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Phase 2a Sam > ILA + EXTRAS > Flashcards

ILA + EXTRAS Flashcards

1
Q

In order to induce anaesthesia quickly, what characteristics should the drug have in terms of its protein binding and lipid solubility?

A
  • Low protein binding
    ==> (if protein bound, its not included in the plasma concentration of the free drug)
  • High lipid solubility
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2
Q

In anaesthetics, why does an additional volatile drug needs to be given as soon as possible

A

Giving the second anaesthetic as a volatile gas means close control of the anaesthesia levels can be maintained.

Because plasma levels of initial drug drop

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3
Q

Where does a drug need to be in order to have its effect?

A

The tissue.

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4
Q

Define and explain the terms agonist and antagonist in relation to drug action and give an example of each.

A

An agonist is a compound with high affinity and efficacy to a receptor i.e. Salbutamol, opiods

An antagonist is a compound with high affinity but low efficacy - binds to ligand i.e. Gliclazide, Beta Blockers, CCBs

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5
Q

Inverse agonist vs Antagonist - What’s the difference?

A

Inverse agonists - Will stop baseline function of a receptor (turn tap off)

Antagonists - stop anything binding, so receptor remains in whatever state it was in. (So if tap was dripping, it stays dripping and nothing can change that will the antagonist

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6
Q

Outline what a competitive agonist is and give an example of it

A

● Competitive= receptor antagonist that binds to a receptor but does not activate it, thus blocking the agonist’s action. Dose response curve = just to right (reversible, surmountable)
o Impact can be overcome by increasing the concentration of the agonist
o E.g., naloxone at opioid receptors

		DECREASE POTENCY. AS MORE OF THE FURG IS THEREFORE NEEDED TO ILLICT THE SAME RESPONSE
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7
Q

Outline what non - competitive antagonist is and give an example of it

A

● Non-competitive= an antagonist that causes a decrease in receptor function either by binding to an allosteric site or irreversibly binding to the receptor (irreversible), dose response curve= to right and down. Binds to an allosteric site on the receptor to prevent activation of the receptor.
o E.g., ketamine at the NMDA-glutamate receptor

	DECREASE EFFICACY AND POTENCY
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8
Q

Define Efficacy
Define Potency

A

Efficacy - how well a ligand activates the receptor

the amount of drug needed to elicit an effect (higher the affinity of the drug, the higher the potency)

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9
Q

Briefly outline morphine metabolism

A

morphine becomes Morphine 6 Glucuronide (10%) and Morphine 3 Glucuronide (90%)

Morphine 6 Glucuronide is the most potent metabolite

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10
Q

Outline the 3 main layers of a vessel wall

A

Tunica externa – normally thinner than the media in all except the largest arteries. Contains collagenous and elastic fibres, and blood supply / nerves that supply the vessel (vasa vasorum, nervi vasorum)

Tunica media – normally the thickest layer of the artery. Contains smooth muscle cells and elastic fibres. External elastic lamina may be present in larger vessels.

Tunica intima – endothelium may appear wavy due to contraction of smooth muscle. Internal elastic lamina in larger vessels. (Internal elastic lamina is absent in veins!)

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11
Q

Outline the pathophysiology of arterial thrombus, that can be compared to a venous thrombus

A

Arterial
occur in high shear conditions
Rich in platelets
Involves disrupted atherosclerotic plaques
White clots
Down to platelet adhesion and aggregation prior to activation of coagulation cascade

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12
Q

Outline the pathophysiology of venous thrombus, that can be compared to an arterial thrombus

A

Develops under low shear stress
Fewer platelets involved
TF generates thrombin prior to platelet aggregation
Made up mainly of coagulation factors
Red clots

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13
Q

Give some symptoms for arterial thrombosis

A

The six P’s of the acutely ischaemic limb (from arterial blockage): pulseless, perishingly cold, paraesthesia, paralysis, pulselessness, pain, pallor.

