Pharmacology Flashcards
1
Q
B-Blockers E.g. Used For: MOA: SE:
A
B1 adrenoreceptor antagonists
E.g. ‘-olols’ Propranolol (nonselective), atenolol (selective)
Used For: Angina, MI, HTN, Hyperthyroidism
MOA: Inhibit binding of Noradrenaline
SE: cold extremities, impotence, vivid dreams, fatigue
2
Q
SAMAs/LAMAs E.g. Used For: MOA: SE:
A
E.g. Ipatropium (SAMA) Tiotropium (LAMA)
Used For: Management of COPD > Management of Asthma
MOA: Antagonise muscarinic receptors on bronchial smooth muscle to prevent bronchoconstriction via cholonergic tone
SE: dry mouth, throat tickle
3
Q
SABA/LABA E.g. Used For: MOA: SE:
A
E.g. Salbutamol (SABA) Sameterol (LABA)
Used For: Treatment of Asthma, COPD
MOA: Stimulation of B2 adrenoreceptors on bronchial smooth muscle —> bronchodilation
SE: Tachycardia due to nonspecific B1 agonist, tremor, palpitations
- Increasing use of SABA or daily use indicates worsening of asthma and requires prompt review
4
Q
Ca2+ Channel Blockers E.g. Used For: MOA: SE:
A
E.g. Verapamil
Used for: HTN, MI, COPD
MOA:
- blocks Ca2+ entry to L-type Ca2+ channels therefore decreasing contractility (negative ionotropic/chronotropic effects)
- Reduce arteriolar resistance in coronary arteries
SE: peripheral oedema, headaches, constipation
5
Q
Inhaled Oral Corticosteriods E.g. Used For: MOA: SE:
A
E.g. Fluticasone
Used For: Treatment of asthma, COPD
MOA: Preventative Treatment —> Reduce airway inflammation and bronchial hyper-reactivity
- do so by preventing synthesis of chemokines by blocking Phospholipase A2 and inhibiting the action of cyclooxygenase
- Reduce freq and severity of exacerbations
SE: oropharyngeal candidiasis, bruising
6
Q
Xanthines E.g. Used For: MOA: SE:
A
-
7
Q
PPIs E.g. Used For: MOA: SE:
A
E.g. Omeprazole
Used For: GORD, Zollinger Ellison Syndrome?
MOA: Irreversibly bind the parietal cell apical K+/H+ ATPase to prevent secretion of acid into the stomach
SE: Headache, nausea, vomiting
8
Q
H2 Antagonists E.g. Used For: MOA: SE:
A
E.g. Cimetidine
Used For: GORD
MOA: Competitively blocks H2-receptors on basal parietal cells reducing paracrine stimulation from ECF cells and gastric acid secretion
SE: Hypotension
9
Q
Treatment for Hypothyroidism
Name:
MOA:
SE:
A
Name: Thyroxine
MOA:
- Acts as exogenous T4
- Long half life
- Drug of choice for primary and secondary hypothyroidism
SE: similar to hyperthyroidism –> nausea, vomiting, gastric discomfort, anxiety
10
Q
Loop Diuretics E.g. Used For: MOA: SE:
A
-
11
Q
Thiazides E.g. Used For: MOA: SE:
A
Diuretic
E.g. hydrochlorothiazide
Used for: HTN
MOA: Inhibit the action of the Na+/Cl- co transporter in the proximal Distal Convoluted tubule –> decrease solute reabsorption therefore water reabsorption –> decrease blood volume
SE: Dizziness, electrolyte disturbances (Hypokalaemia, metabolic alkalosis, orthostatic hypotension
12
Q
Oral Combined Contraceptive Pill
Used For:
MOA:
SE:
A
-
13
Q
HRT
Used For:
MOA:
SE:
A
-
14
Q
ARBs E.g. Used For: MOA: SE:
A
ARBs
E.g. ‘sartans’ Valsartan
Used For: Alternative for ACEi, HTN, Diabetes
MOA: Block Angiotensin Receptor II Class I receptors to prevent vasoconstriction via Ang II
SE: Less incidence of cough
15
Q
Therapy for TB
A
RIPE:
- Rifampicin, isonizid, pyrazinaminde, ethambutol
16
Q
Triple Whammy
What Drugs
MOA
A
