Pharma Paramedicine

Atropine Adenosine Amiodarone

Atropine , blocks rest and digest signals , last 30-60 min,

Bradycardia, airway secretions

Adenosine, slows conduction through conduction through AV node

SVT  

heat block, sick sinus, COPD (causes bronchospasm)

Amiodarone            Blocks K⁺ channels → prolongs repolarization                       

VF, VT

TDP,    WCT 2^nd to hyperK+  (>200ms & <12-bpm) , TCA OD

QAS STEMI ECG criteria and Thrombolysis and pPCI drugs

Normal QRS width and ACS symptoms with

• 1mm contiguous limb leads

• 1mm contiguous limb leads

• V1-V3 STD then> STE V7-V9 0.5mm in One lead

• De winter T wave , Tall symmetric T wave with STD in V1-V6 & STE 0.5mm inaVR

• Sgarbossa criteria in LBBB or paced rythm

 

Lysis

Thrombolytics (plasminogen activators, breaks down fibrin)

Tenecteplase IV (amount requested by consult clinician)

 

Anticoagulants (reduce fibrin formation)

Enoxaparin IV then sub-cut 15 min later (amount requested by consult clinician)

P2Y12I (antiplatelet)

Clopidogrel oral (non-reversable)

Ticagrelor (reversable, faster onset, more potent, more bleeding risk,)

COX-1 I (antiplatelet)

Aspirin

pPCI

Anticoagulants (reduce fibrin formation)

Heparin → (reversable), faster onset, adjusted in hospital

P2Y12I (antiplatelet)

Clopidogrel (non-reversable) OR

Ticagrelor (reversable, faster onset, more potent, more bleeding risk,)

COX-1 I (antiplatelet)

Aspirin

Thrombolysis Drugs QAS

Arterial clot = more platelets

Venous clot = more fibrin

Thrombolytics (plasminogen activators, breaks down fibrin)

Tenecteplase

 

Anticoagulants (reduce fibrin formation)

Enoxaparin → part of lysis, predicable, lasts longer, sometimes home med

 

P2Y12I (antiplatelet)

Clopidogrel (non-reversable)

COX-1 I (antiplatelet)

Aspirin

PCI drugs

Anticoagulants (reduce fibrin formation)

Heparin → PCI referral (reversable), faster onset, adjusted in hospital

P2Y12I (antiplatelet)

Clopidogrel (non-reversable) OR

Ticagrelor (reversable, faster onset, more potent, more bleeding risk,)

COX-1 I (antiplatelet)

Aspirin

Hypertension causes

Increased

• cardiac output

• Peripheral vaso construction

• Blood vessels stiffness

IImpacted renal sodium excretion

Conoary artery disease

Fatty plaque accumulation within conoary arteries, restricts blood flow.

HFrEF

Problem = weak pump

What heart needs = inotropy, stronger squeeze

Adrenaline = good

Fluids = often worsen, pump problem not preload problem

Hx - previous MI, poor perfusion, BB + duretic (spironolactone) + SGL2 I , ARNI

HFpEF

Problem = stiff ventricle , filling problem

What heart needs = preload + rate control, A1 stimulation without B1, Noradrenaline, Phenylephrine

Adrenaline = increased HR = reduced filling time = reduced cardiac output

Fluids = small amounts given slowly (overloading can cause APO)

Hx - elderly hypertensive, LVH, AF, Flash APO, worsened by increased HR, CCB + duretic

TXA

Inhibits plasminogen, stops breakdown of fibrin

Trauma (coats score >3, withing 3 hours)

• entrapment 1

• chest injury 1

• likely abdominal/pelvic injury 1

• temp < 35 1 < 32 2

• systolic < 100 1 < 90 2

Post partum hemorrhage

Severe Epistaxis

Post tonsillectomy hemorrhage

Antiplatelet vs anticoagulant

Antiplatelets inhibit platelet plug formation (arterial clots: ACS, stroke). Anticoagulants inhibit fibrin formation (venous clots: AF, DVT, PE).

What does β-blocker + non-DHP CCB + digoxin overdose look like?

Bradycardia + cold + shocked → think cardiogenic shock.

What does DHP CCB overdose and sepsis look like?

Warm, flushed, vasodilated shock ± tachycardia.

Which prescription drugs increase hyperkalaemia risk?

ACEi, ARB, ARA (spironolactone/eplerenone), ARNIs.

Patient has AF: what medications are they likely on?

Rate control (β-blocker, non-DHP CCB, digoxin) ± anticoagulant ± rhythm control (flecainide/amiodarone).

Patient takes GTN/nitrates: what does this suggest?

History of angina, ACS, APO or IHD (ischemic heart disease)

Patient takes amiodarone: what does this suggest?

Significant arrhythmia history (AF, VT, VF, refractory arrhythmias).

