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Year 1 HLB > HLB Core Drugs > Flashcards

HLB Core Drugs Flashcards

Key Drugs

1
Q

<p>What are cardiac glycosides?</p>

A

<p>- organic compounds (carbon backbone)</p>

<p>- able to increaseinotropic contraction force</p>

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2
Q

<p>What are cardiac glycosides used for?</p>

A

<p>- atrial fibrillation and flutter</p>

<p>- heart failure</p>

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3
Q

<p>What is the most common drug used as a cardiac glycoside?</p>

A

<p>- digoxin</p>

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4
Q

<p>What is the mechanism of action of digoxin, a cardiac glycoside?</p>

A

<p>- inhibits the enzyme ATPase</p>

<p>- stop N+ / K+ ATPase pump</p>

<p>- Na+ ⬆️inside the cell</p>

<p>- Na+ leaves via Na+ / Ca2+ exchanger and Ca2+ ⬆️ inside the cell</p>

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5
Q

<p>Why is N+ / K+ ATPase so important in cells?</p>

A

<p>- maintains resting membrane potential</p>

<p>- maintain electrochemical charge</p>

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6
Q

<p>In normal physiology in cardiomyocytes what does the N+ / K+ ATPase use to move cations against concentrations gradients and what moves into the cell and what moves outside the cell?</p>

A

<p>- ATP used</p>

<p>- Na+ moves out of cell (3)</p>

<p>- K+ moves into cell (2)</p>

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7
Q

<p>What is ATPase?</p>

A

<p>- enzyme inside cells</p>

<p>- hydrolyses ATP to ADP</p>

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8
Q

<p>If Na+ / K+ ATPase is working normally what happens to the cell?</p>

A

<p>- 3 Na+ leave and 2 K+ enter the cell</p>

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9
Q

<p>How does inhibiting N+ / K+ ATPase increase inotropic force?</p>

A

<p>- Na+ remains in cell</p>

<p>- Na+ can leave through Na+ / Ca2+ exchanger</p>

<p>- Na+ leaves and Ca2+ enters</p>

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10
Q

<p>In addition to inhibiting N+ / K+ ATPase and increasing intracellular Ca2+, what other mechanism is digoxin able to work through?</p>

A

<p>- stimulates the vagus nerve (parasympathetic)</p>

<p>- reduced HR through SA and AV node</p>

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11
Q

<p>Why can digoxin, a cardiac glycoside be useful in treating chronic heart failure (CHF) patients?</p>

A

<p>- CHF means heart is weakened</p>

<p>- digoxin ⬆️ inotropic force</p>

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12
Q

<p>What is the renin angiotensin aldosterone system, commonly referred to as RAAS?</p>

A

<p>- hormone system that regulates blood pressure</p>

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13
Q

<p>Why is the renin angiotensin aldosterone system (RAAS) written in this order?</p>

A

<p>- this is the order blood pressure is controlled</p>

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14
Q

<p>What is renin (also known as angiotensinogenase) as part of RAAS?</p>

A

<p>- proteolytic enzyme</p>

<p>- cleaves angiotensinogen released from the liver</p>

<p>- creates angiotensin 1</p>

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15
Q

<p>What is angiotensinogen as part of the RAAS?</p>

A

<p>- alpha 2 globulin</p>

<p>- released by the liver, a precursor for angiotensin 1</p>

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16
Q

<p>When do the kidneys secrete renin in the RAAS system?</p>

A

<p>- when blood flow or blood volume to the kidneys is reduced</p>

<p>- specifically the juxtaglomerular cells in the kidneys</p>

<p>- blood vessels vasoconstrict in attempt to increase blood flow</p>

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17
Q

<p>What is angiotensin I as part of the RAAS?</p>

A

<p>- a weak vasoconstrictor</p>

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18
Q

<p>Is angiotensin II, part of the RAAS the strongest vasodilator in the body?</p>

A

<p>- no</p>

<p>- 2nd strongest vasoconstrictor in the body</p>

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19
Q

<p>What is angiotensin converting enzyme?</p>

A

<p>- enzyme able to cleave amino acid off angiotensin I</p>

<p>- creates angiotensin II</p>

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20
Q

<p>What type of receptor is present on smooth muscles that angiotensin II is able to act upon and cause vasoconstriction?</p>

A

<p>- GPCR - specifically Gaq</p>

<p>- ⬆️ Ca2+ = contraction</p>

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21
Q

<p>To help identify which drugs are ACE inhibitors, what do the drugs names generally end in?</p>

A

<p>- pril</p>

<p>- like ramipril</p>

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22
Q

<p>What is bradykinin?</p>

A

<p>- peptide</p>

<p>- promotes inflammation and vasodilation</p>

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23
Q

<p>What does bradykinin trigger the release of from endothelium cells?</p>

A

<p>- prostacyclin</p>

<p>- nitric oxide</p>

<p>- endothelins (strongest dilator in the body)</p>

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24
Q

<p>What is one of the most commonly prescribed ACE inhibitors?</p>

A

<p>- ramipril</p>

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25
Q

<p>Although ramipril is an effective hypertensive agent, there are some side effects that patients may experience. What are those?</p>

A

<p>- dry cough (due to bradykinin accumulation)</p>

<p>- renal impairment</p>

<p>- hyperkalaemia (can be given with diuretic)</p>

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26
Q

<p>ACE inhibitors such as ramipril are generally used to treat hypertension, but why can they be useful when treating heart failure?</p>

A

<p>- ⬇️ systemic vascular resistance (SVR)</p>

<p>- ⬇️ SVR = ⬇️ afterload (resistance against heart beat)</p>

<p>- heart failure patients have a weak heart</p>

<p>- ⬇️ afterload reduces workload on the heart</p>

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27
Q

<p>What is the normal physiological effect of angiotensin II on aldosterone levels?</p>

A

<p>- stimulates the adrenal cortex</p>

<p>- aldosterone is released from zona glomerulosa cells</p>

<p>- increases blood volume and BP</p>

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28
Q

<p>Angiotensin II is able to stimulate zona glomerulosa cells of the adrenal cortex releasing aldosterone, which can then go on to increase blood volume and BP. How does aldosterone increase blood volume and BP?</p>

A

<p>- signals to distal tubules in renal tubules</p>

<p>- retain Na+ and and H2O</p>

<p>- ⬆️ Na+ and H2O = ⬆️ blood volume</p>

<p>- ⬆️ blood volume = ⬆️ BP</p>

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29
Q

<p>What is the normal physiological effect of angiotensin II on the pituitary gland?</p>

A

<p>- baroreceptors recognise need to ⬆️ BP</p>

<p>- hypothalamus signals pituitary gland</p>

<p>- pituitary gland secretes anti-diuretic hormone</p>

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30
Q

<p>The pituitary gland secretes anti-diuretic hormone (opposite effect of diuretci drugs to treat hypertension) in response to angiotensin II. How does the release of anti-diuretic hormone effect BP?</p>

A

<p>- stimulates kidneys to retain H2O</p>

<p>- ⬆️ H2O = ⬆️ blood volume</p>

<p>- ⬆️ blood volume = ⬆️ BP</p>

<p>- partial arteriole vasoconstrction</p>

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31
Q

<p>Ramipril is an ACE inhibitor, which means it can inhibit the conversion of angiotensin I to angiotensin II. If ACE is inhibited by Ramipril, what are the 3 main effects this can have on the RAAS system?</p>

A

<p>- ⬇️ smooth muscle vasoconstriction</p>

<p>- ⬇️ H2O retention due to anti-diuretic hormone</p>

<p>- ⬇️ Na+ and H2O retention due to aldosterone</p>

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32
Q

<p>When treating hypertension, we need to remember how to calculate BP, which is cardiac output (CO) x systemic vascular resistance (SVR). Therefore what are the main effects on CO and/or SVR that ACE inhibitors have?</p>

