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phase 2a mine > ila > Flashcards

ila Flashcards

1
Q

5 stages of atherosclerosis

A 
fatty streak
intermediate lesion
fibrous cap covered
plaque rupture
plaque erosion
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2
Q

endothelial barrier damaged by what

A 
lipids - LDL cholesterol
smoking toxins 
 - free radical
- CO
- nicotine
hypertension
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3
Q

atherosclerosis occurs where in the vessel

A

intima of arteries

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4
Q

what attracts monocytes to the fatty streak

A

LDL cholesterol is oxidised and modified which send cytokines out

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5
Q

what are foam cells

A

lipid laden macrophages (full of LDL cholesterol) that die full

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6
Q

what cells are in a fatty streak

A

t cells
foam cells
LDL cholesterol

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7
Q

what cells are in an intermediate lesion

A 
t cells
foam cells
LDL cholesterol
platelets
smooth muscle cells
pools of extracellular lipid
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8
Q

where do smooth muscle cells migrate from into intermediate lesion of atherosclerotic plaque

A

tunica media

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9
Q

what is the positive feedback loop in athergenesis

A

foam cells release cytokines (interleukin 1, 6, CRP) to attract more monocytes (that become macrophage foam cells) and T cells

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10
Q

what is the fibrous cap of plaque made of and where does it come from

A

smooth muscle cells secrete collagen and elastin

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11
Q

what do smooth muscle cells produce in atherogenesis

A

collagen
elastin
– these for fibrous cap

calcium
– stiffens plaque

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12
Q

and what stage in atherogenesis does angiogenesis occur

A

fibrous cap covered stage

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13
Q

what makes up the fibrous cap stage of atheroma

A 
t cells
foam cells
LDL cholesterol / pools of extracellular lipid
calcium
platelets
smooth muscle cells
angiogenesis
connective tissue : elastin and collagen
necrotic core (as it gets big!)
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14
Q

race associated with atherosclerosis

A

south asian

white

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15
Q

gender associated with atherosclerosis

A

male

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16
Q

name a condition that increases risk of atherosclerosis

A

diabetes (type 2>1)
hypertension
hyperlipidema
obesity

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17
Q

why does high glucose increase risk of atherosclerosis

A

blood slowed
increase in free radicals
LDL modified –> inflammation

diabetes

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18
Q

why does high cholesterol increase risk of atherosclerosis

A

damages endothelium
more LDL into intima
pro inflammatory when oxidised in fatty streak
hypercoagulation

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19
Q

why does smoking increase risk of atherosclerosis

A

CO, nictotine, free radicals are toxins that damage the endothelium
increases LDL
hypercoagulation

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20
Q

why is low activity arisk factor for atheroma

A

slows blood
more LDL in HDL/LDL balance
higher BP
higher fat

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21
Q

endartectomy =

A

plaque removal

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22
Q

angioplasty

A

stent

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23
Q

atheroma pharmocological treatment

A

statins- reduce cholest
antihypertensives
anticoagulants/antiplatelets
diabetes medication

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24
Q

how does allergen cause mast cell activation

A 
immunological: 
allergen interacts with B cells
b cells --> antibodies igE
ig E attaches to mast cells/ basophils
mast cells activated

non-immunological:
antigen on trigger cell binds directly to mast cell
mast cell activated

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25
Q

what are the mediators of allergic response / allergen attack

A

mast cells

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26
Q

what happens when mast cells activated

A

mast cells release cytokines and inflammatory mediators

so..

wbc recruited
histamine released (from mast cells/basophils)
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27
Q

histamine effect

A

bronchial smooth muscle contraction
vasodilation
vascular permability rises – liquid leaks from vessels

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28
Q

mast cells vs basophils

A

mast cells = mature basophils

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29
Q

proteolytic trigger for anaphylaxis =

A

allergen can cross skin and mucosal barriers

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30
Q

aerodynamic trigger for anaphylaxis=

A

trigger can get into nasal and broncial mucosa

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31
Q

during anaphylaxis, what causes inflammatory cells to infilatrate

A

neutrophil and eosinophil chemotactic factors

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32
Q

which of the anaphylaxis mediators are preformed vs newly formed

A

preformed = HENS
histamine,
eosinophil and neutrophil chemotactic factors
serotonin

newly formed: PT
prostaglandins and thromboxanes

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33
Q

what is the role of prostaglandins and thromboxanes

A

platelet activator factor

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34
Q

what causes the sob, wheeze, shallow breaths of anaphylaxis?