Combination of ACEi or ARB, Diuretic + NSIAD
MOA:
- NSAID inhibit COX –> inhibition of conversion of Arachodonic acid to Thromboxane A2 and Prostaglandins —> Inhibit afferent arteriole dilation —> decreased GFR
- ACEi/ARB —> inhibit efferent arterial constriction —> decreased GFR
- Diuretics: decrease blood volume –> decreases renal blood flow
- Overall –> depress kidney function —> acute renal failure
17
Q
A2 agonist E.g. Used For: MOA: SE:
A
E.g. Clonidine, methyldopa
Used for: HTN, Pre-eclampsia (ACEi contraindicated)
MOA: centrally acting - inhibits the release of catecholamines by reducing sympathetic tone to the adrenal medulla
SE: sedation, dizziness, headaches, headache
18
Q
Sulfonylureas
Used For:
MOA:
SE:
A
Used For: Treatment of Type II DM where ptx still has insulin production
MOA: Inhibits the B-cell Na+/K+ ATPase, increases the resting membrane potential of the B-cell and decreases the stimulation required to elicit insulin secretion
SE: hypoglycaemia
19
Q
Sulphonamides E.g. Used For: MOA: SE:
A
E.g. Sulfilmethazole
Used For: Bacterial Infection
MOA: Inhibit folate production essential for bacterial growth
SE: nausea, vomiting, diarrhoea
20
Q
Aminoglycosides E.g. Used For: MOA: SE:
A
E.g. Gentamicin
Used For: Bacterial Infection
MOA: Irreversibly bind to 30S ribosomal subunit causing cell membrane damage
SE: Nephrotoxic, ototoxic
21
Q
Biguanides E.g. Used For: MOA: SE:
A
E.g. Metformin
Used For: Diabetes Mellitus
MOA: decrease carbohydrate absorbtion in the GIT, decrease hepatic output of glucose
SE: diarrhoea, weight loss
22
Q
B-Lactams E.g. Used For: MOA: SE:
A
Penicillins
E.g. amoxicillin, ampicillin, flucloxacillin
Used For: Treatment of bacterial infection
MOA:
- Interfere with bacterial wall peptidoglycan synthesis
- bactericidal –> lead to cell death
SE:
- Diarrhoea
- Nausea
- allergy
23
Q
Spirinolactone E.g. Used For: MOA: SE:
A
Used for: Hyperaldosteronism (Conns Syndrome)
MOA: Inhibits binding of Aldosterone to principal cells of the DCT and CD —> Inhibits Na+ reabsorbtion from Na+ channel and activity of the Na/K ATPase. Results in secondary decrease in K secretion
SE: Hyperkalaemia
24
Q
Asprin
Used For:
MOA:
SE:
A
-
25
Clopidogrel
Used For:
MOA:
SE:
Used for: antiplatelet therapy
MOA: Binds ADP receptor on platelet to prevent aggregation
SE: Increased risk of bleeding
26
Warfarin
Used For:
MOA:
SE:
Anticoagulant
Used for: HTN, Angina
MOA: Inhibits metabolism of vitamin K and therefore long term synthesis of Vitamin K dependant clotting factors (2,7,9,10)
27
Heparin
Used For:
MOA:
SE:
Anticoagulant therapy
MOA: inhibit formation of Xa
Se: bleeding
28
Progesterone only Contraceptive Pill
Used For:
MOA:
SE:
Used For: Contraception, Pre-HRT
MOA: Negative feedback of GnRH, FSH, LH ---> inhibit ovulation
SE: weight gain
29
Insulin
Used For:
MOA:
SE:
-
30
Management of Incontinence
Drugs Used:
MOA:
SE:
-
31
```
Streptokinase
Drug class:
Used For:
MOA:
SE:
```
-
32
Management of Cholesterol / Cholesterol Lowering:
Drug
MOA
HMG CoA Reductase Inhibitors - Statins
E.g. Atorvastatin
MOA: Prevents synthesis of endogenous Cholesterol production by blocking HMG-CoA reductase (rate limiting step in Endogenous Cholesterol Production)
SE: Myalgia
33
Digoxin
Used For:
MOA:
SE:
-
34
```
Leukotriene Receptor Antagonist
E.g.
