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Med 1011 > Week 12 Sem 1 2014 > Flashcards

Week 12 Sem 1 2014 Flashcards

0
Q

Systemic artery

A

Carry oxygenated blood

High pressure

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1
Q

Artery

A

Vascular tube carries blood away from heart

Direction of flow towards capillary

‘Bigger to smaller tubes’

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2
Q

Pulmonary artery

A

Carry deoxygenated blood

Lower pressure than systemic, but still
Higher than veins

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3
Q

Structure of artery

A

Lumen
Initima (endothelim (most inside) connective tissue)
Media (muscle or elastic fibres)
Adventitia ( collagen fibres

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4
Q

Types of arterial branches

A 
Cutaneous
Muscular
Nutrient (to long bone)
Articular (around joints)
Arteriae nervorum (arteries for nerves)
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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

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6
Q

Muscular artery

A

Lots of smooth muscle in media

Form majority of named arteries

Does lots of branching

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7
Q

Parietal branch

A

Artery close to body wall

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8
Q

Visceral branch

A

Arteries into central body organs

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9
Q

Sinusiods

A

Big capilaries that help transport immune stuff

Have modified endothelium + absent/discontinuos basement membrane

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10
Q

Developemt of artery

A

From

Mesoderm

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11
Q

Avascular structures

A

Epidermis, other surface epithelia
Articular cartilage

‘Blood brain barrier’?

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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

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13
Q

Systolic pressure

A

Pressure due to ventricular contraction

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14
Q

Diastolic pressure

A

Due to recoil of elastic arteries

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15
Q

Pulse pressure

A

Difference bw systolic n diastolic

Wat we feel wen we take radial pulse

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16
Q

Pulsatile flow

A

In elastic n muscular arteries

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17
Q

Continuous flow

A

In capillaries n veins

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18
Q

Haemorrhage

A

Loss of blood from (any type of) blood vessel

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19
Q

First aid for bleeding

A

Rest
Ice
Compression
Elevation

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20
Q

Anastomosis

A

Linkin bw arteries/ arterioles

Links bw veins or bw lymph vessels = ‘communications’

Skeletal muscles have the most anastomoses

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21
Q

True anastomoses

Vs potential anastomoses

A

Links bw artery to artery
Vs
Links bw arteriole to arteriole

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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

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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

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24
Q

Pain threshold

A

Pnt where stimulus becomes painful

Similar for most ppl

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25
Q

Pain tolerance

A

Degree to wich painful stimulus can b tolerated

Varies widely

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26
Q

Biomedial model of pain

A

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?

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27
Q

Gate control theory

A

Pain Nerves activated - opens gate

Activity in other sensory nerves - closes gate (eg rubbin site of pain)

Messages from brain- cognitive influence s

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28
Q

Measures of pain

A

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

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29
Q

End artery

A

Artery that does not link with any other artery

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30
Q

End organ

A

Body part/organ isolated from others

Tend to b supplied by end artery

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31
Q

Blind ending organs

A

Project into/suspended within a cavity
Eg appendix n gall bladder protrude into abdominal cavity

Supplied by end arteries

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32
Q

Visceral segments

A

Organs in large cavity
Of body trunk
Eg kidney n liver

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33
Q

Thromboembolus

A

A bloodclot/part of it that dislodges n is transmitted by blood stream to somewhere else

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34
Q

Vasa vasorum

A

Vessels for blood supply( eg nutrients) for

Media n adventitia

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35
Q

Pulmonary venous system

A

Made of pulmonary veins

Brings oxygenated blood from lungs to into left. Atrium of heart

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36
Q

Systemic venous system

A

Brings deoxygenated blood from body to heart

Drains into right atrium of heart

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37
Q

Azygos vein

A

Feeds into superior vena cava

‘Assymetrical’

Vein that runs up the right side of spinal column

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38
Q

Portal venous system

A

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)

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39
Q

Veins

A

Vascular tubes carry blood to the heart

Direction of flow away from capillary bed

‘Smaller to bigger tubes’

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40
Q

Structure of veins

A

Same as arteries xept
Media- only smooth muscles

Thinner walls n larger lumen

Have valves (unlike arteries)

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41
Q

Venae comitantes

A

Pair of veins that wrap around artery

Intercommunicate

Usually in limbs

Conserve heat

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42
Q

Vascular venous pump

A

Wen arteries next to veins (fanks to venae comitantes) expand, helpin venous flow

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43
Q

Muscular venous pump

A

Wen muscles around the vein contract, helpin venous flow

44
Q

Thoracic venous pump

A

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
Q

Valveless vein

A

In vena caval system, veterbral n azygos system

46
Q

Varicose veins

A

Vein that has abnormal dilation - can become elongated n turtous( = full of twists n turns)

47
Q

Haemorrhoids

A

Dilated veins under surface of anal canal

Associated wit constipation, weightliftin, pregnancy

48
Q

Venous valve incompetence

A

Valve cusps damage (due to eg thrombosis)

Blood can flow in reverse - ISSUE!

