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Human Disease YR3 #1 Flashcards

1
Q

What is the function of an osteoblast?

A

It forms bone

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2
Q

What is the function of an osteoclast?

A

It resorbs bone

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3
Q

What differentiate to form osteoblasts?

A

Mesenchymal progenitor cells

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4
Q

What differentiates to form osteoclsts?

A

Myeloid progenitor cells

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5
Q

Name 5 cell signalling ligands stimulate the activity of osteoblasts?

A 
TNFaIL-1IL-11PTHPGE2
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6
Q

What do osteoblasts release to activate the differentiation of osteoclasts?

A

RANKL

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7
Q

What vitamin is essential for bone health?

A

Vitamin D

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8
Q

Explain the 4 steps in the cycle of vitamin D formation in our body?

A
  1. Photons from sun hit skin2. 7DHC is activated and travels to the liver3. At the liver it is converted to 25(OH)vit D (then stored)4. It then travels to the kidney and becomes 1,25(OH)2 vit D (physiologically active)
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9
Q

What ion is essential for bone formation/turnover?

A

Calcium

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10
Q

If Ca is low what occurs?

A

Bone resportion

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11
Q

If Ca is high what occurs?

A

Bone formation

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12
Q

What are the 5 main substances that aid the control of Ca metabolism? and which organs?

A 
Ascorbic acidVit DCaPTHPO4
BoneGIParathyroid glandKidneyLiver
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13
Q

What is the definition of Paget’s disease of the bone?

A

Localised disorder of bone turnoverIncreased bone resorption followed by increased bone formationLeading to disorganised bone: bigger, less compact, more vascular and more susceptible to deformity and fracture

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14
Q

How is Paget’s disease of the bone transmitted?

A

Genetically (15-30% familial)Anglo-Saxon originsChronic viral infection within osteoclasts

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15
Q

What are the symptoms for Paget’s disease?

A

> 40 age with bone painBone deformityExcessive heat over pagetic boneNeurological complications such as nerve deafness

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16
Q

What are the presentations of Paget’s disease?

A

Isolated elevation of serum alkaline phosphataseBone pain and local heatBone fracture or deformityHearing loss

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17
Q

What is the treatment for Paget’s disease?

A 
Surgical intervention (hard if asymptomatic)Don't treat if raised alkaline phosphatase aloneIV bisphosphonates therapy with one off IV zoledronic acid
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18
Q

What is the difference between Rickets and Osteomalacia?

A

Rickets - before the epiphyseal lines are closed| Osteomalacia - adult disease

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19
Q

What is the definition of Rickets and Osteomalacia?

A

A severe vitamin D or Ca deficiency causing insufficient mineralisationMuscle function is also impaired in low vit D states

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20
Q

How are vitamin D and Ca related?

A

Vit D stimulates the absorption of Ca and PO4 from the gut and Ca and PO4 then becomes available for bone mineralisation

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21
Q

What is the presentation of Rickets?

A 
Stunted growthCurved spineWide joints at elbow and wristCurved legs (splayed)Wide bones and ankles
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22
Q

What are the symptoms for Osteomalacia?

A

Aches and painsInability for muscle coordination Waddle gaitStruggle out of chair

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23
Q

Treatment for Osteomalacia and Rickets?

A

Ca and vit D supplementation

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24
Q

What is the definition of osteogenesis imperfecta?

A

Genetic disorder of CT characterised by fragile bones from mild trauma or everyday acts

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25
Q

What are the 4 most common phenotypes for osteogenesis imperfecta?

A

28 different genetic variation existType I: milder form when child starts to walk but can present in adultsType II: lethal by age 1Type III: progressive deforming with severe bone dysplasia and poor growthType IV: more severe version of type I

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26
Q

What is the presentation for osteogenesis imperfecta?

A 
Growth deficiencyDefective tooth formationhearing lossBlue scleraScoliosisLigamentous laxityEasy bruising
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27
Q

What is the surgical, medical, social and genetic management options for osteogenesis imperfecta?

A

Surgical to treat fractureMedical to prevent fracture via IV bisphosphonatesSocial adaptations to education and socialGenetic via counselling for parents and next generation

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28
Q

What is the definition of osteoporosis?

A

A metabolic bone disease characterised by low bone mass and micro architectural deterioration of bone tissue, leading to enhanced bone fragility and a consequent increase in fracture risk T- score < -2.5 SDs

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29
Q

What other factors increase the risk of bone fractures?

A

AgeBMDFallsBone turnover

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30
Q

What is a good website to calculate the risk of fracture for a patient?

A

Frax

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31
Q

What T-score is needed for an osteoporosis diagnosis?

A

< -2.5 SDs

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32
Q

What type of scan is used to help diagnose osteoporosis?

A

Dual energy x-ray absorptiometry (DXA)

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33
Q

How common is osteoporosis, for men and women?

A

50% of women over 50 will have an osteoporotic fracture before death (Men 1/5)A 50 year old women had a 17% risk of hip fracture

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34
Q

What are the endocrine causes of osteoporosis?

A 
ThyrotoxicosisHyper/HypoparathyroidismCushingsHyperprolactinemiaHypopituitarismEarly menopause
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35
Q

Which rheumatic disease can cause osteoporosis?

A

RAAnkylosing spondylitisPolymyalgia rheumatica

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36
Q

Which GI disease can cause osteoporosis?

A

UC and Crohn’sLiver diseaseMalabsorption

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37
Q

Which medications can cause an increase risk of osteoporosis?

A 
SteroidsPPI (proton-pump inhibitors)Enzyme inducing antiepileptic medicationsAromatase inhibitorGnRH inhibitorsWarfarin
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38
Q

What preventions can be put in place to reduce osteoporotic fractures?

A

Minimise risk factorsEnsure good Ca and vit D statusFall prevention strategiesMedications

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39
Q

What is the treatment for osteoporosis?

A

HRT until 60 years oldSelective oestrogen receptor modulatorsBisphosphonatesDenosumab

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40
Q

What are the side effects of HRT?

A

Increased risk of blood clotsIncreased risk of breast cancerIncreased risk of heart disease and stroke

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41
Q

What are the side effects of SERMS?

A

Hot flushesIncreased clotting risksLack protection at hip site

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42
Q

What are the side effects of bisphosphonates?

A

OesophagitisIritis/UveitisAtypical femoral shaft fracturesNecrosis of the jaw

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43
Q

What is Denosumab?

A

Monoclonal antibody against RANKLReduces osteoclastic bone resorptionSubcut injection every 6 months

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44
Q

What are the side effects for Denosumab?

A

AllergySymptomatic hypocalcemia if given when vit D is depleteAtypical femoral shaft fractures

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45
Q

What are the side effects of Teriparatide?

A

Injection site irritationRarely hypercalcaemiaAllergy

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46
Q

What common features do all CT diseases share?

A

Auto-antibodies presentMainly femaleAll have oral features

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47
Q

What antibody can be used to support a clinical diagnosisof Lupus?

A

ANA (95% +ve in CTD)| Lupus

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48
Q

What are the oral presentations for systemic lupus?

A

1/1000

Oral ulcers (painless)Dry mouth/eyes
(Fatigue, arthralgia and malar rash across nose)
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49
Q

What are the treatments for systemic lupus, specifically oral symptoms?

A

AspirinImmunosuppressive medications )sides thrush and ulcers)(methotrexate and rituximab)Check patients bloodsSuncream, hydroxychloroquine, anti-inflamm and steroids

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50
Q

What are the oral presentations for Sjogren’s syndrome?

A

Dry mouth (xerostomia) –> dental decay and oral infectionSalivary gland swellingsDry eyes (xerophthalmia) –> burning and gritty eyesFatigueArthralgia

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51
Q

How to confirm a suspicions of Sjogren’s?

A

Schirmer’s test, saliva test, blood test (RO and La antibodies)Labial gland biopsy (referral)

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52
Q

What are the 2 types of Sjogren’s?

A

Primary (just the disease)| Secondary (complication of other CTDs)

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53
Q

What is the treatment for Sjogren’s, specifically for oral symptoms?

A

Saliva substitutes: water, BioXtra oral gel, Saliva Othana, Biotene oral gel, High Fl toothpasteSugar free chewing gumRegular dental check ups

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54
Q

What are the 2 types of scleroderma?

A

Localised: morphoeaSystemic: limited and diffuse

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55
Q

What are the presentations for systemic sclerosis?

A

Limited mouth openingPoor dentitionGum recessionSecondary Sjogren’s

Adult onset Raynaud'sSwollen hands/sausage fingersTight waxy skinFatigueDysphagia
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56
Q

What is the treatment for systemic sclerosis?

A

Immunosuppression (methotrexate)Anti-fibroticVascular (ca channel blockers - nifedipine)

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57
Q

What are the presentations for inflammatory muscle disease?

A

Dry mouth and eyes due to secondary Sjogren’sDysphagiaMuscle weaknessRashRapid loss of function (need aid out of chair)

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58
Q

What are the 2 types of inflammaotry muscle disease?