Patient takes flecainide: what does this suggest?

AF/SVT, often in structurally normal hearts.

Patient takes spironolactone

HFrEF, resistant hypertension, hyperkalaemia risk.

Patient takes sacubitril/valsartan (Entresto)

Strong clue for HFrEF

Patient takes frusemide

Heart failure, APO, fluid overload.

Patient takes apixaban/rivaroxaban

AF or DVT/PE history.

Patient takes warfarin

AF, mechanical valve, previous VTE.

Patient takes metoprolol

IHD, HF, AF rate control, post-MI.

Patient takes propranolol

Anxiety, tremor, migraine, portal hypertension.

Patient takes verapamil

AF/flutter, SVT rate control.

Patient takes digoxin

AF rate control ± heart failure.

Patient takes atorvastatin

CAD, dyslipidaemia, cardiovascular risk reduction.

Patient takes dapagliflozin

T2DM ± HFrEF.

Patient takes semaglutide

T2DM and/or weight management.

Patient takes metformin

T2DM, insulin resistance.

Patient takes insulin glargine

Basal insulin requirement (often T1DM).

Patient takes rapid acting insulin only

Meal coverage; think diabetes requiring tighter control.

Patient takes hydrocortisone

Adrenal insufficiency, asthma/COPD, refractory anaphylaxis.

Patient takes dexamethasone

Inflammatory conditions, airway oedema.

Patient takes loperamide

Symptomatic diarrhoea treatment.

Explain Type 1 diabetes

Autoimmune β-cell destruction → absolute insulin deficiency → younger onset → prone to DKA.

Explain Type 2 diabetes

Insulin resistance → compensatory insulin → β-cell dysfunction over time.

Explain gestational diabetes

Pregnancy hormones cause insulin resistance; usually 2nd–3rd trimester.

Explain other diabetes types

Type 3 (brain insulin resistance), Type 3c (pancreatic damage), Type 4 (lean elderly insulin resistance), Type 5 (malnutrition related).

Explain HFrEF vs HFpEF

HFrEF = weak pump/reduced EF. HFpEF = stiff ventricle/filling problem.

Explain why DKA occurs

Severe insulin deficiency → fat breakdown → ketones → metabolic acidosis.

Explain HHS

Severe hyperglycaemia with profound dehydration and hyperosmolarity (high glucose in blood) but minimal ketoacidosis.

Explain Addison’s disease

Primary = adrenal failure. Secondary = pituitary/hypothalamic failure → cortisol deficiency ± aldosterone deficiency.

Cortisol deficiency

Fatigue, weakness, lethargy, weight loss, loss of appetite, nausea/vomiting, abdominal pain, hypoglycemia, dizziness, poor tolerance to stress/illness, hyperpigmentation of skin creases / elbows / knees / scars / pressure areas

Aldosterone deficiency

hypotension, dehydration, salt craving, hyperkalemia, hyponatremia,

Hydrocortisone (preplaces cortisol / helps blood vessels respond properly to adrenaline and noradrenaline, reduces excessive glucose uptake be cells)

Explain cortisol function

Maintains BP, metabolism, glucose regulation, response to stress.

Explain aldosterone function

Regulates sodium, potassium, water and blood pressure.

Explain asthma pathophysiology, and treatments

• Airway inflammation Corticosteroids, _MgSO2

• Bronchoconstriction β₂ Receptor, Anticholinergics, MgSO2

• Mucus production Corticosteroids

→ airflow limitation. Triggers include allergy, infection, pollution and cold exposure

β₂ Receptor antagonists (Bronchodilators) Salbutamol > Adrenaline

Anticholinergics (Muscarinic Antagonists) Ipratropium prevent vagal-nerve-induced muscle tightening

Corticosteroids (Anti-inflammatories) Hydrocortisone, bind to glucocorticoid receptors to switch off inflammatory genes, indirectly assists with bronchoconstriction long-term > lowers airway hyperresponsiveness

Magnesium sulfate, blocks calcium influx into smooth muscle cells, inhibits acetylcholine release,

What medication groups are commonly used in asthma?

β2 agonists (salbutamol),

corticosteroids (hydrocortisone),

anticholinergics (ipratropium), magnesium sulphate.

Explain COPD pathophysiology

Combination of bronchoconstriction, inflammation and mucus plus irreversible air trapping, alveolar destruction and loss of elastic recoil.

Asthma vs COPD

Asthma is more reversible; COPD includes permanent structural lung changes and air trapping.

Explain ipratropium bromide mechanism

Blocks M3 muscarinic receptors → reduces intracellular calcium → decreases bronchial smooth muscle contraction

Explain salbutamol mechanism

β2 agonist → bronchodilation + drives potassium intracellularly via Na/K ATPase activation.

Why can salbutamol lower potassium?

