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MD1 > Cardiology Week 3-4 > Flashcards

Cardiology Week 3-4 Flashcards

1
Q

parts of mediastinum

A

superior

inferior - divided into anterior middle and inferior

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2
Q

demarcation between superior and inferior mediastinum

A

manubriosternal junction - level of T4/5

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3
Q

what vertebrae does heart sit in front of

A

T5,6,7,8

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4
Q

layers in superior mediastinum from superficial to deep

A 
thymus
great veins
aortic arch, vagus+phrenic nerves
trachea
oesophagus
thoracic duct
L recurrent laryngeal N
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5
Q

names of great veins

A

internal jugular vein and subclavian on both sides meet to form brachiocephalic veins

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6
Q

landmark for where IJV and subclavian meet

A

sternoclavicular joint

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7
Q

differences between L and R brachiocephalic veins

A

R - short and vertical

L - longer and more horizontal

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8
Q

where do brachiocephalic veins meet to form SVC

A

behind first costal cartilage

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9
Q

what level does SVC enter right atrium

A

behind third costal cartilage

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10
Q

why do you use R IJV as JVP not left

A

because on the right you have a vertical column

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11
Q

where does azygous vein drain into SVC

A

level of 2nd costal cartilage, empties into back of SVC

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12
Q

what part of mediastinum is arch of aorta

A

all in superior mediastinum

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13
Q

where does arch of aorta become descending aorta

A

T4/5

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14
Q

ligamentum arteriosum

A

remnant of ductus arteriosus from foetus between pulmonary trunk and aorta

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15
Q

great arteries

A

R common carotid and subclavian come off brachiocephalic trunk
L common carotid and subclavian come off as separate branches

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16
Q

where does brachiocephalic trunk divide

A

sternoclavicular joint T4/5

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17
Q

retroesophageal right subclavian artery

A

from left to right coming off aortic arch:
R common carotid
L common carotid (on other side of trachea)
L subclavian
retroesophageal R suclavian artery - comes of the far left but goes behind oesophagus

causes swallowing difficulties

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18
Q

course of Phrenic nerve on right

A

on scalenus anterior
b/w subclavian a and v
anterior to lung root
pierces diaphragm

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19
Q

where does L and R phrenic nerve pierce the diaphragm

A

R - with SVC at T8

L - pierces on its own just near apex of heart

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20
Q

What does the Phrenic nerve supply

A

motor to diaphragm from abdominal surface

sensory to mediastinal +diphragmatic pleura + pericardium (fibrous and parietal serous pericardium)

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21
Q

course of R vagus nerve

A 
descends in carotid sheath as part of neurovascular bundle of neck 
then 
alongside trachea
behind lung root
anterior to oesophagus
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22
Q

course of L vagus nerve

A 
lateral to aortic arch
posterior to phrenic n
crossed by superior IC vein
gives off L recurrent laryngeal nerve 
behind lung root
anterior to oesophagus
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23
Q

where does recurrent laryngeal nerve travel back up

A

groove between trachea and oesophagus - trachoesophageal groove

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24
Q

does oesophagus come away from vertebral column

A

yes - only distally when goes through diaphragm - goes forwards and to the left - swaps places with aorta

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25
Q

3 types of antimicrobial agents

A

antibiotics
chemotherapeutic agents- synthetic
semi-synthetic

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26
Q

why make semi-synthetic antibiotics?

A

alter pharmacological properties - change kinetics, reduce toxicity, modify antimicrobial spectrum
extend patent and make money

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27
Q

tetracyclin

A

naturally occurring but rapidly eliminated by body, modification is doxycyclin

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28
Q

threeclassifications of antimicrobial agents

A

source - natural or synthetic
broad mechanism of action - cidal or static
pharmacological class

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29
Q

bacteriostatic vs bactericidal

A

bacteriostatic - stops bacteria growing

bactericidal - reduces viable count by 99.9% (kills)

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30
Q

they’re both equally effective usually, why would you want to use bactericidal

A

if patient doesnt have functioning innate immune system

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31
Q

infected endocarditis

A

infection sits on heart valves, macrophages cant eat because valves moving
so need bactericidal antibiotics to kill

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32
Q

tetracyclines

A

phamacological type of antibiotic with 5 rings

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33
Q

beta-lactam antibiotics

A

all have square beta-lactam ring

pretty much all of them

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34
Q

penicillin G

administration and toxicity

A

injection

least toxic - can have heaps and wont kill you

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35
Q

penicillin V - administration

A

acid stable so orally available, low toxicity

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36
Q

6-APA

A

precursor for all other penicillins (not G or V)

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37
Q

ampicillin

how is it better than penicillin

A

broader spectrum - rods as well as cocci

orally available, low toxicity

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38
Q

methicillin

A

effective against penicillin resistant staph
but toxic - to kidneys in particular
not orally available

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39
Q

carbenicillin

A

first one effective agaisnt pseudomonas aeruginosa - opportunistic pathogen - problem in hospitals
not orally available

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40
Q

clavulanic acid

A

for streptomyces bacteria

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41
Q

why do antibiotics work as effective treatments

A

because they have SELECTIVE TOXICITY = toxicity for microbe not us

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42
Q

rubidomycin

A

used to treat lymphomas (chemotherapy)

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43
Q

5 targets of antimicrobial agents

A 
cell wall
cytoplasmic membrane
ribosomes
nucleic acid
folic acid
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44
Q

antibiotics against cell wall

A

beta lactams

glycopeptides (vancomycin)

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45
Q

antibiotics against cytoplasmic membrane

why they’re not good

A

polymyxins
polyenes

plasma membrane not good target because similar to ours - they’re quite toxic

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46
Q

antibiotics against ribosomes

A

aminoglycosides

chloramphenicol

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47
Q

antibiotics against nucleic acids and what they do

A

rifamycins - interfere with transcription

quinolones - interfere with folding

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48
Q

antibiotics against folic acid

A

sulphonamides

trimethoprim

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49
Q

why can folic acid be a target of antibiotics

A

because lots of bacteria HAVE to make folic acid for themselves (cant use ready formed)

(we have to get folic acid ready formed from diet)

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50
Q

structure of peptidoglycan

A

polysaccharide backbone of alternating N-acetyl glucosamine and N-acetyl muramic acid (one we dont have)
Off N-acetyl muramic acid have short 4 peptide chain of 4 different peptides (varies between bacteria)
then pentapeptide bridge from 3rd amino acid to 4th of next chain (made of glycine)

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51
Q

why do bacteria use D amino acids

A

they alternate D and L in peptidoglyan to make it rigid - cant fold

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52
Q

biosynthesis of peptidoglycan

A
  • precursors synthesised from intermediates from cytoplasm
  • becomes immobilised on inner aspect of plasma membrane
  • synthesis of building block continues
  • when complete, building block transported to exterior
  • linked to growing peptidoglycan chain
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53
Q

structure of building block of peptidoglycan

A

has carrier pyrophosphate lipid

precursor has an extra D-alanine

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54
Q

cross-linking of peptidoglycan

A

transpeptidases (penicillin binding proteins) catalyse removal of extra D-alanine, glycine attaches
forms link from 3rd (L-lys) to 4th (D-ala)

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55
Q

vancomycin action

A

binds to D-ala D-ala so can’t cross link –> stops cell wall synthesis
causes signal to bacteria to say something wrong with cell wall
bacteria makes catalytic (autolytic) enzymes to remodel cell wall
kills itself

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56
Q

where does most binding of vancomycin occur

A

to terminal D-alanine

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57
Q

basis of vancomycin resistance in enterococci

A

enterococci replaces D-ala with D-lac
still allows peptidoglycan wall to form (because terminal aa doesnt end up in wall)
enterococci has new transpeptidases that can use D-ala D-lac precursor

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58
Q

why are people scared of vancomycin resistant enterococci

A

because enterococci likes to swap genes with other bacteria
vancomycin only antibiotic effective for treatment of golden staph - if enterococci gave genes for vancomycin resistance to golden staph we’d be fucked

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59
Q

vancomycin intermediate resistant SA (VISA)

trouble with treatment?

