, nausea and constipation, mood disturbance, cognitive dysfunction, renal impairment, shortened QT interval and dysrhythmias, hypertension, cardiomyopathy, peptic ulceration, muscle weakness
67
Causes of hypercalcemia
High calcium and parathyroid hormone (PTH) = primary or tertiary hyperparathyroidism
High calcium and low PTH = malignancy
Other - thiazide diuretics, rhabdomyolysis, lithium, theophylline toxicity
68
Manage of severe/symptomatic hypercalcemia
Rehydration saline 0.9% 4-6 hours in 24 hours
Zolendronic acid 4mg over 15 minutes or disodium pamidornate
2nd line options - glucocorticoids, prednisolone, calcitonin, parathyroidectomy
69
Define hypocalcaemia
Mild hypocalcaemia = 1.9-2.12 mmol/L
| Severe = <1.9mmol/L
70
Causes of hypocalcemia
```
Inadequate dietary intake
Hypomagnesemia
Post blood transfusion
Acute pancreatitis
Septic shock
Drug induced e.g. PPIs, anticonvulsants, bisphosphonates, ketoconzole
Rhabdomyolysis
Malignant disease
Chronic renal disease
Vitamin D deficiency
```
71
Signs and symptoms of hypocalcemia
Mild hypocalcaemia is usually asymptomatic
Pins and needles, chyostek and trousseau signs (facial twitching), muscle cramps, personality disorders, seizures, cardiac involvement (prolonged QT interval, arrhythmias and congestive heart failure)
72
Treatment of mild hypocalcemia
Adcal D3 2-3 tablets/day
73
Treatment of severe hypocalcemia
<1.9mmol/L
| 10-20mL calcium gluconate in 100mL of sodium chloride or glucose 5%
74
Phosphate reference range
0.8-1.5mmol/L
75
Define hypophosphatemia
Plasma phosphate level <0.7mmol/L
76
Acute causes of hypophosphatemia
Recovery phase of DKA (supplementation in this setting is not recommended), post partial heptectomy and liver transplant (considered to be due to excessive phosphate renal wasting) , acute alcoholism, refeeding syndrome
77
Chronic causes of hypophosphatemia
Hyperparathyroidism, cushings syndrome, hypothyroidism, chronic aluminium ingestion (e.g. antacids), chronic diarrhoea or vomiting
78
Limitations of using urea to estimate renal function
Urea is protein breakdown of nitrogenous products. It is not a good measure on its own as many factors dictate the level of urea e.g. fluid status, GI bleeds, diet, steroids, shock etc.
Raised urea/creatinine may be dehydration rather than renal impairment
79
Discuss advantages of cockcoft and gault equation
Takes into account body weight
Useful in amputees
Preferred in AKI
Referenced in renal drug handbook
80
Discuss limitations of cockcroft and gault equations
Does not account for difference races - works well in caucasian population, not in other ethnic groups
In accurate at extremes of body weight - may need to use IBW in obese patients (but ABW in muscular patients)
Calculations are based on steady state so are less useful in acute renal failure
81
Discuss pitfalls of eGFR
Significant error is possible e.g. limb amputations.
Likely to be inaccurate at extremes of body type
Confidence intervals are quire wide
Important to look at the trend rather than one off reading
Data based on white/black US citizens
eGFR equations tend to underestimate normal/near normal renal function
Values can differ between labs
Creatinine level must be stable
Not valid for <18 years
82
What is CKD?
Abnormalities of kidney function/structure present for more than 3 months, with implications for health
83
Classify the stage of CKD: eGFR 60-89
Stage 2
84
ACR meaning
Albumin:creatinine ratio
85
Classify the stage of CKD: eGFR 45-59
| ACR 15
Stage 3a A2
86
Classify the stage of CKD: eGFR 30-44
| ACR 19
Stage 3b A2
87
Classify the stage of CKD: eGFR 15-29
| ACR 2.9
Stage 4 A1
88
Classify the stage of CKD: eGFR <15
| ACR 33
Stage 5 A3
| Renal failure
89
Causes of renal anaemia
Lack of circulating iron - increased blood loss, reduced red blood cell survival, dietary inadequacy, poor iron absorption due to uraemia or use of phosphate binders, reduced or impaired erythropoiesis, long term use of immunosuppressants
AND
Lack of erythropoeitin
90
Target blood pressure in CKD
140/90mmHg
91
First line antihypertensive in CKD
ACEi or ARB
Doxazosin as an alternative option
92
What is uraemia?