Stimulates β2 receptors → activates Na/K ATPase → shifts potassium into cells

Explain magnesium sulphate in asthma

Competes with calcium → lowers intracellular calcium → smooth muscle relaxation and bronchodilation.

Explain croup

Viral inflammation/oedema of upper airway (larynx/trachea/bronchi), usually age 6 months–3 years → barking cough + stridor.

Croup medications

Dexamethasone or hydrocortisone ± adrenaline if severe.

Explain allergy vs anaphylaxis

Why can glucagon work in β-blocked anaphylaxis?

Bypasses β receptors by increasing intracellular cAMP directly.

Signs of hypoglycaemia

Sweating, tremor, hunger, tachycardia, anxiety, confusion, weakness, seizures, reduced GCS

Signs of hyperglycaemia

Polyuria, polydipsia, dehydration, abdominal pain, Kussmaul breathing, tachycardia.

Why does HHS cause dehydration?

Glucose pulls water into urine → osmotic diuresis → major fluid loss.

Explain Metformin (include common names)

Common names: Metformin (Glucophage®, Fortamet®, Glumetza®, Riomet®).
Mechanism: Reduces liver glucose production and improves insulin sensitivity.
Indications: T2DM, pre-diabetes, PCOS.
Risks: GI upset, B12 deficiency, lactic acidosis risk.

Explain DPP-4 inhibitors (include common names)

Common names: Sitagliptin (Januvia®), Saxagliptin (Onglyza®), Linagliptin (Tradjenta®), Alogliptin (Nesina®).
Mechanism: Increase insulin release when glucose is present, suppress glucagon, slow gastric emptying.
Indications: T2DM.

Explain Sulfonylureas (include common names)

Common names: Glipizide (Glucotrol®), Glyburide (DiaBeta®, Glynase®, Micronase®), Glimepiride (Amaryl®).
Mechanism: Stimulate pancreatic insulin release → increase endogenous insulin production.
Indications: T2DM, sometimes gestational diabetes.
Risks: Hypoglycaemia, rare reductions in WBC, RBC and platelets.

Explain Thiazolidinediones / TZDs (include common names)

Common names: Pioglitazone (Actos®), Rosiglitazone (Avandia®).
Mechanism: Increase insulin sensitivity and reduce insulin resistance.
Indications: T2DM, sometimes PCOS.
Risks: Fluid retention, peripheral oedema, worsened heart failure, weaker bones, liver toxicity.

Explain SGLT-2 inhibitors (include common names)

Common names: Canagliflozin (Invokana®), Dapagliflozin (Farxiga®), Empagliflozin (Jardiance®), Ertugliflozin (Steglatro®).
Mechanism: Prevent glucose reabsorption → increase urinary glucose loss.
Indications: T2DM, cardiovascular risk reduction.
Risks: UTI, DKA, GI effects.

Explain GLP-1 receptor agonists (include common names)

Common names: Semaglutide (Ozempic®, Wegovy®), Exenatide (Byetta®, Bydureon®), Liraglutide (Victoza®, Saxenda®), Dulaglutide (Trulicity®), Lixisenatide (Lyxumia®).
Mechanism: Increase insulin response and reduce appetite.
Risks: Hypoglycaemia and pancreatitis.

Explain Alpha-glucosidase inhibitors (include common names)

Common names: Acarbose (Precose®), Miglitol (Glyset®), Voglibose (Volix®).
Mechanism: Delay carbohydrate breakdown → slower glucose absorption.
Indications: T2DM, pre-diabetes.
Risks: GI side effects.

Explain Rapid-acting insulin (include common names)

Common names: Insulin Aspart (NovoRapid®), Insulin Lispro (Humalog®).
Onset: ~10–20 min
Peak: ~1–3 hrs
Duration: ~3–5 hrs
Use: Mealtime insulin.

Explain Short-acting insulin (include common names)

Common names: Regular insulin (Humulin R®).
Onset: ~30–60 min
Peak: ~2–4 hrs
Duration: ~5–8 hrs
Use: Mealtime insulin, DKA.

Explain Intermediate-acting insulin (include common names)

Common names: NPH (Humulin N®).
Onset: ~1–2 hrs
Peak: ~4–12 hrs
Duration: ~12–18 hrs
Use: Basal coverage.

Explain Long-acting insulin (include common names)

Common names: Insulin Glargine (Lantus®), Insulin Detemir (Levemir®).
Onset: ~1–2 hrs
Peak: Minimal
Duration: ~20–24 hrs
Use: Basal insulin.

Patient takes Jardiance (empagliflozin) — what does this suggest?

2DM ± cardiovascular risk reduction ± possible HFrEF history.

Patient takes Ozempic — what does this suggest?

T2DM management and appetite/weight reduction strategy.

