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Diploma exam 1 > Clinical services > Flashcards

Clinical services Flashcards

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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.

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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

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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.

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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

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5
Q

Provide some examples of end of bed tests

A 
Temperature
Pulse rate
Respiratory rate
Oxygen saturations
Weight
Blood pressure
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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
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7
Q

TSH reference range

A

0.5-5.5 mU/L

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8
Q

T4 reference range

A

9-25pmol/L

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9
Q

T3 reference range

A

2.5-7.8pmol/l

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10
Q

If T3 and T4 are high but TSH is low what condition does a patient have?

A

Hyperthyroidism

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11
Q

Name three causes of hyperthyroidism

A

Graves disease, tumour of the thyroid, medications e.g. amiodarone

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12
Q

Name common signs and symptoms of hyperthyroidism

A

Sweating, tremor, increased irritability, tachycardia, palpitations, arrhythmias

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13
Q

If TSH is high but T3 and T4 low what condition does the patient have?

A

Hypothyroidism

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14
Q

Provide examples of drugs that can cause hypothyroidism

A

Lithium, amiodarone, dopamine, glucocorticoids

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15
Q

Name commons signs and symptoms of hypothyroidism

A

Lethargy, pale skin, slow speech and mental function, constipation, cold intolerance, weight gain

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16
Q

A request for U&Es will test for what?

A

Serum sodium, potassium, urea and creatinine

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17
Q

How is urea formed?

A

Urea is produced from the breakdown of amino acids in the liver

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18
Q

How is urea removed?

A

Excreted in the kidneys

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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)

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20
Q

What factors can decrease urea levels?

A

Malnutrition, liver disease, pregnancy

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21
Q

Urea reference range

A

2.5-8mmol/L

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22
Q

Why do urea levels rise in dehydration?

A

Urea is an osmotic diuretic, and is reabsorbed in dehydrated states

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23
Q

Define hyperkalemia

A

Plasma potassium level >5.5 mmol/L

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24
Q

Potassium normal reference range

A

3.5-5.5 mmol/l

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25
Q

Name causes of hyperkalemia

A

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.

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26
Q

What might cause pseudohyperkalemia?

A

May occur due to prolonged tourniquet time or if there is a haemolysis of the blood sample

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27
Q

Outline the mode of action of calcium gluconate in hyperkalemia management

A

Stabilises the myocardial membrane, has no effect on the potassium level

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28
Q

How might insulin be prescribed for treatment of hyperkalemia?

A

Give 10 units of actrapid in 50mL of glucose 50% over 10 minutes. Administered via large vien

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29
Q

Outline the mode of action of insulin in hyperkalemia management

A

Shifts potassium into cells

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30
Q

How might salbutamol be prescribed for treatment of hyperkalemia?

A

Prescribed alongside insulin/calcium (should not be used as monotherapy).
Give 10mg over 10 minutes via nebuliser
Note - off label indication

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31
Q

Calcium gluconate is contraindicated in what patients?

A

If adjusted calcium >3.0mmol/L or if patient has digoxin toxicity

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32
Q

Salbutamol nebs should be used with caution in what patients?

A

Ischemic heart disease, previous hx of arrhythmias or open angle glaucoma ,

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33
Q

Define hypokalemia

A

Potassium concentration<3.5mmol/L

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34
Q

Outline the possible causes of hypokalemia

A

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

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35
Q

Why might hypokalemia occur in patients with refeeding syndrome?

A

re-introduction of carbohydrate in malnourished patients results in increased levels o insulin.

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36
Q

What is potassium chloride M/R (slow-K) not recommended?

A

Associated with oesophageal erosions, GI ulceration, and delayed response for replacement therapy

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37
Q

Why is sodium chloride the preferred diluent when administering IV potassium?

A

Initial replacement with glucose infusions stimulates insulin secretion which may further reduce plasma potassium concentrations

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38
Q

What is the maximum concentration that IV potassium can be administered peripherally?

A

40mmol/L

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39
Q

What is the maximum rate that IV potassium can be administered?

A

20mmol per hour

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40
Q

When is high potassium concentrations (40mmol in 500ml) indicated?

A

Only for use in patients with fluid restrictions, not for rapid
replacement in hypokalemia. Should be given centrally wherever possible

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41
Q

How is sodium processed in the kidneys?