A

produce extra peptidoglycan - acts to soak up vancomycin

trouble - can’t give more vancomycin because toxic

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60
Q

how does penicillin work

A

transpeptidases (penicillin binding proteins) which recognise D-ala D-ala also bind to site on Penicillin G which resembles this D-ala D-ala
enzyme now bound there and can’t do anything
cell wall synthesis disrupted, tries to remodel, kills itself
=bacteriacidal

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61
Q

beta-lactamase

A

enzymes produced by bacteria
destroy beta lactam ring - very bond that recongised by penicillin binding proteins
provide bacteria with resistance to beta-lactam antibiotics

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62
Q

two types of resistance to beta-lactams

A

beta-lactamase

altered penicillin-binding proteins

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63
Q

methicillin resistant staph aureus

A

resistant to all penicillins and probably all beta lactam antibiotics
due to low affinity penicillin binding proteins encoded by one gene taken up by the bacteria
–> instant resistance

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64
Q

pneumococcus

A

new gradually accumulated mutations leading to new penicillin binding proteins leading to resistance to beta-lactam antibiotics

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65
Q

why does antibacterial spectrum of beta-lactam antibiotics vary

A

bacteria have different PBPs
accessibility of antibiotic to PBPs varies - gram negative have plasma membrane in the way
susceptibility of antibiotic to beta-lactamase varies

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66
Q

vancomycin effective on gram negative bacteria??

A

NO - because highly charged, lipid insoluble, can’t cross membrane to get to peptidoglycan wall

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67
Q

pseudomonas aeruginosa

A

intrinsically produces a beta-lactamase that destroys penicillin, ampicillin, amoxicillin but NOT carbenicillin

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68
Q

what kind of surface do you need for clotting, provided by what

A

phospholipid surface

platelets

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69
Q

what does normal endothelium produce

A

thrombomodulin, protein C and protein S - to change thrombin from activator to inhibitor

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70
Q

what does fibrinolysis involve

A

release of tissue plasminogen activator (tPA)

binds to fibrin and activates plasmin, plasmin breaks down fibrin

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71
Q

thrombus

A

clotted mass of blood within unruptured cardiovascular system, attached to vessel wall at point of origin, during life (not death)

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72
Q

components of thrombus

A

platelets, fibrin, red and white cells

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73
Q

lines of Zahn

A

red and white layers containing RBCs(red) and platelets and fibrin (white)
let you discriminate between clots formed in live person vs after death

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74
Q

2 types of thrombosis

A

arterial - higher proportion of platelets(and fibrin) - WHITE
- endothelial dysfunction/damage

venous - higher proportion of blood cells (and fibrin)

  • RED
  • blood stasis and hypercoagulability
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75
Q

drugs used for arterial vs venous thrombi

A

arterial - aspirin

venous - warfarin

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76
Q

why to thrombi form

A

imbalance between factors that promote thrombogenesis and those that promote thrombolysis

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77
Q

Virchow’s triad

A

abnormal endothelium
abnormal blood flow
abnormal blood coagulability

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78
Q

2 causes of abnormal endothelium

A

1 - loss of endothelium exposing collagen

2 - endothelial activation or dysfunction (pro-coagulation)

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79
Q

types of abnormal blood flow and what happens

A

turbulence, stasis, loss of laminar flow

“activates” endothelium
brings platelets into contact with vessel wall
allows activated clotting factors to accumulate

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80
Q

Causes of abnormal blood coagulability

A

1 genetic =”primary” - factor V Leiden

2 - Not genetic =”secondary”
oestrogen, cancer, smoking, obesity, age, MI, atrial fibrillation

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81
Q

4 things that can happen to a thrombus

A

1 dissolution - fibrinolysis
2 organisation, sometimes recanalisation
3 propagation (grow bigger)
4 embolisation

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82
Q

embolus

A

intravascular mass carried in blood stream to some site remote from origin
solid, liquid or gas
blocks the vessel it lodges in

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83
Q

2 main types of embolism

A

1 pulmonary embolus - from DVT, can be asymptomatic, cause transient hypoxia or sudden death

2 arterial thromboembolism - from atheroma or heart, block artery downstream, cause ichaemia and infarction

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84
Q

venous thrombosis and embolism risk factors, where do thromboemboli usually arise

A

risk factors: stasis and hyperoagulability - family, surgery, pill

usually arise in deep veins of legs or pelvis

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85
Q

arterial thrombosis and embolism usually involve what

A

turbulence and/or platelets adhering to a dysfunctional blood vessel surface (e.g. atherosclerosis, MI, atrial fib)

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86
Q

what do emboli in heart usually affect

do they go to coronary arteries?

A

can affect any downstream organ

uncommon for emboli from heart chamber to go into coronary arteries

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87
Q

ischaemia

A

not enough blood (causing shortage of O2)

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88
Q

infarction

A

tissue death due to inadequate blood supply

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89
Q

hypoxia

A

not enough oxygen

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90
Q

hypoxaemia

A

not enough oxygen in blood

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91
Q

3 causes of ischaemia

A

local vascular narrowing or occlusion
increased demand for O that isnt met
systemic reduction in tissue perfusion (systemic shock)

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92
Q

3 possible causes of chronic ischaemia

A

stable atherosclerotic disease causing atrophy of lower limbs
renal artery stenosis causing renal atrophy
hyaline arteriolosclerosis causing “benign nephrosclerosis”

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93
Q

angina caused by chronic or acute ischaemia

A

acute

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94
Q

7 P’s of ischaemia

A 
pale
pulseless
painful 
purple (cyanotic)
paralysed
paraesthetic (tingling)
perishingly cold
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95
Q

pale infarction

A

where there is no haemorrhage
due to blocked ‘end artery’
MOST organs
wedge shaped tissue death

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96
Q

red infarction

A

where there is a haemorrhage into infarcted tissue
due to: dual blood supply (lungs, liver), collateral blood supply (intestine), venous infarction, reperfusion after necrosis (brain)

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97
Q

coagulative necrosis

A

‘ghost’ outlines of dead cells

takes at least 4h

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98
Q

digoxin

A

cardiac glycoside - inhibits Na/K ATPase, Ca build up in cell, increase Ca release with each AP
shortens ventricular AP so heart pump more efficiently, risk of dysrhythmias

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99
Q 
glycosides 
TI
tissues effects
toxicity changes
half life
Vd
A

low TI
affects all excitable tissues
increased toxicity with decreased K, high Ca, renal impairment
40h - long - if get dose wrong takes ages to go down
large Vd - binds to muscle with high affinity

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100
Q

Badrenoceptor agonist

A

NA, A
dobutamine - selective B1 agonist

only for short term support of HF

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101
Q

phosphodiesterase inhibitors

A

amrinone

only for short term support of acute HF

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102
Q

two ways of B1 adrenoceptors decreased sensitivity

problem?

