PSA Flashcards

1
Q

Give 6 examples of enzyme inducers:

A

“PC BRAS”
Phenytoin
Carbamazepine
Barbiturates
Rifampicin
Alcohol (chronic excess)
Sulfonylureas

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2
Q

How do enzyme inducers affect drug metabolism?

A

Increase P450 enzyme activity in the liver -> hastening drug metabolism -> reducing the drug’s therapeutic effect

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3
Q

How do enzyme inhibitors affect drug metabolism?

A

Decrease P450 enzyme activity in the liver -> slowing drug metabolism -> increasing the drug’s therapeutic effect

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4
Q

Give 9 examples of enzyme inhibitors:

A

“AO DEVICES”
Allopurinol
Omeprazole
Disulfiram
Erythromycin
Valproate
Isoniazid
Ciprofloxacin
Ethanol (acute intoxication)
Sulphonamides (sulfasalazine)

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5
Q

Name 7 drugs that should be stopped before surgery:

A

“I LACK OP”
Insulin
Lithium
Anticoagulants/antiplatelets
COCP/HRT
K-sparing diuretics
Oral hypoglycemics
Perindopril and other ACEi

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6
Q

How long before surgery should you stop lithium?

A

Day before

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7
Q

How long before surgery should you stop the COCP or HRT?

A

4 weeks before

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8
Q

How long before surgery should you stop perindopril and other ACEi?

A

The day of surgery

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9
Q

Name 9 things to check on every prescription chart:

A

PReSCRIBER:
Patient details
Reactions (any allergies plus the reaction caused)
Signed
Contraindications (any CI for each of the drugs prescribed)
Routes of each drug
IV fluids (do they need any? are they prescribed?)
Blood clot prophylaxis if needed
anti-Emetic if needed
pain Relief if needed

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10
Q

How will erythromycin interact with warfarin?

A

Increases warfarin’s anticoagulant effect, unpredictably raising the INR

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11
Q

Give 3 contraindications to antiplatelets and anticoagulants:

A

Active bleeding
Suspected bleeding
Risk of bleeding (e.g. prolonged PT due to liver disease, risk of haemorrhagic transformation follow ischaemic stroke)

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12
Q

Give 8 side effects of steroids:

A

“STEROIDS”
Stomach ulcers
Thin skin
Edema
Right and left heart failure
Osteoporosis
Diabetes
Infection (including candida)
cushing’s Syndrome

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13
Q

Give 5 safety considerations for prescribing NSAIDs:

A

“NSAID”
No urine (i.e. renal failure)
Systolic dysfunction
Asthma
Indigestion (of any cause)
Dyscrasia (clotting abnormality)

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14
Q

Give two possible side effects of beta blockers:

A
  1. Wheeze in asthmatics
  2. Bradycardia
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15
Q

Give 2 possible side effects of ACEi:

A
  1. Dry cough
  2. Electrolyte disturbances
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16
Q

Give 3 possible side effects of CCBs:

A
  1. Peripheral oedema
  2. Flushing
  3. Bradycardia (only some CCBs)
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17
Q

Give 4 possible side effects of diuretics:

A
  1. Electrolyte disturbances
  2. Renal failure
  3. Gout (thiazide like diuretics)
  4. Gynaecomastia (K-sparing)
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18
Q

Why should you never prescribe trimethoprim and methotrexate together?

A

Both are folate antagonists, together they can cause bone marrow toxicity leading to pancytopenia and neutropenic sepsis

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19
Q

Give an example of when it would be appropriate to stop/pause a patient’s methotrexate prescription:

A

During active infection

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20
Q

What electrolyte disturbances can the following drugs cause?
1. Loop diuretics e.g. furosemide
2. Thiazide diuretics & thiazide-like diuretics e.g. indapamide
3. K-sparing diuretics e.g. amiloride hydrochloride
4. ACEi e.g. ramipril

A

ALL diuretics can cause hyponatraemia (although if they cause dehydration, this can result in hypernatreamia)
1 & 2 = hypokalaemia
3 & 4 = hyperkalaemia

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21
Q

How long should you avoid giving VTE prophylaxis for following a stroke?

A

Varies across the UK but generally not for a few months

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22
Q

All insulin is given s/c - give one exemption to this rule:

A

short-acting insulin on a sliding scale e.g. actrapid and novorapid can be given IV

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23
Q

Give 4 causes of hypernatraemia: (hint - 4Ds)

A

Dehydration
Drugs
Drips - too much IV saline
Diabetes insipidus

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24
Q

Give 4 causes of hypokalaemia:

A

“DIRE”
Drugs - loop diuretics and thiazide diuretics
Inadequate intake or intestinal loss (D&V)
Renal tubular acidosis
Endocrine (cushing’s and conn’s syndrome)

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25
Q

Give 5 causes of hyperkalaemia:

A

“DREAD”
Drugs - K-sparing diuretics and ACEi
Renal failure (AKI and CKD)
Endocrine (addison’s)
Artefact (very common due to clotted sample)
DKA

Plus: rhabdomyolysis, tumour lysis syndrome

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26
Q

A raised urea normally indicates kidney injury - BUT if you have a raised urea with a normal creatinine and your patient is not dehydrated, what other important cause must you rule out?

A

In an upper GI bleed Hb is broken down by gastric acid into urea, and then absorbed into the blood -> raised urea, normal creatinine, not dehydrated!
Check if their Hb has dropped indicating a bleed.

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27
Q

How do you determine if a patient’s levothyroxine dose needs adjusting?

A

Look at TSH levels:
<0.5 mlU/L = decrease dose
0.5-5 mlU/L = no change required
>5 mlU/L = increase the dose

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28
Q

Chest x-ray interpretation:
What does the acronym RIPE prompt you to check?

