Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 3 Sem 1 COPY COPY > PA30325 3. Pharmacology > Flashcards

PA30325 3. Pharmacology Flashcards

1
Q

Whata re the 5 key functions of the kidney?

A
  • Hydroxylation Vitamin D
  • Excretion waste products
  • Control blood pressure
  • Excretion of salt and water
  • RBC production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is ‘Think Kidneys’ ?

A
  • national programme set up with the aim of preventing the avoidable harm caused by acute kidney disease
  • review and, if appropriate, revise prescribing and local policies that relate to assessing the risk of acute kidney injury to ensure these are in line with the NICE guideline on the AKI
  • review and, if appropriate, revise prescribing and local policies that relate to preventing, identifying and managing AKI, to ensure these are in line with the NICE guideline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does NSAIDs / COX II inhibitors effect renal/fluid/electrolyte physiology?

A
  • Altered haemodynamics within the kidney leading to underperfusion and reduced glomerular filtration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the change in side-effects of the following drugs when renal function is reduced?

  • Opioid analgesics
  • Tramadol
  • Benzodiazepiens
  • Aciclovir
A

Opioid analgesics

  • accumulation of active metabolites
  • increased incidence of CNS side effects & respiratory depression

Tramadol
- may accumulate leading to increased sedation, mental confusion and respiratory depression

Benzodiapezines
- accumulation of drug & active metabolites leading to increased sedation & mental confusion

Aciclovir
- accumulation leading to mental confusion, seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is AKI?

A
  • Acute Kidney Injury (AKI) is a sudden reduction in kidney function over hours to days
  • It is not a physical injury to the kidney and usually occurs without symptoms, making it difficult to identify
  • Not a disease itself: result of underlying pathology
  • diagnosed by blood test only
  • Late diagnosis can miss opportunities for early treatment, leading to prolonged and complex treatment and reducing the chances of recovery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is Chronic Kidney Disease?

A
  • abnormality of kidney function and structure that is present for more than 3 months
  • in CKD, the kidney gradually loss function over a longer period of time compared to AKI
  • Can get AKI on background of CKD
  • AKI can lead to CKD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe 3 different stages of AKI

A

RISE in Creatinine, REDUCTION in Urine Output

Stage 1

  • Serum Creatinine 1.5-1.9 times baseline or >26.5 micromol/L increase
  • Urine Output <0.5ml/kg/h for 6-12hrs

Stage 2

  • Serum Creatinine 2.0-2.9 times baseline
  • Urine Output <0.5ml/kg/h for >12hrs

Stage 3

  • Serum Creatinine 3.0 times baseline OR increase serum cretainine to >353.6 micromol/L OR initiation of RRT OR in patients <18yrs, decrease in eGFR to <35ml/min/1.73m2
  • Urine Output <0.3ml/kg/h for >24hrs or Anuria for >12hrs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the causes of AKI?

A

Pre-renal

  • volume depletion (dehydration, bleeding)
  • sepsis
  • cardiogenic (shock)

Intrinsic

  • prolonged pre-renal insult causing tubular necrosis
  • inflammation/glomerulonephritis
  • drugs
Post-renal
- Outflow obstruction
\: Bladder
\: Prostate
\: Ureter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe AKI management

A
  • Treat precipitating insult
  • Stop nephrotoxic medication
    : ACEi/ARB
    : NSAID
    : Aminoglycosides
  • Maintain euvolaemia (normal body fluid volume)
  • Treat electrolyte abnormalities
  • RRT if needed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How do NSAIDs, ACEi and ARB cause AKI?

A
  • NSAIDs inhibit prostaglandin synthesis

- ACEi and ARB cause vasodilation of the efferent blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the roles of Pharmacist in AKI?

A
  • preventing AKI
    : education/risk assessment
  • recognising AKI
  • identify possible drug causes
  • stop nephrotoxic drugs
  • review drugs that may worsen biochemistry e.g hyperkalaemia
  • review doses of other medication that may accumulate
  • review doses/restart medicines when renal function improves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is CKD?

A
  • Chronic Kidney Disease is a progressive and irreversible condition
    : defined as an estimated glomerular filtration rate (eGFR) of <60 mL/min/1.73m2 and/or kidney damage present for at least 3 months
  • The physiological changes that occur in CKD result in subsequent alteration of PK and PD of many drugs
  • Hence, for medications and/or active metabolites that depend on the renal system for their excretion, dosage adjustment is necessary to prevent their accumulation that may eventually lead to toxicity
  • Likewise, medications may also be contraindicated in patients with CKD due to the increased risk of adverse effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe Glomerular filtration rate

A
  • Volume of fluid filtered from glomerular capillaries to Bowman’s capsule per unit time
  • GFR = urine concentration x flow / plasma concentration
  • GFR = clearance rate of a solute
    : free filtered
    : not secreted or reabsorbed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is renal filtration measured?

A
  • waste product from muscle
  • generated at a relatively constant rate in an individual
  • largely removed by filtration alone
  • standarised lab measurement

but. .
- significantly affected by age, race, weight
- non-linear relationship with true GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe Estimated creatine clearance (eCrCl)

A
  • multiple formulae
  • most common is Cockroft-Gault

eCrCl = (140-age) x Weight (kg) x Constant / Serum Cretainine (micromol/L)

  • constant male = 1.23 / female = 1.04
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe different stages of CKD

A

GFR = ml/min/1.73m2

Stage 1

  • GFR >90
  • normal or increased glomerular filtration rate with other evidence of kidney damage

Stage 2

  • GFR 60-89
  • slight decrease in GFR, with other evidence of kidney damage

Stage 3A

  • GFR 45-59
  • moderate decrease in GFR with or without other evidence of kidney damage

Stage 3B

  • GFR 30-44
  • moderate decrease in GFR with or without other evidence of kidney damage

Stage 4

  • GFR 15-29
  • Severe decrease in GFR, with or without other evidence of kidney damdage

Stage 5

  • GFR <15
  • established renal failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the causes of CKD?

A
  • Diabetes
  • Hypertension
  • Glomerulonephritis
  • Reflux nephropathy
  • Polycystic disease
  • Previous acute kidney injury
  • many others, including nephrotoxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the signs and symptoms of CKD?

A
  • increased BP
  • Shortness of Breath
  • Kidney size and shape
  • altered Urine output
  • Blood / protein in urine
  • itching & cramps
  • cognitive function
  • GI symptoms
  • peripheral oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the complications of CKD?

A
  • Electrolyte imbalance
  • renal bone disease
  • hyperetnsion
  • anaemia
  • oedema
  • hyperphosphataemia
  • itching
  • nausea
  • resless legs/cramps
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How is CKD managed?