A

<p>- ⬇️ systemic vascular resistance</p>

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33
Q

<p>What are muscarinic antagonist drugs?</p>

A

<p>- those that inhibit muscarinic receptors</p>

<p>- M1 = Gaq</p>

<p>- M2 = Gai</p>

<p>- M3 = Gaq</p>

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34
Q

<p>What do muscarinic antagonist drugs do to the parasympathetic activity?</p>

A

<p>- reduce the activity</p>

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35
Q

<p>Why are muscarinic antagonist drugs commonly called anti-cholinergic?</p>

A

<p>- muscarinic receptors are a form of cholinergic receptor</p>

<p>- inhibit muscarinic means anti-cholinergic</p>

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36
Q

<p>What is one of the most commonly prescribed muscarinic antagonist drugs?</p>

A

<p>- atropine</p>

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37
Q

<p>What is atropine used for in the heart?</p>

A

<p>- treat people with bradycardia</p>

<p>- patients have low HR</p>

<p>- patients may have lower CO</p>

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38
Q

<p>What is the mechanism of action of atropine?</p>

A

<p>- competitive antagonist</p>

<p>- inhibits acetylcholine and therefore muscarinic receptors</p>

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39
Q

<p>In a normal physiological response what does the muscarinic receptor M2 do to the heart?</p>

A

<p>- inhibit adenylyl cyclase (AC) as part of Gai</p>

<p>- ⬇️ AC = ⬇️ HR and inotropic contraction</p>

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40
Q

<p>Atropine is a non selective competitive antagonist, meaning it can compete with acetylcholine and inhibit its activity when binding to muscarinic receptors. Although it has a wide range of effects, what does atropine do to the heart in patients with bradycardia?</p>

A

<p>- does not inhibit adenylyl cyclase (AC) in Gas</p>

<p>- ⬆️ activation of SA node = ⬆️ HR</p>

<p>- ⬆️ inotropic contraction</p>

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41
Q

<p>What are diuretics?</p>

A

<p>- drugs that ⬆️ urine excretion</p>

<p>- drugs that ⬆️ Na+ and Cl- excretion</p>

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42
Q

<p>What is the most commonly used thiazide diuretic to treat high blood pressure?</p>

A

<p>- bendroflumethiazide</p>

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43
Q

<p>Where in the kidneys is blood filtered to form the filtrate?</p>

A

<p>- blood enters glomerulus</p>

<p>- blood is then filtered into the filtrate</p>

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44
Q

<p>Once the filtrate is formed from the glomerulus, what happens to the fluid as it move through the tubules and out of the collecting duct as urine?</p>

A

<p>- H2O and other molecules are re-absorbed into blood</p>

<p>- what is left is urine</p>

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45
Q

<p>Where are ions mainly re-absorbed in the renal system?</p>

A

<p>- distal convelutedtubules</p>

<p>- location of most diuretics actions</p>

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46
Q

<p>What passively follows ion re-absorption in the distal tubules of the renal system, which ion specifically does it follow?</p>

A

<p>- Na+</p>

<p>- due to osmosis (H2O dilutes Na+ in blood)</p>

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47
Q

<p>In normal physiology how are Na+ and Cl- re-absorbed from the filtrate into the blood from the renal system?</p>

A

<p>- through thiazide sensitive Na+ / Cl- co-transporter into epithelial cells</p>

<p>- Na+ reabosrbed using Na+ / K+ ATPase</p>

<p>- Cl- channels reabsorb Cl-</p>

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48
Q

<p>What is the mechanism of action of bendroflumethiazide on the renal system and thus lower blood pressure?</p>

A

<p>- inhibits thiazide sensitive Na+ / Cl- co-transporter</p>

<p>- Na+ and Cl- excreated out in urine</p>

<p>- H2O follows Na+</p>

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49
Q

<p>How does increased Na+ in the blood cause an increase in blood pressure?</p>

A

<p>- Na+ retains H2O</p>

<p>- ⬆️ volume in blood vessels = ⬆️ pressure</p>

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50
Q

<p>What is one of the most commonly used thiazide like drugs to treat hypertension?</p>

A

<p>- Indapamide</p>

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51
Q

<p>In normal physiological response of smooth muscle vasoconstriction or vasodilation, what happens to the ATP sensitive K+ channels and the Ca2+ voltage gated channels on the smooth muscle cells?</p>

A

<p>- vasoconstriction = ⬇️ K+ ATPase</p>

<p>- ⬇️ ATPase activity = ⬇️ K+ leaves and ⬆️ Ca2+ enters cell</p>

<p></p>

<p>- vasodilation = ⬆️ K+ ATPase</p>

<p>- K+ channel opens ⬆️ K+ inside cell and hyperpolarisation (⬆️ negative)</p>

<p>- ⬆️ K+ leaves and ⬇️ Ca2+ enters cell</p>

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52
Q

<p>In addition to inhibiting the thiazide sensitive Na+ / Cl- co-transporter, Indapamide also acts at lowering blood pressure through a second mechanism, what is this?</p>

A

<p>- dilate blood vessels</p>

<p>- ATPase sensitive K+ channels ⬆️ K+ leaving cell (⬆️ negative inside)</p>

<p>- reduces Ca2+ entry into blood vessels</p>

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53
Q

<p>In addition to bendroflumethiazide and Indapamide, what is the 3rd diuretic drug we are expected to know?</p>

A

<p>- furosemide</p>

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54
Q

<p>What are the 3 thiazide or thiazide like diuretics that are are expected to know? (all end in ide)</p>

A

<p>1 - bendroflumethiazide</p>

<p>2 - indapamide</p>

<p>3 - furosemide</p>

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55
Q

<p>What are some common side effects of diuretics?</p>

A

<p>- Hyponatraemia (Na+) - Hypokalaemia (K+) - Alkalosis (H +) - Hypercalcaemia (Ca2+) - Hypomagnesaemia (Mg2+) - ⬆️ in urate (gout) - ⬆️ blood glucose - ⬆️ lipids</p>

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56
Q

<p>When treating hypertension, we need to remember how to calculate BP, which is cardiac output (CO) x systemic vascular resistance (SVR). Therefore what are the main effects on CO and/or SVR that thiazide and/or thiazide like diuretics have on CO and/or SVR?</p>

A

<p>- blood volume</p>

<p>- blood volume, increases preload</p>

<p>- preload increases SV</p>

<p>- SV increases CO</p>

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57
Q

<p>How can thiazide and thiazide like diuretics cause hyponatraemia (⬇️ Na+), Hypokalaemia (⬇️ K+) and hypercalcaemia (⬆️ Ca2+)?</p>

A

<p>- Na+ and K+ not re-absorbed</p>

<p>- Na+ moves down concentration gradient from blood into epithelial cells</p>

<p>- Na+ / Ca2+ exchanger swaps Na+ anjd Ca2+</p>

<p>- Ca2+ swaps places and leaves epithelail cell into blood</p>

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58
Q

<p>In normal physiology how does Na+ and Cl- get re-absorbed from the distal tubules into the cells?</p>

A

<p>- through the Na+ / Cl- co-transporter</p>

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59
Q

<p>In normal physiology, once Na+ and Cl- have been re-absorbed from the distal tubules through the Na+ / Cl- co-transporter into the epithelialcells, how is Na+ able to be re-absorbed into the blood?</p>

A

<p>- through Na+ / K+ ATPase pump</p>

<p>- 3 Na+ out of cell into blood</p>

<p>- 2 K+ into cell and out of blood</p>

<p>- K+ is able to leave eputhelail cell through K+ channel</p>

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60
Q

<p>In addition to moving from the distal tubules through the Na+ / Cl- co-transporter and back into blood through the N+ / K+ ATPase pump, how can some of the Na+ re-enter the same cell epithelail cellit just left?</p>