Patient takes NovoRapid + Lantus — what does this suggest?

Basal–bolus insulin regimen, commonly Type 1 diabetes.

Patient takes metformin + gliclazide pattern — what does this suggest?

T2DM requiring insulin sensitisation plus increased insulin production.

Explain thrombolysis

Breaks down existing fibrin clot using plasminogen activators.
Indications: STEMI, ischaemic stroke, life-threatening PE.

Explain Tenecteplase

Common name: Tenecteplase
Class: Thrombolytic (plasminogen activator)
Mechanism: Breaks down fibrin clot.
Indications: STEMI, selected stroke, severe PE.

Explain antiplatelets (include common names)

Common names: Aspirin, Clopidogrel, Ticagrelor.
Mechanism: Prevent platelet aggregation → reduce platelet plug formation.
Best for: Arterial clots (ACS, stroke, TIA).

Explain anticoagulants (include common names)

Common names: Warfarin, Heparin, Apixaban, Rivaroxaban, Dabigatran.
Mechanism: Reduce fibrin clot formation.
Best for: AF, DVT, PE.

Explain Heparin

Answer:

Common name: Heparin
Class: Anticoagulant
Mechanism: Reduces fibrin formation.
Notes: Faster onset, reversible, adjusted in hospital.
Indications: PCI referral, PE.

Explain Enoxaparin

Common name: Enoxaparin
Class: Anticoagulant
Mechanism: Reduces fibrin formation.
Notes: Predictable effect, longer duration.
Indications: Part of thrombolysis pathway.

Explain Warfarin

Common name: Warfarin
Mechanism: Inhibits vitamin K clotting factors.
Notes: Requires INR monitoring; affected by dietary vitamin K.
Indications: AF, mechanical valves, DVT/PE history.

Explain Direct Factor Xa inhibitors

Common names: Apixaban (Eliquis®), Rivaroxaban (Xarelto®).
Mechanism: Inhibit factor Xa → reduce clot formation.
Indications: AF, DVT, PE.

Explain Dabigatran

Common name: Dabigatran (Pradaxa®)
Mechanism: Direct thrombin inhibitor.
Indications: AF, DVT, PE.

Explain Aspirin

Common name: Aspirin
Class: COX-1 inhibitor (antiplatelet)
Mechanism: Prevents platelet aggregation.
Indications: IHD, ACS prevention.
OD clue: Tinnitus + metabolic acidosis.

Explain P2Y12 inhibitors

Common names: Clopidogrel (Plavix®), Ticagrelor (Brilinta®).
Mechanism: Antiplatelet action.
Indications: Stents, ACS.
Difference: Ticagrelor = faster, reversible, more bleeding risk.

Explain statins

Common names: Atorvastatin (Lipitor®), Rosuvastatin (Crestor®).
Mechanism: Lower LDL cholesterol.
Indications: CAD, dyslipidaemia.

Ischaemic stroke medication priorities

Antiplatelets become important after imaging; anticoagulants usually avoided initially; thrombolysis selected cases.

PE medication priorities

Anticoagulants are usually primary treatment; thrombolysis reserved for severe/life-threatening cases.

Patient takes Eliquis (Apixaban) — what does this suggest?

AF, DVT or PE history

Patient takes Xarelto (Rivaroxaban) — what does this suggest?

Long-term anticoagulation for AF or VTE (Veinous Thromboembolism) .

Patient takes Warfarin — what does this suggest?

AF, previous DVT/PE or mechanical heart valve.

Patient takes Clopidogrel — what does this suggest?

ACS history, coronary stent or stroke/TIA prevention

Patient takes Ticagrelor — what does this suggest?

More recent ACS or post-PCI antiplatelet therapy.

Patient takes Atorvastatin — what does this suggest?

CAD, vascular risk reduction, dyslipidaemia

Patient takes Entresto + spironolactone + frusemide — what does this suggest?

Strong clue for HFrEF

Patient takes nitrates + statin + antiplatelet — what does this suggest?

Likely established ischaemic heart disease / CAD

Explain Amiodarone

Common name: Amiodarone (Cordarone®)
Class: Antiarrhythmic
Mechanism: Blocks potassium channels (prolongs repolarisation), blocks calcium channels (slows AV node), inhibits sodium channels (slows conduction).
Indications: VF, VT, AF, refractory arrhythmias.
OD: Bradycardia, QT prolongation.

Patient takes Amiodarone — what does this suggest?

Significant arrhythmia history (AF, VT, VF or refractory arrhythmia).

Explain Flecainide (include common name)

Common name: Flecainide (Tambocor®)
Class: Sodium channel blocker antiarrhythmic
Mechanism: Slows conduction.
Indications: AF/SVT (often structurally normal heart).
Risk: Pro-arrhythmic.
OD: Wide complex arrhythmia, arrest.