A

Rotation - is the distance between the spinous processes and the clavicles equal?
Inspiration - is there adequate inspiration? You should be able to see 5-6 anterior ribs or 8-10 posterior ribs
Projection - AP or PA? Remember you cannot comment on heart side on an AP film
Exposure - The left hemidiaphragm should be visible to the spine and the vertebrae should be visible behind the heart.

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29
Q

Chest x-ray interpretation:
What should you check under ‘A’?

A

A = airway
Is the trachea central?
Is the carina visible?
Can you see the left and right main bronchi

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30
Q

CXR Interpretation:
What should you check under ‘B’?

A

B = Breathing
LUNGS
Divide each lung into three zones
Compare left and right lung in each zone:
- Are lung markings present throughout?
- Is there any asymmetry?
- Are there any opacities?
PLEURA
- Fluid in the pleural space? (hydrothorax)
- Blood in the pleural space? (haemothoraz)

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31
Q

CXR Interpretation:
What should you check under ‘C’?

A

C = Circulation/cardiac
Heart size (no more than 50% of thoracic width)

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32
Q

CXR Interpretation:
What should you check under ‘D’?

A

D = diaphragm
Right slightly higher than left
Costophrenic angles - unclear/blunted angles can indicate fluid, consolidation or lung hyperinflation
Gastric bubble under left diaphragm

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33
Q

CXR interpretation:
What should you check under ‘everything else’?

A

Aortic knuckle
Bones
Tubes
Lines
Artificial valves
Pacemaker
ECG nodes
Sternotomy clips (loop like wire loops in the centre of the chest)

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34
Q

Interpreting ABGs:
Describe the 7 steps to interpreting an ABG

A
  1. Look at the PaO2:
    - is it normal? (PaO2>10 kPa on room air, or ~10kPa less than the % inspired concentration FiO2 if receiving O2 therapy)
  2. Look at the pH:
    - <7.35 = acidotic
    - >7.45 = alkalotic
  3. Look at PaCO2:
    High CO2 + low pH = respiratory acidosis
    Low CO2 and high pH = respiratory alkalosis
  4. Look at HCO3-
    - low HCO3- and low pH = metabolic acidosis
    - high HCO3- and high pH = metabolic alkalosis
  5. Look for any compensation:
    - Respiratory compensation = blowing off CO2 to increase pH, or retaining CO2 to decrease pH
    - Metabolic compensation = kidneys increasing HCO3 to raise pH or decreasing HCO3 to decease pH
    - Metabolic compensation takes at least a few days to develop
  6. Look at the base excess
    - >+2 = high HCO3-
    - <-2 = low HCO3-
  7. Check the anion gap:
    Na+ - (Cl- +HCO3-)
    Normal = ~4 to 12
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35
Q

4 causes of a high anion gap

A
  1. DKA
  2. Lactic acidosis
  3. Aspirin overdose
  4. Renal failure
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36
Q

4 features of digoxin toxicity:

A
  1. confusion
  2. nausea
  3. visual halos
  4. arrhythmias
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37
Q

Early, intermediate and late features of lithium toxicty:

A

Early: tremor
Intermediate: tiredness
Late: arrhythmias, seizures, coma, renal failure, diabetes insipidus

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38
Q

5 features of phenytoin toxicity:

A
  1. Gum hypertrophy
  2. Ataxia
  3. Nystagmus
  4. Peripheral neuropathy
  5. Teratogenicity
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39
Q

2 features of gentamicin toxicity:

A

Ototoxicity
Nephrotoxicity

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40
Q

2 features of vancomycin toxicity:

A

Ototoxicity
Nephrotoxicity

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41
Q

Managing over anti-coagulation in a patient who is not bleeding:

A

INR 5-8 = omit warfarin for 2 days then restart

INR >8 = omit warfarin and give 1-5mg PO vit K

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42
Q

Managing over anti-coagulation in a patient with minor bleeding:

A

INR 5-8 = omit warfarin and give 1-5 mg IV vit k

INR >8 = omit warfarin an give 1-5 mg vit k IV

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43
Q

Management of a STEMI (8)

A
  1. ABCDE
  2. O2 15L non-rebreather mask (only if hypoxic, do not give in COPD)
  3. Aspirin 300mg PO
  4. Morphine 5-10mg IV with cyclizine 50mg IV
  5. GTN spray/tablet
  6. Primary PCI (preferred) or thrombolysis
  7. Beta blocker 2.5mg PO unless asthmatic or LVF
  8. Transfer to CCU
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44
Q

Management of an NSTEMI (6)

A

BATMAN:
Beta-blocker unless CI
Aspirin 300mg stat dose PO
Ticagrelor 180mg PO (or clopidogrel 300mg PO)
Morphine 5-10mg IV with cyclizine 50mg IV
Anticoagulant - fondaparinux or LMWH
Nitrates

Give O2 if sats dropping

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45
Q

Management of acute left ventricular failure (8)

A
  1. ABCDE
  2. O2 15L non-rebreather mask (unless COPD)
  3. Sit patient up
  4. Morphine 5-10mg IV with cyclizine 50mg IV
  5. GTN spray/tablet
  6. Furosemide 40-80mg IV (repeat again as required/tolerated)
  7. If inadequate response, isosorbide dinitrate infusion +/- CPAP
  8. Transfer to CCU
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46
Q

What adverse features indicate unstable tachycardia? (4)

A

Tachycardia with:
- shock
- syncope
- MI
- Heart failure

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47
Q

How do you manage unstable tachycardia?

A
  1. Synchronized DC shock, up to 3 attempts
  2. Amiodarone 300mg IV over 10-20 mins and repeat shock; followed by:
  3. Amiodarone 900mg over 24 hrs
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48
Q

What constitutes a ‘narrow’ QRS?

A

<0.12 seconds (3 small squares)

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49
Q

How do you manage re-entry paroxysmal SVT?

What would this look like on ECG?

