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Drugs Flashcards

Learn the drugs and their associated features

1
Q

Mild pain/fever. Reversible inhibitor of PGHS domain.

ADR - liver toxicity, alcohol induces CYP2E1 so increases NAPBQI

A

Paracetamol

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2
Q

Mild pain/inflam. NSAID, competitive inhibitor of PGHS cyclo oxygenase domain. Similar to Aspirin (reversible). Can increase risk of gastric bleeding due to decreased platelet count

A

Ibuprofen

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3
Q

Mild to moderate pain. Opioid receptor agonist. Suppresses synaptic communication can cause addiction and neurological issues. Contraindicated if acute respiratory depression or coma.

A

Codeine

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4
Q

Moderate/unresolved pain. Glucocorticoid steroid agonist (down regulate inflam response). Can cause Cushings (excess cortisol (adrenal gland disorder)) and immune suppression.

A

Prednisolone

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5
Q

Inappropriate. a= opiod analgesic for chronic. b= severe trauma for neuropathic pain.

A

a=morphine b=ketamine.

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6
Q

First abx . high bacterial resistance. Bacteriocidal via b-lactam blocking peptidoglycan synthesis in cell wall (resistance= b-lactamase) ADR = anyphlyaxis

A

Penicillin , give vancomycin if allergic

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7
Q

Good for STI/UTI until resistance increases. Bacteriostatic via quinolone acts as inhibitor of topoisomerase. Prevents bacterial DNA replication (resistance=no binding site)
ADR - Achilles tendon rupture (rare)

A

Ciprofloxacin

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8
Q

‘last resort’ abx but resistance is increasing. Bacteriocidal. Drug -> cell membrane -> ion pores form -> depolarise bacteria -> kill. Resistance S aureus produce MprF (mutated multipoeptide resistance factor) prevents binding. Contraindicated if pregnant

A

Daptomycin

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9
Q

Gastro/duodenal ulcers. Irreversible PPI that blocks HTPase (normally pumps H+ into stomach).
Contra = C difficile, may mask gastric cancers

A

Esomprazole

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10
Q

Gastro/duodenal ulcers. Competitive H2RA so histamine can’t trigger H+ increase. Patients may gain tolerance and mask cancer symptoms.

A

Ranitidine

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11
Q

Acid that neutralises OTC antacids (CaCO3/MgCO3) that are strong alkaline in solution, long term increase in HCl (counter effects). ADR - burping from CO2 liberation.

A

Rennies

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12
Q

Anti coag so increased clot risk (non trauma e.g. turbulent blood flow from AF). Competitive inhibitor of Vit K epoxide reductase (VKOR) so 2,7,9,10. Antidote is Vit K
ADR - haemorrhage, jaundice and pancreatitis.
Contraindicated on NSAIDs

A

Warfarin

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13
Q

Anti platelet in increased risk of vascular trauma platelet activation (eg. post MI) that could lead to vascular clotting (thrombosis). Inhibits platelet P2Y12 ADP receptor (sensitises collagen -> aggregation).
ADR = GI / inter cranial bleeds

A

Clopidogrel

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14
Q

Fibrinolytic (clot buster) used for thrombus causing tissue schema. Recombinant form of tissue plasminogen factor (tPa) mediates plasminogen into plasmin therefore rapidly dissolves by fibrinolysis. Antidote = tranexamic acid
ADR - serious bleeds

A

Tenectaplase

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15
Q

DOACs, don’t need INR monitory and softer than warfarin/heparin

A

Direct acting oral anti coagulants e.g.. Dabigatran

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16
Q

Bronchodilator for acute asthma. B2 adrenoreceptor agonist -> cAMP -> SM dilation.
Contra = CV disease

A

Salbutamol

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17
Q

Bronchodilator for acute asthma. M3 ACh receptor antagonist. Blocks M3 so cGMP down -> SM dilation.
Contra = CV disease

A

Ipratopium

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18
Q

Potent anti inflam steroid drug. Can be used with the others. Forms complex with glucocorticoid receptor -> transcriptional regulator to strongly lower inflam.
Contra = Cushing’s , immunosuppressant.