A

reduced R expression
impaired coupling - cells make B-arrestin to bind to R

problem - ionotropic drugs become less effective as R population falls

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103
Q

ionotropic heart drugs

A

only short term use - increase work on heart, symptoms progress, cardiac remodeling - BAD

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104
Q

3 main causes of HF

A

loss of myocardial muscle - contractility
pressure overload - afterload
volume overload - preload

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105
Q

4 drugs to reduce preload

A

venodilators - nitrates
diuretics - furosemide/frusemide
aldosterone R antagonists
aquaretics - vasopressin R antagonists

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106
Q

spironolactone

A

aldosterone R antagonist

K sparing diuretic

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107
Q

3 drugs to reduce afterload and preload

A

ACE inhibitors
AT1 antagonist
Badrenoceptor antagonist

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108
Q

first line therapy for heart failure

dose titration?

A

ACE inhibitors
improves symptoms, delay progression
must titrate dose due to side effects

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109
Q

why Badrenoceptor antagonists for HF

A

SV increases reduces tachycardia, cardiac work
inhibits renin release
protects against R downregulation

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110
Q

drugs for symptomatic relief vs reduce mortality for HF

A

symptomatic relief: ionotropes, diuretics, venodilators

reduced mortality: angiotensin inhibitors, Badrenoceptor antagonists, aldosterone antagonists

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111
Q

mechanism of vasoconstriction in damaged vessel

A

collagen exposed on damaged vessel
platelets stick and activate
ADP and 5-HT released
5-HT vasoconstrictor

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112
Q

mechanism of platelet activation and adhesion

A

ADP from activated platelets causes aggregation and changing shape
granule contents secreted (5-HT, ADP)
mediators synthesised (thromboxane)
platelets aggregate and adhere via fibrinogen bridging between GPIIb/IIIa Rs

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113
Q

some stimuli for platelet activation

A

collagen
thrombin
thromboxane
ADP

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114
Q

two pathways to activation of thrombin

A

1 - extrinsic - damaged tissues release thromboplastin (something outside blood causing cascade)

2 - intrinsic - exposed collagen or other material (intrinsic to blood itself)

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115
Q

which coagulation cascade pathway faster, extrinsic or intrinsic to

A

extrinsic - because not as many steps

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116
Q

2 ways of controlling blood coagulation

A

antithrombin III - enzyme inhibitor

fibrinolysis by plasmin

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117
Q

cascade leading to fibrinolysis

A

protein C inactivates inhibitor of tissue plasminogen

plasminogen –> plasmin

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118
Q

3 ways coagulation drugs act

A

on coagulation (fibrin formation)
platelets
fibrinolysis

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119
Q

3 types of drugs affecting fibrin formation

A

procoagulant drugs - vit K
injectable anticoagulants - heparin
oral anticoagulants - warfarin

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120
Q

heparin

A

enhances activity of antithrombin III

(antithrombin III inactivates Xa adn thrombin)

ONLY short term use

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121
Q

low molecular weight heparin

A

still not orally available, longer elimination half life, patient administration at home

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122
Q

APTT

A

activated partial thromboplastin time

used to monitor anti-coagulant effect of heparin (measure of intrinsic pathway)

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123
Q

adverse effects of heparin

A

haemorrhage
thrombocytopaenia (platelet deficiency)
osteoporisis

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124
Q

vitamin K essential for what

A

formation of clotting factors 2 7 9 10

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125
Q

warfarin

A

coumarin derivative - oral anticoagulant - inhibit vit K reductase (stops K reduction so cant gamma carboxylate factors )

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126
Q

warfarin - reversible?

adverse effect?

A

reversal with vit K

haemorrhage

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127
Q

problem with warfarin

A

levels and anticoagulant effects v labile - strongly bind to plasma proteins(small change in pp levels (hypermetabolic state, liver damage) will get big change in relative amount of active drug)

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128
Q

what things can lead to increased/decreased warfarin activity

A

increased: vit K deficiency, hepatic disease, hypermetabolic state, drug interactions, competition for cyt p450
decreased: drug interactions, pregnancy

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129
Q

PT

INR

A

prothrombin time

International normalised ratio - ration of patient PT (rate clot forms after addition of Ca and tissue factor) to that of normal
ratio needed varies between patients - e.g. if 3, blood will take 3 times longer to clot than normal

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130
Q

dabigatran

advantage and problem

A

new anticoagulant drug
can be administered in fixed doses
problem - no antidote

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131
Q

3 types of drugs affecting platelet activation and adhesion

A

ADP R antagonists
aspirin
glycoprotein IIb/IIIa R antagonists

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132
Q

clopidogrel

A

ADP R antagonist -

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133
Q

streptokinase

problem?

A

fibrinolytic drug - activates plasminogen to plasmin

antigenic so single use

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134
Q

alteplase

better than streptokinase?

A

fibrinolytic drug - human recombinant tissue plasminogen activators (hrtPA)
non antigenic
clot selective

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135
Q

abciximab

A

GpIIb/IIIa antagonist

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136
Q

as increase HR what happens to diastole

A

shortens

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137
Q

valve incompetence

A

=regurgitation = leaking

-> volume overload

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138
Q

what causes heart murmur

A

turbulence around stenosed or incompetent valves

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139
Q

are LV changes reversible or irreversible in regurgitation and stenosis when symptoms arise

A

irreversible LV changes occur at time of regurgitation symptoms

aortic stenosis symptoms indicate time to intervene - LV changes regres

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140
Q

echocardiography

A

used in assessment of valvular heart disease

can show LV changes before they’re irreversible

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141
Q

interventions for valvular heart disease

A

valve replacements - metal, plastic, bioprostheses
valve repair (mitral)
balloon valvotomy
stent valves

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142
Q

mechanical vs bioprosthetic valve

A

mechanical lasts forever, but thrombus develop so have to be on warfarin

bioprosthetic - no need for warfarin but degrades in 15 yrs

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143
Q

commonest valve lesion

A 
aortic stenosis (fibrosis, calcification)
results in pressure gradient across valve
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144
Q

aortic stenosis LV response

A

pressure overload

concentric hypertrophy

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145
Q

murmur from aortic stenosis

A

crescendo decrescendo

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146
Q

causes of aortic regurgitation

A

aortic leaflets damaged - endocarditis, rheumatic fever

aortic root dilated so leaflets dont close - marfans syndrome, aortic dissection, collagen vascular disorders, syphilis

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147
Q

physiological result of aortic regurgitation

A

increase SV, increase pulse pressure

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148
Q

what happens with prolonged aortic regurgitation

A

eventual decompensation:

LVDV increases, LV function decreases, LVSV increases - at this point irreversible