A

Monitor ECG continuously
1. Use vasovagal manoeuvres
2. Adenosine 6mg IV rapid bolus; if this is unsuccessful then give 12mg; if still unsuccessful give a further 12mg
3. If sinus rhythm is restored this was likely a re-rentry paroxysmal SVT
4. If the re-entry paroxysmal SVT recurs, give adenosine again and consider anti-arrhythmic prophylaxis

If sinus rhythm is NOT restored after step 2 - seek expert help! This could be atrial flutter and would require rate control e.g. beta-blocker

ECG: tachycardia, narrow QRS, regular

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50
Q

What drug is used to manage re-entry paroxysmal SVT?

A

Adenosine

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51
Q

Does re-entry paroxysmal SVT have a narrow or broad QRS?

A

Narrow (<0.12seconds/3 small squares)

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52
Q

How do you manage atrial fibrillation?

What would this look like on ECG?

A

Control rate with beta-blocker or diltiazem (CCB).

ECG: Tachycardia, narrow QRS, irregular, absent p waves, chaotic baseline

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53
Q

Which types of arrhythmia might cause an irregular tachycardia with a broad QRS? (2)

A
  1. Variants of AF (AF w/ BBB, pre-excited AF)
  2. Polymorphic VT
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54
Q

How do you manage tachycardia caused by AF with bundle branch block?

A

The same way you manage AF normally!

Control rate with beta-blocker or ditiazem.

Consider digoxin or amiodarone if evidence of heart failure.

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55
Q

How do you manage polymorphic VT/torsade de pointes?

A

Correct electrolyte imbalance
2g IV magnesium over 10 mins
Should spontaneously resolve - be prepared to shock if not (can develop into ventricular fib)

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56
Q

How do you manage ventricular tachycardia?

What does ventricular tachycardia look like on ECG?

A

Amiodarone 300mg IV over 20-60 mins; then 900mg over 24 hours

Regular tachycardia with broad QRS

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57
Q

How do you manage SVT with BBB?

A

Adenosine 6mg rapid bolus IV
Give 12mg if unsuccessful
Give a further 12mg if still unsuccessful

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58
Q

How do you treat ventricular tachycardia if the patient is stable?

A

Amiodarone: 300mg IV over 20-60 mins, then a further 900mg over 24 hours

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59
Q

Give 2 arrhythmias that might be treated with adenosine:

A
  1. Re-entry paroxysmal SVT
  2. SVT with BBB

(In both cases: 6mg rapid IV bolus, repeat with 12mg if successful, repeat with a further 12mg if still unsuccessful)

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60
Q

How do you manage anaphylaxis? (5)

A

REMOVE THE CAUSE ASAP!
1. ABCDE
2. 15L O2 non-rebreather mask
3. Adrenaline 500 micorgrams of 1:1000 IM (repeat if no improvement after 5 mins)
4. Chlorphenamine 10mg IV (antihistamine is only given once patient is stable)
5. Hydrocortisone 200mg IV

NB:
Treat wheeze if asthmatic
Amend drug allergies box!

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61
Q

Mx of an acute asthma exacerbation:

A

Oh SHIT Me
1. Oxygen
2. Salbutamol 5mg neb
3. Hydrocortisone 100mg IV if severe/life-threatening or predisolone 40-50mg PO if moderate
4. Ipratropium 500 micrograms neb
5. Theophyline or aminophylline if life threatening
6. Magnesium sulphate

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62
Q

How do you treat an acute exacerbation of COPD?

A

Same as asthma exacerbation - Oh SHIT Me, add abx if infective exacerbation

AND be cautious with high flow O2!

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63
Q

A very sick patient (peri-arrest) has known COPD - should you give o2?

A

Yes - give high flow o2 and review quickly after with an ABG
Hypoxia kills quicker than hyprecapnia!

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64
Q

If a patient with COPD is hypoxic but NOT peri-arrest, how should you start O2 therapy?

A

Start with 28% O2 and do an ABG 30 mins later to assess the effect

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65
Q

How do you treat a pneumothorax secondary to lung disease?

A

Chest drain if >2cm or patient has SOB or if patient is >50 years old

Otherwise aspirate

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66
Q

How do you treat a primary spontaneous pneumothorax?

A

If <2cm rim and not SOB discharge and follow-up in 4 weeks

If >2cm rim or SOB aspirate (up to 2 attempts, then try chest drain)

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67
Q

What is the CRB-65 score?

A

Used to decide on tx of pneumonia:
C - confusion
R - resp rate ≥ 30
B - systolic BP <90
65 - 65 years or older

One point for each

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68
Q

What tx would a CRB-65 score of 1-2 indicate?

A

Low risk - give 500mg amoxicillin TDS PO for 5 days

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69
Q

What tx would a CRB-65 score of 3-4 indicate?

A

High risk - consider admitting anyone with a score of 2 or more

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70
Q

How do you manage a PE?

A
  1. High flow O2
  2. Analgesia: morphine 5-10 mg IV with cyclizine 50mg IV
  3. Anticoagulation for at least three months: apixiban, rivaroxaban (can be used in renal impairment), (LMWH can be used in renal failure)
  4. If low BP; give IV fluid bolus and contact ITU and consider thrombolysis
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71
Q

What does class IV haemorrhagic shock consist of? (7)

A

Blood loss >2000ml
Blood loss >40%
Heart rate >140bpm
Blood pressure decreased
Resp rate >40
Urine output <5ml/hr
Confused/unresponsive

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72
Q

How do you manage an acute upper GI bleed? (9)

A
  1. ABC and O2
  2. Cannulas: two large bore
  3. Catheter: monitor strict fluid balance, aim for >30mls/hr urine output
  4. Crystalloid fluid: 500ml hartmann’s or normal saline bolus over 15 mins (250ml if increased risk of overload e.g. HF)
  5. Cross-match 6 units and coagulation screen
  6. Correct clotting abnormalities:
    - if platelets <50 x10^9/L give platelet transfusion
    - if PT/aPTT more than 1.5 times normal give fresh frozen plasma
  7. Camera: endoscopy should be performed on all unstable patients with severe UGIB immediately after resus, within 24 hours
  8. Culprit drugs: stop NSAIDs, warfarin, heparin, aspirin (if bleed was due to warfarin give prothrombin complex!)
  9. Senior help/surgeons!
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73
Q

What is Supraventricular Tachycardia?