A

Fluticasone

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19
Q

Long duration bronchodilation. B2 adrenoreceptor agonist -> cAMP -> SM dilation

A

Salmeterol

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20
Q

Long duration bronchodilator for COPD. M3 Ash receptor antagonist. Blocks M3 decreases cGMP -> SM dilation.

A

Tiotropium

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21
Q

Suppresses eosinophil effects so decreased inflam asthma.

A

Mepolizumab

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22
Q

a/b/c are all po’s (c also via transdermal patch). Reversible ACh esterase inhibitors. Decreased clearance of ACh from synaptic cleft. Before baseline ECG before starting check for arrhythmias (contra).
ADR - abdominal pain.

A

a - Donepezil
b - Galantamine
c - Rivastigmine

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23
Q

NMDA + nAChR receptor antagonist. Decreased glutametergic excitotoxicity (neuronal death). Brain up regulates nAChR to counter effects therefore enhances ACh neurotransmission
ADR - balance goes , Contra - Epilepsy

A

Memantine

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24
Q

For mild pain, local inflammation and fever. NSAID, competitive inhibitor of PGHS cycle oxygenase domain. ADR, if given IV (neonatal). Haemorrhage due to thrombocytopenia

A

Ibuprofen

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25
Q

Histamine (H1) receptor antagonist (suppresses hypersensitive immune response to allergens). ADR, fatigue, drowsiness and dry mouth. Contra, acute porphyria (deficiency to produce heme)

A

Cetirizine

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26
Q

Histamine (H2) receptor antagonist. Blocks acid secretion from gastric and parietal cells. For acid reflux. Contra, if gastric malignancy expected

A

Ranitidine

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27
Q

Why is folate an important supplement in pregnancy?

A

in cases of poor diet it helps in neural tube formation

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28
Q

‘Gas and air’, for contraction pain. Inhalation stimulates endogenous endorphin and endomorphic secretion. ADR, chronic use may be neurologically toxic. Contra, if patient has pneumothorax (or other air cavity injury)

A

Nitrous oxide

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29
Q

Regional anaesthesia/analgesic. Epidural infusion. Voltage gated Na channel block in nociceptive axons. Prevents sensory action potential propagation to CNS. ADR, cardiac arrhythmias, convolutions (CNS disturbances)

A

Bupivacaine

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30
Q

Strong opioid. IM injection. Mu opioid receptor agonist in the CNS suppressing pre synaptic GABA release (causes post synaptic K efflux and hyperpolarisation to decrease pain neurotransmission.

A

Pethidine

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31
Q

Mu opioid receptor agonist suppressing presynaptic GABA release. decreases drug drug interaction potential.

A

Fentanyl

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32
Q

Acts as guanosine analogue blocking viral DNA polymerase when converted to triphosphate form inside infected cells.

A

Aciclovir

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33
Q

Competitive inhibitor of viral neuraminidase. Blocks release of new virus particles from infected host cells. Converted to carboxylate form in hepatocytes

A

Oseltamivir

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34
Q

Used for Hep C. RNA nucleoside mimetic with base paring promiscuity. Causes viral hypermutation during viral RNA synthesis

A

Ribavirin

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35
Q

For HIV, Thymidine analogue inhibits RT. Desreases retroviral gene incorporation into host cells nuclear genome

A

Zidovudine

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36
Q

What is the Baltimore classification of drugs (1-7)

A
  1. dsDNA 2. ssDNA 3. dsRNA 4. ssRNA (sense) 5. ssRNA (antisense) 6. ssRNA-RT 7. dsDNA-RT
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37
Q

Name two PPIs

A

Omeprazole and lansoprazole

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38
Q

What are the indications for use of a PPI ?