A

Filtered by the glomerulus and 95% is reabsorbed in the renal tubules

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42
Q

Define hypernatremia

A

Serum Na>146mmol/

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43
Q

Symptoms of hypernatremia

A

Extreme thirst, headache, confusion, nausea and vomiting, lethargy, seizures ,nystagmus, myoclonic jerks, loss of consciousness

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44
Q

What are the causes of hypernatremia?

A 
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)
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45
Q

How do you treat hypernatremia due to diabetes insipidus?

A

Desmopressin

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46
Q

How do you treat hypernatremia due to dehydrated?

A

Treat with fluids

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47
Q

Define hyponatremia

A

Serum na <130mmol/L

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48
Q

Causes of hyponatremia

A

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

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49
Q

Symptoms of moderate-severe hyponatremia

A

nausea with/without vomiting, confusion, headache, cardiorespiratory distress, abnormal and deep somnolence, seizures, coma/altered GCS

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50
Q

Difference between chronic and acute hyponatremia

A 
acute = onset less than 48 hours
chronic = >48 hours
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51
Q

Management of acute symptomatic hyponatremia with symptoms

A

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

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52
Q

What is the risk of rapid overcorrection of hyponatremia?

A

Rapid overcorrection leads to risk of demyelination syndrome

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53
Q

Provide examples of drugs causing hyponatremia

A 
Anticancer agents
Antidepressants
Antieplileptics
ACEi, amlodipine
Diuretics, thiazides, indapamide, amiloride, loop diuretics and potassium sparing diuretics 
PPIs
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54
Q

Where is Mg primarily stored?

A

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.

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55
Q

Define hypomagnasaemia

A

Mg<0.75mmol/L

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56
Q

Causes of hypomagnasemia

A 
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
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57
Q

MHRA advice regarding PPIs and Mg

A

MHRA recommends that patients newly started on PPIs should have a baseline Mg level taken at the start of treatment and then periodically

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58
Q

Signs and symptoms of hypomagnasemia

A

Cramps, tetany (intermittent muscle cramps), paraesthesia (pins and needles), convulsions, neuromuscular excitability, arrhythmias and ECG changes

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59
Q

When should treatment of hypomagnasemia be commenced?

A

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

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60
Q

First line treatment for mild/asymptomatic hypomagnasmia

A

Magnesium aspartate 10mmol sachets BD

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61
Q

Treatment for severe hypomagnesaemia (<0.5mmol/L)

A

20mmol Magnesium sulphate in 100-1000mL of saline/glucose over 6-12 hours

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62
Q

Treatment of hypermagnesemia

A

saline
diuretics
may need dialysis - while awaiting dialysis prescribe calcium to reduce neuromuscular and cardiac effects

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63
Q

Normal adjusted calcium level

A

2.12-2.62 mmol/L

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64
Q

Why is adjusted calcium used?

A

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
Q

Define hypercalcemia

A

> 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
Q

Symptoms of hypercalcemia

A

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
Q

Causes of hypercalcemia

A

High calcium and parathyroid hormone (PTH) = primary or tertiary hyperparathyroidism

High calcium and low PTH = malignancy

Other - thiazide diuretics, rhabdomyolysis, lithium, theophylline toxicity

68
Q

Manage of severe/symptomatic hypercalcemia

A

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
Q

Define hypocalcaemia

A

Mild hypocalcaemia = 1.9-2.12 mmol/L

Severe = <1.9mmol/L

70
Q

Causes of hypocalcemia

A 
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
Q

Signs and symptoms of hypocalcemia

A

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
Q

Treatment of mild hypocalcemia

A

Adcal D3 2-3 tablets/day

73
Q

Treatment of severe hypocalcemia

A

<1.9mmol/L

10-20mL calcium gluconate in 100mL of sodium chloride or glucose 5%

74
Q

Phosphate reference range

A

0.8-1.5mmol/L

75
Q

Define hypophosphatemia

A

Plasma phosphate level <0.7mmol/L

76
Q

Acute causes of hypophosphatemia

A

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
Q

Chronic causes of hypophosphatemia

A

Hyperparathyroidism, cushings syndrome, hypothyroidism, chronic aluminium ingestion (e.g. antacids), chronic diarrhoea or vomiting

78
Q

Limitations of using urea to estimate renal function

A

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
Q

Discuss advantages of cockcoft and gault equation

A

Takes into account body weight
Useful in amputees
Preferred in AKI
Referenced in renal drug handbook

80
Q

Discuss limitations of cockcroft and gault equations

A

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
Q

Discuss pitfalls of eGFR

A

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
Q

What is CKD?