A

Dermatomyositis| Polymyositis

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59
Q

What is the treatment for inflammatory muscle disease?

A

SteroidImmunosuppressivesIV Immunoglobulins

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60
Q

What is the definition of antiphospholipid syndrome?

A

Sticky blood disorder| have it or its abs

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61
Q

What is the clinical presentation of antiphospholipid syndrome?

A

Recurrent thrombosisRecurrent pregnancy lossPeculiar rash (levido reticularis)

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62
Q

What is the lab presentation of antiphospholipid syndrome?

A

Anticardiolipin antibodyLupus anticoagulantAnti-beta 2 glycoprotein

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63
Q

How to treat someone with antiphospholipid syndrome and what effect does this have on dental procedures?

A

Antiplatelets AnticoagulantsHigh bleeding risk

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64
Q

What are the presentations for Behcet’s disease?

A

Recurrent painful oral ulcers

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65
Q

What are the presentations for giant cell arteritis?

A

Jaw painJaw Cramps/claudicationsTongue pain

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66
Q

What are the presentations for juvenile idiopathic arthrtis?

A

Micrognathia| TMJ involvement

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67
Q

What medications give side effects such as oral ulcers?

A

MethotrexateSulfasalazineFetunomideMycophenolate mofetil

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68
Q

What medications give side effects such as dry mouth

A

Amitriptyline

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69
Q

What medications give side effects such as thrush?

A

Steroids| Immunosuppressants

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70
Q

What medications give side effects such as metallic taste?

A

Penicillamine| Sulfasalazine

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71
Q

What medications give side effects such as gum hypertrophy or staining?

A

Cyclosporin

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72
Q

What are the 2 main causes of autoimmunity?

A

Genetic: susceptible genes that lead to a failure of self-toleranceEnvironmental stimuli: tissue damage leading to presentation of self-antigens activating self-reactive lymphocytes

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73
Q

What is the definition of autoimmune disease?

A

A failure or breakdown of immune system that maintains tolerance to self tissues

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74
Q

How does the immune system change for someone who is autoimmune?

A

Loss of tolerance is due to abnormal selection or lack of control of self-reactive B/T cells

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75
Q

What is the definition of a hypersensitivity response?

A

A harmful immune response that may produce tissue injury or cause serious disease

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76
Q

What is each type of hypersensitivity reaction mediated by?

A

TI-III - antibodies| TIV - T cells

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77
Q

What type of hypersensitivity does autoimmune disease fall under?

A

TII-IV

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78
Q

What is he antibody, ligand, MoA and general name for type I hypersensitivity?

A

IgESoluble antigenAct mast cells and produce mediatorsAllergy

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79
Q

What is he antibody, ligand, MoA and general name for type II hypersensitivity?

A

IgG, IgMCell or matrix antigenOpsonisation, phagocytosis, complement and act of leukocytesRheumatic fever

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80
Q

What is he antibody, ligand and general name for type III hypersensitivity?

A

IgG, IgMSoluble antigenComplement, Fc receptor recruitment and act of leukocytesRA

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81
Q

What is he T cell variation, ligand, MoA and general name for type IV hypersensitivity?

A

Th1 - sol antigen TI diabetes (delayed-type)Th2 - sol antigen MS (T cell mediated)(both produce inflammatory cytokines)CTL - cell antigenTh1 - macrophage activation causing cytokine-mediated inflammTh2 - direct cell killing and cytokine mediated inflammation

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82
Q

Explain the process of type I hypersensitivity?

A
  1. Exposure to allergen2. Act of Tfh cells and stimulation of IgE class switching in B cells3. Production of IgE4. Binding of IgE to FceRI on mast cells5. Repeated exposure to allergen6. Activation of mast cell; releasing medicators7. Mediators such as cytokines and vasoactive amines and lipid
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83
Q

What are the effects of biogenic amines (histamine)

A

Vasodilation| Vasc leakage

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84
Q

What are the effects of lipid mediators (PAF and LTC4)

A

Bronchoconstriction intestinal hypermotility| Inflammation

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85
Q

What are the effects of cytokines (TNF)

A

Inflammation

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86
Q

What are the effects of cationic granule proteins?

A

Killing parasitic cells

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87
Q

What are the effects of enzymes?

A

Tissue damage

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88
Q

Explain the mechanism of action of type II hypersensitivity?

A

Antibody binding to antigenRecruit and activate inflammatory cells (via complement and Fc receptor) (neutrophils and macrophages)Causing tissue injury

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89
Q

Explain the mechanism of action of type III hypersensitivity?

A

Soluble immune complexes of antibodies and antigensRecruit and activate inflammatory cells (via complement and Fc receptor) (neutrophils)Causing tissue injury

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90
Q

What is the MoA of ‘type V’ hypersensitivity

A

Antibody against TSH receptorStimulates the receptor without the ligandIncrease production of thyroid hormoneHyperthyroidism

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91
Q

Name 4 TII hypersensitivity disease?

A

Autoimmune haemolytic anaemiaInsulin-resistant diabetesMyasthenia gravisGraves’ disease

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92
Q

Name 3 TIII hypersensitivity disease?

A

Systemic lupusPolyarthritisPoststreptococcal glomerulonephritis

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93
Q

Name 3 TIV T cell mediated hypersensitivity diseases and their antigen targets?

A

TI diabetes - Islet cellsRA - TII collagenMS - myelin basic protein

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94
Q

Theoretically, how can we treat TIV hypersensitivity?

A

Blockade of CD4 or MHC II molecules with blocking antibodies| Or blockage of CTLA-4 (T-cell inhibitor)

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95
Q

What part of genetics can influence autoimmunity?

A

HLA alleles

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96
Q

What HLA does RA have?

A

DR4

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97
Q

What HLA does Insulin-dependent diabetes have?

A

DR3/DR4

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98
Q

What HLA does MS have?

A

DR2

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99
Q

What HLA does systemic lupus have?

A

DR2/DR3

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100
Q

What gene polymorphisms in HLA can cause increased susceptibility to autoimmune disease?

A

IL-10

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101
Q

What are the potential mechanisms of environmental causes for autoimmunity?

A

Molecular mimicryViral/bacterial superantigensEnhanced presentation and processing of autoantigensBystander activationAct of lymphocytes by lymphotropic viruses

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102
Q

What is the definition of molecular mimicry?

A

Activation of autoreactive T cells by microbial peptides that have sufficient structural similarity to self peptide

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103
Q

What is the definition of viral/bacterial superantigen?

A

Activation of autoreactive T cells that express particular Vbeta segments

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104
Q

What is the definition of enhanced presentation and processing of autoantigens?

A

Enhanced presentation of autoantigens by APC recruited to inflammatory site, followed by priming of autoreactive lymphocytes

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105
Q

What is the definition of bystander activation?

A

Expansion of previously activated T cells at inflammatory site

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106
Q

What is the definition of activation of lymphocytes by lymphotropic viruses?

A

Viral infection of lymphocytes, such as infection of B cells with Hepatitis C virus, resulting in enhanced antibody production and formation of circulating immune complexes

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107
Q

What is a good example for molecular mimicry and MoA?

A

Rheumatic fever:| - streptococcal A antibodies bind M protein, then cross react with cardiac myosin

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108
Q

What are the types of autoimmune disease?

A

Systemic and organ specific

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109
Q

What is the definition of systemic autoimmune disease?

A

Spread throughout the body

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110
Q

What is the definition of organ specific autoimmune disease?

A

Directed towards one organ

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111
Q

What are the oral presentations of systemic lupus?

A 
Mouth ulcersFacial rash (butterfly)
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112
Q

What is TI diabetes’ mainly mediated by and what does it attack?

A

By CD4 and attacks islet cells and insulin and GAD65

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113
Q

What are the oral presentations of oral lichen planus?

A

Papular skin eruptions| Chronic desquamative gingivitis

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114
Q

What is the treatment for oral lichen planus?

A

Mouthwash

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115
Q

What is oral lichen planus’ mainly mediated by and what does it attack?

A

CD8 cells| Targeting keratinocytes

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116
Q

What is the oral presentation of TI diabetes?

A

Increased caries risk

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117
Q

What is the definition of arthritis?

A

Inflammation of joints

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118
Q

What are the symptoms of arthritis?

A

PainStiffnessSwellingFunctional impairment

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119
Q

What are the clinical signs of arthritis?

A

TendernessRestriction of movementHeatRedness

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120
Q

What is the definition of RA?

A

A chronic autoimmune systemic illness characterised by a symmetrical peripheral arthritis and other systemic features, associated with joint damage

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121
Q

Explain the classification for RA?

A 
Categories such as: - joint involvement- serology- acute phase reactants- duration of symptomsA score >6/10 is classified as having definite RA
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122
Q

What are the aetiologies for RA?