A

Dyspepsia
Peptic ulceration
Zollinger Ellison syndrome

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39
Q

What are the causes of Zollinger Ellison syndrome ?

A

Increased gastric acid secretion which leads to peptic ulcers.
Caused by hyperplasia of islet cells in the kidney or from gastrin secreting tumour.

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40
Q

What is the MOA of a PPI?

A

Reduces gastric acid secretion by specific inhibition of H/K ATPase in the gastric parietal cell. Blocks the final step of HCl production.

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41
Q

What type of drug is Ranitidine ?

A

H2RA, H2 receptor antagonist.

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42
Q

What is the MOA of Ranitidine ?

A

Competitive inhibitor of histamine at parietal cell H2 receptor. Suppresses HCl secretion.

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43
Q

Name a lipase inhibitor and describe its MOA

A

Orlistat

Reduces absorption of dietary fat through inhibition of pancreatic lipase.

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44
Q

Name some common systemic and topical corticosteroids, or at least their suffix…

A

HydrocortisONE , PrednisolONE, BeclometasONE.

Budesonide may also be used

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45
Q

What type of drugs could be used in patient presents with acute diffuse inflammatory bowel disease ?

A

Systemic and topical corticosteroids

Aminosalicylates.

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46
Q

What is the MOA of corticosteroids ?

A

Binds with high affinity to cytoplasmic receptors of leukocyte infiltration at the site of inflammation therefore interferes with mediator function.

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47
Q

What are the side effects of corticosteroids ?

A

Adrenal axis and immuno suppression. Hyperglycaemia.

Osteoporosis.

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48
Q

What type of drugs are MesALAZINE and SulfasALAZINE ?

A

Aminosalicylates

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49
Q

What is the MOA of an aminosalicylate ?

A

Metabolised in gut to 5-aminosalicylic acid, an antioxidant that traps free radicals. Decreases inflammatory response by inhibiting prostaglandin production in colon or by blocking cyclyoxygenase.

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50
Q

Name a remedial antispasmodic medication method ?

A

Peppermint oil

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51
Q

What are the indications for use of peppermint oil ?

A

Abdominal colic (wind or obstruction) in IBS.

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52
Q

Out of the anti platelet drugs, which is used acutely and which is used chronically ?

A 
Acute = Aspirin 
Chronic = Clopidogrel
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53
Q

What is the MOA of aspirin?

A

irreversible cyclooxygenase enzyme inhibition. Suppresses prostaglandins and thromboxane synthesis, reducing platelet aggregation.

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54
Q

What is the MOA of a chronic antiplatelet drug (name and method) ?

A

Clopidogrel
Prodrug, active metabolite which reduces platelet aggregation through inhibition of ADP dependant activation of the GP11b/111a receptor.

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55
Q

Name an angiotensin converting enzyme inhibitor and at what age it is indicated ?

A

Ramipril

Hypertension in an under 55 y/o if not afro-caribbean origin.

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56
Q

What is nephropathy and what drug is indicated for treatment ?

A

Kidney damage that can lead to failure

An angiotensin converting enzyme inhibitor, eg. Ramipril.

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57
Q

What is the MOA of ramipril ?

A

Converts to ramiprilat, active metabolite that competes with angiotensin 1 for binding at ACE.

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58
Q

Name an angiotensin 2 receptor antagonist ?

A

Losartan

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59
Q

What are the indications for the use of losartan ?

A

Hypertension (<55 y/o). Heart failure.

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60
Q

What is the MOA of losartan ?

A

Reduce angiotensin 2 vasoconstriction through direct competitive inhibition of AT 1 and 2 receptors.

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61
Q

Name a Ca channel blocker…

A

Amlodipine (dihdropyridine)

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62
Q

What are the indications for Ca channel blockers

hint = age

A

Hypertension (>55 y/o)

Angina, age link yeah…

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63
Q

What is the MOA of amlodipine ?

A

Vasodilation by inhibition of L-type Ca channels, inhibitor vascular SM cell contraction

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64
Q

What type of drug is Indapamide ?