In CKD the kidneys are less able to excrete waste products such as urea and other nitrogenous compounds
It is a serious condition and can result in various medical emergencies such as encephalopathy and pericarditis
Patients with uraemia need dialysis to remove the waste products from their blood
93
Alkaline phosphatase (ALP) reference range
30-85 units/L
94
When is ALP raised?
Cholestasis (biliary obstruction stimulates production), metastatic liver disease, alcohol
95
Which transaminase is more liver specific?
ALT
96
Liver transaminases reference range
10-50units/L
97
Sources of AST
Heart/liver/muscle/kidney/RBCs (AST may be elevated in MI or myositis)
98
What is GGT?
Gamma glutamyl transferase
99
GGT reference range?
5-55units/L
100
Where is GGT found?
Abundant in the liver, also present in the biliary tract, intestines, kidneys, pancreas and prostate. Relatively non-specific so used infrequently
101
What causes a rise in GGT?
Cholestatis (especially if ALP raiseD) obesity, excess alcohol consumption, anticonvulsants
102
How long does it take for GGT levels to return to normal after stopping drinking?
Usually levels return to normal after 2-5 weeks of stopping drinking. If not will indicate permanent liver damage.
103
what is bilirubin?
Bilirubin is a by product of haem metabolism. Bilirubin is conjugated by hepatocytes for excretion.
104
An isolated rise in unconjugated bilirubin likely indicates what?
An isolated raise in unconjugated bilirubin is likely to indicate Gilberts syndrome
105
Albumin reference range
35-50g/dL
106
Half life of albumin
20 days - so low levels could signify chronic liver disease
107
Prothrombin time reference range
10-14 seconds
108
What is an ERCP test?
Endoscopy inserted mouth-small intestine, contrast agent is injected through the tube into the bile and pancreatic ducts then x-rays are taken
109
Examples of medications that can cause acute liver failure
Paracetamol, valproate, statins, oral contraceptive pill
110
Difference between acute and chronic liver failure
If persists >26 weeks = chronic liver failure
111
What is cholestasis?
Reduction/stoppage of bile flow
Bile does not reach the duodenum
Bilirubin from the bile enters the blood stream and accumulates in the blood
112
Symptoms of cholestasis
Jaundice (due to excess bilirubin in skin)
Dark urine (excess bilirubin in the stools)
Light coloured stools
Itchiness due to accumulation in the skin
113
What is bilirubin?
Product of red blood cell breakdown. It is processed in the liver - therefore is a good indicator of excretory function of the liver
114
What causes jaundice?
Excess bilirubin in the blood, accumulates in the skin
115
What is the child-pugh score?
Developed to assess mortality risk in patients with cirrhosis
Grade A (low risk):score 5-6
Grade B score 7-9
Grade C (high risk) score 10-15
116
What is hepatic encephalopathy?
Refers to changes in the brain that occur in patients with advanced, acute or chronic liver disease.
Caused by reduced ammonia metabolism, causing increased ammonia levels reaching the brain
117
How is coagulopathy treated?
Vitamin K for max 3 days
118
What is hepatorenal syndrome?
Portal hypertension leads to arterial vasodilation in the splanchnic (GI) circulation
Vasodilation leads to decreased peripheral resistance, leading to hypotension
This drop in BP activates the renin-angiotensin pathway
Results in renal vasoconstriction and AKI
119
How is heptorenal syndrome treated?
Terlipressin IV 0.5mg BD
| Plus human albumin serm
120
If a drug is very water soluble will it have a high or low volume of distribution?
Low volume of distrubtion
121
Is a drug is lipid soluble will it have a high or low volume of distribution?
High Vd - binds extensively to tissues
122
Carbamazepine target concentration
4-12mg/L (20-50micromol/L)
123
Why does it take a while for carbamazepine to reach steady state after dose changes?
Carbamazepine induces its own metabolism
124
Signs of carbamazepine toxicity
Incoordination, blurred vision, diplopia, drowsiness, nystagmus, ataxia, arrhythmia, nausea and vomiting, diarrhoea, hyponatremia
125
Signs of digoxin toxicity
Arrhythmias, nausea and vomiting, visual disturbances, weakness and lethargy
126
When should digoxin levels be taken?