A 
Genetic:- associated with position 70-74 of DRBeta1Environmental:- smoking- chronic infection (perio disease)
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123
Q

What is the pathology of RA?

A

Synovitis:- bone erosion- swollen and inflamed synovial membrane- inflamed synovium- inflamed joint capsule- destruction of cartilage- long term joint damage

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124
Q

What test to request to identify if a patient has RA?

A

Anti-cyclic citrullinated antibodies test (ACPA)| MRI to identify inflammation

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125
Q

If patient has arthritis, what should you ask about?

A

Where specifically the arthritis is?| If neck, be careful during extra-oral and intra-oral examinations, as neck is very tender

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126
Q

What are the non-specific features of systemic RA?

A

FatigueWeight lossAnaemia

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127
Q

What are the specific features of systemic RA?

A

Mouth, eyes, lungs, nerves, skin and kidneys

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128
Q

What are the long term features of systemic RA?

A

CV disease| Malignancy

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129
Q

What is a good website to assess a patient’s disease score? What are the score ranges?

A

das28.comDAS < 2.4 represents clinical remissionDAS > 5.1 eligibility for biologic therapy

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130
Q

What are the 4 therapeutic categories for the treatment of RA?

A

NSAIDsDisease modifying anti-rheumatic drugsBiologicsCorticosteroids

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131
Q

What is the definition of Disease modifying anti-rheumatic drugs (DMARD)?

A

A group of structurally unrelated, typical small molecule drugs which have demonstrated to have a slow onset effect on disease activity and retard disease progression, but have been associated with toxicity profiles and risk of occasional serious adverse events

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132
Q

Name 4 examples of DMARDs for RA?

A

MethotrexateSulfasalazineHydroxychloroquineLeflunomide

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133
Q

What is the approach for management and treatment of RA?

A

Early and aggressive intervention is key to obtaining optimal outcomesEffective suppression of inflammation

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134
Q

Why is methotrexate the golden standard?

A 
Effective Well-toleratedCheapPeople stay on itCan be combined with DMARD or biologics
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135
Q

What is the definition of biologic DMARDs?

A

Large complex proteins which need to be given via injection, they work rapidly and are well tolerated but with important toxicities

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136
Q

Name 6 biologic DMARDs for RA?

A

TNFa inhibitors (first line)IL-1/6 inhibitorsAnti B/T cell therapiesOral kinase inhibitors

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137
Q

What are the side effects of biologic DMARDs?

A

Injection site reactionInfectionPossible malignancy

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138
Q

When can you use corticosteroids for RA?

A

Short term| In combination with other treatments for RA

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139
Q

What are the outcomes for RA sufferers?

A

50% will be unable to work due to disability within 10 years of diagnosisIncreased number of sick days75% of cases diagnosed during working life

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140
Q

Where to position the blood pressure cuff on the arm?

A

It should be over the brachial artery, above the elbow| Place the stethoscope on the artery to listen for sounds

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141
Q

What are the key Korotkoff sounds?

A

I: artery just opening after reliving of some pressure - SYSTOLICV: silent artery, artery fully open - DIASTOLIC

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142
Q

Process of measuring blood pressure?

A
  1. Place tourniquet over the brachial artery, above the elbow - line on tourniquet should line up with the brachial artery2. Place stethoscope over arteryInflate tourniquet until the artery is fully occluded3. Behind to deflate the tourniquet slowly and once the first sound is heard record the pressure value - this is the systolic pressure4. Continue to release the pressure from the tourniquet, until the artery is fully open and the sound has become silent - this is the diastolic pressure
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143
Q

How should the patient be positioned?

A

Arm on table| Level with heart

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144
Q

What is the definition of osteoporosis?

A

Low bone mass and microarchitectural deterioration of bone tissue

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145
Q

What are the risk factors for osteoporosis?

A

Rheumatic diseaseMalabsorptionEndocrineMedication

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146
Q

What is the absorption and T1/2 of bisphosphonates?

A

Very poor intestinal absorption50% goes to skeleton, rest excreted via kidneyLong skeletal retention, with T1/2 of 10 years

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147
Q

What are bisphosphonates?

A

Pyrophosphate analogues| 2 phosphates linked to C

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148
Q

What is the function of bisphosphonates?

A

Prevent loss of bone density and decrease risk of fractures

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149
Q

How do bisphosphonates work?

A

Stimulate osteoclast apoptosis and inhibit cholesterol synthesis pathwayThis decreases osteoclast numbers and decrease bone resorption

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150
Q

Chemically, how are 2nd and 3rd generation bisphosphonates different?

A

2nd: N side chain3rd: N heterocyclic ring

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151
Q

Name 3 2nd generation bisphosphonates?

A

AlendronateIbrandronatePamidronate

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152
Q

Name 2 3rd generation bisphosphonates?

A

Risedronate| Zoledronate

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153
Q

What is the definition of Medication Related Osteonecrosis of the Jaw (MRONJ)?

A

It is defined as exposed bone, or bone that can be probed through an intraoral or extraoral fistula, in the maxillofacial region that has persisted for more than eight weeks in patients with a history of treatment with anti-resorptive or anti-angiogenic drugs, and where there has been no history of radiation therapy to the jaw or no obvious metastatic disease to the jaws.

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154
Q

What are the systemic risk factors for MRONJ?

A 
GeneticsDiseaseAgeObesityAlcoholSteroid therapyTobaccoSex
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155
Q

What are the medication related risk factor?

A

Total dose| Length of treatment

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156
Q

What are the local factors related to risk factors?

A

MicrotraumaInflamm diseaseOral surgeryOral implantology

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157
Q

What is the pathogenesis of MRONJ?

A 
Inflamm/infectionMicrotraumaAltered bone remodelling or over suppression of bone resorptionANgiogenesis inhibitionSoft tissue BPs toxicityPeculiar biofilm of the oral cavityterminal vascularisation of the mandibleSuppression of immunityVit D deficiency
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158
Q

Risk assessment for MRONJ?

A

No risk - if no medsLow risk - if on meds but not previous diagnosisHigher risk - if on meds for <5 years

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159
Q

Dental advice for a patient with MRONJ?

A 
Healthy diet and reducing sugary snacks and drinksExcellent oral hygieneFl toothpaste and mouthwashStop smokingLimit alcoholRegular dental check ups
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160
Q

What symptoms should an MRONJ patient report to the dentist?

A 
Exposed boneLoose teethNon-healing sores or lesionsPusTinglingNumbness or altered sensationsPainSwelling
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161
Q

What are the treatments for established MRONJ?

A

SurgicalGentle debridement (best)Avoid resectionRemove sequestra

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162
Q

What is a medical management for MRONJ?

A

Teriparatide

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163
Q

Why is stroke relevant to dentists?

A

Seeing older patientsA link between oral health and risk of strokeOH poor after stroke

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164
Q

Risk factors at the dentists for stroke?

A

Invasive treatments

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165
Q

When do most strokes occur across the population?

A

75% over the age of 65

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166
Q

What fraction of patients die within 1 year after their stroke?

A

1/2

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167
Q

What percentage of stroke survivors become dependent on others?

A

50%

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168
Q

How many strokes does the UK have per year?

A

150,000

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169
Q

How much does stroke cost the the NHS?

A

8bn

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170
Q

What is the definition of stroke?

A

It is the sudden onset of focal neurological symptoms caused by ischemia or hemorrhage and lasting more than 24hrsMost strokes are ischaemic

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171
Q

What is the difference between a stroke and a TIA?

A

Symptoms usually resolve within 24hrs (usually an hour)

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172
Q

What is the definition of a hemorrhagic stroke?

A

Blood leaks into brain tissue

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173
Q

What’s the definition of an ischaemic stroke?

A

Clot stops blood supply to an area of the brain

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174
Q

What are the vessels of the anterior supply to the brain?

A

Common carotid

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175
Q

What are the vessels of the posterior supply to the brain?

A

Vertebral arteries

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176
Q

What do the vertebral arteries form?

A

Basilar artery

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177
Q

What does the basilar artery form?

A

Posterior cerebral artery

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178
Q

What does the internal carotid artery form?

A

Middle cerebral artery

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179
Q

What does the middle cerebral artery form?

A

Anterior cerebral artery

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180
Q

How is the posterior and anterior blood supplies of the brain connected?

A

Posterior communicating artery

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181
Q

What does the carotid system of the brain supply?

A

Most of the hemispheres and cortical deep white matter

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182
Q

What does the vertebrobasilar system of the brain supply?

A

Brain stem, cerebellum and occipital lobes

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183
Q

What is the function of the frontal lobe?

A

Judgement, foresight and voluntary movement| Smell

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184
Q

What is the function of the motor coretx?

A

Movement

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185
Q

What is the function of the sensory coretx?

A

Pain, heat and other sensations

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186
Q

What is the function of the parietal lobe?

A

Comprehension of language

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187
Q

What is the function of the temporal lobe?

A

Hearing| Intellectual and emotional functions

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188
Q

What is the function of the Occipital lobe?