A

Abnormalities of kidney function/structure present for more than 3 months, with implications for health

83
Q

Classify the stage of CKD: eGFR 60-89

A

Stage 2

84
Q

ACR meaning

A

Albumin:creatinine ratio

85
Q

Classify the stage of CKD: eGFR 45-59

ACR 15

A

Stage 3a A2

86
Q

Classify the stage of CKD: eGFR 30-44

ACR 19

A

Stage 3b A2

87
Q

Classify the stage of CKD: eGFR 15-29

ACR 2.9

A

Stage 4 A1

88
Q

Classify the stage of CKD: eGFR <15

ACR 33

A

Stage 5 A3

Renal failure

89
Q

Causes of renal anaemia

A

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
Q

Target blood pressure in CKD

A

140/90mmHg

91
Q

First line antihypertensive in CKD

A

ACEi or ARB

Doxazosin as an alternative option

92
Q

What is uraemia?

A

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
Q

Alkaline phosphatase (ALP) reference range

A

30-85 units/L

94
Q

When is ALP raised?

A

Cholestasis (biliary obstruction stimulates production), metastatic liver disease, alcohol

95
Q

Which transaminase is more liver specific?

A

ALT

96
Q

Liver transaminases reference range

A

10-50units/L

97
Q

Sources of AST

A

Heart/liver/muscle/kidney/RBCs (AST may be elevated in MI or myositis)

98
Q

What is GGT?

A

Gamma glutamyl transferase

99
Q

GGT reference range?

A

5-55units/L

100
Q

Where is GGT found?

A

Abundant in the liver, also present in the biliary tract, intestines, kidneys, pancreas and prostate. Relatively non-specific so used infrequently

101
Q

What causes a rise in GGT?

A

Cholestatis (especially if ALP raiseD) obesity, excess alcohol consumption, anticonvulsants

102
Q

How long does it take for GGT levels to return to normal after stopping drinking?

A

Usually levels return to normal after 2-5 weeks of stopping drinking. If not will indicate permanent liver damage.

103
Q

what is bilirubin?

A

Bilirubin is a by product of haem metabolism. Bilirubin is conjugated by hepatocytes for excretion.

104
Q

An isolated rise in unconjugated bilirubin likely indicates what?

A

An isolated raise in unconjugated bilirubin is likely to indicate Gilberts syndrome

105
Q

Albumin reference range

A

35-50g/dL

106
Q

Half life of albumin

A

20 days - so low levels could signify chronic liver disease

107
Q

Prothrombin time reference range

A

10-14 seconds

108
Q

What is an ERCP test?

A

Endoscopy inserted mouth-small intestine, contrast agent is injected through the tube into the bile and pancreatic ducts then x-rays are taken

109
Q

Examples of medications that can cause acute liver failure

A

Paracetamol, valproate, statins, oral contraceptive pill

110
Q

Difference between acute and chronic liver failure

A

If persists >26 weeks = chronic liver failure

111
Q

What is cholestasis?

A

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
Q

Symptoms of cholestasis

A

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
Q

What is bilirubin?

A

Product of red blood cell breakdown. It is processed in the liver - therefore is a good indicator of excretory function of the liver

114
Q

What causes jaundice?

A

Excess bilirubin in the blood, accumulates in the skin

115
Q

What is the child-pugh score?

A

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
Q

What is hepatic encephalopathy?

A

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
Q

How is coagulopathy treated?

A

Vitamin K for max 3 days

118
Q

What is hepatorenal syndrome?

A

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
Q

How is heptorenal syndrome treated?

A

Terlipressin IV 0.5mg BD

Plus human albumin serm

120
Q

If a drug is very water soluble will it have a high or low volume of distribution?

A

Low volume of distrubtion

121
Q

Is a drug is lipid soluble will it have a high or low volume of distribution?