A
  • management of complications
  • proteinuria reduction
  • salt free diet
  • preparation for renal replacement therapy (RRT)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe renal anaemia

A

Reduction in red cell production

  • low EPO (epoetin)
  • functional iron deficiency

Increased red cell turnover
- Uraemia

Treatment

  • EPO replacement
  • iron replacement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe Erythropoiesis Stimulating Agents (ESA) and Hb targets in CKD to treat anaemia

A
  • Initially aimed to normalise Hb
  • Erythropoiesis stimulating agent (ESA) medicines are man-made versions of erythropoietin, which is a hormone (chemical messenger) produced naturally by the kidneys. The role of erythropoietin is to stimulate the bone marrow to produce more red blood cells
  • try to avoid blood transfusion
  • erythropoiesis stimulating agents and iron
  • aim to maintain Hb between 10-12g/dL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe Renal bone disease

A
  1. Reduction in Vit D hydroxylation
    - impaired gut absorption
  2. Hypocalcaemia
    - may cause tingling, cramps etc
  3. Parathyroid stimulation
    - increased sPTH
  4. Calcium release from bones
    - poor mineralisation, phosphate release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How is Mineral Bone disease treated?

A
  • Alfacalidol: post-renal vitamin D
  • Dietary phosphate restriction
  • Phosphate binders
  • Aim to balance serum Ca, PO4 and PTH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe the changes in Absorption in CKD patients

A
  • reduced compliance due to uremic symptoms and polypharmacy
  • gastric oedema
  • phosphate binders
    : bind drugs e.g quinolone antibiotics, levothyroxine
  • PPI and H2 receptor antagonists reduce gastric acidity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe the changes in Distribution in CKD patients

A
  • low albumin reduces the amount of protein binding
  • uraemia causes displacement from protein binding sites
  • increased free drug
    : phenytoin, diazepam, digoxin, sodium valproate, warfarin
  • therapeutic drug monitoring often required for drugs with a marrow therapeutic window
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe the changes in Excretion in CKD patients

A
  • Significant for drugs which are >25% excreted unchanged in the urine
  • Remember metabolites
  • drugs with a narrow therapeutic index
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Ideal drugs in CKD?

A
  • less than 25% excreted in the urine
  • no active metabolites
  • disposition unaffected by fluid balance changes
  • disposition unaffected by protein binding
  • disposition unaffected by tissue sensitivity
  • wide therapeutic index
  • not nephrotoxic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Backgrounds of CKD (JUST READ)

  • Chronic kidney disease is common affecting 1 in 10 adults in UK
  • CKD stage 5 is rare and often preventable
  • Diabetic nephropathy is the most frequently documented primary diagnosis in patients starting RRT aged 35 years and over
  • Other causes of CKD include glomerulonephritis, pyelonephritis, hypertension and renal vascular disease
A

-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the risk factors of CKD progression?

A
  • Cardiovascular disease
  • Proteinuria
  • Acute Kidney Injury
  • Hypertension
  • Diabetes
  • Smoking
  • African, African-Caribbean or Asian family origin
  • Chronic use of NSAIDs
  • Untreated urinary outflow tract obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the indications for starting Renal Replacement in CKD?

A
  • symptoms of uraemia having impact on daily living
  • biochemical measures e.g hyperkalaemia/acidosis
  • uncontrollable fluid overload
  • estimated glomerular filtration rate (eGFR) of around 5 to 7 ml/min/1.73m2 if there are no symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Describe intermittent Haemodialysis

A
  • requires access
    : Arteriovenous fistula, Line, Graft
  • can be done at home or in hospital
  • usually 4 hrs 3 x per week
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Describe Haemodialysis

A
  • Transfer of uraemic solutes from blood by across semi-permeable membrane
  • Solute clearance
  • Water removal
  • Bicarbonate addition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Describe Peritoneal dialysis

A
  • Performed at home
    : continuous ambulatory, automated, assisted
  • Access to peritoneal cavity
    : Tenckhoff catheter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the challenges of dialysis?

A
  • fluid restriction
  • restriction of salt intake
  • restriction of potassium intake
  • phosphate binders to reduce GI absorption of PO4
  • Travel (for-in-centre haemodialysis)
  • restriction in travel within UK
  • continued symptoms
  • access problems
  • infectious problems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the important medicines management considerations in Dialysis?

A

Protein binding
- if patient is uremic, protein binding may be reduced resulting in more free drug available

  • significant if drug has narrow therapeutic index and highly protein bound e.g phenytoin
  • only free unbound drug can pass through pores for dialysis
  • If more than 80% protein bound, consider as not dialysed
  • Excretions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the role of pharmacists in Dialysis?

A
  • advise on drug dosage and interactions
  • ensure medication is given at correct time
    : phosphate binders with meal
    : consider removal by dialysis
  • Encourage patients to have annual infleunza vaccine and pneumonia vaccine every 10 years
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the typical Post-operative considerations?

A
  • Venous thromboembolism (VTE) prophylaxis
  • Antibiotic prophylaxis
  • Post-operative nausea and vomitting
  • Post-operative pain
  • Fluid balance and electrolytes, Nutrition
  • Medicines management and chronic conditions post-op
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the risk factors for VTE

A
  • Active cancer/cancer treatment
  • age over 60 years
  • critical care admission
  • dehydration
  • known thrombophilias
  • obesity
  • one or more significant medical comorbidities
  • personal history of first-degree relative with a history of VTE

Medical patients

  • have had or are expected to have significantly reduced motility for > 3 days
  • expected to have ongoing reduced mobility relative to their normal state and have > one listed risk factors

Surgical patient
- total anaesthetic + surgery time >90mins or 60 minutes if pelvis/lower limb surgery
- acute surgical admission with inflammatory or intra-abdominal condition
- expected significant reduction in mobility
> one of the listed risk factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the methods of VTE prophylaxis?

  • Actions
  • Mechanical
  • Pharmacological
A

Actions

  • mobilise as soon as possible
  • avoid dehydration
  • stop meds which increase risk where possible

Mechanical

  • anti-embolism stockings
  • intermittent Pneumatic Compression devices (IPC)
  • Foot impulse devices

Pharmacological

  • Low molecular weight heparin (LMWH)
  • Unfractionated heparin
  • Rivaroxaban, Dabigatran, Apixaban
  • Fondaparinux
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the VTE prophylaxis regimens for low risk and high risk patients?

A

Low risk

  • Early mobilisation
  • Anti-embolism stockings if not contra-indicated

High risk

  • LMWH / DOAC
  • Intermittent pneumatic compression during surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Describe the duration of VTE Prophylaxis treatment

A
  • continue until returns to usual mobility
  • extended prophylaxis is needed for some procedures
    : fractured neck of femur (hip) 4 - 5 weeks
    : abdominal / pelvic cancer surgery 4 weeks
    : lower limb plaster cast until out of cast
  • patient taught how to give and monitoring required if SC LMWH used
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the consequence of poorly managed pain after surgery?

A

Increase in…

  • length of stay
  • VTE risk
  • BP and pulse
  • anxiety & disturbed sleep

Decrease in…

  • recovery
  • mobility
  • wound healing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is Epidural?

A
  • injection in the back
  • can provide better pain relief than other method
  • usually local anaesthetic + opiate
  • synergistic action with decreased dose of each = less side effects
  • analgesia localised to chest, pelvis, lower limb depending on catheter site
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Describe Patient Controlled Analgesia (PCA)

A
  • strong opiate
    : fentanyl or morphine
  • controlled by patient
    : reduced waiting time for analgesia / less anxiety / increase in patient experience
  • Bolus does when button is pressed with 5 min lockout time
  • Improves quality of recovery but not suitable for all
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Describe post-op nausea and vomitting (PONV)

A
  • affects ~30% patients
  • caused by
    : anaesthetic agents, opioid agents, bowel surgery, antibiotics, U&E disturbances, bowel obstruction

Risk factors
- females at higher risk, history of motion sickness, previous PONV, non smokers higher risk, opiate use

  • Apfel scoring used to assess PONV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How is Post Op Nausea and Vomitting treated?