A

<p>- through Na+ / Ca2+ exchanger</p>

<p>- Ca2+ in renal cells is ⬇️</p>

<p>- creates Ca2+ and Na+ concentration gradient</p>

<p>- higher Ca2+ in distal tubules epithelial cells compared to blood</p>

<p>- Ca2+ moves from epithelailcells into blood</p>

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61
Q

<p>How can thiazide and thiazide like diuretics cause metabolic acidosis?</p>

A

<p>- ⬇️ Cl- re-absorbed- Cl- used to balance carbonic anhydrase with HCO3-</p>

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62
Q

<p>What is aldosterone?</p>

A

<p>- hormone release by adrenal glands</p>

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63
Q

<p>What is the role of aldosterone in the body?</p>

A

<p>- signals kidneys to retain Na+ and H2O and excrete K+</p>

<p>- ⬆️ Na+ and H2O = ⬆️ blood pressure</p>

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64
Q

<p>What do aldosterone antagonists do to the body?</p>

A

<p>- ⬇️ Na+ and H2O re-absorption</p>

<p>- ⬇️ blood volume and BP</p>

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65
Q

<p>What is one of the most commonly prescribed drugs that act as aldosterone antagonists that we need to know?</p>

A

<p>- Spironolactone</p>

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66
Q

<p>What is the structure of the aldosterone antagonists, Spironolactone, similar to?</p>

A

<p>- estrogen</p>

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67
Q

<p>What is the mechanism of action of Spironolactone?</p>

A

<p>-inhibits Na+ pump and ⬇️ Na+ reabsorption from lumen</p>

<p>- inhibits Na+ / K+ ATPase at basolateral membrane (blood)</p>

<p>- Na+ is not re-absorbed</p>

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68
Q

<p>As spironolactone resembles oestrogen in structure, what is one of the most common side effects of spironolactone?</p>

A

<p>- Gynaecomastia (man boobs)</p>

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69
Q

<p>In addition to Gynaecomastia, what are 2 other common side effects of Spironolactone?</p>

A

<p>- Impaired renal function</p>

<p>- Hyperkalaemia (K+)</p>

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70
Q

<p>What are adrenergic receptors?</p>

A

<p>- GPCRs - part of sympathetic system</p>

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71
Q

<p>What hormones activate adrenergic receptors?</p>

A

<p>- catecholamines- adrenaline and noradrenaline (main 2)</p>

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72
Q

<p>What are the 2 main groups of adrenergic receptors?</p>

A

<p>- alpha (a)- beta (B)</p>

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73
Q

<p>What type of transmembrane receptors are all adrenergic receptors?</p>

A

<p>- GPCRs</p>

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74
Q

<p>How many alpha adrenergic receptors are there?</p>

A

<p>- 2- alpha 1 and 2</p>

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75
Q

<p>How many beta adrenergic receptors are there?</p>

A

<p>- 3- B1, B2 and B3</p>

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76
Q

<p>Which GPCR do alpha receptors use to activate intracellular pathways?</p>

A

<p>- a1 = Gaq- a2 = Gai</p>

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77
Q

<p>Which GPCR do beta receptors use to activate intracellular pathways?</p>

A

<p>- all Gas</p>

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78
Q

<p>What is the basic intracellular pathway for Gaq?</p>

A

<p>- phospholipase C is activated and cleaves PiP</p>

<p>- IP3 and DAG are formed</p>

<p>- IP3 increases Ca2+</p>

<p>- Ca2+ binds with DAG and activates protein kinase C</p>

<p>- protein kinase C can phosphorylate inside cell</p>

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79
Q

<p>What is the basic intracellular pathway for Gas?</p>

A

<p>- adenlyly cyclase (AC) is activated</p>

<p>- AC converts ATP into cAMP</p>

<p>- cAMP activates protein kinase A</p>

<p>- protein kinase A can phosphorylate inside cell</p>

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80
Q

<p>What is the primary function of a1 adrenoreceptors receptors during fight or flight?</p>

A

<p>- vasoconstriction (primarily blood vessels)</p>

<p>- bladder sphincter contraction</p>

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81
Q

<p>What is the primary function of a2 adrenoreceptors receptors during fight or flight?</p>

A

<p>- inhibit release of noradrenaline</p>

<p>- inhibit release of acetycholine</p>

<p>- inhibit release of insulin</p>

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82
Q

<p>What is the primary function of B1 adrenoreceptors receptors during fight or flight?</p>

A

<p>- ⬆️ Heart rate</p>

<p>- ⬆️ Inotrophic contractility</p>

<p>- ⬆️ Renin release (fluid and salt retention)</p>

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83
Q

<p>What is the primary function of B2 adrenoreceptors receptors during fight or flight?</p>

A

<p>- Vasodilation (skeletal muscle)</p>

<p>- Bronchodilation</p>

<p>- Gluconeogenesis (⬆️ glucose from liver)</p>

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84
Q

<p>Propranolol was the first ever beta blocker invented. What beta channels does in block?</p>

A

<p>- all as it is a non selective beta blocker</p>

<p>- inhibits B1 and B2 adrenergic receptors</p>

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85
Q

<p>What can Propranolol be used for in treatment?</p>

A

<p>- angina, hypertension, arrhythmias</p>

<p>- migraine, tremor</p>

<p>- anxiety</p>

<p>- thyrotoxicosis (excessive thyroid hormone)</p>

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86
Q

<p>What are beta blockers (specifically beta 1) able do to the heart in relation to BP?</p>

A

<p>- ⬇️ HR</p>

<p>- ⬇️ inotropic force</p>

<p>- ⬇️ afterload (SVR) through reduced renin release</p>

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87
Q

<p>What are 2 common side effects of beta blockers (specifically beta 1) that can occur?</p>

A

<p>- bradycardia</p>

<p>- fatigue</p>

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88
Q

<p>Why canbeta blockers be dangerous in the lungs when using them to treat patients with heart disease?</p>

A

<p>- inhibit B2 adrenoreceptors</p>

<p>- bronchoconstriction</p>

<p>- ⬆️breathlessness</p>

<p>- dangerous in asthma/COPD</p>

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89
Q

<p>Beta blockers (specifically beta 1) are useful drugs when treating the heart, but what are some side effects that they can have on arterioles in the circulatory system?</p>

A

<p>- ⬇️ blood supply to skeletal muscles</p>

<p>- ⬇️ blood supply to skin (cause claudication and cold hands)</p>

<p>- ⬇️ blood supply to penis</p>

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90
Q

<p>What is a useful method for remembering which beta blockers are present in the heart and lungs?</p>

A

<p>- B1 = heart - we have 1 heart</p>

<p>- B2 = lung - we have 2 lungs</p>

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91
Q

<p>What is the most commonly used B1 adrenergic antagonist, also called a beta blockers?</p>

A

<p>- Bisoprolol</p>

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92
Q

<p>Although Bisoprolol does reduce the side effects when compared with Propranolol, there can be one dangerous side effect in patients with diabetes. Hypoglycaemia causes release of adrenaline, causing gluconeogeneis in the liver in an attempt to release glucose. What symptoms can patient with diabetes experience when hypoglycaemic due to adrenaline?</p>

A

<p>- sweating, tremor, irritation and palpitations</p>

<p>- symptoms of adrenaline help patients know they may be hypoglycaemic</p>

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93
Q

<p>Why can it be dangerous for patients who are diabetic to take beta blockers?</p>

A

<p>- B1 adrenergic antagonist/blockers block symptoms associated with hypoglycaemia</p>

<p>- especially dangerous in non selective beta blockers</p>

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94
Q

<p>When treating hypertension, we need to remember how to calculate BP, which is cardiac output (CO) x systemic vascular resistance (SVR). Therefore what are the main effects on CO and/or SVR that adrenergic antagonists/blockers affect?</p>

A

<p>- CO</p>

<p>- ⬇️ inotrophy</p>

<p>- ⬇️ HR</p>

<p>- ⬇️ renin release</p>

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95
Q

<p>What do angiotensin II receptor antagonists do?</p>

A

<p>- inhibit the binding of angiotensin II</p>

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96
Q

<p>What type of membrane receptors are present on smooth muscle to receive stimulus from angiotensin II and vasoconstrict?</p>