A

Thiazide-like diruetic

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65
Q

What is the MOA of Indapamide ?

A

Inhibits active Cl reabsorption at early distal tubule via NaCl transporter.

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66
Q

What are the side effects of using Thiazide-like diuretics ? (4)

A

Hyponatremia (Na down)
Hypokalemia (K down)
Erectile dysfunction
Gout

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67
Q

Name two b-adrenoreceptor blockers … (think suffix)

A

BisoprOLOL

PropranOLOL.

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68
Q

What is the MOA of Bisoprolol ?

A

Competitive antagonist of catecholamines for binding at beta adrenergic receptors.

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69
Q

Why is it possible for propranolol to penetrate the CNS ?

A

It is lipid soluble.

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70
Q

Name two statins …

A

AtorvaSTATIN and SimvaSTATIN.

71
Q

What are the indications for statins ?

A

Primary and secondary CV disease prevention

72
Q

What is the MOA for Simvastatin ?

A

Hydrolysed to active metabolite, competes with HMG-CoA for HMG-CoA reductase. Reduces quantity of mevalonic acid, precursor for cholesterol

73
Q

What is mevalonic acid ?

A

Precursor for cholesterol

74
Q

What are the common side effects of statins ?

A

Hyperglycemia
Muscle toxicity, raised CK, myopathy
Hepatotoxicity

75
Q

Name an Exogenous nitric oxide donor and its method of entry …

A 
Glyceryl trinitrate (GTN) 
Spray sublingually.
76
Q

What are the indications for GTN ?

A

Prophylaxis and treatment of angina.

77
Q

What is the MOA of GTN

A

Converted to NO -> Guanylate cyclase -> cGMP synthesis -> vasodilation in vascular SM -> dephospho rylation of MLC fibre.

78
Q

Why is a 4-12 GTN free period required daily during treatment ?

A

Rapid tolerance build up, so free period prevents efficacy loss

79
Q

What type of drugs are Diltiazem and verapamil?

A

Rate limiting Ca channel blockers (CCBs)

80
Q

What are the indications for CCBs ?

A

Narrow, complex tachycardias

Agina, hypertension

81
Q

What is the MOA of verapamil ?

A

AVN conduction delay through inhibition of L- type Ca channels.

82
Q

What are the side effects of CCBs ? (3)

A

Risk of heart block (avoid concurrent b-blocker use)
Negatively inotropic
Constipation

83
Q

Name 3 antianginals ?

A

Nicorandil, Ivabradine and Ranolazine

84
Q

What are the indications for antianginals and what should’ve been tried first?

A

Angina

If the patient isn’t able to tolerate b-blockers or CCBs.

85
Q

What is the MOA of Nicorandil ?

A

Combines K ATP channel activation with NO donor

86
Q

What is the MOA of Ivabradine ?

A

Sinus node K channel blocker

87
Q

What is the MOA of Ranolazine ?

A

Na channel blocker and myocyte metabolic substrate utilisation

88
Q

What type of drugs are Furosemide and bumetanide ?

A

Loop diuretics

89
Q

When are loop diuretics indicated?

A

symptomatic relief of pulmonary oedema

Peripheral oedema in heart failure or cirrhosis.

90
Q

What are the MOAs of loop diuretics ?

A

Inhibit Na/K/Cl supporter within ascending limb of LoH.

91
Q

What is a side effect of loop diuretics relating to the ear?

A

Ototoxicity, specifically the cochlea or auditory nerve.

92
Q

What are the indications of Parenteral anticoagulants ? (Heparin)

A

Prophylaxis and treatment of venous thromboembolism

Treatment of ACS (LMWH)

93
Q

What is the method of action of Heparin ?

A

Factor Xa inhibition

It’s also a thrombin inhibitor, administered IV.

94
Q

What is HIT ? Which form of Heparin is it most common ?

