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3rd Year BDS > Human Disease > Flashcards

Human Disease 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 
TNFa
IL-1
IL-11
PTH
PGE2
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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 skin
  2. 7DHC is activated and travels to the liver
  3. 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 acid
Vit D
Ca
PTH
PO4
Bone
GI
Parathyroid gland
Kidney
Liver
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13
Q

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

A

Localised disorder of bone turnover
Increased bone resorption followed by increased bone formation
Leading 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 origins
Chronic viral infection within osteoclasts

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15
Q

What are the symptoms for Paget’s disease?

A

> 40 age with bone pain
Bone deformity
Excessive heat over pagetic bone
Neurological 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 phosphatase
Bone pain and local heat
Bone fracture or deformity
Hearing 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 alone
IV 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 mineralisation
Muscle 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 growth
Curved spine
Wide joints at elbow and wrist
Curved legs (splayed)
Wide bones and ankles
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22
Q

What are the symptoms for Osteomalacia?

A

Aches and pains
Inability for muscle coordination
Waddle gait
Struggle 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 exist
Type I: milder form when child starts to walk but can present in adults
Type II: lethal by age 1
Type III: progressive deforming with severe bone dysplasia and poor growth
Type IV: more severe version of type I

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26
Q

What is the presentation for osteogenesis imperfecta?

A 
Growth deficiency
Defective tooth formation
hearing loss
Blue sclera
Scoliosis
Ligamentous laxity
Easy bruising
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27
Q

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

A

Surgical to treat fracture
Medical to prevent fracture via IV bisphosphonates
Social adaptations to education and social
Genetic 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

Age
BMD
Falls
Bone 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 
Thyrotoxicosis
Hyper/Hypoparathyroidism
Cushings
Hyperprolactinemia
Hypopituitarism
Early menopause
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35
Q

Which rheumatic disease can cause osteoporosis?

A

RA
Ankylosing spondylitis
Polymyalgia rheumatica

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36
Q

Which GI disease can cause osteoporosis?

A

UC and Crohn’s
Liver disease
Malabsorption

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37
Q

Which medications can cause an increase risk of osteoporosis?

A 
Steroids
PPI (proton-pump inhibitors)
Enzyme inducing antiepileptic medications
Aromatase inhibitor
GnRH inhibitors
Warfarin
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38
Q

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

A

Minimise risk factors
Ensure good Ca and vit D status
Fall prevention strategies
Medications

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39
Q

What is the treatment for osteoporosis?

A

HRT until 60 years old
Selective oestrogen receptor modulators
Bisphosphonates
Denosumab

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40
Q

What are the side effects of HRT?

A

Increased risk of blood clots
Increased risk of breast cancer
Increased risk of heart disease and stroke

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41
Q

What are the side effects of SERMS?

A

Hot flushes
Increased clotting risks
Lack protection at hip site

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42
Q

What are the side effects of bisphosphonates?

A

Oesophagitis
Iritis/Uveitis
Atypical femoral shaft fractures
Necrosis of the jaw

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43
Q

What is Denosumab?

A

Monoclonal antibody against RANKL
Reduces osteoclastic bone resorption
Subcut injection every 6 months

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44
Q

What are the side effects for Denosumab?

A

Allergy
Symptomatic hypocalcemia if given when vit D is deplete
Atypical femoral shaft fractures

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45
Q

What are the side effects of Teriparatide?

A

Injection site irritation
Rarely hypercalcaemia
Allergy

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46
Q

What common features do all CT diseases share?

A

Auto-antibodies present
Mainly female
All have oral features

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47
Q

What antibody can be used to support a clinical diagnosis?

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

Aspirin
Immunosuppressive medications )sides thrush and ulcers)
(methotrexate and rituximab)
Check patients bloods

Suncream, 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 infection
Salivary gland swellings
Dry eyes (xerophthalmia) –> burning and gritty eyes
Fatigue
Arthralgia

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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 toothpaste
Sugar free chewing gum
Regular dental check ups

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54
Q

What are the 2 types of scleroderma?