A

<p>- GCPR, specifically Gaq</p>

<p>- phospholipase C cleaves PiP2</p>

<p>- forms IP3 and DAG</p>

<p>- IP3 stimulates ⬆️ Ca2+ release</p>

<p>- Ca2+ and DAG activate protein kinase C</p>

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97
Q

<p>Which GPCR are all angiotensin II receptors?</p>

A

<p>- Gaq</p>

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98
Q

<p>What is the most commonly prescribed angiotensin II receptor antagonists (AR-II blockers), and generally the first and most commonly prescribed medication for hypertension?</p>

A

<p>- Losartan</p>

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99
Q

<p>When treating hypertension, we need to remember how to calculate BP, which is cardiac output (CO) x systemic vascular resistance (SVR). Therefore what are the main effects on CO and/or SVR that angiotensin II receptor inhibitors have?</p>

A

<p>- ⬇️ systemic vascular resistance</p>

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100
Q

<p>How many alpha receptors are there?</p>

A

<p>- 2</p>

<p>- alpha 1</p>

<p>- alpha 2</p>

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101
Q

<p>Do adrenergic receptors act on the sympathetic or parasympathetic system?</p>

A

<p>- sympathetic</p>

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102
Q

<p>Which catecholamines act on the adrenergic receptors?</p>

A

<p>- adrenaline</p>

<p>- noradrenaline</p>

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103
Q

<p>What are the main functions of the adrenergic alpha 1 receptors?</p>

A

<p>- smooth muscle vasoconstriction</p>

<p>- sweating</p>

<p>- bladder sphincter closure</p>

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104
Q

<p>What are the main functions of the adrenergic alpha 2 receptors?</p>

A

<p>- inhibit release of noradrenaline</p>

<p>- inhibit release of ACh</p>

<p>- inhibit release of Insulin</p>

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105
Q

<p>Adrenergic receptors are all GPCR, specifically which GPCR are present on alpha 1 and 2 receptors?</p>

A

<p>- alpha 1 = Gaq</p>

<p>- alpha 2 = Gai</p>

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106
Q

<p>What is the basic intracellular pathway once Gaq has been activated?</p>

A

<p>- GCPR, specifically Gaq</p>

<p>- phospholipase C cleaves PiP2</p>

<p>- forms IP3 and DAG</p>

<p>- IP3 stimulates ⬆️ Ca2+ release</p>

<p>- Ca2+ and DAG activate protein kinase C</p>

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107
Q

<p>What is the basic intracellular pathway once Gai has been activated?</p>

A

<p>- inhibits adenylyl cyclase released by Gas</p>

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108
Q

<p>When treating hypertension, we need to remember how to calculate BP, which is cardiac output (CO) x systemic vascular resistance (SVR). Therefore what are the main effects on CO and/or SVR that alpha inhibitors have?</p>

A

<p>- inhibit vasoconstriction of blood vessels</p>

<p>- ⬇️ systemic vascular resistance</p>

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109
Q

<p>What is a common drug prescribed as an alpha 1 inhibitor that we need to know about?</p>

A

<p>- doxazosin</p>

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110
Q

<p>What is the mechanism of action of the alpha 1 inhibitor doxazosin?</p>

A

<p>- binds to alpha 1 receptors</p>

<p>- inhibits Gaq</p>

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111
Q

<p>Is doxazosin a competitive or non-competitive inhibitor?</p>

A

<p>- competitive</p>

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112
Q

<p>Is doxazosin a selective or non-selective alpha inhibitor?</p>

A

<p>- selective alpha 1 inhibitor</p>

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113
Q

<p>Doxazosin is a selective competitive alpha inhibitors. What is the main effect of this drug?</p>

A

<p>- vasodilation of smooth muscle</p>

<p>- ⬇️ systemic vascular resistance and BP</p>

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114
Q

<p>What are the 2 most common side effects of the alpha 1 antagonist doxazosin?</p>

A

<p>- postural hypotension</p>

<p>- tachycardia (reflex tachycardia)</p>

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115
Q

<p>Doxazosin can cause postural hypotension in older patients, why is this?</p>

A

<p>- Doxazosin vasodilates blood vessels</p>

<p>- upon standing blood vessels do not contract quickly</p>

<p>- fall in blood pressure occurs and patients faint</p>

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116
Q

<p>Doxazosin can cause postural hypotension in older patients, which in turn causes tachycardia reflex, commonly known as palpitations. What is tachycardia reflex?</p>

A

<p>- ⬇️ in BP causes ⬆️ in adrenalin</p>

<p>- ⬆️ in HR follows to compensate and maintain CO</p>

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117
Q

<p>What are calcium channel blockers?</p>

A

<p>- drugs that block Ca2+ entering a muscle cell</p>

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118
Q

<p>What are the 2 main groups of calcium channel blockers?</p>

A

<p>1 - dihydopyridines (mainly blood vessel dilation)</p>

<p>2 - non-dihydopyridines (mainly effects on heart)</p>

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119
Q

<p>What is the most commonly prescribed calcium channel blocker in the UK, that is a dihydopyridine?</p>

A

<p>- Amlodipine</p>

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120
Q

<p>What are 2 other drugs that are classed as non-dihydopyridines that can be prescribed as calcium channel blockers?</p>

A

<p>- Diltiazem- Verapamil</p>

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121
Q

<p>Generally out of the 2 groups of calcium channel blockers, which drugs work almost entirely on the smooth muscle and is used to treat hypertension?</p>

A

<p>- drug class = dihydopyridines</p>

<p>- drug name = amlodipine</p>

122
Q

<p>Generally out of the 2 groups of calcium channel blockers, which drugs were almost entirely on the heart?</p>

A

<p>- drug class = non-dihydopyridines</p>

<p>- drug name = Diltiazem and Verapamil</p>

123
Q

<p>Out of the 3 calcium channel blocker drugs that we need to know (Diltiazem, Verapamil and Amlodipine) which one is able to act on the heart and the smooth muscles?</p>

A

<p>- drug class = non-dihydopyridines</p>

<p>- drug name = Diltiazem</p>

124
Q

<p>What are L-type calcium channels?</p>

A

<p>- L means long lasting</p>

<p>- responsible for the excitation-contraction coupling</p>

<p>- located in all muscle cells</p>

<p>- located in endocrine cells of adrenal cortex (involved in aldosterone release)</p>

125
Q

<p>How do L-type Ca2+ channels in cardiac and smooth muscle become activated?</p>

A

<p>- cells receive action potential</p>

<p>- Na+ channel opens</p>

<p>- T-type Ca2+ channel opens</p>

<p>- Na+ and Ca2+ from T-type Ca2+ channels ⬆️ voltage</p>

<p>- L-type Ca2+ channel opens causing action potential</p>

126
Q

<p>What is the mechanism of action of Amlodipine?</p>

A

<p>- non competitive antagonist</p>

<p>- binds to L-type Ca2+ channels</p>

<p>- ⬇️ Ca2+ in cells and inhibit vasoconstriction</p>

127
Q

<p>What effects can Ca2+ channel blockers have on the cardiovascular system?</p>

A

<p>- ⬇️ SA node activity = ⬇️ HR</p>

<p>- ⬇️ cardiomyocyte Ca2+ = ⬇️ inotrope force</p>

<p>- ⬇️ smooth muscle Ca2+ = ⬇️ vasoconstriction</p>

128
Q

<p>Out of the 3 calcium channel blocker drugs that we need to know (Diltiazem, Verapamil and Amlodipine) which one would be used to treat angina?</p>

A

<p>- drug class = non-dihydopyridines</p>

<p>- drug name = Diltiazem</p>

129
Q

<p>Out of the 3 calcium channel blocker drugs that we need to know (Diltiazem, Verapamil and Amlodipine) which one would be used to treat arrhythmia's?</p>