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149
Q

causes of mitral regurgitation

A 
myxomatous degeneration (mitral valve prolapse)
ruptured cordae tendinae (flail leaflet)
infective endocarditis
MI
Rheumatic fever
collagen vascular disease
cardiomyopathy
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150
Q

mitral valve regurgitation initial compensations and prolonged decompensations

A

initially: increase EDV, increased SV, normal ESV

if prolonged: increase LV diastolic volume, reduced SV, increased LV systolic volume –> irreversible changes

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151
Q

resulting problems of mitral regurgitation on atria and pulmonary circulation

A

increase LA pressure and volume
atrial fibrillation - thrombus - risk of embolus

increased pulmonary venous pressure - congestion, oedema, hypoxia

increased pulmonary artery pressure - pulmonary hypertension

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152
Q

mitral regurgitation murmer

A

pansystolic (constant)

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153
Q

mitral stenosis cause

A

rheumatic fever

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154
Q

resulting problems from mitral stenosis

A

increase LA pressure and volume, atrial fibrillation, thrombus in LA - embolism, increased pulmonary venous and artery pressure

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155
Q

hypertrophy

A

an increase in the size of cells resulting in increase in size of organ

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156
Q 
hypertrophy:
no. of cells
production of intracellular structures
nucleus
type of cells
stimuli
A 
same no.of cells
increased
increases in size, can change shape
permanent cells
mechanical stress, GFs, hormones
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157
Q

result of transcription in striated muscle in response to GFs

A

induction of embryonic/foetal genes - increase mechanical performance and decrease work load

increase synthesis of contractile proteins - increase mechanical performance

increase production of GFs

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158
Q

hyperplasia

A

increase in number of cells

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159
Q 
hyperplasia:
stimuli
phys or path
type of cells 
same time as hypertrophy?
A

stem cells stimulated by hormonal or GFs
phys and path!
labile cells (already with active stem cell population) or stable cells
often same time

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160
Q

metaplasia

A

reversible change in which one adult cell type is replaced by another adult cell type

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161
Q

metaplasia:
where occurs
stimuli
phys or path

A

frequently at junctions between different epithelial types
stimuli- altered environment
phys or path!

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162
Q

example of physiological metaplasia

A

onset of menarche - swelling of tissues exposes endocervical mucosa to acidic vaginal environment - simple columnar epithelium to stratified squamous epithelium

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163
Q

example of pathological metaplasia

A

Barrett oesophagus: gastro-oesophageal reflux disease - bile acids induce metaplasia of oesophageal stratified squamous epithelium to intestinal type with goblet cells

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164
Q

neoplasia

A

unregulated cell division that can now occur in absence of stimulus
due to genetic mutation
can be benign or malignant

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165
Q

“premalignant”

A

benign, but often can confer an increased risk for malignancy - the more replications you do the more likely you are to pick up a mutation

166
Q

atrophy

A

a decrease in cell or organ size

167
Q

atrophy
when does it occur (stimulus)
when is reversible

A

occurs when normal growth stimulus decreased or lost

reversible if not accompanied by cell death and fibrosis

168
Q

only cause of hypertrophy that can kill you

how does it happen

A

myocardial hypertrophy

stretch on myocytes directly causes transcriptional changes

169
Q

normal heart weight women and men

A

women

170
Q

microscopic characteristics of myocardial hypertrophy

A

enlarged rectangular nuclei
bi-nucleated myocytes
increased connective tissue

171
Q

nutmeg liver

A

result of left cardiac failure

mixture of haemorrhage and necrosis

172
Q

two causes or aortic valvular disease

A

congenitally bicuspid aortic valve

dystrophic calcification

173
Q

two causes of mitral valvular disease

A

myxomatous valve aka ‘floppy’ - causes prolapse, can cause mitral regurgitation - genetic or related to connective tissue disease

fibrosed mitral valve - from rheumatic valve disease

174
Q

rheumatic fever

rheumatic heart disease

A

streptococcus pyogenes
immune response to strep pyogenes - Ab that looks like something that wants to attack endocardium
can effect all valves - stenosis or regurgitation
most common cause of mitral stenosis

175
Q

infective endocarditis

A

bacteria in blood - end up with collections of bacteria on valves themselves

176
Q

equity vs equality

A

equity - ensuring everyone has equal outcome

equality - giving everyone the same thing

177
Q

social determinants of health

A 
social gradient
stress
early start
social exclusion
work
unemployment
social support
addiction
food 
transport
178
Q

roles of kidney

A

regulation of water and electrolyte balance
endocrine
excretion of endogenous waste
extretion of exogenous compounds

179
Q

where does filtration, secretion and reabsorption occur along nephron

A

filtration - glomerulus
secretion - proximal tubule
reabsorption - proximal tubule, loop of henle, distal tubule, collecting duct

180
Q

where is most of NaCl reabsorbed

A

proximal tubule

181
Q

where is most of water reabsorbed

A

loop of henle

182
Q

where is K+ reabsorbed and secreted

A

reabsorped - proximal tubule, distal tubule

secreted - collecting duct

183
Q

three types of drugs with therapeutic actions on kidney

A

diuretics
drugs that affect urine pH
drugs that alter secretion of organic molecuels

184
Q

action of diuretics

A

decrease Na and Cl reabsorption = increase NaCl excretion = secondary water excretion

185
Q

4 classes of diuretics

A

loop diuretics
thiazide
potassium-sparing
osmotic

186
Q

loop diuretics mechanism of action

A

act on thick ascending loop of henle

inhibit NA/K/2Cl carrier into cells

187
Q

loop diuretics
absorption
plasma protein bound?
duration of action

A

well absorbed - onset

188
Q

loop diuretics adverse effects

A

K+ loss from distal tubule - hypokalaemia
H+ excretion - metabolic alkalosis
reduce extracellular fluid volume (elderly) - hypovolaemia and hypotension

so normally given with K+ supplement

189
Q

loop diuretics clinical uses

A

salt and water overload in acute pulmonary oedema, chronic HF, liver cirrhosis, renal failure

hypertension

190
Q

thiazide diuretics
powerful?
two types

A

moderately powerful - less effect than loop diuretics

“true” thiazides and thiazide-like

191
Q

thiazide diuretics mechanism of action

A

act on distal convoluted tubule

inhibit Na/Cl cotransporter

192
Q

thizide diuretics
oral availability
max effect
duration

A

orally active
max effect 4-6h (slower absorption and onset)
duration 8-12h (longer duration)

193
Q

thizide diuretics adverse effects

A

K+ loss from collecting ducts (same as loop diuretics - K+ supplement)

increased plasma uric acid (inhibition of tubular secretion of uric acid)

indapamide - less effects

194
Q

thiazide clinical uses

A

hypertension

severe resistant oedema (in combo with loop diuretic)

195
Q

potassium-sparing diuretics
why used

where do they act

A

used in combo with K+-loosing (loop and thiazide) diuretics to prevent K+ loss e.g. in patients with HF

act on collecting tubule and ducts

196
Q

spironalactone

A

Potassium-sparing diuretic

aldosterone R antagonist - so get reduced activation of Na+ channel and reduced stimulation of Na+ pump transcription (actions of aldosterone)