A

Primary visual area

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189
Q

What is the function of the Wernicke’s area?

A

Speech comprehension

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190
Q

What is the function of the cerebellum?

A

Coordination

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191
Q

What is the function of the Brain stem?

A

Swallowing, breathing, heartbeat, wakefulness centre and other involuntary functions

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192
Q

What is the function of the Broca’s lobe?

A

Speech

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193
Q

What would occur of there is a small stroke in the deep white matter?

A

Major deficit as the fibres are packed closely together

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194
Q

What are the signs and symptoms of stroke?

A 
Motor: clumsy or weak limbsSensory: loss of feelingSpeech: dysarthria/dysphagiaNeglect/visuospatial problemsVision: loss in one eye or hemianopiaHaze palsyAtaxia/vertigo
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195
Q

What does the posterior circulation supply?

A

PonsMidbrainHindbrainCerebellum

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196
Q

What are the stroke symptoms that may arise from the posterior circulation?

A 
AtaxiaVertigoNystagmusLoss of consciousness (thrombus in basilar artery)Cardiorespiratory control
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197
Q

What are some conditions that present similar symptoms to stroke?

A 
MigraineEpilepsyStructural brain lesionsMetabolic disordersvestibular disorderPsychological disordersDemyelinationMononeuropathy
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198
Q

Name 4 causes for a stroke?

A

Carotid stenosisCarotid diseaseAtrial fibrillationLacunar stroke (small vessel)

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199
Q

Name 2 rare causes for a stroke?

A

Foramen ovale hole (PFO)| Carotid dissection

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200
Q

Name 4 non-modifiable risk factors for stroke?

A

Previous strokeAgeMaleFamily history

201
Q

What is the most important modifiable risk factor for stroke?

A

Hypertension

202
Q

Name 5 other modifiable risk factors for stroke?

A 
Diabetes (3x)Smoking (2x)LipidsAlcoholObesity
203
Q

Over 1 minute of large vessel ischaemic stroke what can a patient lose?

A

1.9 million neurons13.8 billion synapses12km of axonal fibres

204
Q

What is the acronym of FAST?

A

Facial weaknessArm weaknessSpeech problemsTime to call 999

205
Q

What the the immediate management for stroke?

A

Thrombolysis for patients if they present within 4.5 hours| Thrombectomy

206
Q

What is the early management protocol for stroke?

A

Concentrates on:- swallowing- fluids and oxygen- early therapy involvement- good nursing care- aspirin (may wait 24hrs)

207
Q

What is the best thing for someone to do for a person experiencing a stroke?

A

Get them to a hospital as fast as possible| Increases the chance of survival and reduce damage

208
Q

What is the definition of clot retrieval?

A

Enter the artery in the arm| Tip penetrates clot and suctions it out

209
Q

Name the investigations carried out to confirm the diagnosis for a stroke?

A 
CT or MRI scan:- exclude haemorrhage- exclude tumour- define lesionCarotid doppler if anterior circulation signsEcho:- to exclude cardiac cause
210
Q

Why is secondary prevention essential for stroke survivers?

A

7% of patient having a TIA with have another within 1 month20% of stroke survivors will have another within 5 yearsMany de of cardiovascular events

211
Q

Name 5 secondary prevention techniques for stroke survivors and TIAs?

A 
Anti-hypertensivesAnti-plateletsLipid lowering drugswarfarin or DOACSCarotid endarterectomy
212
Q

Why do stroke patients have more oral problems?

A

Nil by mouth| Unable to brush teeth due to physical and swallowing problems

213
Q

Name 6 types of cardiovascular diseases?

A 
AnginaMIHeart failureTransient ischaemic attackThrombotic strokeAtrial fibrillation
214
Q

What is the basic process of the formation of a atherosclerotic vessel??

A

Damage to the vessel wallActivation of platelets and inflammatory cells for abnormal healingIncorporation of cholesterol forming a fibrous cap

215
Q

What can cause damage to the vessel walls?

A

DiabetesHypertensionSmoking

216
Q

What drug groups can be used to reduce wall stress?

A

Beta blockersRenin-angiotensin systemCa blockers

217
Q

Why do we use beta blockers to reduce vessel wall stress?

A

Reduces mortality in IHD and HFReduces symptoms in angina, AF and SVTAnti-hypertensive

218
Q

Name 3 examples of beta blockers?

A

Atenolol (B1)Metoprolol (B1)Propranolol (B1/2)Bisoprolol (B1)

219
Q

Where are Beta 1 receptors found?

A

Aim for beta blockersHeartKidneys: reduce renin release

220
Q

What is the function of beta 1 receptors when activated?

A

Slows HR and conduction (negative chronotropic)Increases diastolic time, reduces BPReduces contractility (negative inotropic)

221
Q

Where are beta 2 receptors found?

A

SM| Skeletal muscle

222
Q

What is the function of beta 2 receptors when activated?

A

Reduces tremor| Lethal bronchospasms for asthmatics, vasoconstriction and PVD

223
Q

What are dental implications or beta blocker use?

A

Protects heart from deleterious effect of adrenaline| Can disguise physiological signs of significant blood loss

224
Q

Why do we use ACE inhibitors and angiotensin receptor antagonists to reduce stress in vessel walls?

A

Reduce mortality and progression of disease in IHD, CVD and renal disease with proteinuriaPrevent aberrant remodeling following MI (reduce aneurysm formation)Reduction in HF symptoms

225
Q

Explain the renin-angiotensin system?

A

Angiotensinogen produced by liverANG converted to ANG I by renin released from kidney in response to reduction in perfusion pressureANG I converted to ANG II by ACE secreted by the lungsANG II acts on adrenals leading to the release of aldosterone

226
Q

What is the function of ANG II?

A

Potent vasoconstrictor:- peripheral vasc- efferent arteriole of the glomerulus

227
Q

What is the function of aldosterone?

A

Retention of NA at the expense of K in the DCT of the kidney

228
Q

Name 3 examples of ACE inhibitors?

A

RamiprilCaptoprilLisinopril

229
Q

What are the positive effects of ACE inhibitors?

A

Reduce BPReduce afterload on heartPrevents aberrant remodelling after MIReduces proteinuria

230
Q

What are the negative effects of ACE inhibitors?

A

Reduces perfusion pressure in glom| Cough

231
Q

Name 2 examples of Angiotensin II receptor blockers?

A

Losartan| Candesartan

232
Q

What are the positive effects for Angiotensin II receptor blockers?

A

Reduce BPReduce afterload on heartPrevents aberrant remodelling after MIReduces proteinuria

233
Q

What are the negative effects for Angiotensin II receptor blockers?

A

Reduces perfusion pressure in glom

234
Q

What are dental implications ACE inhibitors and ARBs?

A

What NSAIDs to prescribe| Avoid if taking ACE inhibitor or has IHD, CVD or heart disease

235
Q

Name 2 examples of aldosterone anatgonists?

A

Spironolactone and eplerenone

236
Q

Why do we use aldosterone antagonists to reduce stress in vessel walls?

A 
Used in HFSpiro used for HT:- enhanced diuretic effect- reduces mortality in IHD and HF- NSAIDs may be a big NO
237
Q

Why do we use Ca channel blockers to reduce stress in vessel walls?

A

Antihypertensive agent| Reduce symptoms for Angina, AF and SVT

238
Q

Name the 2 types of Ca channel blockers?

A

Dihydropyridine| Non-dihydropyridine

239
Q

What is the mechanism of action of dihydropyridine Ca channel blockers and name 2 examples?

A

Block Ca entry into SMLess effect in myocardial pacemaking tissuesAmlodipineFelodipine

240
Q

What is the mechanism of action of non-dihydropyridine Ca channel blockers and name 2 examples?

A

Block CA entry into SMBlocks Ca entry into myocardial pacemaking tissue slow SA and AV conductionVerapamilDiltiazem

241
Q

What are dental implications for Ca channel blockers?

A

Gingival hypertrophy:- specifically with dihydropyridine- poor OH and gingival inflamm as a risk factor (nifedipine and amlodipine)- Common in males and older generation- Not permanent (solve OH and stop taking drug)

242
Q

What drug targets the ADP receptor? (as an antagonist?)

A

ClopidogrelPrasugrelTicagrelor

243
Q

What drug targets phosphodiesterase (as an inhibitor?)

A

Dipyridamole

244
Q

What drug targets fibrinogen receptor (as a blocker?)

245
Q

What drugs target COX I?

A

Aspirin| NSAIDs

246
Q

What drug targets the thrombin receptor? (as an inhibitor)?

A

Vorapaxxar

247
Q

What are dental implications anti-platelet drugs?

A

Interactions with NSAIDs:- potent COX inhibitors- increased bleeding risk (GI)

248
Q

Why do we use Statins to reduce stress in vessel walls?

A

Primary: reduce cardiovascular risk if patient’s 10 year risk >20%Secondary: after cardio event

249
Q

What is the chemical name for a statin?