A

In normal circumstances, electrical impulses are transmitted from the SA node to the AV node. The AV node causes a delay to allow the ventricles to fill completely before contracting. This maintains the normal heart rate.

In SVT an abnormal electrical pathway originating from above the ventricles (i.e. in the atria) bypasses the AV node, accelerating the heart rate and causing ventricles to contract before they’re completely full.

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74
Q

What is re-entry SVT?

A

The AV nodal tissue has two pathways that form a circle.
An impulse will get stuck going round and round this circuit very fast and emitting depolarizing impulses to the rest of the myocardium.

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75
Q

4 differentials for a narrow QRS complex tachycardia:

A
  1. Sinus tachycardia
  2. Supraventricular tachycardia
  3. Atrial fibrillation
  4. Atrial flutter
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76
Q

How do you differentiate between the 4 types of narrow QRS complex tachycardia?

A

Sinus tachy: normal PQRS formation
SVT: regular rhythm
Atrial fib: irregularly irregular
Atrial flutter: atrial rate of ~300 bpm gives ‘sawtooth’ baseline

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77
Q

Management of a seizure: (7)

A
  1. ABC
  2. Recovery position and O2
  3. Lorazepam 2-4mg IV or diazepam 10mg IV or midazolam 10mg IV
  4. Repeat dose if still fitting in after 5 mins
  5. Inform anaesthetist
  6. If still fitting after a further 5 mins give Phenytoin 15-20 mg/kg IV
  7. If still fitting after another 5 mins give propofol and intubate and ventilate
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78
Q

Management of a stroke: (5)

A
  1. ABC
  2. Head CT to exclude haemorrhage
  3. If onset <4.5 hours ago -> thrombolysis
  4. Aspirin 300mg
  5. Transfer to stroke unit
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79
Q

Diagnostic criteria for DKA:

A

Blood glucose >11mmol/l or known diabetes
Ketones >3 mmol/L or +2 on urine dipstick
pH <7.3 or HCO3- <-15

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80
Q

Mx of DKA: (4)

A
  1. ABCDE
  2. IV saline (initially 1L over an hour, then continue at a slower rate)
  3. Fixed rate insulin infusion (0.1 unit/kg/hr)
  4. Monitor continuously (frequent VBGs), should improve within 6-24 hours
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81
Q

Treatment targets for DKA: (4)

A
  1. Decrease in ketones by 0.5 mmol/L/hr
  2. Increase in HCO3- by 3mmol/L/hr
  3. Decrease in CBG by 3mmol/L/hr
  4. Maintain K+ at 4-5.5 mmol/L
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82
Q

3 possible complications of DKA:

A
  1. HypoK leading to VT
  2. Cerebral oedema
  3. High risk of thrombosis/DVT
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83
Q

Diagnostic criteria for hyperosmolar hyperglycaemic state:

A

Hyperosmolarity >320mmol/L
Hyperglycaemia >30mmol/L
No/low ketones <3mmol/L
No acidosis pH>7.3
Hypovolaemia

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84
Q

Management of hyperosomlar hyperglycaemic state:

A
  1. ABCDE
  2. replace fluids slowly
  3. encourage eating and drinking, monitor CBG
  4. continually assess for cerebral oedema, DVT, foot ulcers
  5. ONLY start insulin if glucose does not start to fall with fluids - go low and slow (0.05 units/kg/hr)
85
Q

How do you manage an acute poisoning?

A
  1. ABC
  2. Cannula, catheter, strict fluid balance
  3. Correct any electrolyte imbalance
  4. Reduce absorption if within 1 hour of poisoning:
    - gastric lavage
    - whole bowel irrigation (if lithium/iron)
    - charcoal (dx dependent)
  5. Increase elimination: give generous IV fluids plus specific antidote

+/- pysch input

86
Q

What medication is used to treat paracetamol overdose and when?

A

if paracetamol level at 4 hours or more is over the line on the treatment nomogram give N-acetyl cysteine

87
Q

What medication is used to treat opioid overdose and when?

A

Naloxone if there is slow breathing or GCS is low

88
Q

What is stage 1 HTN?

A

clinic BP ≥140/90 or ABPM ≥135/85

89
Q

At what point should you offer treatment for HTN?

A

Always offer stage 2 and above drug treatment.
Offer stage 1 drug treatment if <80 years old and has any one of:
- end organ damage
- established CVS disease
- renal disease
- diabetes
- 10 year CVS risk equivalent to 10% or more

90
Q

What is stage 2 HTN?

A

Clinic BP ≥160/100, ABPM >155/95

91
Q

What is severe HTN?

A

clinic systolic BP ≥180 or diastolic ≥110

92
Q

Give examples of the following types of drugs used in HTN tx:
ACEi
ARB
CCB
Thiazide-like diuretic

A

ACEi = ramipril
ARB = candesartan, losartan, valsartan
CCB = amolodipine, verapamil, nifedipine
Thiazide-like diuretic = indapamide

93
Q

Draw out the flowchart for the NICE guidance on treating HTN:

A
94
Q

What scoring system is used to help determine whether a patient should be anticoagulated to reduce their risk of having a stroke?

A

CHA2DS2-VASc

95
Q

What makes up the CHA2DS2-VASc score?