A
  • Local hospital policy
  • Aim to prevent vomitting i.e give before end of surgery
  • usually using ondansetron, cyclizine, dexamethasone or prochlorperazine
  • number of medications prescribed depends on risk factors identified
  • Metoclopramide not very effective for PONV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Describe Surgical Antibiotic Prophylaxis

A
  • the use of antibiotics before, during, or after a diagnostic therapeutic, or surgical procedure to prevent infectious complications

Surgical site infections

  • infections of surgical wound or involving the body cavity, bones, joints, meninges or other tissues involved in the operation
  • also includes infections associated with implants or prosthetic devices

In simple terms…
Whether to give prophylatic antibiotics
- depends on type of surgery

Duration depends on degree of contamination

  • 1 dose for clean-contaminated
  • 5-7 days for contaminated
  • Longer for ‘treatment’

Which antibiotic depends on likely causative organism

  • bowel surgery
  • local resitance patterns
  • cost-effectiveness
  • PK (tissue concentration)

To be effective concentration of antibiotic, in the tissue being operated on must be high enough at the time of incision
- high tissue conc at time of incision, IV route preferred

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Describe Nil By Mouth (NBM) Post-op

A
  • following most surgical procedures, patients can eat and drink by lunch/evening
  • post GI surgery may be NBM for several days or have impaired absorption
  • Regular medicines for underlying disease
    : consider alternative routes, essential to be continued?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Describe Electrive Surgical pathway

A

Planned Procedure

  • patient sees GP
  • referred to specialist
  • diagnosis
  • adjunct treatment (e.g chemotherapy)
  • decision made for surgery
  • patient usually seen at pre-op assessment clinic a few weeks pre-op
  • patient sent surgery date
  • patient arrives in Admission in the morning
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Describe Pre-Operative Assessment

A
  • usually nurse led
  • Patient clerked: medical history / HPC
  • procedure explained: consent forms signed
  • opportunity for questions
  • post-operative care and needs on discharge
  • ensures patient ready for surgery
  • Fit for anaesthesia?
  • blood tests: eGFR, Hb, Crossmatch
  • weight: important for medication dose
  • MRSA screen and eradication
  • BP: may need treatment
  • Cardiac function: ECG / ECHO
  • blood glucose: optimise diabetes management pre-op
  • medicaiton history
  • prescribing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Why is Meds Reconciliation pre-op needed?

A
  • if not performed, no accurate source of medication to inform prescribing
  • potential for critical missed dose
  • Pre-op patient is alert, with family/carer, medication is available
  • Post-op patient is drowsy, family not available, medication may have been sent home
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Describe Nil By Mouth pre-op

A
  • pre-operative fast
    : 6 hrs for food, 2 hrs clear fluids
  • risk aspiration of stomach contents during general anaesthetics
  • general rule
    : most regular medication should be given on day of surgery with small sips of water
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What change is needed to Warfarin pre-op?

A
  • long half-life
    : stop 5 days pre-op
  • INR <1.5 for surgery to proceed
  • Emergency surgery
    : give Vit K or beriplex
  • Pre/Post op management depends on indication for anticoagulant and post-op bleed risk
  • Consider risk of thrombo-embolism on stopping
  • Bridging therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Describe Warfarin bridging

A
  • Take last dose of warfarin 6 days before surgery
  • start LMWH at 8am 2 days after stopping warfarin
  • Do not give LMWH on the morning of surgery and stop unfractionated heparin 6 hrs before surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Describe Post-op management of Warfarin

A
  • Usually restart Warfarin ASAP post-op, depending on bleeding risk
  • Role of pharmacist intervention to ensure discharge is not delayed due to delay restarting anticoagulants

If patient at LOW/MODERATE risk
- cover with prophylactic dose LMWH until INR therapeutic

If patient at HIGH risk
- cover with treatment dose LMWH (or IV heparin infusion) until INR therapeutic for 2 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is the disadvantages of DOAC in surgery?

A

Side effect

  • Bleeding
  • GI upset

Lack of optimal reversing agents

New dabigatran reversal agent available but expensive only for immediate surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Describe uses of Cardiac medication in Surgery

A
  • surgery can increase heart rate and BP so continue most cardiac medication
  • ACEi/ARB and diuretics may be omitted due to risk of hypotension but some Trusts advise to give
  • always continue beta-blockers as risk fo rebound tachycardia, arrhythmia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Describe the uses of Long term Steroids in Surgery

A
  • stress of surgery causes plasma adrenocorticotrophic (ACTH) hormone and cortisol levels to rise
  • Patients on oral steroids may have pituitary-adrenal suppression and natural stress response impaired which leads to circulatory collapse
  • Keep steroid use to a minimum. Can affect wound healing, increase infection risk and delay recovery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How is Diabetes managed Pre-op?

A

Type 1 / Type 2 no more than one missed meal

Morning surgery

  • generally omits all oral hypoglycaemics on morning of surgery
  • continue long acting insulin at reduced dose
  • halve A.M dose of biphasic insulin or intermediate insulin
  • Omit A.M and lunch doses of short /rapid acting insulin
  • Close monitoring of blood glucose levels
  • Reintroduce usual diabetic regime when oral intake resumed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

How is Oral contraceptives managed Pre-op?

A
  • Oestrogen containing contraceptives carry 3 fold increase in VTE risk
  • Progesterone only pills no increase in risk
  • SPC, BNF, NICE recommend stopping COCP(Combined Oral Contraceptive Pill) 4-6 weeks before major elective surgery, leg surgery or surgery causing prolonged immobility

-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Describe the uses of MAOIs in surgery

A

Potentially fatal drug interaction
- analgesics
: tramadol increases serotonergic activity leading to CNS toxicity or increased convulsion risk

  • Sympathomimetics
    : risk of hypertensive crisis

Consult with prescriber of MAOIs before deciding to stop

  • reduce down to stop 2 weeks before surgery
  • switch to reversible MAOIs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Describe the use of Lithium in surgery

A
  • narrow therapeutic range
  • renally excreted
  • fluid imbalance can prescipitate toxicity
  • preferably stop 1-2 days before major surgery but consult psychiatrist

If continue…

  • monitor lithium levels
  • monitor fluid balance
  • avoid NSAIDs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Describe the uses of anti-convulsants & Parkinson’s medication

A
  • continuation of treatment essential
    : ensure taken on morning of surgery
  • consider alternative routes of administration if NBM or not absorbing post-operatively
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is required from an anaesthetic?