Used For:
MOA:
SE:
```
E.g. Moteleukast
Used for: Prevention of asthma exacerbation
MOA: Antagonise Leukotriene receptors to prevent leukotriene mediated bronchoconstriction
SE: hyperactivity, behavioural changes, headache, abdo pain
35
Nitrates (Sublingual glyceral trinitrates)
Used For:
MOA:
SE:
Used For: Angina, MI
MOA:
Dilation of venules and arteries:
Metabolised to NO ---> binds to 2nd messenger system ---> Increase cGMP ---> relaxation of SM
Effect: venule dilation: decrease preload, decrease cardiac work
arteriole dilation: decrease afterload and increase blood flow to coronary arteries
SE:
- Headache
- Postural Hypotension
36
Fibrinolytics
Used For:
MOA:
SE:
Used for: MI, Stroke, PE
MOA: Convert plasminogen to plasmin which then breaks down fibrin
SE/Contraindications: Risk of bleeding, Contraindicated in Pregnancy
37
```
ACE inhibitors
E.g.
Used For:
MOA:
SE:
```
E.g. '-prils' Captopril, Perindopril
Used For: 1st line CKD, Diabetes, CHR, Angina, HTN,
MOA: Inhibits Conversion of Ang I to active Ang II
- Decreases constriction of kidney eff arteriole
- Decreases systemic vasoconstriction --> decrease TPR ---> decrease MAP
- Decrease Aldosterone ---> decrease Na+ reabsorption in Kidneys ---> decrease Blood volume
SE: Cough due to inhibition of ACE preventing breakdown of bradykinin in the lungs
38
```
a1 adrenoreceptor Blockers
E.g.
Used For:
MOA:
SE:
```
E.g. prazosin
Used for: HTN
MOA: Weak diuretic
- Arterial and venous dilation due to blockage of a1 adrenoreceptors on vascular SM
SE: Orthorstatic hypotension, dizziness, weakness
39
```
Loop Diuretic
E.g.
Used For:
MOA:
SE:
```
E.g. Furosemide
Used for: Diabetes, HTN,
MOA:
- Inhibit the Na+/K+/2Cl- transporter
- Inhibits K+ Na+ and Cl- movement into the blood
- Inhibits H2O following down its osmotic gradient
SE:
- hypokalaemia
- metabolic alkalosis due to H loss
- depletion of Ca2+ and Mg2+
- hypotension
40
```
Potassium Sparing Diuretics
E.g.
Used For:
MOA:
SE:
```
E.g. Amiloride
Used for:
MOA: Weak diuretic
- inhibit sodium reabsorbtion in DCT by blocking Na+ channels
- Reduce urinary K+ exchange
SE:
- Hyperkalaemia, hyponatraemia, hypochloraemia
- Weakness, headache
- nausea, vomiting
41
Treatment for Hyperthyroidism
- 2 Drug Names
- 2 MOA
- SEs
Drug 1: Carbimazole
- MOA: Inhibition of thyroperoxidase (Iodide --> Iodine conversion)
Drug 2: Polythyrouracil
MOA: At high doses inhibits deiodinase for conversion of T4 to active T3
- SE: Itching, rash, nausea, vomiting, gastric discomfort
42
```
Cephalosporins
E.g.