A

Congestive heart failure
Hypertension
Age >75 (contributes 2 points)
Diabetes
Stroke or TIA previously (2 points)
Vascular disease (PAD or IHD)
Age 65-74
Sex (female)

96
Q

What CHA2DS2-VASc score would indicate the need for anticoagulation?

A

1 = if male

2+ = if male or female

97
Q

If a patient has AF and you want to anticoagulate them, what scoring system could you use to help determine their bleeding risk?

A

HAS-BLED

98
Q

What makes up the HAS-BLED scoring system?

A

Hypertension
Abnormal renal function
Stroke
Bleeding tendency
Labile INR
“Elderly” (>65)
Drugs (aspirin, alcohol, NSAIDs)

99
Q

What does a HAS-BLED score of 1-2 indicate?

A

Low to moderate risk of bleeding, anticoagulation can be considered

100
Q

What does a HAS-BLED score of 3 or more indicate?

A

High risk of major bleeding, alternatives to anticoagnulation should be considered

101
Q

In a patient in acute AF, when would you offer rhythm control?

A

Only if AF is onset less than 48 hours

102
Q

How is rhythm control achieved in AF? (2 options)

A

Cardioversion:
- Electrical
- Pharmacological = flecanide (if no structural heart disease) or amiodarone

NB: Amiodarone should NOT be used for long term rate control

103
Q

In a patient in acute AF, when would you offer rate control and how?

A

If presenting with onset >48 hours ago
Rate control with either bisprolol 2.5mg OD or diltiazem 120mg OD
If monotherapy doesn’t work use dual therapy with any two of: beta-blocker, diltiazem, digoxin

104
Q

Stepwise management of adult asthma:

A
  1. SABA
  2. Add low dose ICS
  3. Add LTRA
  4. Switch to LABA + ICS (+/- LTRA)
  5. Switch to MART (+/- LTRA)
  6. Increase ICS
  7. Seek expert advice
105
Q

Give an example of an LTRA:

A

Montelukast

106
Q

Give an example of a LABA

A

salmeterol

107
Q

Give an example of an ICS

A

beclemetasone

108
Q

Give an example of a SAMA

A

Ipratropium bromide

109
Q

Give an example of a SABA

A

salbutamol

110
Q

What is MART?

A

Maintenance and reliver therapy: a single inhaler is used for both PRN symptom relief and daily maintenance

Will contain a LABA and ICS

111
Q

When should you consider stepping up a patient’s asthma treatment?

A

If using their SABA ≥3 times/week

112
Q

What pattern of spirometry is seen in COPD?

A

Obstructive picture with an FEV1/FVC ratio of <0.7

113
Q

Long term tx for COPD: (4)

A
  • pneumococcal vaccine + annual flu vaccine
  • SABA or SAMA for PRN Sx relief
  • if no asthmatic features: LABA + LAMA
  • if asthmatic/steroid responsive features: LABA + ICS
114
Q

What is alpha-1antitrypsin deficiency?

A

ɑ1AT is a glycoprotein produced largely by the liver
It is responsible for balancing the action of neutrophil-protease enzymes in the lungs
A deficiency in ɑ1AT can lead to increased elastase, breaking down alveolar walls and causing emphysematous changes
It is a genetic condition caused by a mutation on chromosome 14

115
Q

UC:
Where?
Continuous or skip lesions?
Transmural or superficial mucosa affected?

A

An inflammatory bowel disease limited to the colon and rectum
Causes continuous inflammation affecting the superficial mucosa

116
Q

Inducing remission in a mild-moderate UC flare: (3)

A
  1. topical ASA (mesalazine, sulfasalazine)
  2. still not better after 4 weeks? add an oral ASA
  3. still not better? add or swap to short course of steroids
117
Q

Inducing remission in a severe UC flare: (3)

A
  1. IV steroid
  2. consider adding IV clicosporin or infliximab (DMARDs)
  3. consider surgery
118
Q

Maintaining remission in UC:

A

If proctitis/protosigmooiditis: topical and/or oral ASA
If left-sided and extensive UC: low dose oral ASA
Consider adding oral azathioprine or mercaptopurine if had 2 or more flares in prev. 12 months or struggling to maintain remission

119
Q

Crohn’s:
where?
continuous or skip lesions?
transmural or superficial mucosa inflammation?

A

Affects any part of the gut from the mouth to the anus
Skip lesions
Transmural granulomatous inflammation

120
Q

Crohn’s:
investigations (3)

A

Endoscopy = gold standard
May also have a colonoscopy as long as there is no sepsis/perforation
May have barium studies to show strictures/fistulae/rose thorn ulceration

121
Q

How do you induce remission in mild a Crohn’s flare?

A

Prednisolone 20-40mg PO OD

May be given a 5-ASA if very mild disease in the colon only

122
Q

How do you induce remission in a severe Crohn’s flare?

A

Hydrocortisone 100-500mg TDS-QDS IV and supportive care (fluids, nil by mouth, abx)

123
Q

How do you maintain remission in mild-moderate Crohn’s?

A

1st line: azathioprine or mercaptopurine
2nd: methotrexate

124
Q

How do you maintain remission in severe Crohn’s?

A

Infliximab and adalimumab (used for fistulating, can only be used 12mo at a time)

125
Q

Why do you have to check TPMT levels before starting azathioprine?

A

Azathioprine is a pro-drug that is metabolized by the liver to the active agent 6-metacaptopurine.
6-metacaptopurine needs the enzyme TPMT be metabolised to its inactive form.
10% of the population have hereditary low TPMT.
This would lead to a build up of 6-metacaptopurine that can cause liver and bone marrow toxicity.

126
Q

Give three common side effects of sodium valproate:

A
  1. Tremor
  2. Teratogenicity
  3. Weight gain
127
Q

Give 2 important side effects of lamotrigine:

A
  1. rash
  2. steven-johnson syndrome (rare)
128
Q

What is steven-johnson syndrome?