Thrombosis of arteries may build up to these six P’s more slowly, or . Arterial embolus (breaking off a thrombus) may result in these symptoms more quickly.

Both groups are at risk of developing ulcers

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14
Q

Give some symptoms for venous thrombosis

A

WOES

Warm
Oedema
Engorged veins
Swollen

Both groups are at risk of developing ulcers

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15
Q

What are two coagulation tests you can do in thrombus formation?

A

aPTT - activated prothrombin time

PT - Prothrombin time

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16
Q

For both coagulation tests, what pathway does aPTT measure, and what factors does it look at?

A

aPTT - activated prothrombin time

measures intrinsic pathway - (FACTORS 12, 11, 9, 8,), and the common pathway 10, 5, 2 (prothrombin) and 1 (fibrinogen)

Think aPTT - (TT - table tennis = indoors = intrinsic)

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17
Q

For both coagulation tests, what pathway does PT measure, and what factors does it look at?

A

PT - Prothrombin time EXTRINSIC AND COMMON

measures extrinsic pathway (factors 3 and 7) and then common pathway factors 10, 5, 2 (prothrombin) and 1 (fibrinogen)

(T - tennis - outdoors )

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18
Q

What test would use for DVT?

A

D Dimer

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19
Q

Outline the differences between

senstiivty n
specificty

A

Sensitivity - likelihood of detecting a true positive -
High specificity - If the test is positive, you are very likely to have the disease

Specificity - Correctly being able to exclude a negative test
High specifity - if the test is negative, you are very likely TO NOT Have the disease

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20
Q

outline the specificity and sensitivity of D dimer in DVT

A

Its highly sensitive , due to inflammation, (in other words it will always pick up a DVT)

but not specific as you can’t specifically diagnose DVT from it as as positive result can be due to different things that aren’t DVT

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21
Q

What score can you use for DVT and PE?

A

Wells Score

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22
Q

Test for DVT and PE - outline some things seen in the Wells Score

A
  • Cancer
  • Paralysis,
  • Recently bedridden for >3d or major surgery in last 12wks
  • Local tenderness along distribution of deep venous system
  • Entire leg swollen 1 point
  • Calf swelling >3cm 1 point
  • Oedema 1 point
  • Collateral superficial veins (non-varicose) 1 point
  • Previously documented DVT 1 point
  • Alternative diagnosis at least as likely as DVT -2 points
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23
Q

Treatments of DVT:
Outline what heparin/DOACs does

A

Anti coagulants

DOACs - all the apixabans
inhibit factor 10a (remeber bc Xa is in the drug names, inhibtis factor 10a)

Binds to antithrombin and increases its activity (antithrombin inactivates several enzymes of the coagulation system)
Indirect thrombin inhibitor

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24
Q

Treatments of DVT:
How do you monitor the effects of Heparin?

A

Anti coagulants

DOACs - all the apixabans ac

Monitor with Activated partial thromboplastin time (APTT), aim ration 1.2-2.8
Given by continuous infusion