A

<p>- drug class = non-dihydopyridines</p>

<p>- drug name = Verapamil</p>

130
Q

<p>In addition to treating hypertension, what other syndrome can Amlodipine be used to treat?</p>

A

<p>- Raynauds syndrome</p>

<p>- causes severe vasoconstriction</p>

131
Q

<p>What is the most common side effect to Ca2+ channel blockers?</p>

A

<p>- ankle swelling</p>

132
Q

<p>In addition to causing ankle swelling, why would Ca2+ channel blockers cause constipation?</p>

A

<p>- smooth muscle causes peristaltic contractions</p>

<p>- Ca2+ channel blockers inhibit GIT contractions</p>

<p>- stool does not move</p>

133
Q

<p>Ca2+ channel blockers can cause postural hypotension in older patients, which in turn causes tachycardia reflex, commonly known as palpitations. What is tachycardia reflex?</p>

A

<p>- ⬇️ in BP causes ⬆️ in adrenalin</p>

<p>- ⬆️ in HR follows to compensate and maintain CO</p>

134
Q

<p>How can Ca2+ channel blockers cause flushing and headaches as a side effect?</p>

A

<p>- dilating skin and brain blood vessels</p>

135
Q

<p>What do all forms of dihydopyridines, a class of Ca2+ channel blockers end in to help remember them?</p>

A

<p>- pine</p>

136
Q

<p>Dihydopyridines and non-dihydopyridines are both Ca2+ channel blockers, but generally work through different mechanisms. How can you remember that Dihydopyridines primarily work on dilating the blood vessels?</p>

A

<p>- Dihydopyridines start with a D</p>

<p>- D for Dilation of blood vessels</p>

137
Q

<p>Dihydopyridines and non-dihydopyridines are both Ca2+ channel blockers, but generally work through different mechanisms. How can you remember that Non-Dihydopyridines primarily work on the heart?</p>

A

<p>- N D is for Non-Dihydopyridines</p>

<p>- N-D for Node supression in heart (small effect on blood vessels)</p>

138
Q

<p>When looking at Ca2+ channel blockers that we need to know Diltizam, Amolodapine and Verapamil, which would you prescribe for angina?</p>

A

<p>- Diltizam</p>

139
Q

<p>When looking at Ca2+ channel blockers that we need to know Diltizam, Amolodapine and Verapamil, which would you prescribe for arrythmias?</p>

A

<p>- verapamil</p>

140
Q

<p>When looking at Ca2+ channel blockers that we need to know Diltizam, Amolodapine and Verapamil, which would you prescribe for high BP?</p>

A

<p>- amolodapine</p>

141
Q

According to the NICE guidelines what what blood pressure is an indicator to clinicians to start treatment immediately?

A
  • SBP >180 mmHg - stage 3 hypertension
142
Q

According to the NICE guidelines what what blood pressure requires 24 hour monitoring to confirm stage 2 hypertension (due to which coat syndrome) prior to starting treatment?

A
  • BP >160/100 mmHg- stage 2 hypertension
143
Q

According to the NICE guidelines in a patient with end stage organ damage or diabetic, what blood pressure requires treatment to begin?

A
  • BP > 140/90 mmHg - stage 1 hypertension
144
Q

If a patient presents with a high blood pressure, what is the first thing clinicians will tell them to do?

A
  • change lifestyle- lose weight- ⬇️ salt- ⬇️ alcohol- increase exercise/physical activity
145
Q

Using the ABC system below, what would be the first line of treatment for hypertension for a caucasian individual under 55 years of age based on the NICE guidelines?A = ACE-I or AR2BC = Calcium channel blockerD = thiazide diuretic

A
  • A- Ramipril = ACE-I- Losartan = AR2B
146
Q

Using the ABC system below, what would be the second line of treatment for hypertension for any patient based on the NICE guidelines?A = ACE-I or AR2BC = Calcium channel blockerD = thiazide diuretic

A
  • A + C or A + D
147
Q

Using the ABC system below, what would be the third line of treatment for hypertension for any patient based on the NICE guidelines?A = ACE-I or AR2BC = Calcium channel blockerD = thiazide diuretic

A
  • A + B + C
148
Q

Using the ABC system below, what would be the first line of treatment for hypertension for a black or >55 years of age patient based on the NICE guidelines?A = ACE-I or AR2BC = Calcium channel blockerD = thiazide diuretic

A
  • C or D
149
Q

Why are >55 year olds and black patients not prescribed an ACE-I or AR2B as the first line of treatment for hypertension?

A
  • > 55/year = more side effects of ACE-I or AR2B- black = less sensitive to ACE-I or AR2B
150
Q

Based on the NICE guidelines when treating patients for hypertension, what can clinicians do if the combinations of ACE-I, AR2B, Calcium channel blockers and thiazide diuretic are insufficient?

A
  • add in alpha or beta antagonist - add in additional diuretic - prescribe based on other co-morbidities
151
Q

What are the NICE target guidelines for the treatment of hypertension?

A
  • <80 years = <140/90 mmHg- >80 years = <150/90 mmHg- patient with diabetes = <135/85 mmHg
152
Q

<p>What is the first line of treatment in hyperlipidaemia?</p>

A

<p>- lifestyle interventions</p>

153
Q

<p>As there are no surgeries available for hyperlipidaemia what are the 2 treatment options available?</p>

A

<p>- lifestyle interventions</p>

<p>- medications</p>

154
Q

<p>What is 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase?</p>

A

<p>- enzyme that reduces 3-hydroxy-3-methyl-glutaryl-coenzyme A into mevalonate in cholesterol metabolism</p>

155
Q

<p>Where is 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase active in the body?</p>

A

<p>- liver</p>

156
Q

<p>Why is 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase so important?</p>

A

<p>- rate limiting step in cholesterol synthesis</p>

<p>- no HMG-CoA) reductase = no mevalonate and no cholesterol</p>

157
Q

<p>What enzyme is the target for hyperlipidaemia medications?</p>

A

<p>- 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase</p>

158
Q

<p>What are the first line of drugs for anyone with hyperlipidaemia?</p>

A

<p>- statins</p>

159
Q

<p>What are the 2 statins that we need to know?</p>

A

<p>- Atorvastatin (most commonly prescribed)</p>

<p>- Simvastatin (dirty drug)</p>

160
Q

<p>What do statins do to a patients lipid profile?</p>

A

<p>- ⬇️ cholesterol production by liver</p>

<p>- ⬇️ LDL</p>

<p>- ⬇️ total cholesterol</p>

<p>- ⬇️ triglycerides</p>

<p>- ⬆️ HDL</p>

161
Q

<p>In addition to treating hyperlipidaemia, what else are statins effective for when considering the development of atherosclerosis plaques?</p>

A

<p>- -anti-inflammation</p>

<p>- cholesterol in plaques</p>

162
Q

<p>Statins are able to reduce all cause mortality, what does this mean?</p>

A

<p>- reduce death from any cause in patients with arterial disease</p>

163
Q

<p>What are the most common side effect of statins?</p>

A

<p>- myalgia (most common symptom)</p>

<p>- rhabdomyolysis</p>

<p>- arthralgia (joint pain)</p>

<p>- liver dysfunction</p>

164
Q

<p>What does rhabdomyolysis mean?</p>

A

<p>- rhabdo = rod like</p>

<p>- myo = muscle</p>

<p>- lysis = breakdown</p>

165
Q

<p>Prior to statins being developed, what was the main drug of choice to treat hyperlipidaemia</p>

A

<p>- fibrates</p>

166
Q

<p>What is the mechanism of action for fibrates?</p>

A

<p>- activate peroxisome proliferator-activated receptor (PPAR)-alpha</p>

<p>- ⬆️ lipoprotein lipase activity in capillaries</p>

167
Q

<p>Fibrates act on peroxisome proliferator-activated receptor (PPAR)-alpha, what is this?</p>

