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phase 2a pain > ila > Flashcards

ila Flashcards

1
Q

2 main paired arteries supplying brain. arise/ascend where

A

vertebral, internal carotid

arise neck, ascend to cranium

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2
Q

make up CoW?

A 
anterior cerebral
anterior communicating
internal carotid
inferior communicating
inferior cerebral
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3
Q

where ICA’s originate?

A

bifurcation of R&L common carotid at C4

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4
Q

where vertebral originate

A

subclavian arteries

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5
Q

why stroke symptoms contralateral

A

somatic and sensory nerve fibres to and from peripheries decussate @ spinal cord or brainstem (lesion in cerebral cortex on opposite side)

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6
Q

cause of amaurosis fugax

A

stenosis of central retinal artery or ICA

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7
Q

TIA lasts ? it has temporary focal ischaemia but no?

A

24hr then resolves, no infarction

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8
Q

how AF leads to TIA and most common place

A

fibrillating atria = stasis/pooling of blood = increased chance of clot formation
auricular appendage

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9
Q

pre central gyrus functions

A

motor

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10
Q

post central gyrus functions

A

sensory

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11
Q

increased icp triad name and components

A

cushings reflex:
bradycardia
hypertension
erratic breathing

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12
Q

explain why cushings reflex happens

A

icp increase, greater than arterial BP so supply is squashed and brain not perfused properly. alpha 1 adrenergic response, smooth muscle contract to re-perfuse = bp increases, baroreceptors detect this HPN and muscarinic responds by reducing HR. this presses on brainstem leading to resp centre dysfunction and irregular breathing

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13
Q

how does TIA lead to increased ICP

A

necrosis and ischaemia causes inflam response

odema in brain = extra fluid in cranial cavity

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14
Q

define pharmacokinetics

A

effect of body on drug

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15
Q

define pharmacodynamics

A

effect of drug on body

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16
Q

define bioavailability

A

total proportion of drug which reaches target location/can act on target

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17
Q

define first pass metabolism

A

drug is extracted/metabolised by gut wall and liver so not all drug makes it into systemic circulation

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18
Q

4 medical ethics

A

autonomy
beneficence
justice
non-maleficence

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19
Q

function of central nervous sys

A

spinal cord and brain

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20
Q

function of peripheral nervous system

A

connect organs and muscles to CNS - branches into somatic and autonomic

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21
Q

function of somatic nervous system

A

motor control of skeletal muscles

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22
Q

function of sympathetic nervous system

A

fight or flight

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23
Q

function of parasympathetic nervous system

A

rest and digest

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24
Q

function of autonomic nervous system

A

motor control of internal organs - branches into PNS and SNS

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25
Q

sympathetic system - what the neurons release and name of receptor

A

acetylcholine and norepinephrine, adrenergic receptor

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26
Q

parasympathetic system - what the neurons release and name of receptor

A

acetylcholine x2, muscarinic receptor

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27
Q

define agonist drug

A

binds to receptor and activates, mimics endogenous substance
full = same response
partial = partial response

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28
Q

define antagonist drug

A

binds to receptor and prevents its activation
competitive - binds to active site
non-competitive - allosteric site elsewhere

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29
Q

define efficacy of drug

A

how much of a response/how well it works on receptor

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30
Q

define potency of drug

A

how much of a drug is needed to elicit response

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31
Q

enteral administration

A

via gi tract eg. oral, rectal, sublingual

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32
Q

par-enteral administration

A

not gi tract eg. IV IM SC inhale

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33
Q

local administration

A

eg. topical, eye drops, intranasal

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34
Q

3 aspects that affect rate/effectiveness of absorption

A

surface area, pH, perfusion (reduced in shock)

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35
Q

absorption:
water sol drug
lipid sol drug
larger molecule drug

A

water - diffusion
lipid - cross phospholipid membrane
larger - facil diffusion, ATP-dependent, endocytosis

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36
Q

why is IV faster

A

directly into bloodstream so no membrane crossing or first pass metabolism (100% bioavailability)

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37
Q

distribution effectiveness depends on…

A

blood flow to area
permeability of capillaries (lots of slit junc in liver but less in brain so harder)
binding to proteins (drug travels bound, eg. to albumin which makes it slower, but must be free to cross membranes hence anaesthesia needing a low affin for prot)
lipophilicity (lipophilic drugs penetrate membrane easily hence anaesthesia needs to be lipid soluble)

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38
Q

if drug has high vol of distribution then…

A

more drug in tissues than in plasma so higher conc required

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39
Q

how does liver help kidney in drug metabolism

A

kidney cannot excrete/eliminate lipid soluble drugs

liver metabolises them first

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40
Q

2 phases of liver metabolism (and what might interfere with it)

A

phase 1: make drug hydrophilic using cytochrome p450
phase 2: if too lipophilic, make polar = acetylation by adding glutathione
altered by alcohol, inducer which increases Cp450 eg. phenytoin, inhibitor which decreases it eg. ciprofloxacin