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25
What are the advantages and disadvantages of warfarin compared to DOACs
Warfarin - good bc can be used in valve replacements when DOACs cant use, can be reversed with vitamin K easily Disadvantages - need to measure INR all the time with it, so dosing is tricky
26
What are the advantages and disadvantages of warfarin compared to DOACs
Warfafin - good bc can be bused in valve replacemnts when DOACs cant use, can be reveresed with vitamin K easily Disadvateabes - need to measeure INR all teh time with it, so dosing is tricky -- this isnt the case with DOACs Warfarin is Contraindicated in pregnancy!!
27
Outlien how warfarin works.
Prevents synthesis of active factors II, VII, IX, and X Antagonist of vitamin K Long half-life (36 hours) Prolongs the prothrombin time
28
outline how DOACs work
(namely Rivaroxaban which is a Xa inhibitor) Directly acting on factor II or X No blood tests or monitoring Shorter half-lives so bd or od Used for extended thromboprophylaxis and treatment of AF and DVT/PE (equivalent to INR 2-3, not higher, so not heart valves) Not used in pregnancy – as can pass to the baby routine management option for DVT
29
What are some risk factors for DVT???
Old Long haul flight ***COMBIINED CONTRACEPTION PILL***
30
What is the diagnostic criteria for an AKI?
Rise in serum creatinine of 26µmol/l or greater within 48 hours 50% or greater rise in serum creatinine (1.5 times more than baseline) known or presumed to have occurred within 7 days Fall in urine output to less than 0.5ml/kg/hour
31
How can NSAID use lead to an AKI?
Because they inhibit prostaglandin synthesis, *by inhibiting the COX-1 enzyme* so renal vasoconstriction cannot be counteracted NSAIDs can reduce blood flow to the kidneys by causing vasoconstriction, **especially in the afferent arteriole** This narrowing can reduce the amount of blood that flows to the kidneys, which can impair their ability to filter toxins from the bloodstream and can lead to an AKI, **As GFR is reduced** INTRA RENAL CAUSE OF AKI, NEPHROTOXIC
32
What changes does Hyperkalaemia cause on an ECG?
Tall Tented T waves Flattened P waves Prolonged PR Wide QRS
33
name for types of drugs that can have been known to cause/exascerabte an AKI.
DAMN diuretics ACE inhibitors metformin NSAIDs
34
Hyperkalaemia is a complication of AKI, and can lead to a cardiac arrest. How can you manage hyperkalaemia?
3 THINGS - 1. **IV stat of Calcium Gluconate** - Stabilisation of the myocardium 2. **Variable rate insulin with dextrose infusion - to increase cellular uptake of potassium** = Reduction of serum potassium 3. **oral calcium resonium** - Reduction of total body potassium - treat underlying cause
35
How can hypercalcaemia effect the kidneys?
Hypercalcemia induces polyuria by inhibiting the action of antidiuretic hormone on the collecting tubules. Hypercalcemia also impairs renal function by reducing glomerular blood flow through afferent arteriolar vasoconstriction.
36
Why does HR increase when BP is low?
Heart rate increases when BP drops, to compensate for the less stroke volume , to maintain Cardiac output
37
How can hyperkalaemia cause Cardiac arrest?
will lead to more potassium in the cells, meaning that they are more likely to trigger action potential by increasing membrane excitability Membrane potential goes from -84mV to -65 - -45mV
38
Why is metformin contraindicated in renal failure?
Because metformin is cleared by the kidneys, it may accumulate when renal function decreases, with the potential for exposure-dependent toxicity that could precipitate lactate accumulation. **basically can cause lactic acidosis**
39
Fundamental Biological therapies Name a Biologic response modifier that specifically suppresses T cells B Cells
T Cells - Abatacept B Cells - Rituximab T cells end in T B cells end in B *picture = treatment for Rheumatoid Arthritis*
40
Fundamental Biological therapies Name a Biologic response modifier that specifically suppresses TNF alpha Interleukin 1
TNF alpha - infliximab Interleukin 1 - Anakinra *picture = treatment for Rheumatoid Arthritis*
41
What artery is the Superior cerebellar artery Anterior inferior cerebellar artery Posterior inferior cerebellar artery all a branch of
● Superior Cerebellar Artery (SCA) o Branch of Basilar Artery (wraps around Pons before reaching cerebellum) ● Anterior Inferior Cerebellar Artery (AICA) o Branch of Basilar Artery (wraps around Pons before reaching cerebellum) ● Posterior Inferior Cerebellar Artery (PICA) o Branch of vertebral artery