A

<p>- a ligand-activated transcriptional factor</p>

<p>- upregulation offatty acid beta-oxidation (produce energy)</p>

168
Q

<p>What is the main fibrate we need to be aware of?</p>

A

<p>- Bezafibrate</p>

169
Q

<p>What are fibrates, specifically Bezafibrate able to do to the lipid profile?</p>

A

<p>- ⬇️ LDL</p>

<p>- ⬇️ TAG (main effect)</p>

<p>- ⬆️ HDL</p>

170
Q

<p>What are side effects of fibrates, specifically Bezafibrate?</p>

A

<p>- GI disturbance (diarrhoea)</p>

<p>- myalgia (muscle pain)</p>

<p>- rhabdomyolysis</p>

171
Q

<p>In addition to statins and fibrates there are bile salt sequestrants. How do these drugs affect cholesterol levels?</p>

A

<p>- bind to bile acids and stops re-absorption - liver has to use cholesterol to make more bile acids - ⬇️ cholesterol</p>

172
Q

<p>What is the name of the bile salt sequestrants that we need to be aware of?</p>

A

<p>- Cholestyramine</p>

173
Q

<p>What is the main side effect of Cholestyramine, a bile salt sequestrants?</p>

A

<p>- GI disturbance (diarrhoea)</p>

<p>- ⬇️ fat soluble vitamines (A.D.E.K)</p>

174
Q

<p>Instead of using Cholestyramine, what is a more commonly used bile salt sequestrants?</p>

A

<p>- Ezetimibe</p>

175
Q

<p>What is proprotein convertase subtilisin/kexin type 9, more commonly referred to as PCSK9?</p>

A

<p>- an enzyme involved in cholesterol regulation</p>

<p>- regulates the number of LDL receptors</p>

176
Q

<p>What do PCSK9 inhibitors do?</p>

A

<p>- ⬆️ number of LDL receptors</p>

<p>- cholesterol</p>

177
Q

What was the first cardiovascular event risk score?

A
  • Framlington risk score- 10 year risk score
178
Q

What is the Framlington study?

A
  • study of the town Framlington- study of cardiovascular risks on population
179
Q

What are the 2 cardiovascular event risk scores used in the UK, and which is used more commonly?

A
  • Q-risk (most common)- JBS3 risk
180
Q

At what point should a patient be prescribed statins based on the NICE guidelines?

A
  • > 10% risk of CVD event in the next 10 years- score is based on Q-risk score
181
Q

When treating a patient with statins, how long should a clinician leave it before checking lipids profile?

A
  • 3 months
182
Q

What is the aim for LDL reduction in any intervention?

A
  • > 40% reduction in LDL
183
Q

<p>What are nitrates?</p>

A

<p>- salts containing polyatomic ion</p>

184
Q

<p>What is the nitrate drug that we need to know?</p>

A

<p>- glyceryl trinitrate (GTN)</p>

185
Q

<p>What does glyceryl trinitrate do to the body?</p>

A

<p>- vasodilates blood vessels (⬇️ pre and afterload)</p>

<p>- ⬇️ systemic vascular resistance</p>

<p>- ⬇️ inotropic effect in heart</p>

186
Q

<p>What is the preferred administration of glyceryl trinitrate in acute situations?</p>

A

<p>- sublingually</p>

<p>- under the tongue</p>

187
Q

<p>Is glyceryl trinitrate a pro drug?</p>

A

<p>- yes</p>

<p>- only active once metabolised</p>

188
Q

<p>How does glyceryl trinitrate enter the body?</p>

A

<p>- releases nitrate ions</p>

<p>- converted to nitric oxide (NO) by enzymes in the blood</p>

<p>- NO, a hydrophobic gas diffuses into cells</p>

189
Q

<p>What is the mechanism of action of glyceryl trinitrate enter the body?</p>

A

<p>- activates guanylyl cyclase (GC)</p>

<p>- GC activates protein kinase G (pKG)</p>

<p>- pKG activates myosin phophotase (MP)</p>

<p>- pKG phosphorylates Ca2+ pump</p>

<p>- MP dephosphorylates light myosin chain</p>

190
Q

<p>What are corticosteroids used for in respiratory medicine?</p>

A

<p>- anti-inflammatory medication</p>

<p>- vasodilation</p>

191
Q

<p>What cells can corticosteroids receptors be found upon in the body?</p>

A

<p>- all cells</p>

192
Q

<p>What type of receptors do corticosteroids use to influence the body?</p>

A

<p>- nuclear receptors</p>

193
Q

<p>What compounds in the body do corticosteroids get grouped as which allows them to cross the transmembrane barrier of cells and bind with nuclear receptors?</p>

A

<p>- steroid</p>

<p>- hormone and steroid are able to bind to nuclear receptors</p>

194
Q

<p>How do corticosteroids generally have their affect on cells?</p>

A

<p>- cross plasma membrane</p>

<p>- bind with nuclear receptor</p>

<p>- modulate gene expression</p>

195
Q

<p>What are the 2 key corticosteroids drugs that we need to be aware of?</p>

A

<p>- prednisolone (oral tablet or intervaneously)</p>

<p>- beclomethasone (inhaler)</p>

196
Q

<p>What are the benefits and risks of giving a patient the corticosteroids prednisolone intravenously?</p>

A

<p>- systemic and fast acting</p>

<p>- not affected by inhaler technique</p>

<p>- higher risk of side effects</p>

197
Q

<p>What are the benefits and risks of giving a patient the corticosteroids beclomethasone via an inhaler?</p>

A

<p>- localised action</p>

<p>- fewer side effects</p>

<p>- disease may impair absorption</p>

198
Q

<p>Which corticosteroids is given as an inhaler?</p>

A

<p>- beclomethasone</p>

199
Q

<p>Beclomethasone is a corticosteroids that is given as an inhaler. Although it can be very effective, what are the most common side effects?</p>

A

<p>- reduced immune effect</p>

<p>- fungal infections occur (oral candidiasis)</p>

<p>- dysphonia (horse voice)</p>

200
Q

<p>Oral candidiasis (fungal infection) is a common side effect when giving Beclomethasone as a corticosteroids inhaler, how can this be minimised for patients?</p>

A

<p>- oral mouthwash</p>

<p>- use spacers</p>

201
Q

When treating patients with asthma or COPD is it preferential to increase a dosage of a specific drug or add another drug to the patients medication?

A
  • add another drug
202
Q

What are the combination therapy options for continued management of a patient that are are commonly used from the following:- Inhaled corticosteroids (ICS)- Short Acting Beta 2 agonists (SABA)- Long Acting Beta 2 agonists (LABA)- Short Acting Muscarinic antagonists (SAMA)- Long Acting Muscarinic agonists (LAMA)

A
  • ICS + LABA- LABA + LAMA- ICS + LABA + LAMA
203
Q

In addition to treating a patients respiratory symptoms , what is another key effect of medication?

A
  • improved quality of life
204
Q

What are the 3 common antibiotics given to patients with suspected respiratory infections?

A
  • amoxicillin- clarithromycin- vancomycin (MRSA)
205
Q

If a patient has Streptococcus pneumonia, which antibiotic should be prescribed?

A
  • amoxicillin (bacterial wall target)- clarithromycin (ribosome target)
206
Q

The NHS provides advice to patients when treating asthma based on the British Thoracic Society (BTS) and Scottish Intercollegiate Guidelines Network (SIGN). What are the 3 basic things patients with asthma are instructed to do to manage their symptoms?

A

1 - smoking cessation2 - remove allergens3 - inhaler

207
Q

What treatments are given to patients in the form of a preventer to treat asthma on a day to day basis?

A
  • inhaled corticosteroids (ICS) is first line of treatment- LABA with ICS if symptomatic
208
Q

What treatments are given to patients in the form of a reliever to treat asthma during an exacerbation?

A
  • SABA
209
Q

According to the stepwise guide to asthma management, what is the first line of treatment for a patient with asthma?

A
  • inhaled corticosteroids (ICS)
210
Q

According to the stepwise guide to asthma management, if a patient controls their asthma symptoms well, what could you consider doing the dose of their medication?