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41
Q

what may inducers and inhibitors of cp450 result in

A 
inducer = sub-therapeutic dose
inhibitor = toxicity
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42
Q

where are drugs excreted

A

most excreted in liver
doses/drugs altered if renal failure
some excreted by liver in bile then faeces

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43
Q

treat paracetamol overdose if acute liver injury and overdose within last 8 hrs

A

IV N-acetylcysteine

44
Q

describe phase 2 metab of paracetamol

A

para conjugates with glucuronide sulfates

excreted in urine

45
Q

describe phase 1 cytochrome p450 metab of paracetamol

A

becomes NAPQI - highly reactive intermediate metabolite

this is conjugated with glutathione to make it non toxic

46
Q

what happens to metab pathway in paracetamol overdose

A

phase 2 pathway becomes saturated/overwhelmed so more paracetamol shunted to phase 1 reaction leading to increase of NAPQI
Glutathione available is overwhelmed and NAPQI remains in liver where it reacts with cellular membrane molecules = hepatocyte damage = acute liver necrosis

47
Q

treat paracetamol overdose if staggered over 1 hour

A

base treatment off paracetamol levels and further blood tests

48
Q

if severe liver damage from paracetamol overdose

A

acidic blood, high blood lactate, poor clotting, hepatic encephalopathy = liver transplant

49
Q

side effects of NSAIDs

A

GI upset, GI bleeding, renal impairment

50
Q

side effects of anti-histamines

A

older ones can cross BBB and cause sedation

anti emetics bc H1 receptors in vom centre too

51
Q

side effects of beta 2 agonist

A

can agonise b2 receptors in other tissue eg. sweating, tachycardia

52
Q

side effects of ACE-I

A

dry cough due to bradykinin

dilates afferent glom arteriole so worsens kidney function

53
Q

side effects of PPI

A

prolonged use in elderly can incr fracture risk

54
Q

side effects of opioids

A

resp depression - give naloxone

n&V, constip, addiction, withdrawal

55
Q

side effects of diuretics

A

hyperkalaemia

increased freq and dehydration

56
Q

define zero order

A

enzymes saturated by high drug doses, rate of metabolism is constant

57
Q

define first order

A

catalysed by enzymes, rate of metabolism directly proportional to drug concentration

58
Q

high blood flow organs

A

brain heart kidney liver lungs

if site of action here then redistribution = termination of drug action

59
Q

why is additional drug given to maintain anaesthesia

A

Well perfused tissues will receive drug first, lowering overall plasma conc
If a second anaesthetic agent is not given then as the plasma concentration of drug decreases the patient will start to wake up

60
Q

what is thiopentone and how does it work

A

ultra-short acting depressant of the CNS
due to high lipid solubility, can cross blood brain barrier and membranes
distrib rapidly to highly perfused areas
continued muscle uptake lowers the blood concentration & indirectly the brain concentration
therefore fast recovery from drug

61
Q

4 drug targets

A

receptors, ion channels, enzymes, carrier molecules

62
Q

score for DVT assess

A

well’s score

63
Q

suspected DVT, what is performed first

A

within 4hrs US doppler

if not then d dimer and LMWH, then US doppler within 24 hrs

64
Q

arterial thrombosis signs

A 
pulseless
pallor
perishingly cold
paraesthesia
paralysis
pain
65
Q

3 long term treatment DVT

A

warfarin - vit k antagonist
DOAC
LMWH

66
Q

purpose of coag cascade

A

maintain haemostasis by repairing damaged vessel to prevent blood loss

67
Q

primary haemostasis forms

A

unstable platelet plug at site of injury, then coag cascade activated

68
Q

heparin mechanism

A

catalyzes the inactivation of thrombin

69
Q

warfarin mechanims

A

vitamin k antagonist - inhibs synthesis of CF 10 9 7 2

prolongs prothrombin time

70
Q

doac mechanism

A

direct acting oral anticoagulant

increases activity of endogenous antithrombin

71
Q

high creatinine suggests…

A

kidney disfunction

72
Q

define GFR

A

vol of fluid filtered from glomerulus to bowman’s space

73
Q

AKI ECG findings

A

tall tented t waves
wide QRS
PR elongation
flattened p wave

74
Q

which drug CI in AKI

A

NSAIDs - nephrotoxic med

75
Q

3 classes of AKI

A

pre renal - inad blood supply to kidney, dehydration, hypotension, hf, low bp
renal - damage to kidney
post renal - blockage in urinary tract, tumours, renal stone

76
Q

change in AKI symptoms with hydration

A

HR reduced, BP increased

77
Q

how does insulin correct hyperkalaemia in AKI

A

stimulates activity of sodium ATPase pump = k+ into cell

insulin also reduces glucose so dextrose given to compensate

78
Q

atherosclerosis and complications?