A
  • abolition of sensation
  • aboilition of pain
  • Triad of General Anesthesia
    : unconsciousness
    : analgesia
    : muscle relaxation
  • multiple drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Describe the 4 stages of anaesthesia

A

Stage 1: analgesia
- conscious, drowsy, antinociception, amnesia

Stage 2: excitement
- loss of consciousness but delirium, irregular cardiorespiration, apnea, spasticity, gagging, vomitting

Stage 3: anaesthesia
- regular respiration, loss of reflex and muscle tone

Stage 4: medullary paralysis
- depression of cardiorespiration, death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Describe different types of anaesthetics

A

Inhalation: gasses or vapours

  • controllable
  • rapid blood-gas exchange
  • usually halogenated ethers or hydrocarbons

Intravenous

  • injections
  • very rapid, short acting
  • induction or anaesthesia
68
Q

Describe Protein Theory regarding General Anaesthesia

A
  • based on the supposition that anaesthetics interact with membrane proteins (e.g receptors and ion channels) and alter their function
  • although anaesthetics can bind protein molecules, the levels of anaesthetics required to affect protein conformation or enzyme activity are much greater than those required for anaesthesia
69
Q

Describe Somatic Motor innervation

A
  • single motor neuron connecting CNS to the skeletal muscle
  • cell bodies are in the brain stem

Motor Unit
- the motor neurone + muscle fibre it nnervates

70
Q

Describe ACh release at the Neuromuscular junciton

A
  • Action potential conducted along the motor nerve
    : depolarisation
    : influx of calcium at nerve terminal
  • ACh released from storage vesicles into the synapse
  • High density of nicotinic receptors
  • ACh metabolised by acetylcholine esterases
71
Q

Describe Nicotinic receptors on skeletal muscle motor end plate

A
  • ligand-gated ion channel
  • contain alpha, beta, delta and gamma subunits
  • Two ACh molecules bind
  • Cation channel opens for 1 millisecond
    : Na+ in and K+ out
    : End plate depolarisation
  • CNS and ganglion nAChR have different subinits
72
Q

Describe Neuromuscular Junction plate

A
  • ACh binding to nicotinic receptors leads to Na+ influx
    : End Plate Potential
  • initiates opening of voltage-gated Na+ channels
    : action potential in muscle cell membrane
73
Q

Describe NMJ blocking drugs

A
  • interfere with post-synaptic action of ACh
  • Non-depolarising agents
    : act by blocking ACh
  • Depolarising blocking agents
    : weak nicotinic agonists
74
Q

How does Tubocurarine effect the Neuromuscular transmission?

A
  • nerve stimulation initiates end-plate potential (epp)
  • initiates action potential
  • Tubocurarine reduces the epp amplitude so that no action potential is generated
75
Q

What are the unwanted effects of non-depolarising blockers? (NMJ)

A
  • hypotension
    : due to ganglion blockade
  • Histamine release from mast cells
    : bronchospasm
  • Respiratory failure
    : assisted ventilation used
76
Q

Describe Depolarsing blocking agnets

A
  • initially bind and activate nicotinic receptor
  • opens end-plate voltage-sensitive Na+ channels
    : depolarises muscle
  • slowly hydrolysed by cholinesterases
  • depolarisation maintained at the end-plate
  • loss of electrical excitability
  • produces initial twitching of skeletal muscle prior to causing block
77
Q

What are the advantages of using depeolarising Neuromuscular blocker?

A

e.g
Suxamethonium
- rapid onset, short duration of action
- surgery during pregnancy/caesarean section
- less likely to elicit histamine release

78
Q

What are the unwanted effects of depolarising blockers? (NMJ)

A
  • Bradycardia
    : due to direct muscarinic action
  • Potassium release
  • post-op pain
  • increased intraocular pressure
  • prolonged paralysis
  • Malignant hyperthermia
79
Q

what are the key differences between depolarising and non-depolarsing neuromuscular blockers?

A
  • Non-depolarising
    : drugs ending with ‘-curonium’ or ‘-curium’
  • Depolarising
    : Suxamethonium
  • non-depolarising block is reversible by increasing ACh concentration
    : depolarising block no effect or potentiated
  • depolarising block produces initial fasciculation (small involuntary twitches)
  • Suxamethonium is hydrolysed by plasma cholinesterase and is shorter-acting than most non-depolarising drugs
80
Q

Describe different levels of Critical Care

A

Level 0
- patients whose needs can be met through normal ward care in an acute hospital

Level 1
- patients at risk of their condition deteriorating, or those recently relocated from higher levels of care, whose needs can be met on an acute ward with additional advice and support from critical care team

Level 2
- patients require more detailed observations or interventions, including support for a single failing organ system or post-operative care and those ‘stepping down’ from higher levels of care

Level 3

  • patients require advanced respiratory support alone or basic respiratory support together with the support of at least two organ systems
  • this level includes all complex patients requiring support for multi-organ failure
81
Q

What are the common reasons for admission to Critical Care?

A
  • post-operative
  • overdose / poisoning
  • post cardiac arrest
  • respiratory failure
  • pancreatitis
  • trauma
  • sepsis
  • circulatory shock
  • renal failure requiring RRT
  • severe neurological conditions
82
Q

Main reason for admission to ICU is the need for ‘advanced respiratory support’

What is the reason for invasive respiratory support?

A
  • protect the airway
    : e.g facial trauma, unconscious patient
  • treat profound hypoxaemia
    : e.g pneumonia, cardiogenic shock and pulmonary oedema
  • postoperative care
    : e.g after major, complicated or prolonged surgery
  • allow removal of secretions
    : e.g myasthenia gravis, Guillain-Barre syndrome
  • rest exhausted patients
    : e.g respiratory rate >30/min
  • avoid or control hypercapnia
83
Q

Why is sedation needed in Critical care?

A
  • alleviation of pain
  • facilitation tolerance & reduce distress
  • endotracheal tubes
  • to augment the effectiveness treatment
  • seizure control or management of intra-cranial pressure
  • to reduce anxiety and control agitation
84
Q

AKI is common in critically ill patients.

Why is this and how is it managed?

A

AKI common in critically ill patients due to

  • impaired renal perfusion
  • medication
  • primary renal disease

Managed by..

  • correcting circulation and optimising perfusion
  • avoid nephrotoxic medications
  • may need renal replacement therapy
85
Q

Describe infection and Sepsis in Critical Care

A
  • can be a cause for admission to an ICU or as a complication of other severe illness
  • sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection
86
Q

How is sepsis treated?

A
  • fluid resuscitation
  • aim for initial MAP of 65mmHg
    : fluids
    : vasopressors (noradrenaline)
  • send cultures then treat the underlying infection
    : IV antibiotics in under 1 hr
    : Viral/fungal?
    : optimise PK
  • support failing organs
87
Q

Describe different types of Shock (circulation)

A

Cardiogenic

  • Low CO, high SVR
  • heart failure, valvular heart disease

Hypovolaemic

  • Low CO, low CVP
  • haemorrhage, burns, diarrhoea, vomitting

Distributive

  • High CO, low SVR
  • Sepsis, anaphylaxis

Dissociative

  • High CO, inability to release O2 to tissue
  • carbon monoxide poisoning

Obstructive

  • Low CO, vessel blocked, resistance increased
  • PE, tension pneumothorax
88
Q

How is Shock (circulation) treated?

A
  • recognise cause
  • maintain circulating volume
    : fluids
    : crystalloid vs colloids
  • Vasopressors / inotropes
    : noradrenaline usually 1st line
    : essentially keeps you alive
  • other
    : steroids in sepsis
89
Q

What is Phenylketonuria?