A
  • reduce the dosage
211
Q

Why is a personalised action plan for asthma important?

A
  • ⬆️ adherence and control - ⬇️ A&E attendance- ⬇️ GP contact time
212
Q

If a patient with an acute asthma exacerbation attends A&E, one of the first things to detect is SaO2. How is this monitored and what would we want to keep this above?

A
  • pulse oximetry - >92%
213
Q

If a patient with an acute asthma exacerbation attends A&E and they are at risk of type 1 respiratory failure with an SaO2 <92% detected by pulse oximetry, what would be the next 2 tests to perform?

A
  • Arterial blood gas- Chest X-ray
214
Q

If a patient with an acute asthma exacerbation attends A&E and they are at risk of type 1 respiratory failure with an SaO2 <92% detected by pulse oximetry, what beta or muscarinic drugs might be prescribed?

A
  • high dose SABA + SAMA (nebuliser)- SABA = salbutamol- SAMA = ipratropium bromide
215
Q

In a patient with COPD, what is the most important thing to discuss with a patient to help alleviate their symptoms?

A
  • smoking cessation
216
Q

In a patient with COPD, smoking cessation is crucial. In addition, if they are hypoxic what treatment should they be prescribed?

A
  • long term O2 therapy
217
Q

If a patient with an acute asthma exacerbation attends A&E and they are at risk of type 1 respiratory failure with an SaO2 <92% detected by pulse oximetry, which steroid would be administered, and how would it be administered?

A
  • steroid via intravenous- prednisone
218
Q

If a patient with an acute asthma exacerbation attends A&E and they are at risk of type 1 respiratory failure with an SaO2 <92% detected by pulse oximetry, what salt can be administered in severe asthma flair ups?

A
  • magnesium sulphate
219
Q

If a patient with an acute asthma exacerbation attends A&E and they are at risk of type 1 respiratory failure with an SaO2 <92% detected by pulse oximetry, what may need to be administered if the patient has an infection??

A
  • antibiotic- amoxicillin- clarithromycin- vancomyosin
220
Q

If a patient with an acute asthma exacerbation attends A&E and they are at risk of type 1 respiratory failure with an SaO2 <92% detected by pulse oximetry, what other drug that is able to cause bronchodilation can be prescribed?

A
  • methylxanthines
221
Q

Is oxygen considered to be a drug?

A
  • yes- must be prescribed
222
Q

What is the normal O2 concentration in the air we breathe?

A
  • 21%
223
Q

When would you prescribe O2 to a patient with respiratory symptoms?

A
  • type 1 and 2 respiratory failure - O2 is <7.8 kPA or <58mmHg
224
Q

When giving a patient with type 1 respiratory failure, what is the target for SaO2?

A
  • 94-98%
225
Q

When giving a patient with type 2 respiratory failure, what is the target for SaO2?

A
  • 88-92%
226
Q

In a patient who is suspected to have type 2 respiratory failure (T2RF), why is it important to ensure they are given controlled O2?

A
  • cause iatrogenic T2RF- CO2 retention- death
227
Q

If a patient is breathless, but not in type 1 or 2 respiratory failure, or receiving palliative care, would you provide O2 therapy?

A
  • no
228
Q

What are the 3 basic masks that patients with type 1 respiratory failure, who do not need controlled oxygen be given?

A
  • standard face mask- re-breathe mask- nasal cannula
229
Q

In a patient who is suspected to have type 2 respiratory failure (T2RF), what type of mask is used to give controlled O2?

A
  • venturi mask
230
Q

What is a short acting Beta 2 agonist?

A
  • drug that enhances B2 receptors
231
Q

What are the main functions of Beta 2 adrenergic receptors?

A
  • bronchodilation- vasodilation of blood to smooth muscle - gluconeogenesis
232
Q

What is the main effect when administering a SABA to an asthmatic patient?

A
  • bronchodilation
233
Q

In addition to bronchodilation, what else can SABA medication be useful for in asthma?

A
  • stabilise mast cells, inhibiting inflammation- enhance mucociliary clearance- ⬇️ vascular permeability
234
Q

Which SABA drug do we need to know about?

A
  • salbutamol (ventolin)
235
Q

Which LABA drug do we need to know about?

A
  • salmeterol
236
Q

How quickly do SABA drugs take to work and last for?

A
  • 10 minutes - 3-5 hours lasting
237
Q

What are the 2 most common side effects of SABA?

A
  • muscle tremors (B2 receptors)- tachycardia (B1 receptors)
238
Q

How quickly do LABA drugs take to work and last for?

A
  • 30 minutes- 10-12 hours lasting
239
Q

What is the only way LABA can be administered?

A
  • inhaled
240
Q

Is LABA ever prescribed in isolation?

A
  • no
241
Q

What should LABA be prescribed with?

A
  • inhaled corticosteroids- LAMA
242
Q

How do muscarinic antagonists work?

A
  • inhibit muscarinic receptors- ⬇️ ACh effects
243
Q

Which short acting muscarinic drug do we need to know about?

A
  • Ipratropium bromide
244
Q

Ipratropium bromide is a muscarinic antagonist, which muscarinic receptor do short acting muscarinic antagonists (SAMA) target, and which GCPR is present?

A
  • M3 receptors - Gaq
245
Q

Ipratropium bromide is a muscarinic antagonist of M3, how long can these drugs take to alleviate symptoms and last for?

A
  • 30 minutes effective- 6 hours lasting
246
Q

Is ipratropium bromide, a muscarinic antagonist, given as an inhaler or intravenously?

A
  • generally inhaler
247
Q

Is ipratropium bromide, a muscarinic antagonist, given as a daily inhaler for asthma and COPD?

A
  • just COPD
248
Q

When is Ipratropium bromide, a muscarinic antagonist, given to asthma and COPD patients?

A
  • during acute exacerbation- given as nebuliser
249
Q

Are SAMA or SABA a more effective bronchodilator?

A
  • SABA
250
Q

In addition to acting as a bronchodilator ipratropium bromide, a muscarinic antagonist, can also help with what in the lungs?

A
  • reduce mucus production- enhance mucociliary escalator
251
Q

Why can the use of SABA and SAMA be effective?

A
  • SABA enhances sympathetic - SAMA reduces parasympathetic
252
Q

Which long acting muscarinic antagonist (LAMA) drug do we need to know about?

A
  • Tiotropium
253
Q

Tiotropium is a long acting muscarinic antagonist (LAMA), by inhibiting muscarinic receptors, what effects do they have on the lungs?

A
  • cause bronchodilatation- ⬇️ bronchospasm- ⬇️ mucus production
254
Q

Tiotropium is a muscarinic antagonist, how long can this drugs last for?

A

12-24 hours

255
Q

Is tiotropium, a muscarinic antagonist, given as an inhaler or intravenously?

A
  • generally as an inhaler
256
Q

Is Tiotropium, a muscarinic antagonist, given as a daily inhaler for asthma and COPD?

A
  • just COPD
257
Q

When would tiotropium, a muscarinic antagonist, been given to asthma and COPD patients?

A
  • during acute exacerbation- given as nebuliser
258
Q

What are the most common side effects of SAMA and LAMA drugs?