A

High Vd - binds extensively to tissues

122
Q

Carbamazepine target concentration

A

4-12mg/L (20-50micromol/L)

123
Q

Why does it take a while for carbamazepine to reach steady state after dose changes?

A

Carbamazepine induces its own metabolism

124
Q

Signs of carbamazepine toxicity

A

Incoordination, blurred vision, diplopia, drowsiness, nystagmus, ataxia, arrhythmia, nausea and vomiting, diarrhoea, hyponatremia

125
Q

Signs of digoxin toxicity

A

Arrhythmias, nausea and vomiting, visual disturbances, weakness and lethargy

126
Q

When should digoxin levels be taken?

A

Should be taken at least 6 hours after a dose

127
Q

When should gentamicin levels be taken?

A

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
Q

Target gentamicin concentrations (peak and trough)

A

Peak 5-10mg/l
Trough <2mg/l

for endocarditis:
peak 3-5mg/l
trough <1mg/l

129
Q

Signs of lithium toxicity

A

GI disturbances, visual disturbances, polyuria, muscle weakness, fine tremor, CNS disturbances

130
Q

When should lithium samples be taken?

A

12 hours post dose

131
Q

What are the target lithium levels?

A
  1. 4-1mmol/L (lower end if elderly)

0. 8-1mmol/l if acute mania

132
Q

Signs of phenytoin toxicity

A

Nystagmus, diplopia, slurred speech, ataxis, confusion and hyperglycemia

133
Q

Target pheyntoin concentrations

A

10-20mg/L (or 40-80micromol/L)

134
Q

How is theophylline metabolised?

A

In the liver

135
Q

Target plasma theophylline concentrations

A

10-20mg/L is needed for satisfactory bronchodilation

136
Q

When should plasma theophylline levels be taken?

A

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
Q

When are vancomycin levels taken?

A

Trough levels- immediately before the next dose

Peak levels are not usually required

138
Q

Target vancomycin levels

A

10-15g/L

139
Q

In haematology what does MCV stand for?

A

Mean corpuscular volume = this is the average volume of a single red blood cell

140
Q

Will MCV be high or low in microcytic anaemia?

A

Low MCV = microcytic anaemia

141
Q

Will MCV be high or low in macrocytic anaemia?

A

High MCV = macrocytic anaemia

142
Q

What does MCH stand for?

A

Mean corpuscular haemoglobin (MCH) = average amount of Hb in a red blood cell

143
Q

What does MCHC stand for?

A

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
Q

Anaemia definition in men

A

Hb <130g/L

145
Q

Anaemia definition in women

A

120g/l (110g/L throughout pregnancy)

146
Q

what serum ferritin level confirms iron deficiency?

A

Ferritin level <15mcg/L

147
Q

Treatment for iron deficiency anaemia

A

Dietary changes alone are not enough to correct iron deficiency
Prescribe ferrous sulphate 200mg 3 times a day

148
Q

How long should PO iron treatment continue for when treating iron deficiency anaemia?

A

Treatment should continue for 3 months after iron deficiency has been corrected

149
Q

What monitoring is required when treating iron deficiency anaemia?

A

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
Q

When might ongoing iron supplementation (at prophylactic dose) be indicated?

A

In people who have recurring anaemia, poor diet, malabsorption, menorrhagia

151
Q

What action should be taken if a patient doesn’t respond to PO iron?

A

Assess compliance
Consider testing for h.pylori
IV iron

152
Q

Define B12 deficiency

A

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
Q

Define folate deficiency

A

Serum folate <3mcg/L

154
Q

What is pernicious anaemia?

A

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
Q

What medications can cause B12 deficiency?

A

Colchicine, metformin, nitrous oxide, PPIs, H2 antagonists

156
Q

What is the schilling test?

A

Test to see if B12 is being absorbed

Radioactive B12 is given by mouth and urine is collected over 24 hours

157
Q

How is folate deficiency treated?

A

Folic acid 4mg OD

In most people treatment wil be required for 4 months

158
Q

Why must b12 deficiency be treated BEFORE folate deficiency?

A

May precipitate subacute combined degeneration of the spinal cord

159
Q

What is ESR?

A

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

Diploma exam 1 (3 decks)

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