Used For:
MOA:
SE:
```
E.g. Cephalexin
Used For: Treatment of bacterial infection
MOA: interfere with bacterial cell wall peptidoglycan synthesis leading to cell death (bacteriocidal)
SE:
- Diarrhoea, nausea, vomiting
43
```
Glycopeptides
E.g.
Used For:
MOA:
SE:
```
E.g. Vancomycin
Used For: Bacterial infection
MOA: Prevent formation of glycoprotein polymers
SE: Nephrotoxic
44
```
Tetracyclines
E.g.
Used For:
MOA:
SE:
```
E.g. Doxycycline
Used For: Bacterial Infection
MOA: Bacteriostatic, inhibit bacterial protein synthesis by reversibly binding to 30S subunit
SE: nausea, vomiting, diarrhoea
45
Outline which diuretics cause hypokalaemia, which cause hyperkalaemia?
-
46
Outline which bacterial classes inhibit the following
- Bacterial cell wall
- Protein synthesis
- Bacterial metabolism
- Bacterial DNA synthesis
- Bacterial cell wall: Penicillins, B-Lactams, Glycopeptides
- Protein synthesis: Tetracycline, Macrolides
- Bacterial metabolism: Sulfonamides
- Bacterial DNA synthesis: Quinolones
47
```
Macrolides
E.g.
Used For:
MOA:
SE:
```
E.g. Clarythromycin
Used For: Bacterial infection
MOA: Bacteriostatic, bind to 50S subunit of ribosome to inhibit protein synthesis
SE: Nausea, vomiting, diarrhoea
48
Which Antibiotics are Bacteriocidal? Which are bacteriostatic?
Bacteriocidal: Quinolones, Penicillins, Glycopeptides
Bacteriostatic: Sulfonamides, Tetracyclines, Macrolides
49
```
Quinolones
E.g.
Used for
MOA:
SE:
```
E.g. Ciprofloxacin
Used for: Bacterial Infection
MOA: Inhibit bacterial DNA synthesis by blocking topoisomerase
SE: Nausea, vomiting, diarrhoea
50
Treatment for H. Pylori
Omeprazole, amoxicillin, clarithromycin
51
Cromones
Used for
MOA
SE
Used for: add on therapy as prophylaxis for asthma, esp exercise induced. No use in COPD
MOA: Chloride channel blockers --> stabilise mast cell and prevent degranulation
SE: hard to use?
52
```
Anti-epileptics: Phenytoin
Class:
Used for:
MOA
SE
```
Class: Na+ Channel Blocker
Used for: Partial and generalised seizures (not effective in absence seizures)
MOA: Bind to Na+ Channels preferably in inactive state --> prolong inactivation and preventing return to active state --> reduce the # of active sodium channels
* Bind preferentially to Na+ channels with a high firing frequency (those that occur w seizures)
SE: Nausea + vomiting, agitation, sedation, dizziness, blurred vision, vertigo
*Narrow therapeutic range + metabolised by liver therefore other drugs metabolised by liver will affect kinetics
Used as a second line treatment
53
```
Anti-epileptics: Carbamazapine
Class:
Used for:
MOA
SE
```
Class: Na+ channel blockers
Used for: generalised and focal seizures
MOA: Bind to Na+ Channels preferably in inactive state --> prolong inactivation and preventing return to active state --> reduce the # of active sodium channels
* Bind preferentially to Na+ channels with a high firing frequency (those that occur w seizures)
SE: Drowsiness, ataxia, dizziness, blurred vision, diplopia, headache, rash
* Induces liver P450 enzymes --> increase metabolism of drugs metabolised by liver e.g. phenytoin
Used as first line treatment for focal seizures
54
```
Anti-epileptics: Lamotrigine
Class:
Used for:
MOA
SE
```
Class: Na+ channel blockers
Used for: Generalised and focal seizures, can be used in absence seizures