197
Q

spironolactone:
oral availability
onset
half life

A 
orally active
slow onset (due to its action on transcriptional changes)
short half life (10mins) but metabolite long half life (16h) =long duration
198
Q

spironolactone:
adverse effects
clinical use

A

hyperkalaemia
GIT upset

combo with loop or thiazide diuretics
HF
hyperaldosteronism

199
Q

triamterene and amiloride

A

K+-sparing diuretic

block luminal sodium channels in collecting tubules and ducts

inhibit Na+ reabsorption, inhibit K+ secretion

200
Q

triamterene and amiloride
absorption
onset
duration

A

triamterene - well absorbed, 2h onset, duration 12-16h

amiloride - poorly absorbed, slow onset, duration 24h

201
Q 
osmotic diuretics
pharmacological 'action'
reabsorbed?
main effect where 
action
A 
pharmacologically inert
filtered but NOT reabsorbed
main effect on water permeable parts of nephron - proximal tubule, descending limp of loop, collecting tubules
reduce passive water reabsorption
only small reduction in Na+ reabsorption
202
Q

osmotic diuretics clinical uses

A

raised intracranial or intraocular pressure, prevention of acute renal failure

203
Q

3 types of compounds with adverse effects on kidney

A

heavy metals
antibiotics
antineoplastic agents

204
Q

why kidney susceptible to toxicity

A

receives 25% of blood supply
substances may be concentrated
kidney able to carry out metabolism - reactive species

205
Q

mechanisms of direct toxicity or via metabolite

A

ROS - drug metabolism can lead to reactive O species - this may be why drug damaging, not actual drug

interfere with Ca metabolism

protein/enzyme building - inhibition of enzyme function, initiation of immune response (body thinks its foreign)

206
Q

mercury
mechanism of toxicity
damage primarily where

A

direct toxicity and vasoconstriction
binds to thiol groups in proteins
damage primarily in proximal tubule

207
Q

gentamicin
what used for
site of action
mechanism of action

A

Gram neg infections

site of action apical membrane of proximal tubule

binds phospholipids, changes Ca intracellular, impairs mitochondrial respiration, cell injury

208
Q

gentamicin toxicity greater in patients with :

problem with elimination

A

existing renal disease, or taking other potentially nephrotoxic drugs

elimination is renal - nephrotoxicity can improve excretion - vicious cycle

209
Q

antineoplastics - cisplatin :
what is it
causes what

A

cytotoxic anticancer agent - treatment of prostate tumours

causes dose-limiting nephrotoxicity

210
Q

cisplatin mechanism of nephrotoxicity

A

activated inside cells, forms reactive species, binds to neucleophilic cell components in distal tubule and collecting ducts

211
Q

total cholesterol/HDL cholesterol ratio

A

increased ratio - increased heart disease risk

212
Q

LDL vs HDL

A

LDL bad - increases risk of heart disease

HDL - good - decreases risk of heart disease

213
Q

cholesterol hydrophobic or philic

A

NEITHER LOL

amphipathic

214
Q

4 fates of cholesterol made in liver

A

transport
bile acids
steroid hormones and vit D
membranes

215
Q

cholesterol made in liver for transport

A

assembled into VLDL (very low density lipoprotein) for transport to tissues

216
Q

role of cholesterol in membrane

A

optomise mammalian membrane fluidity - fits into kinks of unsaturated fatty acyl chains to make membrane less fluid

217
Q

membrane rafts

A

higher levels of cholesterol, glycolipids and sphingolipids - little regions where membrane v rigid

218
Q

cholesterol synthesis

A 
acetyl-CoA generated in mitochondria
acetyl CoA converted to HMG CoA
HMG CoA converted to mevalonic acid
mevalonic acid converted to cholesterol 
cholesterol feeds back to inhibit HMG CoA reductase (regulatable step)
219
Q

HMG CoA reductase

A

converts HGM CoA into mevalonate

220
Q

how is cholesterol carried around body

A

esterify cholesterol to make it more hydrophobic - incorporate into lipoproteins

221
Q

chylomicrons

A

formed in intestinal mucosa
package triacylglycerol and cholesterol-ester from gut and take to tissue
remnants taken to liver

222
Q

VLDL

A

takes TAG and cholesterol-ester stored/generated in liver to tissue
remnants taken to liver

223
Q

LDL

A

some cholesterol-ester transferred from VLDL to LDL - LDL not taken up by liver as well so continues to circulate to supply cholesterol-ester to tissues

224
Q

HDL

A

scavenger - takes cholesterol from membranes an cells to liver for bile salt formation

acts on macrophages to stop them becoming foam cells

225
Q

apolipoprotein

A

protein part of lipoprotein

involved in structure, uptake and activation of lipoprotein lipase

226
Q

lipoprotein lipase

A

breaks down TAG in lipoproteins into free fatty acids

227
Q

Apo-B100

A

apolipoprotein in LDL and VLDL - structure and uptake

228
Q

Apo-CII

A

apolipoprotein in VLDL and chylomicrons - activates lipoprotein lipase

229
Q

ApoA1

where made

A

precursor of HDL

made in liver and intestine

230
Q

SR-B1 Receptor

A

scavenger receptor in liver - HDL binds to transfer cholesterol-ester

231
Q

ACAT

A

in liver - helps VLDL form

232
Q

LCAT

A

in plasma - helps HDL scavenge cholesterol from membranes

233
Q

dyslipidaemia

A

disorders of LP metabolism

234
Q

hypercholesterolaemia

A

increase total (free and esterified) cholesterol in blood - above 6.2mM

235
Q

hypertriglyceridaemia

A

increase blood triglycerides

236
Q

high circulating LDL =

A

higher risk of heart disease

237
Q

process of LDL causing atherosclerosis

A

oxidised LDL accumulates in artery wall
endothelial cells react by displaying adhesion molecules
WBCs (monocytes and T cells) invade and secrete cytokines
macrophages appear - take up modified LDLs with scavenger receptors
macrophages engorged with cholesterol =foam cells
fibrous tissue develops to trap foam cells
foam cells produce tissue factor - can lead to blood clot on rupture of plaque

238
Q

how reduce serum cholesterol levels

A

block HMG-CoA reductase (rate limiting enzyme in cholesterol synthesis)

239
Q

statins

A

competitive inhibitors of HMG-CoA reductase

240
Q

ischaemic heart disease definition

A

imbalance between myocardial O supply and demand

241
Q

acute and chronic forms of ischaemic heart disease

A

acute - unstable angina, MI, sudden cardiac death

chronic - stable angina, chronic myocardial ischaemia

242
Q

factors limiting coronary blood flow

A

perfusion pressure
coronary vascular resistance (coronary artery atherosclerosis)
external compression - vessels of subendocardium particularly get squeezed between muscles and pressure in ventricle
intrinsic regulation (endothelium and local metbolites)

243
Q

non-transmural infarcts

A

just subendocardium

244
Q

transmural infarct

A

subendocardium through whole wall

245
Q

why is endocardium spared?