A

Heparin induced thrombocytopenia
Heparin dependant IgG antibodies bind to heparin to activate platelets and produce a hypercoagulable state.
Unfractionated heparin > LMWH.

95
Q

Name one and give the indications for oral anticoagulants … (2)

A

Warfarin
Prophylaxis and treatment of venous thromboembolism.
Prevention of stroke and systemic emboli in AF

96
Q

What is warfarin’s MOA ?

A

Inhibits Vit K epoxide reductase shuttle, inhibits synthesis of factors 2,7,9,10

97
Q

Salbutamol and Salmeterol, which is long and which is short acting ?

A 
Salbutamol = short 
Salmeterol = long
98
Q

What is a Tocolytic agent ?

A

Drugs that slow down or halve contraction force of uterus during labour

99
Q

What is the MOA of Salbutamol ?

A

Specific b2 receptor agonist, causes bronchodilator through SM relaxation

100
Q

What type of drugs are Ipratropium and Tiotropium?

A

Antimuscarinic bronchodilators

101
Q

What are the MOAs of antimuscarinic bronchodilators ?

A

Inhibit M1-M3 muscarinic receptors. Cause bronchodilator through SM relaxation.

102
Q

Name 2 inhaled corticosteroids

A

Beclomethasone and fluticasone

103
Q

What is the MOA of fluticasone ?

A

Binds with high affinity to specific cytoplasmic receptors. Inhibits leukocyte infiltration to inflammation site.

104
Q

Codeine and morphine, which is moderate and which is severe pain ?

A 
Codeine = moderate
Morphine = severe
105
Q

What is the name of the drug that can be used for biliary colic and obstetric pain relief

A

Pethidine, causes decreased risk of neonatal respiratory suppression.

106
Q

What structure metabolises codeine into morphine ?

A

CYP2D6. 2D6 is under genetic control, may cause apparent lack of efficacy in some individuals

107
Q

What might methadone be preferred over morphine even though it is less sedating ?

A

It has a longer half life

108
Q

What type of drugs are CycliZINE and PromethaZINE ?

A

Antihistamines
Promethazine is used in pregnancy.
Antihistamines are also a class of antiemetic drugs.

109
Q

Where might antiemetic drugs be indicated ? (4)

A

Postoperative nausea and vomiting
Treatment of chemo/radiotherapy nausea and vomiting
Treatment of migraine associated nausea and vomiting (metoclopramide)
Treatment of motion sickness (Cyclizine)

110
Q

What drugs are indicated for focal seizures ?

A

Carbamazepine or lamotrigine

Antiepileptic drugs

111
Q

What drugs are indicated for generalised seizures ?

A

Sodium valproate or lamatrigine

112
Q

What is the MOA of carbamazepine ?

A

Voltage operated Na ion channel inhibitor. Strong hepatic enzyme inducer. Reduces own half life form 30 -> 15 hours.

113
Q

What drug has this MOA? : Na/Ca ion channel blocker. Increases GABA in the CNS

A

Sodium valproate

114
Q

What is the MOA of lamotrigine ?

A

Potent Na channel blocker

115
Q

What are the common side effects of Valproate ? (4)

A

alopecia, weight gain, teratogenic. May increase plasma conc of lamotrigine to toxic levels.

116
Q

What type of agent is mebeverine and what condition is it commonly used for ?

A

Antispasmodic agent

IBS

117
Q

What is the overall effect of mebeverine on gastric SM cells ?

A

Decrease Ca entry into gastric SM cells, particularly in the colon. Reduces episodes of painful gut SM spasms.

118
Q

If somebody starts taking a new drug and experiences indigestion, constipation, rash, urticaria. What drug is most likely?

A

Meberverine

119
Q

What is Loperamide ?

A

Antidirrhoeal, used for acute non infective diarrhoea

120
Q

Name the antidiarrhoeal agent that is an Mu opioid receptor agonist. It decreases myenteric plexus electrical activity that then relaxes GI SM tone increasing peristalsis.