MOA: Bind to Na+ Channels preferably in inactive state --> prolong inactivation and preventing return to active state --> reduce the # of active sodium channels
* Bind preferentially to Na+ channels with a high firing frequency (those that occur w seizures)
SE: Diplopia, blurred vision, dizziness, ataxia, headache, somnolence, hyperkinesia, nausea, vomiting, severe skin rashes (Steven-Johnsons Syndrome) occurs in 0.8% of children and 0.3% adults
* newer drug, wider therapeutic index
55
```
Anti-epileptics: Valproate
Class:
Used for:
MOA
SE
```
Class: Na+ channel blocker; weak inhibitor of GABA transaminase
Used for: Infantile seizures*, adolescent seizures*, absence seizures (1st line), myoclonic + tonic clonic (1st line)
*particularly useful due to lack of sedative properties
MOA:
- Bind to Na+ Channels preferably in inactive state --> prolong inactivation and preventing return to active state --> reduce the # of active sodium channels
* Bind preferentially to Na+ channels with a high firing frequency (those that occur w seizures)
- Weak inhibitor of GABA transaminase --> increase GABA levels
SE: teratogenic, Nausea, vomiting, increased appetite, weight gain, tremor
56
```
Anti-epileptics: Ethosuximide
Class:
Used for:
MOA
SE
```
Class: T-type Ca2+ channel inhibitor
Used for: absence seizures
MOA: Blocks T-type calcium channels pacemaker current that underlies the thalamic rhythm in spikes & waves seen in absence seizures
SE: Anorexia, nausea, vomiting, epigastric pain, weight loss, hiccup, drowsiness, dizziness, ataxia, headache, euphoria
57
```
Anti-epileptics: Gabapentin/Pregabalin
Class:
Used for:
MOA
SE
```
Class: Voltage gated T type Ca2+ channel blocker
Used for: Partial seizures
MOA: Blocks voltage-gated calcium channels Ca2+ entry into neurons inhibit neurotransmitter (including glutamate & substance P) release
**Structurally similar to GABA but do not affect GABA levels
SE: sedation, fatigue, dizziness, drowsiness, confusion
58
```
Anti-epileptics: Benzodiazapenes
Class:
Used for:
MOA
SE
```
Class: GABA receptor agonist
Used for: 2nd line in generalised, focal and absence seizures, status epilepticus
MOA: Bind to GABAa receptors, prolong frequency of opening --> influx of Cl- ---> hyper-polarises cell and prolongs effect of GABA
SE: drowsiness, sedation, confusion, lightheadedness
* typically not used in continuous treatment bc tolerance develops after 6mo
59
```
Anti-epileptics: Phenobarbitol
Class:
Used for:
MOA
SE
```
Class: GABA receptor agonist
Used for: 2nd line for generalised, focal and absence seizures
MOA: Bind to GABAa receptors, prolong duration of opening --> influx of Cl- ---> hyper-polarises cell and prolongs effect of GABA
SE: Sedation, confusion, depression, cognitive impairment, altered mood and behaviour
60
```
Anti-epileptics: Vigabatrin + Valproate
Class:
Used for:
MOA
SE
```
Class: GABA transaminase inhibitor
Used for: 2nd line generalised, focal and absence seizures (Valproate 1st line for absence, myoclonic and tonic clonic)
MOA: Inhibit GABA transaminase metabolism of GABA GABA
SE: Visual field defect in 20-40%, diplopia, fatigue, sedation
61
```
Anti-epileptics: Topiramate
Class:
Used for:
MOA
SE
```
Class: Glutamate receptor agonists
Used for: 2nd line generalised and focal seizures
MOA: blocks glutaminergic receptors (NMDA/AMPA receptors) ---> decrease release of glutamate ---> decrease excitation of neurons
SE: sedation?