A

O from ventricle lumen diffuses

246
Q

vascular supply of heart:

  • anterior wall and 2/3 septum
  • lateral wall
  • posterior wall
A

LAD
LCX
PD

247
Q

MI caused by

A

acute plaque event - plaque forming an occlusive thrombus

248
Q

angina/reversible injury

A

no macroscopic or microscopic changes

intracellular changes
rapid loss of contractility

249
Q

minutes -hours of MI

A

irreversible injury - disruption of cell membrane (sarcolemma)

250
Q

what does disruption of sarcolemma cause

A

leaking of cardiac proteins (troponin, CK)

leaking of current - STEMI, NSTEMI, myocardial irritability (more likely to spark arrhythmia)

251
Q

STEMI

A

ST elevation MI - severe ECG change - due to transmural infarct

252
Q

NSTEMI

A

non-ST elevation MI - due to non-transmural infarct - less severe ECG changes

253
Q

hours of MI

A

irreversible injury
cell death
haemorrhage
oedema

254
Q

12-24h post MI

A

contraction band necrosis, neutrophil invasion (acute inflammation)

255
Q

1-3 days post MI

A

acute inflammation - heavy neutrophil infiltration, necrosis

256
Q

peak of destruction of heart muscle in MI

A

troponin peak - 3 days

257
Q

3-7 days post MI

A

end of acute inflammation, start of early granulation - macrophages ingest dead monocytes, fibroblasts and vessels appear, collagen at 5-6 days

258
Q

3 ways to rupture wall

A

1 - rupture of free ventricular wall - blood into pericardium “haemopericardium”, compresses heart until stops “cadiac tamponade”

2 - rupture of papillary muscle

3 - rupture of IV septum

2 and 3 –> cadiogenic shock = acute severe cardiac failure

259
Q

1-8 weeks post MI

A

vascular granulation tissue becomes fibrous granulation tissue

collagen - flexible and may stretch (aneurysm = infarct expansion) causing thinning of wall

260
Q

8 weeks post MI

A

fibrosis/scar - fixed

261
Q

stable angina vs unstable angina presentation

A

stable - chest pain on exertion, goes away with rest

unstable - chest pain, may occur at rest

262
Q

stable angina due to

A

atherosclerotic narrowing of vessel, endothelial dysfunction, symptoms at 70% stenosis

263
Q

unstable angina due to :

resolves?

A

acute plaque event, coronary artery thrombosis

RESOLVES - no irreversible damage

264
Q

chronic myocardial ischaemia

A

small areas of subendothelial ischaemia, patchy myocyte necrosis and replacement by fibrosis

265
Q

sudden cardiac death

A

unexpected death in short time period (

266
Q

cardiac arrest

A

sudden cessation of cardiac output and effective circulation
usually precipitated by ventricular fibrillation and or ventricular asystole

267
Q

3 examples of aminoglycosides

A

gentamicin, tobramycin, amikacin

268
Q

mechanism of aminoglycosides action

A

two stag system: at low concentrations: binds to particular site on ribosome, causes abnormal reading of genetic code,incorrect proteins made,
cell wall weakene

higher concentrations get in - then get total ribosomal blockade

269
Q

way bacteria get around aminoglycosides

A
  1. enzymatic covalent modification - add extra charge groups
  2. ribosomal mutation (aminoglycoside cant bind)
  3. active eflux
  4. modified outer membrane - reduced entry
270
Q

4 mechanisms of resistance to antimicrobial agents

A
  1. drug inactivation
  2. altering the target of drug action
  3. reduce access of drug to target
  4. failure to activate inactive precursor of drug
271
Q

metronidazole - action

A

strictly on anaerobes

nitroreductase converts to active form

272
Q

3 things apart from infection antibiotics important for

A

surgical procedures
malignancies (protect them when immune system down)
immunodeficiencies, cystic fibrosis

273
Q

where does antibiotic resistance originate

A
  1. innate resistance - (gram neg for vancomycin, enterococci for sulfonamides (no folic acid synthesis))

acquired - change in bacterial phenotype reflecting altered genotype due to:
mutation
acquisition of new genes via horizontal transfer

274
Q

transfer of genes between bacteria occurs by:

A

transformation
phage-mediated transduction
plasmid-mediated conjugation

275
Q

process of transformation

A
  • lysis of cell or DNA release
  • uptake into competent cell (must be closely related)
  • homologous recombination
276
Q

what is necessary for transformation to occur

A
  • DNA has to be methylated in a particular way so its not restricted
  • homologous recombination

so can only occur between closely related bacteria

277
Q

lysogenic and lytic cycle of bacteriophages

A

lysogenic - temperate phage - replicates harmlessly with bacteria

lytic - virus replicates in bacteria, makes lots of copies, kills bacteria

278
Q

largest cause of antibiotic resistance

A

harmless comensals - every time we take an antibiotic they want to be resistant to not get removed
mutations make harmless bacteria pathogenic

279
Q

transduction

A

rarely an abnormal phage produced: phage that has taken up bacterial DNA
Then goes and transfers this DNA to another bacteria by infecting it

280
Q

plasmid mediated conjugation

A

plasmid from one bacteria to another
plasmid encodes cytoplasmic bridge - allows transfer of DNA
can occur between entirely unrelated bacteria

281
Q

3 factors that favour the development of resistance

A

evolutionary advantage:
vast numbers
rapid growth
promiscuity

282
Q

3 factors that favour emergence /persistence of AMR

A

way antimicrobials act - selective pressure to become resitant
power of natural selection

283
Q

muli-resistance plasmid

A

BAD because with one genetic step - organisms go from being susceptible to all to being resistant to like 12 antibiotics

284
Q

why is resistance increasing

A

using antimicrobials promotes resistance

285
Q

time for bacteria to develop resistance

A

getting shorter! bacteria getting better at getting resistant

286
Q

MIC

A

measure of susceptibility - test of bacteriostatic

287
Q

MBC

A

minimum bactericidal concentrations

288
Q

E-test strip

A

MIC by diffusion - where the oval stops is MIC

289
Q

considerations regarding choice of antibiotic

A 
antimicrobial spectrum
efficacy
route of administration
route of excretion
pharmacokinetics/dynamics
availability 
cost
290
Q

common prescribing errors

A
  1. prescribing an antimicrobial when not needed
  2. prescribing wrong antimicrobial
  3. using correct one inappropriately - wrong dose, course, route, patient
291
Q

rationale for antibiotic combinations

A 
temporary measure when unknown cause
delay emergence of resistance
mixed infections
reduce toxicity 
synergistic effect
292
Q

antagonism in antibiotic combinations - e.g.

A

bactericidal with static

293
Q

mechanisms of synergy

A
  1. block sequential steps of metabolic pathway
  2. inhibit enzymatic degradation
  3. enhance antimicrobial uptake by bacterial cell
294
Q

synergy example - blocking steps of metabolic pathway

A

sulphonamides with trimethoprim in folic acid synthesis

=co-trimoxazole

295
Q

synergy example - inhibit enzymatic degredation

A

beta-lactam + beta-lactamase inhibitor

amoxycillin + clavulanate

296
Q

synergy example - enhance antimicrobial uptake

A

beta-lactam + aminoglycoside

297
Q

4 mechanisms of antagonism

A
  • inhibition of bactericidal activity by bacteriostatic
  • induction of enzymatic degradation
    -competition for binding to same target
    inhibition of target
298
Q

Jawetz’s laws

A

bacteriostatic + bacteriostatic = additive or indifferent
bacteriostatic + bactericidal = antagonistic
bactericidal + bactericidal = synergistic

299
Q

dyslipidaemia

A

abnormal lipid profile

300
Q

are “normal “ total cholesterol levels necessarily healthy?