42
What symptoms would a stroke in the posterior circulation have?
Would be blocking the posterior cerebellar artery/vertebral/basillar artery Loss of consciousness Isolated homonymous hemianopia Brainstem/cerebellar syndrome
43
Explain in pathophysiological/coagulation terms how AF leads to a TIA
Fibrillating atria - pooling of blood and increased blood stasis - increased chance of clot formation Can become dislodged and may be carried as an embolus through the heart. ==> into the carotid arteries
44
How can a TIA/sichaemic stroke lead to raised ICP?
Ischaemic/necrosing tissue creates an inflammatory response. This in turn perpetuates swelling and oedema, that will lead to an increase in ICP
45
How can a raised ICP lead to further brain tissue ischaemia?
Raised ICP will lead to CSF, venous system, and then arteries have all become squashed. the cerebral perfusion pressure in the arteries is not high enough to properly perfuse the brain, and it starts to become more ischaemic.
46
What is cushings reflex?
- Bradycardia, hypertension, irregular breathing
47
How can raised ICP lead to the symptoms seen in Cushing's reflex
In response to raised ICP, The arterial smooth muscle will increase the blood pressure by vasoconstricting to try to reperfuse the brain Which will lead to an increase in BP - which will stimulate the baroreceptors in the aorta, which will result in **bradycardia**, seen in Cushing's reflex
48
What do you give for an ischaemic stroke if its been over 4.5 hours?
Can't give alteplase Give 300mg aspirin Clopidogrel Or mechanical thrombectomy
49
What is mechanical thrombectomy? What is the time limit for it
Thrombectomy, also known as mechanical clot retrieval, is the surgical removal of a blood clot in an artery. It is used to treat some strokes caused by a blood clot (ischaemic stroke) and it aims to restore blood flow to the brain. has to be done within 24 hours
50
Misc Med School drugs - what is dobutamine used for, and what type of drug is it?
Its an ionotropic agent and so can treat hypotension by raising BP Dobutamine - B1 agonists - and acts as a postive inotrope Increases heart contractility **Inotrope - refers to STRENGHT OF HEART BEATS** **Chronotope - REFERES TO RATE/SPEED OF HEARTBEATS**
51
Misc Med School drugs - when is Oxybutynin used, and how does it work?
its an Antimuscarinic Relaxes bladder muscles so you don’t feel the need to pee as much Overreative bladder, also used in MS
52
Misc Med School drugs - when is Rivaroxaban used, and how does it work?
DOAC Factor Xa inhibitor, so blood is less likely to clot, used to treat AF Deep vein thrombosis
53
Misc Med School drugs - what drug do you use to treat erectile dysfunction, and how does it work?
Sildenafil its a phosphodiesterase type V inhibitor enhances erection on sexual arousal by **increasing the quantity of cyclic guanosine monophosphate** in the corpora cavernosa- helps vessels dilate
54
Misc Med School drugs - when is tramadol used, and how does it work?
inhibits serotonin and norepinephrine reuptake enhancing **inhibitory effects on pain transmission** in the spinal cord
55
What drug is often used as a muscle relaxant before surgery?
Suxamethonium - Ach Analogue Suxamethonium has a longer duration of effect than acetylcholine, and is not hydrolyzed by acetylcholinesterase. By maintaining the membrane potential above threshold, it does not allow the muscle cell to repolarize.
56
Define anaphylaxis
Anaphylaxis a severe, life-threatening, generalised or systemic hypersensitivity reaction. It is characterised by rapidly developing life-threatening airway and/or breathing and/or circulation problems usually associated with skin and mucosal changes
57
What are some signs/symptoms of anaphylaxis?
o Occurs within minutes and lasts 1-2 hours o Vasodilation o Increased vascular permeability o Bronchoconstriction o Urticaria (hives) Tachycardia, Hypotension
58
Outline what happens in the initial, "priming stage" of anaphylaxis
● Type 1 hypersensitivity reactions are IgE mediated. o The IgE antibodies are formed to an antigen (or allergen), with an individual’s tendency towards making IgE being determined by factors including genetics, T cell responsiveness and antigenic burden. o The IgE binds to high-affinity IgE receptors on the surfaces of mast cells and basophils, and these cells are now primed to react the next time the cells come into close proximity with the allergen.