A

histamine

  • bronchoconstriction of smooth muscle
  • vasodilation and vascular permeability –> swelling of throat and tongue
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35
Q

what causes the low BP and light headed , confusion, collapsing symptoms of anaphylaxis

A

histamine

-vasodilation and leaky vessels (increase permeability)

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36
Q

what causes the rash in anaphylaxis

A

histamine

- redness due to vasodilation

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37
Q

what causes the tachycardia /arrythmia in anaphylaxis

A

histamine

  • due to vasodilation and increased vascualr permability, reduced perfusion –> abdominal cramps, vomiting
  • heart works harder to compensate for reduced perfusion – baroreceptors
  • histamine increases heart rate
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38
Q

if a patient with anaphylaxis is having breathing problems, how should they be positioned

A

sat upright

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39
Q

if a patient with anaphylaxis is unconcious, how should they be postioned

A

recovery position

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40
Q

if a patient with anaphylaxis has low bP how should they be

A

lying flat - feet raised

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41
Q

after ABCDE, patient positioning and trigger removal what is the next key step for anaphylaxis treatment

and how much

A

adrenaline
IM 500 μg microgrmas

repear dose every 5 mins if shock persists

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42
Q

action of adrenaline
on alpha adrenoreceptor
(how does this affect heart)

A
  • peripheral vasoconstriction, vascular resistance
  • BP increases
  • coronary perfusion increases
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43
Q

action of adrenaline on beta 2 adrenoreceptors

A
  • dilates airways

- reduces oedema (less leaky vessels

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44
Q

action of adrenaline on beta 1 adrenoreceptors

A
  • increases HR (chonotropic)

- increases force of contraction (inotropic)

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45
Q

general action of adrenaline with both beta adrenoreceptors

A

suppresses histamine and other inflammatory mediator release

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46
Q

other treatment of anaphylaxis

A

antihistamine
steroids
oxygen (may be hypoxic)
IV fluid (may be hypotensive)

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47
Q

name an antihistamine

A

chlorfemine

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48
Q

how do steroids act against anaphylaxis (by doing what specifically)

A

suppress immune response: suppress prostaglandin and leukotryin mediators

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49
Q

how can you confirm the patient’s condition is anaphylaxis

A

blood test

  • rapid increase in tryptase = enzyme released from mast cells in any immune response)
  • too early/ late may give false negative
  • histamine levels
  • take multiple samples, spread by few hours (and compare to baseline)
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50
Q

antibody associated with anaphylaxis

A

igE

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51
Q

histamine effect on liver

A

stimulates glycogenolysis

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52
Q

histamine effect on fat

A

triggers lipolysis

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53
Q

protein binding property of a drug=

A

allows drug to be carried by a protein (eg albumin) in blood to destination

  • so lower plasma/unbound conc
  • there is competition for binding
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54
Q

effect of having high unbound conc of drug?

A

effect increases, potentially can be toxic

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55
Q

does bound or unbound drug cross the membrane

A

unbound

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56
Q

lipid soluble property of a drug =

A

high lipophlicity = more lipid soluble

  • drug can be absorbed in gut more easily
  • drug can cross biphosphate lipid membrane from blood into cells/tissues mostly passively
  • so more potent and more fast-acting
57
Q

what kind of drug molecules are able to cross the blood brain barrier

A

unbound
lipid soluble
unionised

58
Q

distribution of a drug

A

low distribution = high proportion at the effect site (and little elsewhere)

59
Q

how does a drug distribute around the body (order)

and how does this relate to why an additional booster of drug may be given

A

first to highly perfused areas (brain, lungs, liver). then gradually to less perfused areas too (muscle). this lowers the plasma concetration and so concentration distrubuted to highly perfused areas decreases (inc brain- which is where we want for anaesthetic for eg)
- so booster given to boost brain amount- to keep patient asleep

60
Q

agonist

A

binds to receptor to activate / stimulate it to obtain a response

61
Q

inverse agonist

A

something that biinds to a receptor to activate it but has the opposite action/effect of the agonist

62
Q

antagonist

A

reduced the effect of an agonist by reducing/removing stimulus and thus response
- competitive and non-competitive antagonists