A

Loperamide

121
Q

What is the proper name for Imodium ?

A

Loperamide

122
Q

Name the anti inflammatory agent that is commonly used in UC.

A

Prednisolone

123
Q

What is the action of Prednisolone ?

A

Gene transcription regulator. Increases anti inflammatory protein synthesis

124
Q

If a patient has an ADR of cushings with associated weight gain, immune/adrenal suppression what drug would come to mind ?

A

Prednisolone

125
Q

Cinchocaine can be used for haemorrhoids along with what drugs ?

A

Hydrocortisone , local anaesthetic and an anti inflammatory (eg. NSAID/steroid)

126
Q

What is the action of local anaesthetics ?

A

Blocks Na voltage gated channels in nociceptive nerve fibres. Forces nerve to increase refractory period and prevents pain action potential propagation along axons to CNS

127
Q

How might GI pathologies affect oral drug absorption ? What might you do to compensate ?

A

Decrease an oral drug availability. Consider a different route of administration.

128
Q

What factors should you be aware of when considering drug oral availability ? (8)

A

Dysphagia , vomiting , rapid GI transit times , chronic GI inflammation
Thickening of GI wall tissues eg. malignancy
Trauma (scarring) to GI absorptive SA
Deranged stomach pH (for drugs whose ionisation is dependant on local pH)
Bacterial infection (drugs metabolised by GI bacteria before absorption).

129
Q

What is the cause of T1DM?

A

autoimmune mediated destruction of pancreatic B cells. Stops insulin synthesis and secretion

130
Q

How might an overdose of insulin be treated ?

A

Hypoglycaemic so give glucose and glucagon

131
Q

Why are beta blockers a contraindication for insulin ?

A

They enhance and mask hypoglycaemia

132
Q

What drug forms an active complex with nuclear glucocorticoid receptors ?

A

Hydrocortisone

133
Q

What are the common ADRs for hydrocortisone ? (4)

A

Weight gain, fluid retention, hypoglycaemia, Cushings (long term).

134
Q

What can synthetic thyroxine be converted into ?

A

T3

135
Q

What can bind to nuclear thyronine receptors causing transcriptional regulation of metabolically associated genes ?

A

T3 and T4.

136
Q

What are the common ADRs for Levothyroxine (5)

A

Tremor, cardiac arrthymias , excitability, diarrhoea , flushing

137
Q

If the patient has known ischeamic heart disease what drug are you unlike to give them relating to endocrine function ?

A

Levothyroxine

138
Q

What is carbimazole converted into and what is its method of action ?

A

Prodrug that’s converted to methimazole. This inhibits thyroid peroxidase (blocks iodination of thyroglobulin needed for T3 and T4).

139
Q

What are the common ADRs of carbimazole ? (5)

A

Joint pain, headache, fever, rash, taste disturbances

140
Q

Why is warfarin a contraindication when on Carbimazole ?

A

Carbimazole may enhance anti-coagulation effect of coumarin class drugs.

141
Q

What are the effects of rate control drugs ?

A

Slow or quicken the heart i.e. chronotropic effects

142
Q

What is bisoprolol ?

A

Cardioselective b-1 adrenoreceptor antagonist.

-ve chronotropic effect for AF

143
Q

What effect does blocking the b-1 receptor have on cation levels ?

A

decreases cAMP activity, limits cation influx into cardiomyocytes and pacemaker cells.

144
Q

Which phase is prolonged in pacemaker potential when cation influx decreases ?

A

4 , decrease freq of impulse from SAN

145
Q

Why might rhythm control drugs be used first even though they have worse ADRs?

A

they’re faster to extinguish arrhythmias than Rate control drugs

146
Q

Name the drug that can be used to prolong phase 3 of aberrant cardiac APs in AF ?

A

Amiodarone

147
Q

What VM class is Amiodarone?

A

3, blocks voltage gated K channels. ^ repolarisation phase. Tissue can’t be stimulated by or contribute to aberrant electrical impulses during this period

148
Q

What is a severe ADR for Rhythm control drugs ?