A

Hydroxy-methyl-glutaryl CoA reductase inhibitor (HMGCoA)

250
Q

Name 3 examples of statins?

A

SimvastatinRosuvastatinAtorvastatin

251
Q

What are dental implications for statins?

A

Clarithromycin contraindicated with simvastatin and increases risk of myositis (muscle aches and pains)

252
Q

Why do we use diuretics to reduce stress in vessel walls?

A

Antihypertensive effectPromote Na and water loss in kidneyReduce total contentReduce BP

253
Q

Name 2 examples of thiazide diuretics?

A

Indapamide| Bendroflumethizide

254
Q

Name 2 examples of loop diuretics and their indication?

A

FurosemideBumetanideFor HF

255
Q

What are dental implications for diuretics?

A

Nephrotoxic effect in combo with NSAIDs

256
Q

Why do we use anti-coagulants to reduce stress in vessel walls?

A

Primary or secondary prevention in CVD associated AF

257
Q

Name 2 examples of Vit K antagonists?

A

Warfarin| DOACs

258
Q

What are dental implications for anticoagulants?

A 
Enhanced effect: Inhibition of cP450:- clarithromycin, azoles and antifungalsReduced effect:Induction of cP450- rifampicin
259
Q

Name 1 antianginal? and its implication for dentistry?

A

Nicorandil| Can cause ulceration

260
Q

Name 2 antiarrhythmics? and its implication for dentistry?

A

Digoxin| Amiodarone - theoretically reduces toxic dose of lignocaine

261
Q

What occurs during immediate response to injury?

A

Attempts to maintain tissue structure/functionMinimise deleterious effects of injuryOverlaps with the inflammatory process

262
Q

What is the definition of regeneration?

A

Replaces damaged cells with new cellsLeaves no trace of injuryTissue requires ongoing mitotic activity

263
Q

What is the definition of repair?

A

Replaces damaged cells with fibrous CTLeaves permanent scarOccurs in non-mitotic tissues and with more severe injuries

264
Q

What is the definition of stromal regions?

A

Support tissue:- CT, ECM, BVs and nervesNon-mitotic

265
Q

What is the definition of parenchymal tissues?

A

Functional cells of organsHighly specialisedHepatocytes and kidney tubular cellsMitotic cells

266
Q

What is the definition of a labile cell?

A

Continuous division| Often exposed to damage/abrasion and need constant replacement

267
Q

Name 4 examples of labile cells?

A

SkinOral cavityGI tractUterus

268
Q

What is the definition of stable cells?

A

Division stops when growth is complete| Still has potential for division (regen)

269
Q

Name 3 examples of stable cells?

A

HepatocytesKidney tubular cellsSM cells

270
Q

What is the definition of fixed cells?

A

Incapable of mitotic divisionIf damaged they are replaced by fibrous scar tissuesScar lacks any functional capacity

271
Q

Name 3 examples of fixed cells?

A

Nerve cellsSkeletal muscles cellsCardiac muscle cells

272
Q

What is the definition of inflammatory mediators?

A

Released by WBCs such as monocytes and macrophages

273
Q

Name 6 examples of inflammatory mediators?

A 
TNF-aILInterferonsArachidonic acidLeukotrienesProstaglandins
274
Q

What is the function of inflammatory mediators?

A

Coordinate:- blood clotting (initial vasoconstriction)- recruit immune cell infiltration (delayed vasodil- phagocytosis of debris and bacteria- new cell growth and fibroblast infiltration- angiogenesis

275
Q

What is the definition of growth factors?

A

Released by fibroblasts, macrophages and endothelial cells

276
Q

Name 5 examples of GFs?

A 
PDGFFGFEGFVEGFTGF
277
Q

What is the function of GFs?

A

Coordinate:- inflammatory response - chemotaxis- proliferation and differentiation- generation of ECM- angiogenesis

278
Q

What GF related function do fibroblasts, macrophages, epithelial cells and neutrophils allow?

A

ChemotaxisProliferationDifferentiationProduce ECM

279
Q

What is the definition of the ECM?

A

Locally secreted milieu that surrounds and supports the cells in 3D

280
Q

Name the 3 different types of ECM composition?

A

StructuralWater-hydrated gelsAdhesive glycoproteins

281
Q

What is the function of fibrous ECM? and examples of them?

A

Scaffolding of ECM provides framework and tensile strengthCollagenElastin

282
Q

What is the function of water-hydrated gel ECM? and examples of them?

A

Provides lubrication, resilience and flexibilityProteoglycanshyaluronic acid

283
Q

What is the function of adhesive glycoprotein ECM? and examples of them?

A

Provide cohesion between matrix components and cellsFibronectinLaminin

284
Q

What are the 2 different forms of ECM?

A

Basement membrane| Interstitial matrix

285
Q

What is the definition of basememnt membrane?

A

ECM sheet that epithelial, endothelial and SM cells lie onPhysical/chemical barrierGiving structural support and strength

286
Q

What is the definition of interstitial matrix?

A 
Found between cells within tissueAbundant and consistency varies(nerves sparse but bone dense)Provides adherence (like glue)Also protects against tissue compression
287
Q

How does the ECM aid in tissue repair?

A

Help regulate cell prolif, diff and movementContains regulatory molecules for repairPrived a tissue framework for repair/regenHowever, repairing damaged tissue needs largely intact ECM

288
Q

What occurs in tissue repair if the ECM is excessively damaged?

A

Impaired controlDisorganisationCausing delayed or dysregulated repair

289
Q

What are the 3 key phases for wound healing?

A

InflammatoryProliferativeRemodelling

290
Q

What is the initial phase of wound healing?

A

InjuryStop bleeding via vasoconstrictionPlatelet activation and aggregation forming a fibrin clot

291
Q

What occurs during the inflammatory phase of wound healing?

A

Vasodilation and increased vessel permeabilityThis recruits plasma and WBCs to the wound siteNeutrophils and macrophages ingest debris and fibrinNeutro secrete GFs to attract other immune cellsMacrophages secrete GFs and stimulate angiogenesis0-2 days

292
Q

What occurs during the proliferative phase of wound healing?

A 
Macrophage GFs stimulate:- continued angiogenesis- influx and activation of fibroblastsFibroblasts:- variety of ECM components- secrete GFs to activate angiogenesis or further fibroblasts recruitment- this forms the granulation tissue2-21 days duration
293
Q

What is the defintion of granulation tissue?

A

Precursor to scar tissueMoist, red CT and develops into a mature scarProvides a framework for scar formation

294
Q

What is the process of angiogenesis during granulation tissue formation?

A

Growth of new capillary buds from existing vesselsVisible at wound surfaceeventually from new vasculatureProvide blood supply

295
Q

What is the process of fibrogenesis during granulation tissue formation?

A

Influx/activation of fibroblasts secrete:- hyaluronic acid and fibronectin (loose ECM)- then proteoglycans (local oedema and moistness)- finally collagen (progression to mature scar)

296
Q

What occurs during the late proliferative phase?

A

Inflammation no longer apparentFibroblasts persit producing collagen and strength the ECMGranulation tissue migrates upwards leaving scar behind (scar avascular)Upper epithelial layer proliferates, using granulation tissue as matrixSeals wound with new epithelialSome cell division replaces keratinocytes and epiderma strata

297
Q

What occurs during the remodelling phase?

A

Fibroblasts continue to secrete collagen ALso secrete collagenase:- breakdown collagen fibres- prevents wound separation- remodels, shrinks and re-oriented scarScar contracts inwards (contractile fibroblasts)

298
Q

What are the characteristics of mature scar tissue?

A 
Forms from granulation tissueFormed during late proliferative phasePale (few BVs)Quiescent, spindle fibroblastsDense collagenElastic fibresWound site filled in
299
Q

How does regeneration differ to repair?

A 
May show different profile of GFsFewer fibroblasts and less ECM fill inGreater emphasis on division of regenerating cellsMinor scarMore function
300
Q

What factors influence healing?

A

InfectionSeparationForeign bodiesAffected by extent of injury and tissue loss

301
Q

What factors are required for healing?

A 
NutritionO2Blood flowImmune functionInflammatory function
302
Q

Difference between primary intention and secondary intention?

A

Primary is minor damage| Second is major damage

303
Q

What is included on a Full Blood Count (FBC)?

A 
Red cells (description of cells)White cells (+subtypes)Platelets
304
Q

How to send a FBC?

A

EDTA sample to haematology lab

305
Q

Describe the structure of a neutrophil?

A

Multi-lobed nucleus| Granular cytoplasm

306
Q

Describe the structure of a eosinophil?

A

Multi-lobed and granular| Increased in allergy, inflamm and myeloproliferative disease

307
Q

When are basophil found in the blood, in response to?

A

Increased in allergy and myeloproliferative disorders

308
Q

Describe the structure of a monocyte?

A

Larger| Lobulated nuclei

309
Q

What to double check if platelets are very low?