A
  • very common inherited error in metabolism
  • results from deficiency in Phenylalamnine hydroxylase (PAH) which converts S-Phe to S-Tyr
  • overall incidence is ~1 in 10,000-15,000 in Caucasians and East Asians and ~1 in 25,000 in Latin Amaericans
  • It results in accumulation of S-Phe and reduced levels of S-Tyr in cells
  • High blood levels of S-Phe result
  • This causes gross neurological defects such as microcephaly and mental retardation
  • More subtle injuries occur with milder disease
  • Because of high incidence neonatal screening is performed
90
Q

Describe the normal metabolic pathway for phenylalanine

A
  • pathway occurs in the liver
    1. S-Phe to…
    2. S-Tye to…
    3. 3,4-dihydroxyphenylalanine (L-DOPA) to..
    4. Dopamine to..
    5. Noradrenaline to..
    6. Adrenaline
91
Q

Describe the phenylalanine hydroxylase (PAH) reaction

A
  • PAH is an allosteric liver enzyme with respect to S-Phe
  • ~90% of S-Phe is converted to S-Tyr in normal subjects and released into blood
  • The S0.5 value is ~145 micromolar
  • The enzyme is a tetramer with each monomer possessing catalytic, regulatory and tetramization domains
92
Q

How is phenylketonuria diagnosed?

A
  • all new born infants are screened for PKU soon after birth
  • current methods use mass spectrometry / mass spectrometry (MS/MS) to quantify levels of S-Phe in the blood
  • several other amino acids and metabolites are also quantified including S-Tyr. This allows differentiation of PKU due to PAH-deficiency, BH4 deficiency and other amino acidaemias
  • blood levels of S-Phe can be as high as 1200 micromolar
  • Blood S-Phe levels can fluctuate quite a lot during the day and over longer periods
  • it is Central Nervous System levels that appear to determine disease progression
93
Q

What is the consequence of phenylketonuria?

A
  • highly elevated S-Phe levels cause severe mental retardation in the patient
  • the standard treatment is therefore to restrict S-Phe dietary intake
  • Blood S-Phe levels of > ~800micromolar appear to increase reaction oxygen species production (inflammation)
  • Having PKU also appears to disturb nitric oxide (NO) levels, which is also a neurotransmitter
  • reduced levels of S-Tyr also often result in hypopigmentation
  • patients are prone to fractures due to poor bone metabolism
94
Q

Describe treatment of PKU with Large Neutral Amino Acid (LNAAs)

A
  • increased levels of LNAAs (tyrosine, tryptophan and branched aliphatic amino acids) appears to decrease absorbance of S-Phe from digestive system an hence lower blood S-Phe levels
  • LNAAs also compete for the amino acid transporter allowing access of amino acids to the brain
  • inclusion of LNAAs in the diet appears to have positive infleunce of executive function
95
Q

Just READ

- PKU

A

PKU is an extremely common ‘rare’ inborn error in metabolism

Due to severity and high incidence all children are screened shortly after been born

The main treatment is a low phenylalanine diet

Poor control of blood Phe levels results in irreversible brain damage

Use of Sapropetrin can allow relaxation of diet or in faviourable cases no dietary therapy

96
Q

What are the challenges of prescribing in pregnancy?

A
  • almost all women take some medication during pregnancy e.g paracetamol
  • about 1/3 are prescribed drugs in pregnancy but only about 1/2 take what is prescribed
  • women often make independent decisions about taking medicine in pregnancy
  • almost all medicine packaging states ‘if pregnant seek a medical opinion before taking’
97
Q

Describe ‘pregnancy trimesters’

A

pregnancy is divided into 3 trimesters

  • 1st is up to 13 weeks
  • 2nd is 13-28 weeks
  • 3rd is after 28 weeks
98
Q

Describe the change in Drug Absorption in Pregnancy

A

Morning sickness
- tablet may not stay down long enough to be absorbed
: can change timing
: can give with anti-emetic

Progesterone slows gastric emptying and can lead to slower absorption and lower peak drug conc.
Bigger problem with single doses as opposed to long term medication. Can be a problem with analgesics as time taken to be effective is longer

99
Q

Describe the change in Drug Distribution in Pregnancy

A
  • Total body water increase by about 81
  • This should dilute concentration of a drug but serum albumin also falls and pregnancy steroids displace drugs from their binding proteins so ‘free’ levels may actually rise
  • eg thyroxine, we use TSH not T3 or T4 to check thyroid functio
100
Q

Describe the change in Drug Metabolism in Pregnancy

A
  • catabolism of ‘active’ drugs to inactive metabolites AND anabolic activation of inactive precursor drugs
  • pregnancy affects both often acting through CYP450 enzymes
  • A clinically important example is that the enzyme which inactivates lamotrigene is induced by pregnancy
    : doses of lamotrigene need to be increased to get same effect
101
Q

Describe the change in Drug Excretion in Pregnancy

A
  • higher cardiac output leads to an increase of 50% in GFR
  • therefore renally excreted drugs e.g penicillin are excreted faster. Therefore in pregnancy we use 500mg ampicillin tds not 250mg tds
102
Q

Describe the change in Pharmacodynamics in Pregnancy

A
  • some drugs become less effective because of the underlying physiological changes of pregnncy
  • e.g b-blockers are less likely to cause bradycardia because of the tachycardia which exists in pregnancy.
    Ca channel blockers are less likely to decrease the total peripheral resistance because this is already reduced
103
Q

What is ‘Teratogenesis’?

A
  • 1-2% of babies born with a congenital abnormality
  • <1 in 20 of these can be attributed to drugs
    : difficult to estimate because most of the abnormalities can also occur spontaneously
  • if a tetratogenic agent is taken during the period embryogenesis (upto 8 weeks) the result will be an anatomical malformation
  • later in pregnancy function will be affected
104
Q

What is the cause of Teratogenesis?

A
  • methotrexate and thalidomide are unusual
    : if there are given to a pregnant women the majority of fetuses will be affected
  • with other drugs the risk of teratogenicity is small and dependent on other factors which are poorly understood
  • most cong abnormalities are multi-factorial
105
Q

Describe the placental transfer

A
  • most drugs cross placenta by simple diffusion
  • this depends on
    : conc gradient, molecular weight
  • in practice many drugs given to the mother in therapeutic concentration will eventually reach the fetus
  • Fetal metabolism also important
    :e.g iodine is concentrated in fetal thyroid and labetalol accumulates in the amniotic fluid
106
Q

What are the characteristics of teratogenic effect?

A

Species differences
- corticosteroids
: cleft palate in mouse, cardiac malformation in rabbits
- drug which is benign in animals may affect humans

Genetic differences

  • Gestational age
    : maximum susceptability is between 3-11 weeks of pregnancy during organogenesis
107
Q

What are the absolutely contraindicated drugs in pregnancy?

A
  • Cytotoxics
    : methotrexate, cyclophosphamide
  • Vitamin A
  • Cardiovascular
    : ACEi
  • Endocrine
    : radioactive iodine, sex hormones
  • Antibiotics
    : trimethoprim
  • Antifungal & anti-helminthics
108
Q

What are the relatively contraindicated drugs in pregnancy?