59
Outline what happens in anaphylaxis when a patients primed Mast cells are exposed to the allergen
o The cross-linking of **IgE on the cell surfaces causes rapid (mast cell) cellular degranulation** and liberation of a number of chemical mediators. The mediators released by mast cell degranulation include the preformed molecules **histamine, protease enzymes, proteoglycans and chemotactic factors.** o Reaction of antigen with IgE on mast cells also stimulates synthesis and release of **platelet activating factor (PAF), leukotrienes and prostaglandins.**
60
What are some of the physiological responses to anaphylaxis?
▪ Smooth muscle spasm in the respiratory and GI tracts ▪ Vasodilation ▪ Increased vascular permeability ▪ Stimulation of sensory nerve endings ▪ Increased mucous secretion and bronchial smooth muscle tone, as well as airway oedema ▪ Cardiovascular effects result from decreased vascular tone and capillary leakage. **Hypotension, cardiac arrhythmias** Tacycardia, syncope and shock can result from intravascular volume loss
61
What is the Treatment for anaphylactic shock?
ABCDE assessment IM Adrenaline (500mg) - If ineffective then give second IM 500mg Adrenaline Dose Then Chlorphenamine - Anti-histamine (H1) Hydrocortisone - Steroid
62
Why is a Second dose of Adrenaline given if the first dose is ineffective?
Adrenaline has a very short 1/2 life and therefore if it has not worked first time round this may be due to the concentration of adrenaline dropping too quickly to have a good effect
63
What is the blood test to confirm anaphylaxis?
SERUM MAST CELL TRYPTASE: Most specific reading for most cell degranulation
64
Define Prevalence?
Number of cases at a given point in time
65
Define Incidence?
Number of new cases in a given time frame
66
What properties of a drug will help induce anaesthesia quickly?
What properties of a drug will help induce anaesthesia quickly?
67
Define sensitivity - what would a highly sensitive test mean?
Sensitivity refers to a test's ability to designate an individual with disease as positive. A highly sensitive test means that there are few false negative results, and thus fewer cases of disease are missed.
68
Define specificity - what would a highly specific test do?
The specificity of a test is its ability to designate an individual who does not have a disease as negative. A highly specific test means that there are few false positive results.
69
What is the difference between plasmaphereses and plasma exchange?
Plasmapheresis refers to a procedure in which the plasma is separated from the blood either by centrifugation or membrane filtration. Once separated the plasma can be manipulated in a variety of ways. Plasma exchange refers to discarding the plasma totally and substituting a replacement fluid.
70
What is the treatment, route and dose for anaphylaxis in Type 1 HS recation?
Adreanline, IM, 500mcg
71
Name some causes of Hypercalcaemia
CKD Myeloma Dehydration hyperparathryoidism Sarcoidosis **Neoplastic syndromes**, eg (squamous cell lung ca) Drugs eg - **Thiazide diuretics**
72
What would Hypercalcaemia cause on an ECG?
Short ST segment, and Widened T wave, Shorted QT interval
73
What would Hypocalcaemia cause on an ECG?
Prolonged ST segment Prolonged QT interval
74
What signs would you see in someone with acute appendicits? What examinations would you do?
- **Right iliac fossa tenderness:** rebound tenderness (pain when pressure is taken off) or percussion tenderness (pain during percussion) suggests localised peritonism - **Guarding** - **Rovsing’s sign:** pain in the right iliac fossa is worsened by pressing on left iliac fossa - **Psoas sign:** pain is worsened by extending the hip - **Obturator sign:** pain is worsened by flexing and internally rotating the hip **Tachycardia, hypotension and generalised peritonism:** suggests perforation
75
What are some common side effects of statins?
Myalgia is a very common side effect of statins Angio-oedema and rhabdomyolysis are also side effects of statins but are very uncommon.
76
How long after a TIA should you not drive?
Do not notify the DVLA but no driving for 1 month – this is the correct management for a TIA

Phase 2a Sam (18 decks)

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