A

Check for platelet clumping on the blood count

310
Q

Male Hb reference range for 12-70 yo?

A

140-180 g/L

311
Q

Male Hb reference range for >70 yo?

A

116-156 g/L

312
Q

Female Hb reference range for 12-70 yo?

A

120-160 g/L

313
Q

Male Hb reference range for >70 yo?

A

108-143 g/L

314
Q

What is the definition of anaemia?

A

Reduction in red cells or their haemoglobin content

315
Q

Name 4 causes of aneamia?

A

Blood lossIncreased destructionLack of productionDefective production

316
Q

Describe the signs and symptoms of anaemia?

A

Tiredness/FatigueDizziness/LightheadednessBreathlessness (on exertion)Chest painsPaleGlossitisAngular stomatitisKoilonychia (spoon-shaped nails)Due to oxygen deprivation

317
Q

What does MCV stand for?/

A

Mean cell volume (cell size)

318
Q

What does MCH stand for?

A

Mean cell haemoglobin

319
Q

Diagnosis for Low MCV and MCH and and a further test?

A

Hypochromic microcyticTest for Serum ferritin (low)

320
Q

Diagnosis for Raised MCV and a further test?

A

MacrocyticTest for B12/Folate and bone marrow (low)

321
Q

Name 4 causes of hypochromic microcytic anaemia?

A 
Blood lossIncreased requirementsReduced intakeNormal ferritin (Thalassaemia)Anaemia of chronic disease
322
Q

Name 4 causes of macrocytic (megaloblastic) aneamia?

A 
B12:- autoimmunity (pernicious anaemia)- binds to intrinsic factor which has autoantibodies against them- gastric diseaseFolate:- dietary- malabsorption- increased requirementsMyelodysplasiaLiver diseaseDrugsAlcoholThyroid disease
323
Q

Diagnosis for normal MCV and MCH and a further test?

A

Normochromic normocytic anaemia| Reticulocyte count

324
Q

Diagnosis for a low/normal reticulocyte count?

A

Marrow replacementHypoplasia(secondary anaemia)

325
Q

Diagnosis for a increased reticuloycte count?

A

Acute blood loss| Haemolysis

326
Q

Describe what occurs for haemolytic anaemia?

A

Accelerated red cell destructionCompensation by BM (increased reticulocytes)Level of Hb balance between red cell production and destruction

327
Q

How long does a RBC last in the circulation?

328
Q

How are RBCs broken down?

A

By the reticuloendothelial system

329
Q

What are RBCs broken down into?

A

GlobinIronProtoporphyrin

330
Q

What does globin get converted into?

A

Amino acids

331
Q

What does iron get converted into?

A

Binds to transferrin

332
Q

What does protoporphyrin get converted into?

A

BilirubinTransported to liverBound to glucuronidesExcreted in urine as urobilinogen or in the faeces as stercobilinogen

333
Q

Name 3 types of congenital haemolytic anaemia and tests for their diagnosis?

A 
Hereditary spherocytosis (HS)Enzyme deficiency (G6PD)Haemoglobinopathy (HbSS)
334
Q

Name the acquired types fof haemolytic anaemia?

A

Autoimmune haemolytic anaemia (extravascular)

335
Q

Name 3 intravascular acquired types of haemolytic anaemia?

A

Mechanical (valve)Severe infectionPET/HUS/TTP

336
Q

Describe the signs and symptoms of haemolytic anaemia?

A

Jaundice| Yellow sclera

337
Q

Explain the mechanism of action for Warfarin?

A

Orally active vitamin K antagonistReduces functional factors II, VII, IX and XMonitored by INR

338
Q

Indications for Warfarin?

A

Atrial fibrillationProsthetic heart valvesOther arterial thromboembolismVenous thromboembolism

339
Q

What are the disadvantages for warfarin?

A 
Wide individual variation in dose to achieve target INRHigh drug intersDietary inters (vit K rich food)Fatal bleeding 1% per year
340
Q

What is warfarin target enzyme and what is it metabolised by?

A

Vit K epoxide reductase| P450

341
Q

What is warfarin target INR?

A

2.0-3.0Can go up to 3.0-4.0In therapeutic range for 60%

342
Q

What are the considerations a dentist must take when a patient on warfarin attends the surgery for an extraction?

A

INR <4.0 dental procedures are allowedOxidised cellulose, collagen sponges and sutures can be considered5% tranexamic acid mouthwash for 2 days can be consideredAvoid NSAIDsIANB - anecdotal risk of bleeding with airway compromise (INR >3.0)Single dose antibiotic prophylaxis unlikely to affect INR

343
Q

Name the immediate and gradual reversal of warfarin?

A

Immediate:- coagulation factor concentrate (II, VII, IX and X), IntravenousGradual:- vitamin K, PO/IV

344
Q

Explain the mechanism of action for heparin?

A

Inhibits thrombin and F Xa indirectly

345
Q

Indications for heparin?

A

Prophylaxis of venous thrombosisTreatment of arterial and venous thrombosisNeed interruption of treatment at least 24hrs pre procedure

346
Q

Describe what the ideal antithrombotic drug should do?

A 
Orally activePredictable dose-responseNo monitoring requiredMinimal drug intersminimal effect of diet
347
Q

Name 3 new Anti-Xa oral anticoagulants?

A

Rivaroxaban (3A4 and 2J2)Apixaban (3A4)Edoxaban (3A4)

348
Q

Name 1 new antithrombin oral anticoagulant

A

Dabigatran

349
Q

Explain the mechanism of action for Dabigatran?

A

Inhibits thrombinMetabolised in the liverExcreted via the kidneys

350
Q

Explain the mechanism of action for new Anti-Xa anticoagulants?

A

Metabolised by the Liver| Excreted via faeces and kidney

351
Q

What to suggest to patients on DOACS for a low and high bleeding risk procedures?

A 
Low:- treat without interruptionHigh:- omit dose on morning of procedure- omit for longer (48/72) if have renal disease
352
Q

Explain the mechanism of action for aspirin?

A

Irreversible inhibitor of platelet COXreduce platelet aggregabilityImpairs primary haemostasis

353
Q

Explain the mechanism of action of Clopidogrel/Ticagrelor/Prasugrel?

A

Block the platelet ADP receptor (P2Y12)

354
Q

Explain the mechanism of action of dipyridamole?

A

Blocks platelet phosphodiesterase and adenosine deaminase

355
Q

Indications for aspirin?

A

For secondary prophylaxis of arterial thrombosisUsed in combo with:- dipyridamole in stroke- clopidogrel after coronary intervention- rivaroxaban in peripheral/coronary artery disease

356
Q

How long do aspirin’s effects last for?

357
Q

How long do clopidogrel effects last for?

A

over 5 days

358
Q

What should you advice to a patient taking anti-platelet drugs for a extraction?

A

Treatment should be fine without interruption of drug as the risk/benefit to stopping the drug is much higher risk

359
Q

Name the 2 causes of reduced survival for thrombocytopenia?

A

Immune thrombocytopenic purpura| Drug induced

360
Q

Name the 5 causes of reduced production for thrombocytopenia?

A 
ChemotherapyBone marrow malignancy/failureMegaloblastic anaemiaDrug inducedAlcohol excess
361
Q

What is the normal platelet count?

A

> 140 x10^9/L

362
Q

What is the mild thrombocytopenia platelet count?

A

80-140 x10^9/L

363
Q

What is the moderate thrombocytopenia platelet count?

A

20-80 x10^9/LIncreased bleeding after trauma

364
Q

What is the severe thrombocytopenia platelet count?

A

<20 x10^9/LSevere bleeding after trauma

365
Q

Platelet count threshold for simple elective procedures?

366
Q

Platelet count threshold for simple extraction?

367
Q

Platelet count threshold for complex extraction?

368
Q

Platelet count threshold for LA?

A

> 30| Avoid IAN

369
Q

Platelet count threshold for Minor oral surgery?

370
Q

Platelet count threshold for major oral surgery?

371
Q

Describe Immune thrombocytopenic purpura?

A 
AutoimmuneAgainst plateletsTriggered by infection or medsVariable severityResponsive to immunosuppressants or splenectomy
372
Q

What coagulopathy are associated with liver disease?

A

All clotting factors and fibrinogen are reduced| Enlarged spleen due to portal hypertensions leads to thrombocytopenia

373
Q

Reduced clotting factor + thrombocytopenia = ?

374
Q

Reduced natural anticoagulants = ?

A

Thrombosis

375
Q

How to manage patients with liver disease?

A

Striking balance between preventing bleeding and thrombosis| Often avoid replacement of clotting factors unless hemorrhagic

376
Q

Signs and symptoms of acquired haemophilia?

A

New onset bruisingNo previous bleeding disorder historyIsolated prolonged APTT and low levels of VIIIAntibody to VIII

377
Q

Management of acquired haemophilia?