A

fatty deposit, hardening of arterial wall
chronic inflam/activation of immun sys
plaque rupture - thrombus can cause ischaemia

79
Q

define stenosis

A

narrowing/reduction of blood flow

80
Q

qrisk 3 >10% score …

A

start atorvastatin

81
Q

secondary prevention 4a’s for athersclerosis

A

atorvastatin
aspirin
atenolol
ACE inhib

82
Q

3 layers of vessel wall and constituents

A

adventitia - connective tissue layer, contains: CT, elastin, vaso varum (blood supply to vessels), nerve fibres
media - smooth muscle, external elastic lamina
intima - endothelium, basement membrane, internal elastic lamina

83
Q

atheroscle: LDL conc inside lumen higher than inside lumen…

A

LDLs infiltrate damaged/altered endothelium deposits in tunica intima and becomes oxidised, trapping them in intima

84
Q

prim, secon, preventions of atherosclerosis

A
  1. prevent disease: exercise, reduce red meat

2. prevent progression of disease: aspirin, atorvastatin, atenolol, ACE inhib

85
Q

co benefit def and example

A

change to peoples life that will benefit climate and health

eg. walk instead of drive

86
Q

non mod RF for atherosclerosis

A

1st degree fam hist, old age, race - south asian, male

87
Q

mod risk factors for atherosclerosis

A

poor sleep, stress, sedentary, smoking, high chol diet, obese

88
Q

atheroscle: trapped oxidised LDLs in intima activates what?

A

endothelial cells to express receptors on luminal surface. WBC adhere to these receptors allowing monocytes and THC from blood to also penetrate and differentiate into macrophages

89
Q

atheroscle: what do macrophages do once in intima

A

engulf LDLs = foam cells
these cells promote migration of smooth muscle cells from media to intima via IGF-1
and promote smooth muscle cell proliferation
=intima growwwwwsss

90
Q

atheroscle: what does increased smooth muscle cells do in intima

A

increases synthesis of collagen by fibroblasts = plaque hardens

91
Q

atheroscle: what happens when foam cells die (apoptosis)

A

DNA material attracts neutrophils and pro inflam cytokines = inflam in plaque area
lipid content moves into plaque and grows it which increases pressure and leads to rupture

92
Q

atheroscle: what happens when plaque ruptures

A

coag cascade occurs to stop plaque entering lumen = thrombus forms = impedes blood flow

93
Q

triggers of anaphylaxis

A 
flucloxacillin
peanuts
pollen
mould
bee stings
shellfish
plasters/latex
94
Q

symptoms of anaphylaxis

A 
SOB
low o2 SATS
high resp rate
wheeze
low bp
high hr
distressed
itching
95
Q

type 1 hypersensitivity reaction

A

Classical allergy, mediated by the inappropriate production of specific IgE antibodies to harmless antigens

96
Q

type 2 hypersensitivity reaction

A

Caused by IgG and IgM antibodies that bind to antigens cells or tissues leading to cell or tissue damage

97
Q

type 3 hypersensitivity reaction

A

Caused by antibody-antigen complexes being deposited in tissues, where they activate the complement system and cause inflammation

98
Q

type 4 hypersensitivity reaction

A

A delayed type hypersensitivity reaction caused by T helper cells traveling to the site of antigens, recruiting macrophages and causing inflammation e.g. rheumatoid arthritis, contact dermatitis

99
Q

define anaphylaxis

A

severe, life-threatening, generalised or systemic hypersensitivity reaction - rapidly developing life-threatening airway and/or breathing and/or circulation problems usually associated with skin and mucosal changes.

100
Q

first exposure in anaphylaxis?

A

inappropriate antigen specific immune response to a benign pathogen

  1. allergen detected by antigen presenting - present antigens on surface
  2. T-helpers recognise and inform B-cells of antigen presence
  3. b cells trigger their proliferation into plasma cells via interleukin-21.
  4. Interleukin-4 ensures that these plasma cells secrete IgE antibodies
  5. mast cells have FC receptors bind to IgE and present them
101
Q

subsequent exposure of anaphylaxis - within minutes

A

minutes = IgE on mast cell recog allergen, cross-linking, degranulation of histamine = vasodilation, bronchoconstriction, increase vasc perm and oedema

102
Q

subsequent exposure of anaphylaxis - within hours

A

Leukotrienes → increased vascular permeability and bronchoconstriction → swelling and breathing trouble)
prostaglandins → bronchoconstriction → breathing problems
eosinophil chemotactic factor of anaphylaxis (ECF-A) → attracts eosinophils

103
Q

initial manage anaphylaxis

A

Airways → Ensure and secure patent airway
Breathing → Provide O2 if needed or salbutamol if wheezing
Circulation → IV fluid bolus to support circulation and BP
Disability → lie flat to increase cerebral perfusion
Exposure → expose skin and look for flushing, angioedema (swelling), urticaria

104
Q

manage anaphylaxis once confirmed

A

IM adrenaline (epipen, repeat after 5 mins if required) → vasoconstriction and prevent anaphylactic shock
Antihistamines (oral chlorpheniramine or cetirizine) → block the effects of histamine by blocking histamine 1 receptors
Steroids (IV hydrocortisone) → reduce inflammatory response

105
Q

second dose of adrenaline in anaphylaxis?

A

short half life (Half life is the time taken for the concentration of the drug to reduce by 50% within the patients body)

106
Q

anaphylaxis diagnostic bloodtest

A

mast cell tryptase is raised

phase 2a pain (27 decks)

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