62
Bisphosphonates
Used for:
MOA:
Se:
Bisphosphonates
Used for: Osteoporosis
MOA: inhibit osteoclasts
Se: oesophagitis, osteonecrosis of the jaw, must be given before breakfast sitting up
63
Explain how estrogen therapy is used for the treatment of osteoporosis? What are some drawbacks of estrogen therapy
Oestrogen upregulates the expression of OPG which binds RANK-L preventing activation of osteoclasts, oestrogen also modulates the expression of cytokines such as IL-1, IL-6, TNFa which stimulate osteoblasts to activate osteoclasts, and downregulates M-CSF
Drawbacks: not recommended for use 5 years post menopause due to increased breast ca risk, increases blood coaguability
64
Denosumab
Used for:
MOA:
Se:
Denosumab
Used for: Osteoporosis
MOA: monoclonal antibody that binds RANKL similar to OPG, inhibits osteoclast function and survival
SE: fatigue, headache
65
```
SERMS
e.g.
Used for:
MOA:
SE
```
```
Selective estrogen receptor modulators
E.g. raloxifene
Used for: Osteoporosis
MOA: acts as a estrogen receptor agonist at the bone osteoblasts but as an antagonist at the mammary gland, therefore decreases risk of both osteoporosis and breast cancer
SE: increased risk thromboembolism
```
66
Calcitriol
Used for:
MOA:
SE:
Calcitriol
Used for: osteoporosis esp in CKD patients where final conversion to active vit D by 1a hydroxylase cannot be achieved
MOA: Vit D is synthesised from the skin from cholesterol in the presence of UV light, it is then hydroxylated in the liver and finally in the kidneys by 1ahydroxylase to its active form. Vit D acts at the intestine to increase Ca2+ absorption by generating the synthesis of calcibindin an IC protein that binds 4 Ca2+ ions, it also acts in the kidneys to increase HPO4 reabsorbtion and Ca2+ absorbtion, and in bone to lead to resorption and reformation
67
```
DMARDs: Antimalarials
E.g.
Used for:
MOA:
SE:
```
E.g. Hydroxychloroquine
Used for: RA, SLE
MOA: anti-inflammatory, immunosuppressive, interefere T cell proliferation, IL production
SE: corneal opacity (require yearly eye check), rash, dermatitis
TAKE 3MO BEFORE ONSET
Others: Sulfalazine, Lefolimide
SE: sulfalazine myelosuppression, leflunomide teretogenic
68
DMARDS: Methotrexate
Used for:
MOA:
SE:
Used for: RA, Chemotherapy for haem malignancy
MOA: Immunosuppressive, folate antagonist, reduces production of ILs
SE: N+V, stomatitis, myelosuppression, alopecia, liver toxicity,
TAKE 3MO BEFORE ONSET
69
bDMARDS
E.g.
MOA
SE
E.g. Infliximab (cytokine production - TNFa), Rituximab (, Abatacept
MOA: inhibit TNFa (Infliximab), B-cells (Rituximab), T cells (Abatacept)
SE: myelosuppression,
GENERALLY FAST ACTING BUT ONLY USED IN CONJUNCTION WITH MTX
70
Alteplase rtPA
Indication:
MOA:
SE:
Class: thrombolytic
Indication: Stroke re-perfusion
MOA: recombinant tissue plasminogen activator --> binds fibrin and converts plasminogen to plasmin --> clot degradation
SE: increased bleeding risk
71
Antipsychotics - typical
E.g.
MOA
SE
E.g. Halopiridol, Chloropromazine
MOA: Inhibit D2 receptors with >80% affinity --> decrease mesolimbic pathway (positive ssx),
SE: also bind Histamine receptors (sedation), alpha receptors (hypotension), and effect the other dopaminergic pathways (tubuloinfundibular - prolactinaemia; nigrostriatal - basal ganlia - EPSE)
EPSEs may be relieved by anticholinergic co administration - e.g. cogentin
72
Antipsychotics - atypical
E.g.
MOA
SE
E.g. Clozapine, respiridone
MOA: inhibit D2 receptors with less affinity --> decrease EPSE
SE: sedation, hyperglycaemia, cholesterol and lipid abnormalities, EPSE
EPSEs may be relieved by anticholinergic co administration - e.g. cogentin
73
Antidepressants - SSRIs
E.g.