A
  • Lithium
  • Warfarin
  • B-blockers
  • Diuretics
  • Tetracycline, ciprofloxacin, nitrofurantoin
  • Phenytoin, valproate, Phenobarbitone
  • NSIADs in third trimester
109
Q

Describe how Diabetes is managed in Pregnancy

A
  • Glucose tolerance decreases with advancing gestation because of the anti-insulin effects of human placental lactogen, glucagon & cortisol
  • Therefore blood glucose levels will rise during pregnancy. Need to alter insulin doses almost daily
  • Aiming for normoglycaemia as much as possible
  • Poorly controlled diabetics have a high incidence of cong abnormalities
  • Optimise blood glucose control using either more frequent doses of insulin or metformin
  • Increase frequency of BS monitoring
  • > 4x daily injections of insulin / insulin pumps
110
Q

Describe how Epilepsy is managed in Pregnancy

A
  • Carbamazepine, valproate, phenytoin & phenobarbitone are all teratogenic
  • NTDs esp. valproate & carbamazepine
  • Congenital cardiac defects
  • Orofacial cleft linked with phenytoin usage
  • risk increases with polypharmacy
  • with valprooate the effect is dose-dependent
  • Lamotrigene similarly dose-dependent
- Minor malformations associated with use of anti-convulsants in pregnancy includes 
\: low-set ears
\: broad nasal bridge
\: irregular teeth
\: hypoplastic nails and digits
  • Mechanism may be folate deficiency. Evidence week but all epileptic women advised to take folate 5mg daily
  • Overall benefit of treatment outweighs risk
111
Q

Describe how High BP is managed in Pregnancy

A
  • important because women can have high BP pre-pregnancy
  • pre-eclampsia

Anti-hypertensives used commonly in pregnancy

  • Alpha-methyl dopa
  • Nifedipine
  • labetalol
  • hydralazine
  • ACEi, diuretics, ATII receptor blockers are contra-indicated
112
Q

When/Why access information in pregnancy?

A

Before concenption
- if on regular medicines

Whilst pregnant (antenatal)
- not considered medication a risk, unplanned pregnancy or no choice due to illness

After giving birth (postnatal)
- problem with baby and took medication in pregnancy

113
Q

What is the information needed before carrying out a research in pregnancy?

A
  • stage of pregnancy at time of exposure or if pregnant yet
  • medication involved
  • dose, frequency and route
  • indication
  • other options tried
  • pregnancy history
  • medical history
  • who is asking
114
Q

What are the information sources in Pregnancy?

A
  • BNF and BNF-C
  • Manufactures SPCs
  • Online resources e.g Toxbase
  • National MI specialist service (UKTIS)
  • Bumps: best use of medicines in pregnancy
115
Q

What are the potential adverse effects from medication use in pregnancy?

A
  • spontaneous abortions
  • intra-uterine growth retardation
  • prematurity
  • still births
  • obstetric complications
  • neonatal side-effects
  • mental impairment
116
Q

Describe the advantages of Breast feeding for baby

A

Immune function

  • maternal IgG antibodies cross the placenta
  • IgM is produced in response to infection
  • IgA initially only if baby receives colostrum an breast milk

Also reduces incidence of

  • diarrhoea
  • iron related anaemias

Reduced SID (sudden infant death) by 50%

Reduced adult obesity, diabetes, osteroporosis

117
Q

What is the advantage of Breast feeding for mother?

A
  • lower blood pressure & reduced blood loss postpartum
  • decreased risk of hip fracture, osteoporosis & RA
  • Protection against breast cancer
  • possible reduced risk of ovarian cancer
  • reduced risk postmenopausal CV disease
  • reduced response to stress
118
Q

Medication safety in BF depends on the significant of the excretion into the breast milk an the absorption by the baby

Describe different drug properties and how they distribute in breast milk

A

Acid-base balance

  • pH gradient between maternal plasma and breast milk
  • breast milk is slightly acidic compared to blood
  • weak acids e.g penicillins will have levels in breast milk less than half that in maternal plasma
  • weak bases become ionised in milk e.g isoniazid will have levels in breast milk that may be greater than in maternal plasma

Protein binding capacity
- medicines highly protein bound in maternal plasma will have low levels in breast milk

Lipid solubility

  • breast milk is a fat-in-water emulsion
  • medicines with a high lipid solubility are morelikely to pass into breastmilk because they are able to pass through the lipid membrane of the alverolar epithelium
  • fat can be a small proportion of milk volume so lipid solubility is not always a good predictor of drug accumulation in milk

Molecular weight
- medicines with MW <300 appear in breast milk quickly after maternal administration

Half-life
- drugs with longer half-lives have an increased risk of accumulating in the baby, increasing the risk of side effects

Bioavailability
- low or minimal oral bioavailability will not lead to significant systemic concentrations in the infant

119
Q

What are the factors producing poor excretion into breast milk?

A
  • high MW
  • highly protein bound
  • weak acid
  • short acting medication or preparation
  • no active metabolites
120
Q

Why should Codeine be avoided in pregnancy?

A
  • it can pass to the baby through breast milk and potentially cause harm
    : pro-drug partly metabolised by CYP2D6 enzyme to morphine
    : some individuals can be ultra-rapid metabolisers
  • Dihydrocodeine , tramadol as alternatives
121
Q

Describe VTE risk in pregnancy and how it is managed

A
  • VTE is upto 10 times more common in pregnancy with the pouerperium being the time of highest risk
  • RCOG guidelines advise that LMWHs and warfarin are not contraindicated in breastfeeding mothers
  • Dalteparin high MW, Warfarin highly protein bound hence safe in breastfeeding
122
Q

Describe how lactation is stimulated and suppresssed in pregnancy

A

Drugs used to stimulate lactation (galactagogues)
- dopamine D2 antagonist domperidone causes an increase in prolactin secretion and can improve milk production if absolutely necessary

Drugs used to suppress lactation
- dopamine receptor agonist cabergoline is licensed for suppression of lactation

123
Q

What are the common paediatric conditions to be aware in community pharmacy?