A

Torsade de pointes arrhythmia.

149
Q

How would you manage uncomplicated back pain?

A

Avoid using severe txs, better to manage with ibuprofen and physiotherapy.

150
Q

What medication would be used for first line strong back pain ?

A

Naproxen, long lasting alternative to ibuprofen with an inflammatory component

151
Q

What is the MOA of Naproxen?

A

NSAID, selectively blocks PGHS1+2 enzymes. PGE2 sensitises local nociception and potentiates local inflammatory responses.

152
Q

What drug should be given with Naproxen ?

A

A PPI cover eg. Esomprazole because Naproxen predisposes to GI ulceration.

153
Q

What are the contraindications for Naproxen ?

A

Already on an NSAID, renal impairment, existing GI ulcer

154
Q

What is Triamcinolone ?

A

Powerful steroid anti inflammatory often given as epidural

155
Q

What drug; up regulates anti inflammatory mediators and down regulates pro inflammatory mediators?

A

Triamcinolone

156
Q

What are the ADRs of Triamcinolone ? (4)

A

Cushing’s, weight gain, hyperglycaemia, immune suppression

157
Q

If a px presents with severe back pain but also has Cushing’s, what tx are you likely to give them after Naproxen?

A

Oxycodone, Trimcinolone is contraindicated when px has Cushing’s.

158
Q

What type of drug is Oxycodone?

A

strong mu opioid analgesic acts on brain/spinal cord.

159
Q

What ion movements are caused due to Oxycodone?

A

GPCR mediated K efflux and Ca channel closing in neurones which suppresses release of pain NT and deepens pain pathways.

160
Q

What are the contraindications for Oxycodone ?

A

Acute respiratory depression, ^ ICP, if on/dependant on another opioid.

161
Q

What are the ADRs of oxycodone ?

A

Constipation, nausea, resp depression, dependence.

162
Q

What is Ramipril ?

A

ACE inhibitor, antihypertensive that limits AT2 mediated LV remodelling in cardiac failure.

163
Q

What are the ADRs of Ramipril?

A

Causes hyperkalaemia by blocking AT2/aldosterone mediated Na reuptake from urine in CD. Na reuptake would normally drive K secretion/loss into urine

164
Q

Name a loop diuretic, when is it indicated ?

A

Furosemide. 1st line when cardiac failure fluid overload causes oedema

165
Q

What drug blocks the Na/K/Cl symporter in ^ LoH to cause potent diuresis ?

A

Furosemide

166
Q

What is the ADR of Furosemide ?

A

Trapping Na in urine in LoH means ^Na (that would normally have been reasborbed) now flows down past the CD cells where its uptake drives K secretion/loss into urine = hypokalaemia

167
Q

What is Digoxin ?

A

Thiazide like diuretic. Positive inotrope indicated for systolic CF in elderly and sedentary px

168
Q

How does Digoxin produce +ve inotropy ?

A

Blocks the Na/K ATPase which ^ Ca in cardiomyocytes

169
Q

What is the ADR of Digoxin?

A

Digoxin competes with K for the Na/K ATPase so prevents K from entering cells so hyperkalaemia.

170
Q

What is the effect of Aldosterone in the kidney ?

A

Up regulate epithelial Na channels in the principal cells of the CD so Na reabsorption ^ and K lost.

171
Q

What is the action of Spironolactone ?

A

K sparing diuretic. Blocks mineralocorticoid receptors normally activated by aldosterone so less Na reabsorption and K is preserved.

172
Q

Px has OD on Digoxin, what would their ECG show ?

A

Hyperkalaemia. Peaked T waves, prolonged QRS. Eventually lost P waves , bradycardia or even systole because of high serum K.

173
Q

How would hypokalaemia present on an ECG ?

A

Large P waves, T wave flattening or inversion, ST depression, U waves, prolonged PR interval.

test (14 decks)

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