A 
Bypassing agents (Novoseven) to control bleeding episodesImmunosuppression with high dose steroid (+/- cyclophosphamide)Refractory cases may require B cell depletion with Rituximab
378
Q

Vitamin C deficiency can cause acquired bleeding disorder?

A 
YesCofactor in collagen synthesisRequire 40mg dailySmokers need moreCan lead to scurvy
379
Q

Signs and symptoms of scurvy?

A 
Normocytic anaemiaBleeding with normal platelets and coagulationSkin and gum changesHigh risk:- alcoholics - malignancy
380
Q

What are the risk factors for essential hypertension?

A 
ObesityAlcoholSalt intakeStressGenetics
381
Q

What is the definition of secondary hypertension?

A

Due to other diseases such as kidney dysfunction or hormonal disturbances

382
Q

Explain how to manage a patient with high BP?

A

Weight lossLow salt dietModeration of alcohol intakeIf risk too high pharmacological measures are indicated

383
Q

Blood pressure value to be diagnosed with hypertension?

A

> 160/100 mmHgTreatment

384
Q 
Blood pressure value to be diagnosed with borderline hypertension (High CV risk)?
A

140-159/90-99 mmHgTreatment

385
Q 
Blood pressure value to be diagnosed with borderline hypertension (High CV risk)?
A

140-159/90-99 mmHgLifestyle changes

386
Q

What is the definition of postural hypotension?

A

Where one’s BP falls on standing up with subsequent brief loss of consciousnessThis is especially seen when a patient gets up from the dentist’s chairCan be further exacerbated with the use of sedation during dental procedures

387
Q

What antihypertensive drug causes gingival overgrowth?

A

Some Ca channel blockers such as nifedipine

388
Q

What BP reading will make dental treatment not suitable?

A

180/110 mmHg

389
Q

What recommendations would you give to a hypertensive patient needing a dental procedure in the future?

A

hypertensive patients take their medication on the day of the dental procedure and have their BP checked a few minutes following injection. Always seek medical advice where there is any concern.

390
Q

What is the definition of stable angina?

A

Angina is a temporary obstruction of blood flow to the heart, with no associated damage to the myocardium. This typically presents as chest pain radiating to the jaw or left arm that resolves within minutes.Where pain occurs with exercise, this is known as ‘stable angina’.

391
Q

What is the definition of unstable angina?

A

Where pain is experienced at rest or on minimal exertion, this is ‘unstable angina’.

392
Q

What is the definition of ischaemic heart disease?

A

Occurs when there is inadequate blood supply and, hence, oxygen supply to the heart muscle.

393
Q

What is the definition of myocardial infarction?

A

Myocardial infarction is a complete obstruction of blood flow to the myocardium leading to muscle death. This presents as angina-like pain that is more severe and persistent and is associated with nausea, vomiting and shortness of breath. The patient is often pale and clammy

394
Q

What are the risk factors for Ischaemic heart disease?

A

AgeGenderGenetics

HypertensionHigh cholesterolDiabetesObesityExcess alcohol consumption
395
Q

Explain the development of an atherosclerotic plaque in a coronary artery?

A

Develop at sites of pre-exisiting arterial wall damage caused by hypertension smoking or high blood cholesterolFatty plaques become large enough to occlude vesselPlaque also promotes thrombus development leading to complete occlusion

396
Q

What modifiable risk factors can a patient with IHD reduce?

A 
Exercise with a balanced dietSmoking cessationBP controlDIabetes controlReduction of cholesterol
397
Q

Name 3 drugs that are indicated for MI, and angina?

A

AspirinStatinsACE inhibitors

398
Q

Describe the mechanism of action for aspirin?

A

By inhibiting circulating platelets from forming a clot, preventing obstruction of the arteries

399
Q

Describe the mechanism of action for statins?

A

Reduce LDLs| Inhibiting HMG-CoA reductase

400
Q

Describe the mechanism of action for ACE inhibitors?

A

Inhibiting the enzyme ACE

401
Q

What surgical intervention is GS for treatment of IHD?

A

Percutaneous angioplastyInsertion of a stent via a peripheral artery into a stenosed coronary arteryIf this fails, a coronary artery bypass graft can be undertaken (from patient’s leg)

402
Q

How long should treatment be avoided after an acute MI?

403
Q

What is the definition and symptoms of congestive heart failure?

A

This is the situation where the oxygenated blood pumped out from the heart is inadequate to meet the metabolic demands of the body.This mismatch can result in a variety of symptoms, the commonest being fluid retention in dependent areas such as the legs and, more significantly, in the lungs.Patients subsequently have difficulty breathing, and are unable to lie flat. They have poor exercise tolerance, also limited by difficulty breathing. In the severest form, patients are short of breath at rest and are unable to mobilise at all.

404
Q

What medications are indicated for HF and their aims?

A 
Diuretics (loop) - remove extra fluidACE inhibitors (promote cardiac function)B-blockers (promote cardiac function)
405
Q

What are the dental implications for a patient with HF?

A

Difficulty lying flat| If uncontrolled, avoided unless an emergency

406
Q

Name 2 analgesics to be wary when prescribing for a patient with kidney or liver problems?

A

NSAIDs| Opioids

407
Q

Why you need to be wary when prescribing for a patient with kidney or liver problems?

A

Dosages are metabolised at different rates due to the loss of function can exacerbate disease and have higher levels in the blood

408
Q

How can NSAIDs cause damage?

A

Direct damage to kidneys with long-term use| Cause fluid retention exacerbating HF symptoms straining the myocardium

409
Q

How can opioids cause damage?

A

Avoid morphine as liver damaged individuals can lead to drug accumulation

410
Q

What is the definition of an ECG?

A

The electrocardiograph (ECG) is a trans-thoracic interpretation of the electrical activity of the heart.

411
Q

What does the P wave represent?

A

Atrial contraction

412
Q

What does the PR interval represent?

A

Passage of electrical current between atria and ventricles

413
Q

What does the QRS complex represent?

A

Ventricular contraction

414
Q

What does the T wave represent?

A

Ventricular relaxation

415
Q

What’s the definition of a cardiac arrhythmia?

A

occur when there is an abnormality within the cardiac conduction system. They may manifest as dizziness, palpitations, collapse, shortness of breath or sudden cardiac death. There may be no symptoms at all.

416
Q

Bradycardia?

417
Q

Tachycardia?

418
Q

When can sinus bradycardia be seen?

A

Sinus bradycardia is often seen in athletes; it may also be seen in patients with hypothermia or hypothyroidism.

419
Q

When can sinus tachycardia be seen?

A

Experienced during exercise. It is also seen with fever and in hyperthyroidism.

420
Q

What is the definition of atrial fibrillation?

A

It occurs when electrical activity within the atria becomes disordered and chaotic.Consequently, the muscle fibres of the atria no longer contract in synchrony; instead they ‘fibrillate’ making the atria mechanically ineffective.

421
Q

How does AF look on an ECG?

A

Lack of P waves and by an irregularly irregular ventricular rate`

422
Q

What are the signs and symptoms for a patient presenting with AF?

A 
PalpitationsShortness of breathCollapseDIzzinessFatigue
423
Q

Name 5 conditions that can cause AF?

A 
ISHRheumatic HDHypertensionMitral valve diseaseCardiomyopathy
424
Q

How to manage a patient withAF?

A

Rhythm control:- cardioversion with shocking or amiodarone/flecainideRate control:- via b blockers (bisoprolol and digoxin)Stroke prevention:- anticoagulation such as warfarin

425
Q

What is the definition of heart block?

A

occurs when there is a delay in the conduction of electrical current as it passes through the cardiac conduction system

426
Q

What are the signs and symptoms for heart block?

A

Many symptom freeFatigueDizzinessCollapse

427
Q

Name the 2 types of heart block?

A

AV block| Bundle branch block

428
Q

What is the definition of AV block?

A

Block at the level of the AV node

429
Q

What is the definition of bundle branch block?

A

There is an abnormality lower down in the conducting system

430
Q

Name the 3 degrees of heart block?

431
Q

Describe 1st degree heart block and ECG findings?

A

when there is delayed electrical conduction to the ventricles following atrial activation. However, every impulse reaches the ventricles.Prolonged PR interval

432
Q

Describe 2nd degree heart block and ECG findings?

A

Occurs when there is intermittent block of impulses to the ventricles. The heart may beat slowly, irregularly or both.

433
Q

Name the 2 types of 2nd degree heart block?

A

Mobitz 1| Mobitz 2

434
Q

How does Mobitz 1 show via ECG?

A

Failed conduction of QRS complex due to progressive elongation of PR interval

435
Q

How does Mobitz 2 show via ECG?

A

Dropped QRS complex| 2 P waves to a single QRS complex

436
Q

Describe 3rd degree heart block and ECG findings?

A

Occurs when there is complete failure of conduction to the ventricles from the atria. Life is maintained by so called ‘escape rhythms’ generated in conducting tissue within or distal to the AV node. This results in a very slow heart rateThere is no relationship between P waves and QRS complexes and the ventricular rate is slow.