MOA
SE
E.g. Sertraline, Fluoxitene
MOA: inhibit 5HT reuptake from the post synaptic cleft
SE: N+V, diarrhoea, insomnia
74
Antidepressants - SNRIs
E.g.
MOA
SE
E.g. Duloxitine
MOA: inhibit the reuptake of 5HT and NE at the post synpatic cleft
SE: N+V, hypertension
75
Antidepressants - NRIs
E.g.
MOA
SE
E.g. Buproprion
MOA: inhibit reuptake of NE at post synaptic cleft
SE: headache, dry mouth
76
Antidepressants - MAOIs
E.g.
MOA
SE
E.g. Phenelzine
MOA: inhibit the breakdown of monoamines by MAO-A and MAO-B
SE: interact with tyramine containing foods --> malignant hypertension (tyramine is a sympathomimetic broken down by MAOs)
77
```
Antidepressants - TCAs
Indications:
E.g.
MOA
SE
```
E.g. Amytriptaline
Indications: depression, tension headaches
MOA: inhibit reuptake of 5HT and NA
SE: Sedation, anticholinergic effects
78
Benzodiazepines
Indications
MOA
SE:
Indications: management of acute psychosis, intense agitation, high risk of immediate danger, status epilepticus
MOA: increase the affinity of GABA receptors for GABA --> increase Cl- influx into the neuron --> inhibtion
SE: addictive, respiratory depression, muscle weakness
79
Analgesics: Opioids
E.g.
MOA
SE
E.g. Morphine
MOA: act preferentially on mu receptors to provide supraspinal analgesia, inhibit Ca2+ entry and increase K+ efflux, inhibiting AC and cAMP --> inhibit pain perception
SE: arteriodilation and venodilation, sedation, gi motility + constipation, addiction
80
```
Muscle relaxants - Depolarising agents
Indications
E.g.
MOA
SE
```
E.g. Succinylcholine
Indications: orthopeadic surgery - allow for intubation, surgical anaesthetics for manipulation
MOA: competitive agonists for nicotinic ACh receptors - similar structure to ACh --> cause prolonged depolarisation leading to closure of the inactivation gate and prevention of further muscle APs
SE: muscle soreness, rapidly hydrolysed by plasma butrylcholinesterase
Progression: muscle fasisculations over chest --> rapid paralysis
81
```
Muscle relaxants - Non-depolarising
Indications
E.g.
MOA
SE
```
E.g. Rocuronium
Indications: Surgery
MOA: Competitive antagonist for Ach receptors --> prevent muscular depolarisation
Progression --> small fasiculations --> small muscle paralysis --> larger muscle paralysis --> reversal from large to small
82
```
Anticholinesterases
Indications
E.g.
MOA
SE
```
E.g. Neostigmine
Indications: myasthenia gravis, reversal of muscle relaxants
MOA: inhibit the breakdown of ACh in the post synaptic cleft --> increase avaliability
SE: hypotension, bradycardia, N+V
83
Dantrium
Indication
MOA
Indication: treatment for malignant hyperthermia, severe spasticity in non ambulatory ptx
MOA: blocks the release of Ca2+ from SR
84
Propofol
Indication
MOA
SE:
Indication: induction anaesthesia, maintainence anaesthesia, status epilepticus
MOA: binds GABAa receptors in prefrontal cortex and hippocampus
SE: amnesia (hippocampus), N+V, depression of airway reflexes, decrease in BP
85
Ketamine
Indication:
MOA:
SE
Indication: induction/maintenance anaesthesia, neuropathic pain
MOA: NMDA receptor antagonist in thalamus and limbic system. Some analgesia
SE: sympathetic NS activation --> increase HR, BP, CO
86
Tranaxemia Acid
Indications:
MOA
SE
Indications: surgery, bleeding disorder
MOA: inhibits the formation of plasmin therefore increasing time for fibrinolysis
SE: increased clotting propensity