63
Q

competitive antagonist

A

binds to the same (orthosteric) site as agonist does. this means the agonist is unable to bind.

can be reversible (surmountable) or irreversible (insurmountable)

64
Q

non competitive antagonist

A

binds to a different (allosteric) site as the agonist does. this causes a shape change that means the agonist can no longer bind.

only irreversible (insurmountable)

65
Q

orthosteric vs allosteric binding sites

A

same vs different binding sites

described compet/noncompet inhibitors to an agonist

66
Q

different targets of drugs

A

receptors

  • ligand gated ion channels( ligand binds to ion channel to open it)
  • g protein couples receptors (ligand binds to recptor on cell surface to activate g protein on inside –> signally cascade)
  • kinase linked receptors (ligand in active site causes conformational change that allows enzme activity inside target cell)
  • cytosolic/nuclear receptors (ligand enters cell (imported) and binds to DNA, switching on transcription for a specific gene)

enzymes

transporters

ion channels

67
Q

enzyme drug targets

A

drug binds to enzyme to decrease its activity

68
Q

receptor drug targets

A

lignad binds to recpetors to cause response within target cell

69
Q

bioavailability

A

fraction of drug absorbed into blood/ systemic circulation

70
Q

bioavailability of morphone IV/ IM/ oral

A

100% IV
nearly 100% IM – goes from muscle directly to blood
50% oral

71
Q

why is the bioavailability of oral drugs what it is?

A

first pass :
(gut)

liver:
elimination

72
Q

first pass effect on bioavailability

A

not all oral drug absorbed due to:

intestine lumen - digestive enzymes metabolise drugs + colonic bacteria

intestinal wall - contains enzymes that transport drugs back to lumen

surgery may reduce surface area of absorption sites
so some drug excreted in faeces

sometimes liver is counted within this (another flashcard)

73
Q

elimination(liver) effect on bioavailability

A

gut absorption –> blood –> portal vein –> liver –> metabolised aka eliminated (splanchnic circulation)

IV: drug passes elsewhere before reaching liver

74
Q

converting IV dose to oral (morphine)

A

2x

to compensate

75
Q

effect of reduced renal function on morphine

A

kidney cant excrete so more in system

  • more potent
  • smaller dose given for renal patients
76
Q

name 5 ideal qualities in a drug

A
  1. low protein binding
  2. high ionising proporion
  3. lipophilic
  4. no side effects
  5. cheap
  6. long lasting shelf life
  7. stable in solution
  8. rapid clearance and no active metabolites (= cant cause damage once metabolised, so less renal failure)
77
Q

name 3 signs and 3 symptomson arterial thrombosis

A
  1. perishingly cold
  2. pulselessness
  3. pallor
  4. paralysis
  5. pain - in muscle (+ cramps)
  6. paraethesia numbness/tingling -
78
Q

venous thrombosis signs/symptoms

A 
red
hot
swollen
increased pulse
pain, cramps
stiffness
(looks like inflammation)
79
Q

virchows triad

A

= 3 factors that contribute to thrombus development (pathologically)

  • stasis of blood
  • endothelial damage/injury
  • hypercoagulability
80
Q

name 3 causes of blood stasis

A
  1. AF (blood in atria)
  2. pregnancy
  3. low mobility
  4. sickle cell anaemia
  5. venous insufficiency - valves not working
81
Q

name 3 causes of endothelial injury

A
  1. smoking
  2. hyperlipidimia
  3. hypertension
    (same as atherosclerosis causes)
  4. atherosclerosis?
82
Q

name 5 causes of hypercoaguability and state whether they are inherited or aquired

A

inherited:

  1. haemophilia = unable to make coagulation factors 8 or 9
  2. coagulation factor deficiecy

aquired:

  1. malignancy/cancer
  2. dehydration
  3. oral contraceptive pill / post pregnancy / HRT (increase in prothrombin/ fibrinogen)
  4. infection
  5. heparin-induced thromocytopenia (isnt this the opposite of thrombogenesis?)

also have since thought - polycythaemia (inc but not only rubra vera), DIC

83
Q

undisturbed healthy endothelium prevents thrombus formation by:

A

producing prostacyclin

  • vasodilation
  • inhibits platelet activation

producing NO

  • vasodilation
  • inhibits platelet aggregation
84
Q

what in the endothelium is exposed with endothelial injury

what part do these play

what is released from damaged endothelium

A

collagen and von willebrand factor

collagen: releases endothelin 1 –> vasoconstriction

von Willebrand: platelets bind to vW at glycoprotein 1b

also – tissue factor is released

85
Q

platelets release what 3 things, and what is their effect

how do they release them

A

ATP and ADP - platelet amplification
thrombin- platelet activation

each have positive feedback loops

released in secretory vesicles (Exocytosis)

86
Q

what is activated platelet called

A

pseudopodia.
it is spiculated
it has more gcoprotein receptors exposed

87
Q

fibrinogen binds to what

effect

A

glycoprotein receptors on activated platelets

effect= platelet aggregation (clump together)

88
Q

what do platelets release after platelet aggregation

effect

A

thromboxin A2

-> vasoconstriction and platelet activation (pos feedback)

89
Q

tissue factor effect

A

extrinsic pathway of coagulation cascade : tissue factor causes
prothrombin –> thrombin. thrombin causes fibrinogen to fibrin.
fibrin = insoluble

90
Q

what is clot made of

A

insoluble fibrin + aggregated activated platelets

91
Q

which gender is at higher risk of thrombosis

A

men

92
Q

well’s score =

A 
likelihood of getting a DVT (/PE)
based on symptoms  / risk factors
 - calf/whole leg swelling
- superficial veins present
 - pitting oedema
 - local tenderness
 - paresis
 - paralysis
- cancer
 - immobilisation/surgery
 - previous DVT
- other diagnoses unlikely
93
Q

test for DVT

A

D dimer elevation
- this is a degradation product of fibrin (degraded by plasmin)

positive result (elevation) isnt definitive (not specific - malignancy, pregnancy, operations)

but negative result (no elevation) can rule DVT out!!

ultrasound

94
Q

DVT treatment

+ explain action

A

heparin

  • indirect thrombin inhibitor (binds to antithrombin which binds to factor 10a and prevents thrombin functioning in the cascade)
  • increases prothrombin time

warfarin

  • antagonist to vitamin k so stops blood clotting factors (1972) as these are activated by vit k
  • increases prothrombin time
95
Q

what is heparin reversed by

A

protamine

96
Q

what is warfarin reversed by

A

vitamin k

97
Q

warfarin half life

A

36h = long

so is hard to reverse (Wait for half life + wait for vit k to activate factors again before they can work)

98
Q

INR

stands for
what is normal

A

international normalized ratio
measure of blood clotting
usually between 2 and 3

99
Q

measure of blood clotting

A 
INR
prothrombin time (differs place to place)
100
Q

DVT complications

A
  • PE
    • sudden, severe
  • post thrombotic syndrome
    • long term affects due to scarring and damage to veins/valves or due to some blockage remaining. causes impaired venous return
101
Q

name 5 PE symtpoms

A 
1 SOB/ trouble breathing/ 2 rapid breathing
3 chest pain
4 coughing, maybe blood
5 fainting/light headed
6 sweating/clammy
7 tachy
8 blueish
9 anxiety/restless
102
Q

name 5 sympyoms of post thrombotic syndrome

A 
1 pain /ache/ cramping
2 heaviness
3 swelling, oedema
4 parasthesia - itching/pins needles
5 redness /discoluration
6 ulcers
7 mobilisation is a releiving factor
103
Q

what is chronic venous insufficiency

A

the name fro post thrombotic syndrome when there has never been a DVT

104
Q

AKI diagnosis criteria

A

increase in serum creatinine of 26+ μmol/L within 48h

increase in serum creatinine of 1.5+ xbaseline from within past 7d

urine volume less than 0.5mL/kg/h for 6h

105
Q

AKI severity staging

A

stage 1 : 1.5-1.9 xbaseline serum creatinine

stage 2 : 2.2.9 xbaseline serum creatinine

stage 3 : 3+ x baseline serum creatinine or renal replacement therapy

106
Q

if you have 1 kidney can you still have normal kidney function?