A
  • inhibition of the parasympathetic system- slowing of rest and digest
259
Q

<p>What is anaemia?</p>

A

<p>- low haemoglobin in the blood</p>

260
Q

<p>What is the main cause of anaemia?</p>

A

<p>- inability to transport sufficient O2 around the body</p>

261
Q

<p>What are the 2 general causes of anaeimia?</p>

A

<p>1 - low number of RBCs</p>

<p>2 - low haemoglobin level in blood</p>

262
Q

<p>Why is iron so important in RBCs?</p>

A

<p>- binds O2 and haemoglobin together</p>

<p>- no iron means no O2</p>

263
Q

<p>Whenis ferrous sulphate prescribed?</p>

A

<p>- iron supplement</p>

<p>- prescribed when patients have low levels of iron</p>

<p></p>

264
Q

<p>How long is ferrous sulphate generally prescribed for?</p>

A

<p>- 3 months</p>

265
Q

<p>What is B9?</p>

A

<p>- man made version of folic acid</p>

266
Q

<p>Folic acid, the man made version of B9 can be prescribed if patients are low in folic acid. How long are they generaly prescribed this?</p>

A

<p>- 3 months</p>

267
Q

<p>Why are treatments for anaemia generally prescribed for 3 months?</p>

A

<p>- life cycle of RBS (100-120 days</p>

<p>- see if treatment has relieved aneamia</p>

268
Q

<p>What foods can vitamin B9 be found naturally?</p>

A

<p>- green leafy vegetables generally</p>

269
Q

<p>What is vitamine B12 and where can it be found?</p>

A

<p>- compound found in animal meatand dairy products</p>

270
Q

<p>How is vitamin B12 prescribed?</p>

A

<p>- can be prescribed orally</p>

271
Q

<p>If a patient has B12 deficiency due to absorption problems, how can it be administered?</p>

A

<p>- intravenously every 3 months</p>

272
Q

<p>Why is folate so important for RBCs?</p>

A

<p>- important for making RNA and DNA</p>

<p>- important for the production of cells that rapidly turn over like RBCs</p>

273
Q

<p>Why is vitamin B12 (also known as cobalamin) so important for RBCs?</p>

A

<p>- acts as a co-enzyme for folate to synthesis DNA</p>

<p>- if B12 is low then folate cannot function properly</p>

274
Q

<p>What are anti-platelet medications?</p>

A

<p>- drugs that inhibit coagulation</p>

275
Q

<p>What is a day to day drug that is commonly used for headaches that can be used as anti-platelet medication?</p>

A

<p>- aspirin</p>

276
Q

<p>What is the mechanism of action of how aspirin acts as an anti-platelet medication?</p>

A

<p>- inhibits cyclo-oxygenase-1 (COX-1)</p>

277
Q

<p>What is the role ofcyclo-oxygenase-1 (COX-1) in platelet coaggulation?</p>

A

<p>- convertsArachidonic acid intoThromboxane A2</p>

<p>-Thromboxane A2 activates platelets</p>

<p>- Activation, Adhesion and Aggregation of platelets follows</p>

278
Q

<p>Why is a low dose of aspirin better as an anti-platelet medication than a larger dose?</p>

A

<p>- higher doses inhibit COX-1 and prostacyclin</p>

<p>- prostacyclin inhibits platelet aggregation so not a good thing</p>

<p>- low does inhibit COX-1 but notprostacyclin</p>

279
Q

<p>In addition to aspirin, what is the second drug that we need to be aware of?</p>

A

<p>- clopidogrel</p>

280
Q

<p>What is the mechanims of action ofclopidogrel?</p>

A

<p>- inhibits the P2Y12 receptor on platelets</p>

<p>-P2Y12 triggersActivation, Adhesion and Aggregation of platelets</p>

281
Q

<p>Do aspirin and clopidogrel work on the intrinsic or extrinsic coagulation cascade?</p>

A

<p>- intrinsic</p>

<p>- directly on platelets</p>

282
Q

<p>What are anticoagulant medicines?</p>

A

<p>- anticoagulantsare medicines that help prevent blood clots</p>

<p>- generally thin the blood</p>

283
Q

<p>What was the first anticoagulant drug discovered, and the one we need to know?</p>

A

<p>- Warfarin</p>

284
Q

<p>What is the mechanism of action of Warfarin as an anti-coaggulant medication?</p>

A

<p>- inhibits vitamin K factors II (2), VII (7), IX 9 and X (10) - coagulation</p>

<p>- proteins S and C = anti-coagulation</p>

285
Q

<p>What is the mnemonic for remebering the mechanism of Warfarin?</p>

A

<p>- 1972 was the year of diSCo</p>

<p>- factors 9, 7, 2 and 10</p>

<p>- proteins S and C</p>

286
Q

<p>When administering Warfarin, it can initially making clotting worse, generally in the first 36 hours. Why is this the case?</p>

A

<p>- inhibits proteins S and C</p>

<p>- proteins S and C are anti-coaggulators</p>

287
Q

<p>Warfarin has a narrow therapuetic window and interacts with a number of factors including alcohol, green vegetables, P450 and antibiotics, making it a drug that is not commonly used. However, what 2 cases is Warfarin still used for?</p>

A

<p>- mechanical heart valves</p>

<p>- mitral valve stenosis with atrial fibrillation</p>

288
Q

<p>What are direct acting oral anticoagulants (DOACs)?</p>

A

<p>- drugs taken orally to reduce the risk of thrombosis (blood clot)</p>

289
Q

<p>Direct acting oral anticoaggulants (DOACs) are able to inhibit the coaggulation pathway andreduce the risk of thrombosis (blood clot). Which DOAC acts directly on the coaggulation cascade by inhibiting factor X (10)?</p>

A

<p>-Rivaroxaban</p>

290
Q

<p>Rivaroxaban is a drug that is able to inhibit factor X (10) in the coaggulation cascade. Why is factor X (10) so important in the coaggulation cascade?</p>

A

<p>- it sits between intrinsic and extrinsic pathways so powerful</p>

<p>- sits in the common pathway</p>

291
Q

<p>In the names of drugs that inhibit factor X (10) of the coagulation cascade there is a helpful way of identifying these drugs, what is it?</p>

A

<p>- they have XA in their name, which is factor XA (10a)</p>

<p>-Rivaro<strong><u>XA</u></strong>ban is an example</p>

292
Q

<p>Direct acting oral anticoaggulants (DOACs) are able to inhibit the coaggulation pathway andreduce the risk of thrombosis (blood clot). Which DOAC acts directly on the coaggulation cascade by inhibiting factor II(2), more commonly known as thrombin?</p>

A

<p>-Dabigatran</p>

293
Q

<p>Dabigatran is a DOAC drug that is able to inhibit factor II (2), more commonly known as thrombin. Why is thrombin important in the coaggulation cascade?</p>

A

<p>- thrombin converts fibrinogen to fibrin</p>

294
Q

<p>What is heparin?</p>

A

<p>- name heparin is because original heparin was found in liver</p>

<p>- anti-coaggulant medication</p>

295
Q

<p>What is the mechanism of action of heparin?</p>

A

<p>- anti-thrombin III is made and produced by the liver</p>

<p>- thrombin III inhibits aspects of the coagulation cascade</p>

<p>- heparin binds to anti-thrombin III and activates it</p>

296
Q

<p>Once heparin has bound to anti-thrombin III to inhibit the coagulation cascade it is able to inhibit a number of factors. What is an easy way to remember which aspects of the coagulation cascade heparin can inhibit?</p>

<p></p>

A

<p>- 2 + 7 = 9 then comes 10, 11, 12</p>

<p></p>

297
Q

<p>Heparin is a very effective drug, but the effects of the drug can vary depending on the batch. This is due to the high molecular weight of unfractioned heparin. What is fractionated and unfractionated heparin?</p>

A

<p>- unfractionated is physioloigical heparin and contains HMW and LMW heparin</p>

<p>- fractionated is processed heparin and contains only LMW heparin</p>

298
Q

<p>Is fractionated and unfractionated heparin used more commonly?</p>

A

<p>-fractionated</p>

299
Q

<p>What are the 2 fractionated heparin drugs that we need to know about?</p>

A

<p>-Enoxaparin and Tinzaparin</p>

<p>- both end in <u><strong>aparin</strong></u></p>

300
Q

<p>Fractionated heparin is used more commonly more that unfractionated heparin due to efficacy and safety. But what is one of the main times when fractionated low molecular weight heparins are not used?</p>

A

<p>- needs to be cleared by the kidneys</p>

<p>- if patient has significant renal impariment</p>

Year 1 HLB (25 decks)

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