A

An immune-complex mediated hypersensitivity disorder ranging from mild skin and mucous membrane lesions to a severe, sometimes fatal, systemic illness - toxic epidermal necrolysis (TEN).

Most commonly caused by drugs.

129
Q

What is levetiracetam? Give 3 common side effects:

A

AKA keppra - used to treat partial-onset/myoclonic/tonic-clonic seizures

fatigue, mood disorders, agitation

130
Q

What is carbamazepine used for? (2)

A

Anticonvulsant used to treat epilepsy and neuropathic pain (e.g. trigeminal neuralgia, diabetic neuropathy)

131
Q

5 common side effects of carbamazepine:

A
  1. rash
  2. dysarthria
  3. ataxia
  4. nystagmus
  5. Low Na
132
Q

Name four types of laxative:

A

stool softners
bulking agents
stimulant laxatives
osmotic laxatives

133
Q

Give an example of a stool softner:
When are stool softners useful?

A

Sodium docusate*
When there is faecal impaction

*NB: stimulant at higher doses!

134
Q

Give an example of a bulking agent laxative:
When are they contraindicated? (3)
How quickly do they work?

A

Isphagula husk
CI: faecal impaction, colonic atony, reduced gut motility
Can take days to develop effect

135
Q

Give two examples of stimulant laxatives:

A

senna
bisacodyl
NB: can worsen abdo cramps

136
Q

Give two examples of osmotic laxatives:

A

lactulose
phosphate enema (CI in IBD!)
NB: may exacerbate bloating

137
Q

How do you treat chronic non-infective diarrhoea?

A

loperamide 2mg PO up to 3 hourly
or codeine 30mg PO up to 6 hourly (to also relieve pain)

NB: must be proven non-infective by negative stool cultures and microscopy

138
Q

At what time of day should you give corticosteroids? Why?

A

In the morning - cause insomnia

139
Q

Hypnotics to assist with insomnia should be avoided as much as possible - if you had to, what would you give?

A

start with zopiclone 7.5mg PO nightly in adults, 3.75mg in the elderly

140
Q

GO THROUGH CONTRACEPTIVES - UKMEC

A
141
Q

Gout:
- chronic prevention

A

allopurinol to reduce uric acid level

142
Q

Name a blood pressure medication that is teratogenic in the first trimester:

A

ramipril

143
Q

REVISE HRT

A
144
Q

What is a high dose regimen of gentamicin?

A

5-7 mg/kg once daily

145
Q

How is gentamicin prescribed for a patient with severe renal failure or endocarditis?

A

A divided daily dose (1mg/kg) 12 hourly in renal failure

A divided daily dose (1mg/kg) 8 hourly in endocarditis

146
Q

Your patient weighs 50kg and has a creatinine clearance of 15mL/min - what dose of gentamicin should you give and at what frequency?

A

Creatinine clearance <20 = severe renal failure
Dose = 1mg/kg 12 hourly

1 x 50 = 50mg every 12 hours

147
Q

How frequently are gentamicin normally monitored?

A

Once daily - exact regimen varies locally e.g. 6-14 hours after the previous infusion started

148
Q

What chart do you use to check gentamicin levels and how?

A

7mg/kg dose = Hartford nomogram
5mg/kg = urban and craig nomogram

Plot the blood concentration of genetamicin on the y-axis, against the time of sampling against the x-axis.
If the plot point falls within the 24 hour area continue with the same dose.

If it falls in the 36hr area, change to 36 hourly dosing interval.
If it falls in the 48hr area, change to 48 hourly dosing interval.
If it falls above the 48hr area, repeat the level and only give the next dose once gentamicin concentration is <1mg/L

149
Q

What medications are used to manage chronic heart failure and why? (5)

A
  1. ACEi: improves ventricular function, reduces mortality (switch to ARB if not tolerated)
  2. Beta-blocker: reduces heart rate, myocardial oxygen demand and RAAS activtation
  3. Loop diuretic if fluid overloaded (titrate to clinical response)
  4. Low dose aldosterone anatgonist (if still symptomatic despite 1, 2 & 3)
  5. Third line HR drugs (see next card)
150
Q

6 types of drug that can cause hyperkalaemia:

A
  1. ACEi
  2. ARBs (candesartan, losartan)
  3. NSAIDs/COX 2 inhibitors
  4. Digoxin (in toxicity)
  5. Trimethoprim
  6. K-sparing diuretics
  7. Beta-blockers
  8. Nicorandil
  9. Heparin
  10. Ciclosporin
  11. Tacrolismus
  12. Potassium supplements
  13. Renin-inhibitors (aliskiren)
151
Q

3 ECG changes seen in hyperK:

A

tall tented t waves
flattened p waves
broad qrs complex

152
Q

When should you treat hyperkalaemia?

A

K+ ≤ 6mmol/L with otherwise stable renal function: no urgent tx, consider changing diet/medications

K+ ≥ 6mmol/L with ECG changes: urgent tx
K+ ≥ 6.5mmol/L: urgent tx

153
Q

First line tx for hyperkalaemia?

A

Insulin: actrapid 10 units
AND
Dextrose: 50mls of 50%

+ clacium gluconate to protect the myocardium and prevent arrhythmias

154
Q

Other than giving insulin, how can you treat hyperkalaemia?

A
  • Salbutamol neb (temporarily drives k+ into cells)
  • IV fluids (to increase urine output, caution in renal failure)
  • Oral calcium resonium (draws K+ out of gut slowly, for mild cases)
  • Dialysis (for severe/persistent hyperK associated with renal failure)
155
Q

3 notable side effects of metformin:

A

Diarrhoea
Abdominal pain
Lactic acidosis

156
Q

Metformin carries a risk of lactic acidosis, it is therefore contraindicated if: (2)

A

creatinine >150
or
eGFR <30mL/min/1.73m^2

157
Q

When prescribing vancomycin, what is the most important baseline parameter to check and why?