A

yes

107
Q

prerenal causes of AKI pathophysiology

A

decrease in effective blood flow to kidney to decreased GFR
kidneys recieve 20-25% of cardiac output so any failure of circulating blood volume / intra renal circulation has profound effect on renal perfusion

108
Q

prerenal causes list

A

volume depletion- hypovolemia

  • haemorrhage
  • severe vom/diar
  • burns
  • over diuresis (renal fluid loss)
  • peritonitis

edematous states

  • HF
  • hypotension

CV

  • HF
  • hypotension
  • cardiogenic shock
  • MI
  • PE

systemic vasodilation

  • liver cirrhosis
  • ACE i / antihypertensives
  • anaphylaxis

increased cascular resistance

  • NSAIDs
  • renal vasoconstriction / thrombosis / stensosi
  • surgery
  • anasthesia

severe infections/ sepsis

109
Q

intrinsic AKI causes - glomerulus

A
  • glomerulonephritis = inflammation of glomeruli / small vesselss causing them damage
110
Q

intrinsic AKI causes!!!! - tubules

list

A

ISCHAEMIC - reduced blood flow so less oxygen/ nutrients/ ATP

    • shock
    • haemorrhage
    • trauma
    • bacteraemia
    • pregnancy
    • pancreatitis
NEPROTOXIC
exogenous
 - antibiotics
- contrast media
 - anasthetic
 - heavy metals
 - organic solvents
 - antineoplastic drugs
endogenous
 - rhabdomyolysis = break down of damaged skeletal muscle = toxic to kidney
- myoglobin
- haemoglobin
- uric acid

ATN- acute tubular necrosis = tubules damaged (normally by pre-renal damage)

111
Q

intrinsic AKI causes - vascular pathophysiology

A

injury to intra renal vessels . this decreases renal perfusion and diminishes GFR

112
Q

intrinsic AKI causes- vascular

list

A

large vessels
- renal artery stenosis/ thrombosis (bilateral)

small vessels

  • vasculitis (inflammation + scarring to blood vessels –> stiff, weak, narrow)
  • hypertension
  • atherosclerotic/thrombotic emboli
113
Q

intrinsic AKI causes -

interstitum

A

infections (bacterial/viral)

medications (antibiotics, diuretics, NSAIDs)

AIN - acute intersitial nephritis = inflammation of kidneys as allergic to certain drugs( eg NSAIDs) or an infection

114
Q

post renal AKI causes pathophysiology

A

disease states downstream of kidney, often obstruction.
this increases tubular pressure and so decreases GFR. May also lead to impaired renal blood flow and inflammatory process (decreases GFR)

115
Q

post renal AKI causes list

A 
EXTRA RENAL OBSTRUCTION
prostate hypertrophy (BPH/cancer)
imporperly placed catheter
bladder cancer
cervical cancer
retroperitoneal fibrosis
INTRA RENAL OBSTRUCION
kidney stone (nephrolithilasis)
obstructed urinary catheter
bladder stones
blood clots
ureter cancer (bilateral)
116
Q

nephrotic vs nephritic

A 
NEPHROTIC (kideny disease)
loss of protein - big proteinuria (but no blood)
hypoalbuminemia
peripheral oedema
hyperlipidiaemia

NEPHRITIC (glomeruli inflammation)
loss of blood - haematuria - cola coloured urine
little proteinuria
oligurai

117
Q

decreased blood volume causes what (RAAS)

A

kidney cells produce renin. this converts angiotensinogen to angiotensin 1. this is converted to angiotensin 2 by ACE (from lungs). angiotensin 2 causes

1) vasoconstriction
2) aldosterone production (adrenal cortex) - so tubules reabsorb more Na and water into blood
3) ADH (from hypothalamus) - so thirst increases and water is reabsorbed in kidney tubules and collecting duct (aqua porin 2)

118
Q

increase in BP effect on HR

A

detected by baroreceptors (carotid sinus, aortic arch) –>

HR decreases

119
Q

NSAID effect on kidneys

A

NSAIDS are toxic to kidneys, can induce AKI

NSAIDs inhibit COX enzyme
COX enxyme synthesises prostaglandins
prostaglandins cause afferent arteriolar vasodialtion (and diminished vascular resisitance)

so NSAIDs –> afferent arteriole vasoconstriction, higher vascualr resistance, reduced renal perfusion, slower GFR,

120
Q

AKI ECG

A 
hyperkalemia
so tall tented T waves
loss of P waves - flatteneed
pathological Q wave
wide QRS
may then cause bradycardia
121
Q