Should be taken at least 6 hours after a dose
127
When should gentamicin levels be taken?
In patients with normal renal function, concentrations should be measured after 3 or 4 doses of multiple daily dose regimen. Take blood samples approx. 1 hour after IV administration (peak) and just before the next dose (trough concentration)
128
Target gentamicin concentrations (peak and trough)
Peak 5-10mg/l
Trough <2mg/l
for endocarditis:
peak 3-5mg/l
trough <1mg/l
129
Signs of lithium toxicity
GI disturbances, visual disturbances, polyuria, muscle weakness, fine tremor, CNS disturbances
130
When should lithium samples be taken?
12 hours post dose
131
What are the target lithium levels?
0. 4-1mmol/L (lower end if elderly)
| 0. 8-1mmol/l if acute mania
132
Signs of phenytoin toxicity
Nystagmus, diplopia, slurred speech, ataxis, confusion and hyperglycemia
133
Target pheyntoin concentrations
10-20mg/L (or 40-80micromol/L)
134
How is theophylline metabolised?
In the liver
135
Target plasma theophylline concentrations
10-20mg/L is needed for satisfactory bronchodilation
136
When should plasma theophylline levels be taken?
Measured 5 days after starting oral treatment and at least 3 days after any dose adjustment
A blood sample should usually be taken 4-6 hours after an oral dose of a M/R preparation
137
When are vancomycin levels taken?
Trough levels- immediately before the next dose
Peak levels are not usually required
138
Target vancomycin levels
10-15g/L
139
In haematology what does MCV stand for?
Mean corpuscular volume = this is the average volume of a single red blood cell
140
Will MCV be high or low in microcytic anaemia?
Low MCV = microcytic anaemia
141
Will MCV be high or low in macrocytic anaemia?
High MCV = macrocytic anaemia
142
What does MCH stand for?
Mean corpuscular haemoglobin (MCH) = average amount of Hb in a red blood cell
143
What does MCHC stand for?
Mean corpuscular haemoglobin concentration MCHC
This is the average concentration of Hb per 100mL of RBCs (and it is a measure of how tightly packed with Hb the red blood cells are)
144
Anaemia definition in men
Hb <130g/L
145
Anaemia definition in women
120g/l (110g/L throughout pregnancy)
146
what serum ferritin level confirms iron deficiency?
Ferritin level <15mcg/L
147
Treatment for iron deficiency anaemia
Dietary changes alone are not enough to correct iron deficiency
Prescribe ferrous sulphate 200mg 3 times a day
148
How long should PO iron treatment continue for when treating iron deficiency anaemia?
Treatment should continue for 3 months after iron deficiency has been corrected
149
What monitoring is required when treating iron deficiency anaemia?
Recheck Hb levels after 2-4 weeks of PO iron
| Hb concentration should rise by about 2g/100mL over 3-4 weeks of treatment
150
When might ongoing iron supplementation (at prophylactic dose) be indicated?
In people who have recurring anaemia, poor diet, malabsorption, menorrhagia
151
What action should be taken if a patient doesn't respond to PO iron?
Assess compliance
Consider testing for h.pylori
IV iron
152
Define B12 deficiency
There is no gold standard test for measuring vitamin B12 deficiency, but the likelihood of deficiency can be determined by measuring serum cobalamin
A serum cobalamin level <200ng/L to diagnose vitamin B12 deficiency
153
Define folate deficiency
Serum folate <3mcg/L
154
What is pernicious anaemia?
An autoimmune disorder which results in reduced production of intrinsic factor. It is the most common cause of severe vitamin B12 deficiency, stops B12 being absorbed
155
What medications can cause B12 deficiency?
Colchicine, metformin, nitrous oxide, PPIs, H2 antagonists
156
What is the schilling test?
Test to see if B12 is being absorbed
| Radioactive B12 is given by mouth and urine is collected over 24 hours
157
How is folate deficiency treated?
Folic acid 4mg OD
| In most people treatment wil be required for 4 months
158
Why must b12 deficiency be treated BEFORE folate deficiency?
May precipitate subacute combined degeneration of the spinal cord
159
What is ESR?
Erythrocyte sedimentation rate
Can test for infection/inflammation - cells will settle at a faster rate if there is an increased level of proteins, especially acute phase reactants