A

Serum creatinine

Vancomycin is renally eliminated. Clearance is reduced in patients with renal dysfunction - you must take this into account when choosing the dosing regimen.

158
Q

Statins carry a risk of myopathy - any patient at a higher risk of developing this side effect must have what checked at baseline?

A

creatinine kinase level

159
Q

Which patients are at a higher risk of developing myopathy when taking a statin? (6)

A

Anyone with any of the following risk factors:
1. Personal or family hx of muscle disorders
2. High alcohol intake
3. Prev hx of muscular toxicity
4. Renal impairment
5. Hypothyroidism
6. The elderly

160
Q

If a patient has no risk factors for myopathy, what baseline parameter should you check before starting a statin?

A

serum AST or ALT

statins are metabolised by the liver, if AST/ALT is >3xs normal, or in active liver disease -> statin is CI

161
Q

When is the recommended sampling time for lithium?

A

12 hours after the last dose

162
Q

What is the normal reference range for lithium levels?

A

0.4-0.8mmol/L

163
Q

At what level will toxic effects of lithium manifest?

A

serum concentrations above 1.5mmol/L

164
Q

How frequently should you check the FBC of a patient on lithium?

A

Once before treatment initiation - no requirement for regular measurement during treatment

165
Q

How frequently should lithium levels be checked?

A

Weekly after treatment intiation or any change to dosing, until lithium conc. stabilises.
Then once stable check every 3 months.

166
Q

How does sodium affect the risk of lithium toxicity?

A

Sodium depletion increases the risk of toxicity. Patients should be advised to avoid making dietary changes that would lead to increased or decreased sodium intake.

167
Q

How is methotrexate excreted?

A

Predominantly renally excreted - therefore toxicity is more likely in the presence of renal dysfunction

168
Q

How frequently should you monitor FBC in a patient on methotrexate?

A

every 2-3 months once treatment has stablised

169
Q

Drug monitoring: two possible side effects of olanzapine that require monitoring

A

Hypercalcaemia & diabetes -> check at baseline and regular intervals

170
Q

Drug monitoring for amiodarone:

A
  1. Baseline serum potassium
  2. Baseline CXR (risk of pulmonary toxicity)
  3. TFTs at baseline & every 6 months (continue for several months after stopping treatment)
171
Q

How is digoxin eliminated/excreted?

A

The majority is (50-70%) is excreted by the kidneys - therefore those with CKD/AKI etc are at an increased risk of toxicity

172
Q

What monitoring is required for patients taking sodium valproate?

A

baseline & regular LFTs (risk of hepatotoxicity)

173
Q

A patient taking sodium valproate develops severe abdominal pain radiating to their back, what side effect has occurred? How should you alter the valproate?

A

Pancreatitis
Stop!

174
Q

All antipsychotics require monitoring of which hormone?

A

Prolactin - baseline, 6 months, then yearly

175
Q

Venous thromboprophylaxis following total hip replacement:

A

LMWH for 10 days followed by aspirin for 28 days
OR
LMWH for 28 days with stockings
OR
Rivaroxaban (look up dose)

176
Q

Hypoglycaemia: what blood glucose level requires medical treatment?

A

<4mmol/L

177
Q

How do you manage hypoglycaemia with a CBG of <4mmol/L? (1st and 2nd line)

A

First line: oral glucose - repeat every 15mins up to 3xs
Second line (if unable to swallow or doesn’t respond to 1st line): 10% glucose IV infusion

178
Q

3 examples of NSAIDS:

A

Ibuprofen
Diclofenac
Naproxen

179
Q

3 examples of anti-platelet medications:

A
  1. Aspirin (COX inhibitor)
  2. Clopidogrel (ADP receptor inhibtor)
  3. Ticagrelor (ADP receptor inhibitor)
180
Q

4 types of anticoagulant drugs:

A
  1. Factor Xa inhibitors: apixaban, rivaroxaban, fondaparinux
  2. Unfractionated heparin
  3. LMWH: dalteparin, enoxaparin
  4. Warfarin (a coumarin, limits availability of vit K)
181
Q

Other than the usual side effects (STEROIDS acronym), what can glucocorticoids contribute to in the elderly?

A

Confusion

182
Q

How might you manage breakthrough pain in a patient using a fentanyl patch?

A

Patients receiving at least 25 micrograms of transdermal fentanyl per hour can use nasal fentanyl for breakthrough pain (look up dose)

183
Q

A week prior to elective surgery a patient’s anticoagulation is stopped. Their INR is checked on the day before surgery, how you should respond to the result?

A

if INR > 1.5 the day before surgery, give phytomenadione (vit K) 1-5 mg PO or IV (check dose)

184
Q

1 nanogram = ?micrograms

A

1 nanogram = 0.001 micrograms

185
Q

Cholestatic jaundice can commonly occur during/shortly after treatment with flucloxacillin - this is especially common in which demographic?

A

Men and patients >65 years

186
Q

Phenytoin has zero-order kinetics and therefore a very narrow therapeutic index - you need to increase a patient’s dose, how much should you do this by?

A

by the minimum amount possible!

187
Q

What is gelofusine? When is it used?

A

A blood plasma replacement used to treat low blood volume in hypovolaemic shock, burns and cardiopulomnary bypass

188
Q
A

A solution of albumin protein, used in

189
Q

UKMEC 4 criteria for the progesterone only impact/nexplanon:

A

Active breast cancer
(also UKMEC4 for progesterone only pill)

190
Q

UKMEC 1 to 4 meaning:

A

1 = no restriction
2 = benefits > risks
3 = risks > benefits
4 = absolutely contraindicated

191
Q

UKMEC 3 criteria for COCP:

A

BMI >35

192
Q

UKMEC 4 criteria for COCP: (give 4 examples)

A

Uncontrolled HTN
Migraine with aura/sensorimotor sx
History of VTE
>35 years and smoking>15/day
Major surgery
Vasc disease or stroke
IHD, AF or cardiomyopathy
Liver cirrhosis or tumours
SLE or antiphospholipid syndrome

193
Q

Someone with epilepsy taking phenytoin, carbamezepine, barbituates, primidone, topiramat or oxcarbazepine should be recommended which type of contraceptive?