A
  • chicken pox
  • shingles
  • measles
  • mumps
  • food allergies
  • whooping cough
  • Croup
  • Impetigo
  • Slapped cheek syndrome
  • hand, foot and mouth
124
Q

Describe chicken pox, its referral symptoms and how it is managed

A
  • caused by the varicella zoster virus, a herpes virus
  • has a relatively long incubation period (10-20 days)
  • fever, headache & sore throat seen first followed a few days later by rash

Referral symptoms

  • secondary infection due to scratching
  • signs of chest infection
  • severely ill
  • any signs of chicken pox in pregnancy or new born

Treatment

  • for majority of children, chicken pox is uncomplicated and treatment is purely symptomatic
  • antipyretics: avoid ibuprofen
  • antihistamines
  • calamine
  • lifestyle advice
125
Q

Describe Shingles

A
  • may occur following a case of chicken pox
  • caused by varicella zoster virus lying dormant in dorsal root nerve ganglia
  • many occur at anytime
  • referral needed
126
Q

Describe Measles

A
  • infants and children regularly immunised against
  • incubation period of ~10days
  • highly infectious

Symptoms

  • fever 39degrees
  • cough and cold
  • sore throat
  • reddish eyes
  • sensitivity to light
  • Koplik’s spots
127
Q

describe Mumps

A
  • Paramyxo virus
  • incubation period 14-25 days
  • contagious about a week before breakout
  • spread by saliva

Symptoms

  • begins with 2 days of discomfort
  • increasing temperature
  • headache, ear ache, sore throat and pain on opening mouth
  • jaw stiffness
  • swollen parotid glands
  • earlobes may stick out
128
Q

Describe food allergens in children

A

most common foods that cause an allergy are

  • milk
  • eggs
  • peanuts
  • fish
  • shell fish
  • tree nuts

Signs to spot
- itching in mouth, throat or ears, skin rash, angioedema, vomiting, anaphylaxis

Referral needed to discuss potential allergy, especially if more significant reaction is seen

129
Q

Describe impetigo

A
  • caused by bacterial infection S.aureus
  • most common in young children
  • often is self-limiting, and will heal without scaring
  • stay away from school/nursery/work till healed
130
Q

Describe slapped cheek syndrome

A
  • spread via droplets
  • systemic infection presents 1st
    : high temp, sore throat and headache
  • birhg red rash develops on cheeks after 1-3 days
  • body rash may develop later
131
Q

Describe Han, foot and mouth disease in community pharamcy (paediatric)

A
  • acute viral infection, often mild and self limiting
  • spread via droplets, fluid filled vesicles and faeco-oral transmission
  • most common in young patient groups
  • few serious complications
  • sore throat, fever and rash as described
  • often self-limiting self care, analgesics, hygiene care to avoid transmission
132
Q

Describe Scarlet fever

A
  • Bacterial infection caused by Streptococcus pyogenes
  • sore throat, fever, headache, N&V and red sandpaper like rash
  • highly contagious via saliva or mucus
  • care to avoid spread
  • refer for antibiotic treatment and ND
133
Q

Describe Glandular fever

A
  • caused by Epstein Barr virus
  • long incubation period
  • in most people, infection lasts 2-3 weeks
  • consider referral if symptoms severe in adults and children
  • analgesics, rest within reason but not imposed bed rest, avoid spreading
134
Q

Why should Breast feeding be prompted?

A
  • unique, complex fluid containing energy, all essential nutrients and protection against infection and allergies
  • more convenient
  • cheaper, sterile, easier to digest
  • closer bonding, antural
135
Q

What is safeguarding?

A
  • protecting people’s health, wellbeing and human rights, and enabling them to live free from harm, abuse and neglect. It’s fundemental to high-quality health and social care
  • often focused on those who are in the most vulnerable circumstances and least able to protect themselves, often by virtue of being the weaker side in a power balance
  • safeguarding children and vulnerable adults is a key priority for all health care professionals and a statutory responsibility for local authorities
136
Q

Who are ‘children’ and ‘vulnerable adults’ under context of safeguarding legislation?

A

Children
- those who are under 18 years of age

Vulnerable adult

  • aged 18 years or over and at risk of abuse or neglect because of their needs for care and or support
  • elderly or frail
  • learning disabilities
  • suffers from mental illness
  • physical disability
  • substance misuser
  • homeless
137
Q

What types of abuses exist in terms of safeguarding issues?

A
  • Physical
  • Domestic
  • Sexual
  • Psychological
  • Financial or material
  • Modern slavery
  • Discriminatory
  • Organisational
  • Neglect and acts of omission
  • Self-neglect
138
Q

Why is prescribing more difficult in older people?

A
  • Frailty
  • multiple pathology
  • polypharmacy
  • difficulties with adherence
  • altered drug handling
    : physical changes, PK, PD
139
Q

Describe frailty in elderies

A
  • most often defined as a syndrome of physiological decline in late life, chractacterised by marked vulnerability to adverse health outcomes
  • Frail older adults are less able to adapt to stressors such as acute illness or trauma than younger or non-frail older adults
  • Increasingly, frailty in older patients is considered the hallmark geriatric syndrome and a forerunner to many other geriatric syndromes, including falls, fractures, delirium and incontinence
  • importantly, old age itself does not define frailty
140
Q

Describe Multiple Pathology in elderies

A
  • many disease states more common in older people
  • interactions between disease states and medicines
  • lack of appropriate trial data
141
Q

Define the following terms and how they are improved in eldery patients

  • Compliance

- Adherence

A

Compliance
- the extent to which the patient’s behaviour matches the prescriber’s recommendations

Adherence
- the extent to which the patient’s behaviour matches agreed recommendations from the prescriber

Non-adherence: unintentional

  • physical difficulty with packing or devices
  • poor swallow
  • confusion / memory problems
  • poor communication / lack of information
  • polypharmacy / complicated regimen

Non-adherence: intentional

  • deliberate adjustments
  • lack of confidence in medicines or prescriber
  • side effects or concerns about these
  • poly pharmacy / complicated regimen
  • poor communication / lack of information

Improving adherence

  • assess use of medicines
  • large print labels and leaflets
  • plain tops on bottles
  • medication reminder card
  • multi-compartment compliance aids e.g Dosette box
142
Q

For safe use of Multi-compartment compliance aids (MCAs) what checks need to be done from the patient?

A
  • knowledge
  • visual issues
  • manual dexterity
  • cognition
  • supply
143
Q

Describe the PK changes in eldery patients

A

Absorption

  • reduced rate by all routes but extent unchanged
  • reduced salivary flow, gastric emptying time, surface area for absorption, blood flow
  • increased gastric pH

Distribution

  • reduced perfusion = slower distribution throughout body
  • reduced body water = increased plasma concentration of water-soluble drugs
  • increased body fat = prolonged effects of fat-soluble drugs
  • reduced albumin = increased free concentration of protein-bound drugs
  • reduced muscle = increased free concentration of muscle-bound drugs

Metabolism

  • reduced hepatic perfusion
  • reduced first pass metabolism = increased blood levels
  • reduced hepatic enzymes

Elimination

  • most important PK change in elderlies
  • predictable age-related decrease in kidney function = accumulation of renally eliminated drugs
144
Q

Describe the change in PD in elderly patients

A
  • ‘Changes in target receptor sensitivity’
    : increased effects of CNS-acting drugs
    : decreased efficacy of beta blockers
  • changes in target organ responsiveness
  • loss of homeostatic mechanism
145
Q

What are the reasons for inappropriate prescribing

A
  • failure to recognise an adverse effects
  • patients’ or relatives demand or refusal of a drug
  • filure to individualise treatment
  • inadequate review
  • under prescribing because ‘old’
146
Q

What are the key paramters to monitor in elderly patients?

A
  • Haematology
    : FBC
- Biochemistry
\: LFTs
\: U&amp;Es
\: Blood sugar
\: TFTs
\: Blood lipids
  • Body mass index or equivalent
  • Drug therapeutic target ranges
147
Q

What is osteoporosis and how is it managed?