A

nope - its ratio of LDL to HDL

as ratio increases, risk of adverse events increases

301
Q

treatment for dyslipidaemia

A
  1. establish fasting plasma lipid profile for diagnosis
  2. consider cardiovascular status and risk factors
  3. treat secondary causes (obesity, diabetes)
  4. manage modifiable risk factors
302
Q

which fats contribute mostly to cholesterol

A

saturated and trans

303
Q

rate limiting step in cholesterol synthesis

A

HMG-CoA reductase

cholesterol has negative feedback on it

304
Q

4 fates of cholesterol

A
  1. stored in liver for export in VLDL
  2. bile acids
  3. steroid hormones and vit D synthesis
  4. membrane synthesis adn maintenance
305
Q

chylomicrons

A

transport dietary triglycerides and cholesterol

306
Q

cholesterol transport and metabolism

A
  • dietary chol into chylomicrons, from liver in VLDL
  • circulates to tissues - broken down by lipoprotein lipase in capillaries and tissues - hydrolysis of triglycerides, release of FFAs - energy for tissues
  • chylo and VLDL remnants taken up by liver or converted to LDL
307
Q

HDL

A

reverse cholesterol transport: when liver needs cholesterol for bile acids, increase HDL removes cholesterol from tissues and takes back to liver

308
Q

LDL

A

bad - contains apolipoprotein B-100 - can transport lipids into artery walls

309
Q

statins

A

HMG-CoA reductase reversible competitive inhibitors

- primary treatment for hypercholesterolaemia

310
Q

action of statins

A
  • decrease synthesis of mevalonic acid, so reduces cholesterol synthesis in liver
  • so compensatory upregulation of LDL Rs - so increase LDL clearance
  • increase levels of HDL
  • decrease TG
311
Q

statin ceiling effect

A

increasing dose has little effect

312
Q

problem with statin compliance

A

perceived lack of efficacy

313
Q

precautions with statins

A
  • common cytP450 - drugs and grapefruit juice
  • statin levels increased by some drugs and decreased by others
  • elevation of aminotransferase (liver damage)
  • increase creatine kinase (muscle pain)
314
Q

statins in pregnancy?

A

no - impaired fetal myelination

315
Q

bile acid sequestrants/resins

A

bind bile acid, preventing gut absorption - increase bile excretion
- increase demand for bile acid synthesis - upreg of hepatic LDL Rs, removal of LDL from plasma,

316
Q

ezetimibe

A 
specifically inhibits cholesterol absorption in intestine - binds sterol transporter
lowers LDL
(but dietary chol  doesnt contribute much to circulating chol)
317
Q

when ezetimibe used

A

used as adjunct to statin, or in statin-intolerant patients

318
Q

nicotinic acid/niacin

A

mechanism unclear:

  • decrease VLDL secretion from liver
  • reduce plasma LDL and triglyc
  • increase LDL R
  • increase HDL
  • lowers potentially atherogenic lipoprotein (a)
319
Q

lipoprotein (a)

A

formed from LDL, found in plaques, inhibits thrombolysis

320
Q

nicotinic acid/niacin widely used?

A

not really - bad side effects (reduced with lengthy use, but lack of patient compliance)

321
Q

fibrates

A

treat hypertriglyceridaemia
- agonist at PPA nuclear R - increases synthesis of lipoprotein lipase (LPL)
- increase lipolysis of lipoprotein triglyceride
- reduction in plasma triglyc
(variable effects on LDL)
- increase HDL

322
Q

fish oils

A

treatment of hypertriglyceridaemia:

  • omega 3 fatty acids
  • reduce triglyc and VLDL
  • increase HDL
323
Q

stable angina

A

chest pain wiht exertion, stress

arteries/arterioles already dilated, stiff walls - can’t dilate to meet oxygen demand

324
Q

ways to increase O2 supply

A
  • dilate coronary arteries

- reduce HR - heart longer in diastole, coronary arteries longer to fill

325
Q

ways to decrease O2 demand

A
  • decrease CO
  • reduce preload (dilate veins, reduce venous return)
  • reduce afterload (dialate arterioles, decrease resistance)
326
Q

4 drugs to treat stable angina

A
  1. nitrates - preload
  2. Ca channel blockers - afterload, myocardium
  3. B-adrenoceptor antagonists - HR/SV
  4. ivabradine - HR
327
Q

nitrates mechanism of action

A
  • drug undergoes biotransformation (prodrug)
  • release NO
  • stimulats guanyate cyclase in vascular smooth muscle
  • GTP to cGMP
  • dephosphorylates myosin light chain
  • relaxation
328
Q

short and long acting nitrates

A

short - glyceryl trinitrate (GTN)

long - isosorbide dinitrate (prodrug to isosorbie-5-mononitrate)

329
Q

GTN - 1st pass metabolism, route of administration (3 types)

A

1st pass metabolism - inactive metabolite so not oral

  • sublingual for acute attack
  • transdermal for prophylaxis
  • IV for emergency
330
Q

isosorbide dinitrate

1st pass metabolism, rout of administration

A

prodrug!

oral for anticipation of effort or prophylaxis

331
Q

GTN and viagra

A

GTN - increases cGMP
viagra - phosphodiesterase inhibitor (phosphodiesterase breaks down cGMP) - would get massive increase in cGMP - fatal BP drop

332
Q

GTN and tolerance

A

has tolerance! - drug free period required

  • depletion of tissue thiols required or NO production from GTN
  • increase sensitivity to vasoconstrictors
333
Q

verapamil and nifedipine

A

L-type calcium channel blockers for heart disease

334
Q

verapamil ad nifedipine vascular or cardiac selective

A

verapamil - non-selective

nifedipine - vascular selective

335
Q

adverse effects of verapamil

never taken with

A

(ca channel blocker)
flushing, headache, oedema, bradycardia, AV block

never taken with beta blocker

336
Q

adverse effects nifedipine

A

vascular selective ca channel blocker

flushing, headache, oedema, hypotension, reflex tachycardia

337
Q

selective B1 antagonist

A

atenolol

338
Q

ivabradine

A

“pure” HR reduction:

- “specific” selective inhibition of inward Na-K If(ifunny) current in SA node

339
Q

when ivabradine used in patients

A

patients with IHD, LV dysfunction, HR>70bpm

340
Q

variant angina

A

coronary vasospasm at rest

341
Q

treatment for variant angina

A

relieve coronary vasospasm with short acting nitrate

prophylaxis with dihydropyridine ca channel blocker

342
Q

give beta blockers to variant angina patient??

A

NO- alpha-adrenoceptor mediated vasospasm may be worse if B2 coronary dilation blocked

343
Q

treatment for unstable angina

A

as for stable, add aspirin

344
Q

naming of parietal pleura

A

cervical
mediastinal
costal
diphragmatic

345
Q

costodiaphragmatic recess

A

where parietal pleura touches parietal pleura

346
Q

does pleural cavity peak out of thoracic cage anywhere?

A

yes - either side of vertebral column where T12 attaches

347
Q

why do we have a pulmonary ligamnet

A

so pulmonary veins can expand in times of hypercapacitance

348
Q

pyothorax

A

puss in the pleural cavity

349
Q

pain from visceral vs parietal pleura

A

visceral pleura - dull ache b/c only visceral nerve supply

parietal - V PAIN - somatic nerve supply

350
Q

where does trachea begin

A

neck at C6

351
Q

RMB different to LMB?