A

Depot injection, IUD or IUS = UKMEC1

(COCP and POP = UKMEC3)
(implant = UKMEC 2)

194
Q

What is the treatment for acute oculogyric/dystonic crisis?

A

Procyclidine 5-10mg

195
Q

Which hormones are low in primary adrenal insufficiency/Addison’s?

A

Dependent on the layer of the adrenal medulla that is affected:
- Zona Glomerulosa = low aldosterone
- Zona Fasicualata = low cortisol
- Zona Reticularis = low androgens (testosterone precursor specifically)

196
Q

Symptoms of Addison’s disease:
How do these relate to the hormones affected by this disease?

A

Low aldosterone = High K+, Low Na+, hypovolaemia, metabolic acidosis

Low cortisol = low blood sugar at times of high stress, increased melanocyte stimulating hormone causing skin hyperpigmentation

197
Q

How do you test for primary adrenal insufficiency?

A

Short synacthen test: measure baseline cortisol, give synthetic ACTH, measure again after 30 mins, measure again after 60 mins

Cortisol should at least double in response to ACTH, if it fails to double = primary adrenal insufficiency

198
Q

What is Cushing’s syndrome?

A

A syndrome involving excessive cortisol, which effects the body in the following ways:
1. Anti-insulin → hyperglycaemia, lipolysis & fat mobilisation
2. Muscle protein degradation → muscle wasting
3. Immunosuppression/anti-inflammation → easy bruising, poor wound healing

199
Q

Symptoms of Cushing’s syndrome: (10)

A

C - cataracts
U - ulcers
S - skin bruising and thinning
H - hypertension, hirtuism
I - infection
N - necrosis of the femoral head
G - glycosuria
O - obesity (buffalo hump, central adiposity) and osteoporosis
I - irritability/depression/lethargy
D - diabetes

200
Q

What is Cushing’s disease?

A

A pituitary tumour secreting ACTH leading to bilateral adrenal hyperplasia → excessive cortisol

201
Q

What is a phaeochromocytoma?

A

A rare adrenal tumour that secretes cathecholamines (dopamine, norepinephrine, epinephrine).

Presents with a classic triad of: excessive sweating, episodic headache, tachycardia.

Other Sx: paroxysmal HTN, palpitations, tremor, SOB

202
Q

Describe the pathophysiology of type 1 diabetes:

A

Autoimmune destruction of pancreatic beta cells leading to absolute insulin deficiency.
Associated with HLA-DR4 and HLA-DR3 genes.

203
Q

5 investigations used to diagnose type 1 diabetes:

A

Fasting glucose > 7
Random glucose > 11
OGTT: measure fasting glucose, drink 75 g glucose drink, measure again in two hours → >11.1
Islet cell antibodies and GAD antibodies
C-peptide - measures endogenous insulin

204
Q

Blood glucose and HbA1c targets for type 1 diabetes:

A

CBG on waking: 5-7
CBG before meals: 4-7
HbA1c measured every 3-6 months, target of 48 or lower

205
Q

3 types of insulin regimen:

A
  1. Basal-bolus: intermediate/long acting insulin before bed, rapid/short-acting before meals (this if first line for adults)
  2. Once daily: one long acting before bed (gargaline/detemir)
  3. Twice daily: one injection before breakfast, one injection before dinner, both contain a mix of short and intermediate acting insulin
206
Q

Diagnostic criteria for type 2 diabetes:

A

HbA1c ≥ 48
Fasting glucose ≥ 7
Random plasma glucose ≥ 11
OGTT at two hours ≥ 11

207
Q

Pre-diabetes criteria:

A

HbA1c 42-47
Fasting glucose 6.1-6.9
OGTT: plasma glucose at 2 hours is 7.8 -11.1

208
Q

1st, 2nd, 3rd, 4th line treatment for type 2 diabetes:

A

1st: lifetsyle changes ± metformin
2nd: if HbA1c rises to 58 → dual therapy of metformin + one other DM2 drug (see below)
3rd: triple therapy or switch to metformin + insulin regimen
4th: switch one of the drugs to a GLP-1 mimetic or try insulin therapy

DM2 drugs:
- Metformin
- Pioglitazone
- Sulfonylurea e.g. gliclazide
- DPP-4 inhibitors e.g. sitagliptin
- SGLT-2 inhibitors e.g. empagliflozin
- GLP-1 mimetics e.g. exenatide

209
Q

Name 6 types of drug used to manage type 2 diabetes and how they work:

Which ones can cause hypoglycaemia?

A
  1. SGLT-2 inhibitors e.g. empagliflozin: increase glucose excretion in the urine (“glucose flozin the urine”)
  2. GLP-1 mimetic e.g. exenatide: incretins (like GLP-1) increase insulin secretion and slow GI absorption making you feel fuller (“exenatide tides you over till your next meal”)
  3. DPP-4 inhibitors e.g. sitagliptin: inhibit DDP-4 enzyme which inhibits GLP-1 (DPP-4 inhibitors Pack a Punch giving you a fat lip = sitagLIPtin)
  4. Thiazolidinedione e.g. pioglitazone: increase insulin sensitivity, decrease gluconeogenesis in the lliver (all contain “zone”)
  5. Sulfonylureas e.g. glicazide
  6. Metformin - increases insulin sensitivity

Hypoglycaemia: sulfonylureas (gliclazide), GLP-1 mimetics (low risk)