A
  • Osteoporosis is defined by a T-score of -2.5 SD or below on DXA scanning
  • T-score relates to the measurement of BMD using central DXA scanning
  • The aim of osteoporosis management is to reduce the risk of fracture by increasing bone mineral density and correcting deficiencies in calcium and vitamin D
  • current guidelines recommend oral bipohsphates first line for primary and secondary prevention of fractures
  • undesirable side effects and strict administration requirements assosicated with these medicines can lead to poor adherence
  • Second- and Third- line options include IV biphosphates, denosumab, raloxifene
148
Q

What are the lifestyle information and advice for managing osteoporosis?

A
  • take regular exercise to improve muscle strength
  • eat a blaanced diet as this may improve bone health
  • stop smoking if needed, as it is a risk factor for fragility fracture
  • Drink alcohol within recommended limits, as alcohol is a dose-dependent risk factor for fragility fracture
149
Q

Describe Age divisions in pre-18y/o

A

Preterm new-born
- <37 weeks gestation

Neonates
- 37+ weeks gestation & < 1 month post-natal age

Infants

  • 1 month to 2 years
  • early growth spurt

Child

  • 2 y/o to 11 y/o
  • gradual growth phase

Adolescent
- 12-18y/o

150
Q

What are the causes of prescribing errors?

A
  • incorrect prescribing
  • incorrect calculations
  • incorrect administration
  • incorrect equipment
  • interface issues
  • medication prescribed thati s contra-indicated
151
Q

Describe change in Absorption in paediatric patients

A
  • Gastric pH 6-8 at birth and reaches adult values at 2-3 years of age
  • ionisation of drugs is pH dependent so certain pH’s are required for certain drugs
  • Neonates also have reduced peristalsis and prolonged gastric emptying compared to adults leading to slower and unpredictable absorption
  • gastric emptying times normalise around 3y/o

Intramuscular
- erratic in neonates as muscle mass is low and blood flow through muscle is reduced and variable

Percutaneous
- inversely proportional of the thickness of the surface layer the stratum corneum and the hydration of the skin
- increased systemic absorption of topical substances in neonates and infants
: higher surface area to body weight ratio
: thin SC
: well hydrated skin

Rectal

  • may be incomplete/slow due to variable blood supply to the rectum
  • useful when the oral or parenteral routes are not available or appripriate
152
Q

Describe change in Distribution in paediatric patients

A

Increased total body volume

  • the % of body mass, total body water and extracellular fluid volume decreases with increasing age
  • neonates have a higher volume of distribution for water soluble drugs so they need higher doses than adults on a weight-to-weight basis
  • normal adult levels reached by 12 yrs of age
  • proportion of body fat increases rapidly in the first year. Starts to decrease as child becomes mobile
  • fats soluble drugs in neonates need smaller doses
  • reduced plasma protein concentration, binding capacity and affinity in neonates and infants as total protein concentrations and serum albumin are lower
  • may need to reduce doses of highly protein bound drugs in neonates
153
Q

Describe change in Metabolism in paediatric patients

A

Enzyme systems mature at different rates

  • hepatic phase I reactions appear to mature over the first few months of life and similar to adult at 6 months of age
  • hepatic phase II reactions increase significantly over the first 2-3 months of life and fully mature by about 3y/o
154
Q

Describe change in Excretion in paediatric patients

A
  • renal excretion depends on glomerular filtration rate, tubular secretion and tubular reabsorption which all mature at different rates
  • clearance of renally excreted drugs is prolonged in infants and especially in premature babies
155
Q

Define the following licensing temrs

  • Licensed
  • Unlicensed
  • Off-label
A

Licensed

  • shown to be safe and effective if used as licensed
  • is of a suitable quality

Unlicensed
- not licensed for any age group or indication

Off-label
- used outside the terms of the license

156
Q

What is Obesity and its impact expected in UK by 2020

A
  • excess accumulation of body fat sufficient to endanger health
  • 8 out of 10 men and 7 out of 10 women by 2020
157
Q

What is the treatment of obesity recommended by NICE?

A
  • Dietary changes
  • Behaviour modification
  • Exercise
  • Drug therapy
  • Surgery
158
Q

Who is Bariatric surgery for?

A
  • BMI of 40kg/m2 or more, between 35kg/m2~40kg/m2 and other significant disease that could be improved if they lost weight
  • All appropriate non-surgical measures have been tried but the person has not achieved or maintained adequate, clinically beneficial weight loss
159
Q

Describe surgery for Obesity

A

Gastric restriction

  • intra-gastric balloon
  • gastric banding
  • vertical banded gastroplasty
  • horizontal banded gastroplasty
  • sleeve gastrectomy

Malabsorptive surgery
- jejuno-ileal bypass

Gastric restriction & Malabsorptive surgery

  • gastric bypass
  • bilio-pancreatic bypass
  • duodenal switch
160
Q

What is the main physiological changes in Bariatrics surgery?

A
  • massive reduction in surface area of stomach
  • reduced gastric volume
  • bypass of main areas of drug absorption
  • pH changes
  • resultant weight loss
161
Q

Describe reduction in Gastric Surface Area after bariatrics surgery

A
  • all procedures result in reduced available surface area of stomach
  • only limited number of drugs are absorbed through the stomach wall
  • disintegration and dissolution occur in stomach
  • drugs in aqueous solution more rapidly absorbed than those in oily solutions, suspensions or solid forms
  • time for complete disintegration and dissolution affect absorption and resultant bioavailability
  • particular caution with drugs with narrow therapeutic index and sustained/modified release preparations
162
Q

Describe reduction in gastric volume after bariatrics surgery

A
  • stomach volume reduced to ~30ml
  • post-op oedema may further reduce stomach volume and opening into stomach
  • solid oral medicines may get stuck
  • avoid effervescent formulations
163
Q

Describe bypass of absorptive areas after bariatrics surgery

A
  • gastric bypass procedures create a malabsorptive state for food and oral drugs
  • main absorptive site for drugs: duodenum
  • absorptive sites for some drugs totally bypassed
  • For drugs absorbed throughout GIT
    : reduced surface area, time for absorption, enterophepatic circulation distrupted
    : unpredictable reductions in bioavailability
  • drugs with long absorptive phases that remain in the intestine for extended periods are likely to exhibit decreased bioavailability
164
Q

Describe pH changes after bariatrics surgery

A
  • partitioning of stomach results in decreased production of HCl
  • May affect bioavailability of drugs/formulations whose absorption is pH-dependent e.g iron and calcium
  • may be possible to use alternative salt forms or to artificially alter gastric pH
165
Q

Describe changes in volume of distribution after bariatrics surgery

A
  • patients may rapidly lose weight post-op
  • hence, altered volume of distribution
  • drugs that are highly lipid-soluble will have an altered volume of distribution
  • close monitoring essential
  • dose adjustment may be needed
166
Q

Describe pre-op and post-op considerations in bariatrics surgery

A

Pre-op

  • often complex polypharmacy due to co-morbidities
  • advise on appropriate peri-operative medicines management
  • VTE prophylaxis
  • initiate formulation/drug changes proactively

Post-op

  • close monitoring for efficacy of orally administered drug therapy
  • if lack of efficacy then suspect poor absorption
  • consider change of formulation or route
  • prone to deficiencies in fat-soluble vitamins, calcium and iron: supplements

Year 3 Sem 1 COPY COPY (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions