Week 12 Sem 1 2014 Flashcards
0
Q
Systemic artery
A
Carry oxygenated blood
High pressure
1
Q
Artery
A
Vascular tube carries blood away from heart
Direction of flow towards capillary
‘Bigger to smaller tubes’
2
Q
Pulmonary artery
A
Carry deoxygenated blood
Lower pressure than systemic, but still
Higher than veins
3
Q
Structure of artery
A
Lumen
Initima (endothelim (most inside) connective tissue)
Media (muscle or elastic fibres)
Adventitia ( collagen fibres
4
Q
Types of arterial branches
A
Cutaneous Muscular Nutrient (to long bone) Articular (around joints) Arteriae nervorum (arteries for nerves)
5
Q
Elastic arteries
A
Lots of elastic tissue in media
Yellow in appearence in media
Arteries that r largest n closest to heart eg aorta
6
Q
Muscular artery
A
Lots of smooth muscle in media
Form majority of named arteries
Does lots of branching
7
Q
Parietal branch
A
Artery close to body wall
8
Q
Visceral branch
A
Arteries into central body organs
9
Q
Sinusiods
A
Big capilaries that help transport immune stuff
Have modified endothelium + absent/discontinuos basement membrane
10
Q
Developemt of artery
A
From
Mesoderm
11
Q
Avascular structures
A
Epidermis, other surface epithelia
Articular cartilage
‘Blood brain barrier’?
12
Q
Blood pressure
Ie pressure on vessel wall
A
= pressure wave from contraction of heart
+ hydrostatic pressure (pressure of volume of blood on blood vessel wall due to gravity
13
Q
Systolic pressure
A
Pressure due to ventricular contraction
14
Q
Diastolic pressure
A
Due to recoil of elastic arteries
15
Q
Pulse pressure
A
Difference bw systolic n diastolic
Wat we feel wen we take radial pulse
16
Q
Pulsatile flow
A
In elastic n muscular arteries
17
Q
Continuous flow
A
In capillaries n veins
18
Q
Haemorrhage
A
Loss of blood from (any type of) blood vessel
19
Q
First aid for bleeding
A
Rest
Ice
Compression
Elevation
20
Q
Anastomosis
A
Linkin bw arteries/ arterioles
Links bw veins or bw lymph vessels = ‘communications’
Skeletal muscles have the most anastomoses
21
Q
True anastomoses
Vs potential anastomoses
A
Links bw artery to artery
Vs
Links bw arteriole to arteriole
22
Q
Arteriovenous anastomoses
A
Link bw artery n vein
Occur in exposed part eg nose penis fingertips toes ( to reduce heat loss so go straight from artery to vein
23
Q
Anatomical end artery vs fuctional end artery
A
Both dont have anastomoses wit other arteries but
FUNctional end art= has potential anastomoses bw its arterioles
24
Pain threshold
Pnt where stimulus becomes painful
| Similar for most ppl
25
Pain tolerance
Degree to wich painful stimulus can b tolerated
| Varies widely
26
Biomedial model of pain
Nerve stuff
Says that the more damage there is the more pain there is- pain is proportional to tissue damage
Does everyone wit same injury get same pain?
27
Gate control theory
Pain Nerves activated - opens gate
Activity in other sensory nerves - closes gate (eg rubbin site of pain)
Messages from brain- cognitive influence s
28
Measures of pain
Self reporting scale eg numeric ratin scale, mcgill pain questionnare
Behavioural measurement eg pain complaints, food uptake, number of visits to dr, number of treatments, nonverbal indicators eg facial expression
(Physiological measures) eg tissue damage, fever
29
End artery
Artery that does not link with any other artery
30
End organ
Body part/organ isolated from others
Tend to b supplied by end artery
31
Blind ending organs
Project into/suspended within a cavity
Eg appendix n gall bladder protrude into abdominal cavity
Supplied by end arteries
32
Visceral segments
Organs in large cavity
Of body trunk
Eg kidney n liver
33
Thromboembolus
A bloodclot/part of it that dislodges n is transmitted by blood stream to somewhere else
34
Vasa vasorum
Vessels for blood supply( eg nutrients) for
| Media n adventitia
35
Pulmonary venous system
Made of pulmonary veins
Brings oxygenated blood from lungs to into left. Atrium of heart
36
Systemic venous system
Brings deoxygenated blood from body to heart
Drains into right atrium of heart
37
Azygos vein
Feeds into superior vena cava
'Assymetrical'
Vein that runs up the right side of spinal column
38
Portal venous system
Wen one capillary bed pools into another capillary bed through veins, at low pressure
Eg hepatic portal system (drains blood from GIT(gut) into liver)
39
Veins
Vascular tubes carry blood to the heart
Direction of flow away from capillary bed
'Smaller to bigger tubes'
40
Structure of veins
Same as arteries xept
Media- only smooth muscles
Thinner walls n larger lumen
Have valves (unlike arteries)
41
Venae comitantes
Pair of veins that wrap around artery
Intercommunicate
Usually in limbs
Conserve heat
42
Vascular venous pump
Wen arteries next to veins (fanks to venae comitantes) expand, helpin venous flow
43
Muscular venous pump
Wen muscles around the vein contract, helpin venous flow
44
Thoracic venous pump
Oscillation of pressure of respiration contribute to venous flow
INSPIRATION- diaphragm descends, shortens IVC (inferior vena cava), wich empties -lengthens SVC, which fills
EXPIRATION- diaphragm ascends, IVC lengthens n fills- SVC shortens n empties
45
Valveless vein
In vena caval system, veterbral n azygos system
46
Varicose veins
Vein that has abnormal dilation - can become elongated n turtous( = full of twists n turns)
47
Haemorrhoids
Dilated veins under surface of anal canal
Associated wit constipation, weightliftin, pregnancy
48
Venous valve incompetence
Valve cusps damage (due to eg thrombosis)
Blood can flow in reverse - ISSUE!
49
Venous sinuses
Normal dilations of veins
50
Perforatin vein
Vein bit bw deep vein n superficial vein
51
Dural venous sinuses
Venous sinuses bw inner n outer layers of dura matter surrounding brain
52
EmissAry veins
Vein bits bw intracranial n extracranial veins
53
Portal systemic anastomosis
Communications bw portal system n systemic system
2 major sites- lower end of oesophagus n at anal canal
54
Venous plexus
Where there r intercommunicating networks with NUMeRous veins
55
Types of pain:
Nociceptive vs
Pathological
Nociceptive- Under normal circumstances
Where potentially damagin noxious signals activate nociceptors
Pathological- pain due to neural damage in pain mechanisms
56
Pain as perception: process
Appraisal > beliefs (neg expectation of ones ability to control over pain) > copin strategies (will increase risk of inactivity)
57
Flow in lymph vessels
Relies on 3 one-way-valve pump systems:
Vascular
Muscular
Thoracic
58
Lacteals
Lymphatic capillaries that absorb dietary fats in villi of small intestines
59
Lymphangitis
Swollen inflammation of lymphatics in the subcutaneous tissue
60
Lymphadenitis
Swollen , inflammation of lymph nodes
61
Major node groups
(All palpable)
Cervical (drains tonsils)
Auxillary
Inguinal
62
Lymph ducts
There r 2:
Thoracic duct
Right lymphatic duct
63
Plasmid
Circular
Self replicating
Double-stranded DNA
64
Resistance plasmid (R plasmids)
Basically bacteria has plasmid that can transfer itself from one bac to another
N has all these genes that is resistant to all these chemicals eg mercury, fusidic acid etc
65
Conjugative plasmid
Plasmid that can b transfered from one bac to another during process of conjugation
66
Conjugation
Wen bac make a copy of plasmid, keeps a copy n transfer the other to other bac
67
Transposons
' Jumping genes'
Mobile genetic bits that transfers dna within cell from
Plasmid to plasmid n bak
Plasmid to chromo n bak
Types:
Insertion sequences (IS elements)
Composite transposons
68
HGT
Horizontal Gene Transfer
Wen bac continuously pass genes bw them from the bac in their enviro
69
Transduction
Dna transfered from one bac to another via virus
70
Gene cassette
Mobile genetic element that has a gene (often antibiotic resistance gene) and a recombination site (cassette attachment site)
Can b on plasmids/come in via HGT
71
Integron
Genetic units that can capture seperate gene cassettes and reorder genes on its sequence of genes that it had collected
Mechanism for bac to collect huge regions of their chromo/plasmids that contain 'resistance' genes they'd like to keep
Can b on chromosomes or plasmids, may or may not b on transposon
72
Thrombosis
Formation of blood clot (thrombus) in blood vessel which blocks the vessel
Blocks SITE OF ORIGIN
72
Embolism
When a blood clot that has broken free from initial site of thrombus formation ( ie embolus) travels down the blood stream and blocks a DISTANT SITE
72
Virchow's triad
3 broad categories of factors that contribute to thrombosis
1. Damage to vessel wall
2. Stasis/alteration to blood flow
3. Hypercoagulability- alterations in constitution of blood
73
Vascular injury
Atherosclerosis= fatty stuff+ cellular debris stuck on artery walls, likely to rupture, exposing subendothelium n release of tissue factor
Vasculitis= inflammation of blood vessels, can cause occlusion
Myocardial infarction= aka heart attack. Necrosis of part of cardiac muscle due to obstruction in coronary artery due to atherosclerosis/thrombus/spasm
74
Stasis
Stoppin blood flow
75
Hypercoagulability
Tendency to coagulate more than normal due to component imbalance (where coagulants r favoured over anticoagulants)
In inherited conditions, this may merely result from anticoagulant deficiencies, not procoagulant overactivation
76
Coronary artery thrombosis
Due to atherosclerosis, can lead to mycardial infarction, myocardial ischaemia, angina
77
Ischemia
Insufficient blood supply to organ
78
Angina
Pain (due to pressure in chest cuased by ischemia to the heart)
Feelins of 'chokin, suffocation'
79
Carotid and cerebral artery thrombosis and embolism