K normal range

A

3.5-5.4

122
Q

how to correct for hyperkalemia

A

insulin

  • drives K into cells using sodium- potassium ATPases
  • insulin also drives glucose into cells

SO
need to give dextrose (glucose) with it to counter this

123
Q

how much dextrose given per insulin

A

10 units of insulin in 50 ml of 50% dextrose over 10-15 mins

124
Q

TIA vs stroke

A

TIA symptoms resolves spontaneously, within 24h

this is because the clot dissolves/moves on on its own

125
Q

amaurosis fugax

  • =
  • cause
A

fleeting sudden onset loss of vision in one or both eyes. painless.

lots of causes but for TIA/stroke is atherosclerosis or thromboembolism in

  • -internal carotid artery
  • -opthalmic artery
  • -retinal artery
  • leading to temporary retinal hypoxia
126
Q

what is the name for transient visual disturbance of loss in one or both eyes

A

amaurosis fugax

127
Q

stroke relation to AF

A

atrial fibrillation –> rapid, irregular palpitations , uncoordinated atrial contraction
–> blood collects and pools –> stasis–> clot formation –> stroke

128
Q

stroke affecting lower limb is clot where?

A

anterior cerebral artery

129
Q

stroke affecting upper limb/ face is clot where?

A

middle cerebral artery

130
Q

cause of increased intracranial pressure in haemorrhagic stroke (2)

A

blood itself –> takes up space –> increased ICP

+

blood comes into contact with cerebral neurons → inflammatory response→ swelling and oedema → increased intracranial pressure

131
Q

cause of increased intracranial pressure in ischaemic stroke

A

ischaemic/ necrosing tissue → inflammatory response → swelling and oedema → increased intracranial pressure

132
Q

total anterior circulations stroke (TACS)

  • where
  • which arteries
  • criteria
A

Large stroke in cortex

anterior or middle cerebral arteries

Criteria: all of the following
Unilateral weakness and/or sensory deficit of face/limbs
Homonymous hemianopia (losing same side of vision in both eyes)
Higher cerebral dysfunction
133
Q

Partial anterior circulation stroke (PACS)

  • where
  • which arteries
  • criteria
A

In cortex

Anterior or middle cerebral arteries

Criteria: 2 or the following
Unilateral weakness and/or sensory deficit of face/limbs
Homonymous hemianopia (losing same side of vision in both eyes)
Higher cerebral dysfunction
134
Q

Lacunar stroke (LACS)

  • where
  • which arteries
  • criteria
A

Subcortical

In small deep perforating arteries – internal capsule, midbrain

Criteria
Pure motor, sensory or sensorimotor (2 of face, arm, leg)
Ataxic hemiparesis (weakness + clumsiness + lack of control - affects leg more than arm)

135
Q

Posterior circulation stroke (POCS)

  • where
  • which arteries
  • criteria
A

Posterior cerebral artery (Cortical), basilar artery + branches (cerebellum) vertebral artery (brainstem)

Criteria:
Cerebellar or brainstem syndrome
Loss of consciousness
Isolated homonymous hemianopia

136
Q

what is the affect of increased intracranial pressure

A

CSF, venous system, arteries == squashed!!

Cerebral perfusion pressure in the arteries is not high enough to perfuse the brain properly
ICP> mean arterial blood pressure (perfusion pressure)… arteriole compresses

Brain not perfused → brain more ischaemic

137
Q

what symptoms do you see with increased intracranial pressure?

what is this reflex called?

A

hypertension
bradycardia
irregular breathing (dyspnea–> apnea)

= cushings reflex

and papilloedema

138
Q

what is the explanation between the symptoms of increased intracranial pressure

A

cerebral ischemia → sympathetic (fight/flight)

    • Stimulatees alpha 1 adrenergic receptors = vasoconstriction → hypertension
  • -Stimulates beta 1 receptors→ increased heart rate (Tachy)

hypertension –> Stimulates baroreceptor in aortic arch → parasympathetic → decrease heart rate (brady) via m2 receptors

Hypertension → presses on respiratory centre on brain stem→ irregular breathing

139
Q

when you see cushing reflex , what does this indicate

A

increased intracranial pressure

this is an acute emergency

brain herniation/ death is imminent

phase 2a mine (38 decks)

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