437
Q

Aetiology of First degree heart block?

A

Athletes and young patientsStructural heart disordersDrugs

438
Q

Aetiology of Second degree heart block?

A

Young peopleAthletesStructural abnormalitiesAcute myocardial infarction

439
Q

Aetiology of Third degree heart block?

A

Complete heart blockElderly (degenerative)Young patients (ischemic)

440
Q

Treatment for first degree heart block?

A

Rarely warranted

441
Q

Treatment for 2nd and 3rd degree heart block

A

Artificial pacemaker

442
Q

What is the definition of bundle branch block?

A

Occurs when there is complete or incomplete interruption to the flow of electrical current through the right or left bundle branches

443
Q

What is the difference between right and left bundle branch block?

A

Right:- healthy individuals as an isolated congenital abnormality- result from cardiac or respiratory condition- damage to heartLeft:- more severe- from IHD, aortic valve disease or secondary to chronic hypertension

444
Q

Name the 12 complications of hypertension?

A 
HaemorrhageStrokeCognitive declineRetinopathyPeripheral vascular diseaseRenal failureDialysisTransplantationLeft ventricular hypertrophyHFCHDMI
445
Q

How does IHD and stroke risk change with a 2 mmHg rise in BP?

A

7% for IHD| 10% for stroke

446
Q

At what BP is a patient hypertensive?

A

NICE: 140/90

447
Q

What is the definition of Stage 1 hypertension?

A

Clinic blood pressure is 140/90 mmHg or higher| ABPM daytime average 135/85 mmHg or higher.

448
Q

What is the definition of Stage 2 hypertension?

A

Clinic blood pressure is 160/100 mmHg or higher| ABPM daytime average 150/95 mmHg or higher.

449
Q

What is the definition of Severe hypertension?

A

Clinic systolic blood pressure is 180/120 mmHg or| higher

450
Q

Name the 7 risk factors for hypertension?

A 
Cigarette smokingDiabetesRenal diseaseMaleHyperlipidemiaPrevious MI/StrokeLeft ventricular hypertrophy
451
Q

How is BP controlled systemically?

A

By an integrated system of the| sympathetic and renin angiotensin aldosterone systems.

452
Q

What occurs during activation of the sympatheic nervous system of the heart?

A

VasoconstrictionReflex tachycardiaIncreased COAll increasing the BP

453
Q

When is the Renin-angiotensin-aldosterone system stimulated?

A

Fall in BPFall in blood volumeNa depletion

454
Q

What is the aetiology of hypertension?

A

Polygenic:- major and poly genesPolyfactorial:- environment

455
Q

Name 2 theories on hypertension aetiology?

A

Increased reactivity of resistance vessels and resultantincrease in peripheral resistance– as a result of an hereditary defect of the smooth muscle liningarterioles• A sodium homeostatic effect– In essential hypertension the kidneys are unable to excreteappropriate amounts of sodium for any given BP. As a resultsodium and fluid are retained and the BP increases

456
Q

Name 9 risk factors that contribute to hypertension?

A 
AgeGeneticsEnvironmentWeightAlcohol intakeRace Birth weightNa intake
457
Q

Name the 2 types of hypertension?

A

Primary| Secondary

458
Q

What is the definition of secondary hypertension and its causes?

A 
Caused by other diseaseRenal diseaseDrug inducedPregnancy (pre-eclampsia)EndocrineVascular (coarctation of aorta)Sleep Apnoea
459
Q

Name 4 types of renal disease that cause 2nd HT?

A

Chronic pyelonephritisFibromuscular dysplasiaRenal artery stenosisPolycystic kidneys

460
Q

Name 3 types of drug inducers of 2nd HT?

A

NSAIDsOral contraceptiveCorticosteroids

461
Q

Name 6 types of endocrine causes of 2nd HT?

A 
Conn’s Syndrome– Cushing's disease– Pheochromocytoma– Hypo and hyperthyroidism– Acromegaly
462
Q

How to accurately diagnose HT?

A

Must use ABPM Ambulatory Blood pressureMonitoring– or HBPM Home Blood pressure Monitoring

463
Q

HT risk calculator?

A

assign-score.com

464
Q

BHS target pressure to reach?

A

<135/80-85 mmHg

465
Q

Why do we treat hypertensive patients?

A

reduce cerebrovascular disease by 40-50%| – reduce MI by 16-30%

466
Q

How do we approach treatment for hypertensives?

A

Stepped approachLow doses of several drugsMinimises adverse events and maxismises patient compliance

467
Q

BIHS guidelines for young and elderly patient with HT?

A 
Young:- ACE inhibitor or ARBElderly:- Ca ch blocker- Thiazide (diuretic)
468
Q

Step 1 treatment for a HT patient?

A

<55 offer ACE inhibitor/ARBcontraindicated for afro-caribbean and women of childbearing age(avoid teratogenicity)(low renin state and a lower cardiac output, with increased peripheral resistance)

469
Q

Step 2 treatment for a HT patient?

A

Add thiazide diuretic such as indapamide to CCB or ACEI/ARB

470
Q

Step 3 treatment for a HT patient?

A

Add CCB, ACEI and diuretic together

471
Q

Name 3 ACE inhibitors?

A

RamiprilPerindoprilLisinopril

472
Q

Contraindications of ACE inhibitors?

A

Renal artery stenosisRenal failure Hyperkalaemia

473
Q

ADR of ACE inhibitors?

A 
CoughFirst dose hypotensionTaste disturbanceRenal impairmentAngioneurotic oedema
474
Q

Name 3 types of ANG II antagonists (ARB)?

A

ValsartanCandesartanIrbesartanSimilar sides and ntersNo cough

475
Q

Name 4 types of Ca ch blockers?

A 
Vasodilators:- amlodipine- felodipineRate limiting:- verapamil- diltiazem
476
Q

Contraindications of Ca ch blockers?

A

Acute MIHeart failureBradycardia (rate limiting CCBs)

477
Q

ADRs of CA ch blockers?

A 
FlushingHeadacheAnkle oedemaIndigestionReflux oesophagitis
Also cause bradycardia and constipation
478
Q

Name 2 thiazide type diuretics?

A 
IndapamideChlorthalidone1st line for afro-caribbeanCan be comboHelp in stroke and MI
479
Q

Mechanism of action for thiazide diuretics?

A

Urinary excretion of Na

480
Q

ADRs of thiazide diuretics?

A

Gout| Impotence

481
Q

Name 1 alpha antagonist for HT?

482
Q

Name 2 centrally acting agent for HT?

A

Methyldopa| Moxonidine

483
Q

Name 2 vasodilators for HT?

A

Hydralazine| Minoxidil

484
Q

Mechanism of action for doxazosin?

A

Selectively block postsynaptic alpha 1-adrenoceptors| Oppose vascular smooth muscle contraction in arteries

485
Q

ADRs of Doxazosin?

A

First dose hypotensionDizzinessDry mouthHeadache

486
Q

Indications for methyldopa?

A

HT in pregnancy

487
Q

Mechanism of action for methyldopa?

A

Converted to alpha-methylnoradrenaline which acts onCNS alpha adrenoceptors which decrease centralsympathetic outflow

488
Q

ADRs for methyldopa?

A 
SedationDrowsinessDepressionDry mouthNasal congestionOrthostatic hypotension
489
Q

Mechanism of action for moxonidine?

A

Centrally acting imidazoline agonist

490
Q

Describe the treatment regimen for patient over 55 YO?

A 
CCB+ thiazide diuretic+ ACE inhibitor+ Beta blocker+ less commonly used agent
491
Q

Describe the treatment regimen for patient under 55 YO?

A 
ACE inhibitorChildbearing age CCB or beta blocker+ thiazide diuretic+ CCB+ b-blocker+ less commonly used agent
492
Q

What interactions can occur between HT and pregnancy?

A

Develop gestational HTSometimes BP rises severely from about 20 weeksBP>140/90 mmHg and proteinuria >300 mg/24h —Preeclampsia

493
Q

Treatment for HT pre-pregnancy?

A

NifedipineMethyldopaAtenololLabetalol

494
Q

Treatment for HT during pregnancy?

A

+ thiazide diuretic| + amlodipine

495
Q

Potential complications for hypertensive pregnant women?

A 
Postural hypertensionRenally impairedBradycardiaCollapseDrug inters
496
Q

What is the clinical value for a anaemic patient?

A

< 13.5 g/dl in M| < 11.5 g/dl in F

497
Q

What are the signs and symptoms of anaemia?

A 
FatigueHeadachesLoss of appetiteWeight lossBreathlessnessPale skinIncreased HRNausea
498
Q

What are the oral symptoms of anaemia?

A 
Angular cheilitisGlossitisBurning mouth/tongueAphthous ulcerOral candidiasisDelayed wound healing

CSP1 YR5 (10 decks)

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