49
Q

Venous sinuses

A

Normal dilations of veins

50
Q

Perforatin vein

A

Vein bit bw deep vein n superficial vein

51
Q

Dural venous sinuses

A

Venous sinuses bw inner n outer layers of dura matter surrounding brain

52
Q

EmissAry veins

A

Vein bits bw intracranial n extracranial veins

53
Q

Portal systemic anastomosis

A

Communications bw portal system n systemic system

2 major sites- lower end of oesophagus n at anal canal

54
Q

Venous plexus

A

Where there r intercommunicating networks with NUMeRous veins

55
Q

Types of pain:
Nociceptive vs
Pathological

A

Nociceptive- Under normal circumstances
Where potentially damagin noxious signals activate nociceptors

Pathological- pain due to neural damage in pain mechanisms

56
Q

Pain as perception: process

A

Appraisal > beliefs (neg expectation of ones ability to control over pain) > copin strategies (will increase risk of inactivity)

57
Q

Flow in lymph vessels

A

Relies on 3 one-way-valve pump systems:

Vascular
Muscular
Thoracic

58
Q

Lacteals

A

Lymphatic capillaries that absorb dietary fats in villi of small intestines

59
Q

Lymphangitis

A

Swollen inflammation of lymphatics in the subcutaneous tissue

60
Q

Lymphadenitis

A

Swollen , inflammation of lymph nodes

61
Q

Major node groups

A

(All palpable)

Cervical (drains tonsils)
Auxillary
Inguinal

62
Q

Lymph ducts

A

There r 2:
Thoracic duct
Right lymphatic duct

63
Q

Plasmid

A

Circular
Self replicating
Double-stranded DNA

64
Q

Resistance plasmid (R plasmids)

A

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
Q

Conjugative plasmid

A

Plasmid that can b transfered from one bac to another during process of conjugation

66
Q

Conjugation

A

Wen bac make a copy of plasmid, keeps a copy n transfer the other to other bac

67
Q

Transposons

A

’ 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
Q

HGT

A

Horizontal Gene Transfer

Wen bac continuously pass genes bw them from the bac in their enviro

69
Q

Transduction

A

Dna transfered from one bac to another via virus

70
Q

Gene cassette

A

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
Q

Integron

A

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
Q

Thrombosis

A

Formation of blood clot (thrombus) in blood vessel which blocks the vessel

Blocks SITE OF ORIGIN

72
Q

Embolism

A

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
Q

Virchow’s triad

A

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
Q

Vascular injury

A

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
Q

Stasis

A

Stoppin blood flow

75
Q

Hypercoagulability

A

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
Q

Coronary artery thrombosis

A

Due to atherosclerosis, can lead to mycardial infarction, myocardial ischaemia, angina

77
Q

Ischemia

A

Insufficient blood supply to organ

78
Q

Angina

A

Pain (due to pressure in chest cuased by ischemia to the heart)

Feelins of ‘chokin, suffocation’

79
Q

Carotid and cerebral artery thrombosis and embolism

A

Causes ischaemic attacks and strokes

80
Q

Venous thromboembolism

A

Describes both
Deep vein thrombosis (DVT) snd
Pulmonary embolism (PE)

81
Q

DVT

A

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
Q

PE

A

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
Q

Dyspnoea

A

Difficulty or laboured breathin

84
Q

Inherited risk factors for DVT or PE

A

Family history

Factor V leiden (a genetic disorder)

Prothrombin gene mutation

Deficiency of antithrombin,Protein C, Protein S

85
Q

Acquired risk factors for DVT and PE

A 
Surgery n trauma
Increase in age
Cancer
Previous thrombosis
Oral contraceptives
Antiphospholipid antibodies
86
Q

Diagnosis of DVT

A

Compression ultrasound

Venogram

87
Q

Diagnosis of PE

A

Ventilation-perfusion (V/Q) scan

CT-pulmonary Angiogram (CTPA)

88
Q

Placental thrombosis

A

Increase risk of miscarriage by virtue of interferrin with oxygenation of fetal blood

89
Q

Management of DVT/PE

A

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
Q

Haemostasis

A

Formin blood clot to stop bleedin by containin blood within damaged vessels

91
Q

Blood coagulation tests

PT and APTT

A

Measures time taken to clot

If Factor deficiency or inhibitor, time to clot will be longer

92
Q

PT (INR)

A

Prothrombin time

Extrinsic pathway

93
Q

aPTT

A

Activate partial thromboplastin time

Intrinsic pathway

94
Q

Mixing studies (to identify clottin issues)

A

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
Q

Disseminated intravascular coagulopathy

A

Activation of coagulation mechanisms, leadin to blood clots inside blood vessels throughout the body n EXHAUSTION OF COAGULATION FACTORS

96
Q

Thrombocytopenia

A

Disease from DECREASED BLOOD COUNT due to

  1. Increased platelet consumption/destruction
  2. Splenic sequestration
  3. Decreased platelet production
97
Q

Platelet defects

A

Show mucocutaneous hemorrhages, petechiae, epistaxis/bleeding gums

98
Q

Coagulation protein defects

A

Show larger intramuscular/intra-articular hemorrhages, n sometimes hemarthrosis

99
Q

Fibrinolysis

A

Choppin down fibrin
Clot breakdown n dissolution

Plasminogen to plasmin then plasmin cuts fibrin mesh

100
Q

Anticoagulant proteins

A

Stop formation of fibrin ie regulate clot size (by stopping it from growin)

Eg antithrombin, protein C, protein S

101
Q

Extrinsic pathway ( in haemostasis)

A

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
Q

Intrinsic pathway

A

Platelets activate F12,
Wich converts F11,
Wich converts F9 (& wit its cofactor F8)
Activate common pathway

103
Q

Platelet degranulation

A

Releases:
ADP (attracts more platelets)
Thromboxane A2 - promotes platelet aggregation,degranulation n further vasoconstriction
Serotonin-a vasoconstrictor

104
Q

Haemostasis process

A
  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
Q

Common pathway (in haemostasis)

A

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

Med 1011 (12 decks)

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