Causes ischaemic attacks and strokes
80
Venous thromboembolism
Describes both
Deep vein thrombosis (DVT) snd
Pulmonary embolism (PE)
81
DVT
Deep vein thrombosis
Occurs in veins of calf and lower limbs,n less commonly in upper limb
Causes pain n swellin, can lead to chronic venous insufficiency (veins cant pump enough blood bak to heart)
82
PE
Pulmonary embolism
Blood clot travels from DVT in lower limbs, through heart, to pulmonary arteries
Can b asymptomatic or hav Symptoms: acute shortness of breath/dyspnoea, pleuritic chest pain, or death
83
Dyspnoea
Difficulty or laboured breathin
84
Inherited risk factors for DVT or PE
Family history
Factor V leiden (a genetic disorder)
Prothrombin gene mutation
Deficiency of antithrombin,Protein C, Protein S
85
Acquired risk factors for DVT and PE
```
Surgery n trauma
Increase in age
Cancer
Previous thrombosis
Oral contraceptives
Antiphospholipid antibodies
```
86
Diagnosis of DVT
Compression ultrasound
Venogram
87
Diagnosis of PE
Ventilation-perfusion (V/Q) scan
CT-pulmonary Angiogram (CTPA)
88
Placental thrombosis
Increase risk of miscarriage by virtue of interferrin with oxygenation of fetal blood
89
Management of DVT/PE
Inititally, THROMBOPROPHYLAXIS IS IDEAL but for MANAGENT:
Anticoagulation (to prevent further clot formation) via heparin/low MW (molecular weight) heparin, oral vitamin K antagonists eg warfarin for longer term
Antiplatelet agents eg aspirin/clopidorgrel NOT used for treatment of DVT/PE but have some benefit in prevention of recurrent DVT
90
Haemostasis
Formin blood clot to stop bleedin by containin blood within damaged vessels
91
Blood coagulation tests
| PT and APTT
Measures time taken to clot
If Factor deficiency or inhibitor, time to clot will be longer
92
PT (INR)
Prothrombin time
| Extrinsic pathway
93
aPTT
Activate partial thromboplastin time
| Intrinsic pathway
94
Mixing studies (to identify clottin issues)
Patient's plasma mixed wit normal plasma
If aPTT corrects, there is a CLottin factor DeFICiENCY (n is compensated for in the normal plasma)
If aPTT fails to correct, there is a coagulation factor INHIBiTOR that is affectin both sets of plasma
95
Disseminated intravascular coagulopathy
Activation of coagulation mechanisms, leadin to blood clots inside blood vessels throughout the body n EXHAUSTION OF COAGULATION FACTORS
96
Thrombocytopenia
Disease from DECREASED BLOOD COUNT due to
1. Increased platelet consumption/destruction
2. Splenic sequestration
3. Decreased platelet production
97
Platelet defects
Show mucocutaneous hemorrhages, petechiae, epistaxis/bleeding gums
98
Coagulation protein defects
Show larger intramuscular/intra-articular hemorrhages, n sometimes hemarthrosis
99
Fibrinolysis
Choppin down fibrin
Clot breakdown n dissolution
Plasminogen to plasmin then plasmin cuts fibrin mesh
100
Anticoagulant proteins
Stop formation of fibrin ie regulate clot size (by stopping it from growin)
Eg antithrombin, protein C, protein S
101
Extrinsic pathway ( in haemostasis)
Tissue factor (F3) released from damaged tissue , wit the aid of Ca2+, activates F7 (wich then activates common pathway)
Quicker, dominant to intrinsic pathway
102
Intrinsic pathway
Platelets activate F12,
Wich converts F11,
Wich converts F9 (& wit its cofactor F8)
Activate common pathway
103
Platelet degranulation
Releases:
ADP (attracts more platelets)
Thromboxane A2 - promotes platelet aggregation,degranulation n further vasoconstriction
Serotonin-a vasoconstrictor
104
Haemostasis process
1. Vasoconstriction
2. Exposure of subendothelium
3. Platelet plug formation (PRIMARY HAEMOSTASIS) (wen platelets come n stick to collagen + von Willebrand factor
4. Coagulation (SECONDARY HAEMOSTASIS) wen u get fibrin meshes:extrinsic/intrinsic pathway, then common pathway
5. Clot breakdown n dissolution
105
Common pathway (in haemostasis)
Factor 7 n 9 will eventually activate factor 10.
F10 (+ some other factors) converts
PROTHROMBIN to THROMBIN
Thrombin converts FIBRINOGEN TO FIBRIN
FIBRIN initally forms loose mesh
Then FACTOR 13 forms COVALENT CROSSLINKS, convertin fibrin to DENSE INSOLUBLE FIBRIN MESH