A

RMB shorter, wider and more vertical

352
Q

muscle making up posterior aspect of trachea

A

trachealis muscle

353
Q

each segmental bronchus supplies a

A

bronchopulmonary segment

354
Q

right apical segment lower lobe (bronchopulmonary segment)

A

bronchopulmonary segment something aspirated when patient on back will likely go (first segmental bronchus that comes off directly posteriorly)

355
Q

right lung fissures and lobes

A

3 lobes and 2 fissures

356
Q

left lung fissures an lobes

A

oblique fissure, 2 lobes

357
Q

lingular

A

on left lung - functions as middle lobe (same no. of bronchopulmonary segments)

358
Q

position of veins and bronchi at hilum

A

veins - anterior and inferior

bronchi posterior

359
Q

two branches of Right main pulmonary artery

A

pulmonary artery

right uper love branch of pulmonary artery

360
Q

two branches of RMB

A 
bronchus intermedius (continuation of RMB)
right upper lobe bronchus
361
Q

lymphatics in lung

A

superficial (just beneath visceral pleura) and deep (within tissue of lung)

362
Q

first port of call for superficial and deep lymphatics of lung

A

hilar lymph nodes

363
Q

series of lymph nodes from lung

A

hilar
bronchopulmonary
tracheobronchial
bronchomediastinal

364
Q

more xrays vs fewer xrays, e-density, black or white

A

more xrays get through, high e-density - white

less x rays through, low e-density - black

365
Q

when can interface in x ray be seen

A

if tissues of different e-densities next to each other

366
Q

requirements for erect PA (posterior to anterior) CXR

A
  • full inspiration
  • PA
  • scapulae moved away from chest wall
  • erect
  • straight
367
Q

how do you make sure someone is straight on CXR

A

sternal notch line up with spinous processes

368
Q

how do you know if full inspiration on CXR

A

must see 7 anterior ribs in mid clavicular line

369
Q

how do you know if heart enlarged on CXR

A

heart diameter 50% or less of inside diameter of rib cage

370
Q

CXR divided into what zones

A

upper middle lower
lower 1/2 or lower zone is base
upper 1/2 of upper zone is apex

371
Q

air or fluid in pleural spaces goes where

A

fluid - sinks to bases

air - rises to apices

372
Q

hydrothorax

A

fluid accumulation in pleural cavity

373
Q

hydropneumothorax

A

air and fluid in pleural cavity

374
Q

meniscus in CXR

A

fluid in pleural cavity

375
Q

what happens when xrays hit film (what chemically are they doing)

A

convert silver-halide crystals to silver

376
Q

does CT use film?

how take CT

A

NO - radiation detector

spiral scan

377
Q

hounsfeild units

A

absolute measure of xray attenuation

digital “grey scale” rather than film density

378
Q

CT spatial and contrast resolution compared with X-radiography

A

poorer spatial and better contrast than X-ray

379
Q

what is the orientation of a CT slice

A

from feet up, toes up

380
Q

reconstruction orientation : axial coronal and sagittal

A

axial - from feet up
coronal - from front
sagittal - from left

381
Q

post processing

A

after data acquired and patient gone home - make things better looking and easier to understand

382
Q

cons of CT

A 
ionising radiation (dramatic icnreased exposure)
expensive
383
Q

disorders of haemoglobin type of genetic inheritace

A

autosomal recessive

384
Q

alpha-like globin genes:

  • where located
  • what are they
A
  • chromosome 16

- alpha 1 and 2, pseudo zeta and alpha (not expressed), zeta

385
Q

beta-like globin genes

  • where located
  • what are they
A
  • chromosome 11

- beta, deta, pseudo beta, G gamma and A gamma(two versions, only differ by one base), epsilon

386
Q

LCR

A

locus control region - essential for regulation fo B-like globin genes

387
Q

embryonic Hbs

A

zeta2epsilon2
zeta2gamma2
alpha2epsilon2

388
Q

fetal Hb

A

alpha2gamma2

389
Q

HbA

A

alpha2beta2

390
Q

HbA2

A

alpha2delta2

391
Q

time course of Hbs in life

A
  • first 3 months - embryonic and foetal
  • 2nd trimester - fetal, some HbA
  • last trimester to birth - cross over of fetal and HbA
392
Q

alhpa and beta thalassaemias

A

decreased synthesis of one or more globin chains

393
Q

structural variants haemoglobinopathies

A

altered globin polypeptide without altering rate of synthesis (e.g. sickel cell)

394
Q

types of haemoglobinopathies

A
  • alpha and beta thalassaemias
  • structural variants
  • hereditary persistence of fetal haemoglobin
395
Q

what results from thalassaemias

A

imbalance in relative amounts of alpha and beta chains - get homotetramers instead of heterotetramers

396
Q

alpha thalassaemias mostly caused by what mutation

A

large deletions

397
Q

beta thalassaemias mostly caused by what mutation

A

point mutations

398
Q

B+ and B0

A 
B+ = reduced B
B0 = no B
399
Q

two issues in thalassaemia

A

homotrimers form aggregates, accumulate and precipitate in RBCs causing damage, RBCs destroyed prematurely

ineffective erythropoiesis/ dyserythropoiesis leads to breakdown of erythroid precursors in bone marrow

both lead to haemolytic anaemia

400
Q

pathophysiology of untreated beta thalassaemia

A

liver enlargement - goes back to making RBCs

  • bone marrow expands - trying to make more RBCs
  • splenomegaly - abnormal RBC breakdown
401
Q

microscopic features of RBCs in B-thalassaemia

A

microcytic, hypochromic

tear drop shaped (due to aggregates of alpha)

402
Q

usually more or less HbA in B-thalassaemia

A

more - compensatory mechanism

403
Q

treatment of B-thalassaemia

A
  • transfusions
  • splenectomy - prefer to remove before it ruptures
  • chelation therapy - remove iron
404
Q

alpha-thalassaemias

  • which Hbs it effects
  • what homotetramers produced
A
  • effects fetal and adult Hbs

- homotetramers that are less soluble

405
Q

why is carrier genotype important

A

south east asian - 1/4 chance of hydrops fetalis (4 alpha genes absent)
whereas mediterranean mutation - produce all alpha-/alpha-

406
Q

what kind of mutation causes sickle cell disease, what happens

A

point mutation
–> polar residue to hydrophobic one, forms aggregates - forms sickle cell shape
blocks capillaries

407
Q

treatment of sickle cell

A

hydroxyurea

408
Q

can you detect sickle cell with MVC/MCH

A

no - may be normal or reduced, need to look for abnormal cells

409
Q

compound heterozygotes

A

individuals with two different mutations (e.g. B-globin and sickle cell , or two different B-globin mutations

410
Q

double heterozygote

A

B-globin and alpha-globin mutation

411
Q

gene therapies for thalassaemia

A
  • alter imbalance of chains (e.g. knock down alpha chains in beta-thalassaemia
  • epigenetic modificcations to induce HbF
412
Q

why is there a high rate of alleles for haemoglobinopathies in some parts of the world

A

carriers have some resistance to malaria

MD1 (5 decks)

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