A

Localised: morphoea
Systemic: limited and diffuse

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55
Q

What are the presentations for systemic sclerosis?

A

Limited mouth opening
Poor dentition
Gum recession
Secondary Sjogren’s

Adult onset Raynaud's
Swollen hands/sausage fingers
Tight waxy skin
Fatigue
Dysphagia
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56
Q

What is the treatment for systemic sclerosis?

A

Immunosuppression (methotrexate)
Anti-fibrotic
Vascular (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’s
Dysphagia

Muscle weakness
Rash
Rapid 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

Steroid
Immunosuppressives
IV 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 thrombosis
Recurrent pregnancy loss
Peculiar rash (levido reticularis)

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62
Q

What is the lab presentation of antiphospholipid syndrome?

A

Anticardiolipin antibody
Lupus anticoagulant
Anti-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
Anticoagulants

High 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 pain
Jaw Cramps/claudications
Tongue 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

Methotrexate
Sulfasalazine
Fetunomide
Mycophenolate 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-tolerance
Environmental 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

IgE
Soluble antigen
Act mast cells and produce mediators
Allergy

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79
Q

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

A

IgG, IgM
Cell or matrix antigen
Opsonisation, phagocytosis, complement and act of leukocytes
Rheumatic fever

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80
Q

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

A

IgG, IgM
Soluble antigen
Complement, Fc receptor recruitment and act of leukocytes
RA

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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 antigen
Th1 - macrophage activation causing cytokine-mediated inflamm
Th2 - direct cell killing and cytokine mediated inflammation

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82
Q

Explain the process of type I hypersensitivity?

A
  1. Exposure to allergen
  2. Act of Tfh cells and stimulation of IgE class switching in B cells
  3. Production of IgE
  4. Binding of IgE to FceRI on mast cells
  5. Repeated exposure to allergen
  6. Activation of mast cell; releasing medicators
  7. 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 antigen
Recruit 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 antigens
Recruit 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 receptor
Stimulates the receptor without the ligand
Increase production of thyroid hormone
Hyperthyroidism

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91
Q

Name 4 TII hypersensitivity disease?

A

Autoimmune haemolytic anaemia
Insulin-resistant diabetes
Myasthenia gravis
Graves’ disease

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92
Q

Name 3 TIII hypersensitivity disease?

A

Systemic lupus
Polyarthritis
Poststreptococcal glomerulonephritis

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93
Q

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

A

TI diabetes - Islet cells
RA - TII collagen
MS - 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 mimicry
Viral/bacterial superantigens
Enhanced presentation and processing of autoantigens
Bystander activation
Act 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 ulcers
Facial 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

Pain
Stiffness
Swelling
Functional impairment

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119
Q

What are the clinical signs of arthritis?

A

Tenderness
Restriction of movement
Heat
Redness

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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 symptoms
A 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 DRBeta1
Environmental:
- 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

Fatigue
Weight loss
Anaemia

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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.com
DAS < 2.4 represents clinical remission
DAS > 5.1 eligibility for biologic therapy

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130
Q

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

A

NSAIDs
Disease modifying anti-rheumatic drugs
Biologics
Corticosteroids

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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

Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide

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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 outcomes
Effective suppression of inflammation

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134
Q

Why is methotrexate the golden standard?

A 
Effective 
Well-tolerated
Cheap
People stay on it
Can 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 inhibitors
Anti B/T cell therapies
Oral kinase inhibitors

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137
Q

What are the side effects of biologic DMARDs?

A

Injection site reaction
Infection
Possible 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 diagnosis
Increased number of sick days
75% 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 - SYSTOLIC
V: 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 artery
  2. Place stethoscope over artery
    Inflate tourniquet until the artery is fully occluded
  3. Behind to deflate the tourniquet slowly and once the first sound is heard record the pressure value - this is the systolic pressure
  4. 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 disease
Malabsorption
Endocrine
Medication

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146
Q

What is the absorption and T1/2 of bisphosphonates?

A

Very poor intestinal absorption
50% goes to skeleton, rest excreted via kidney
Long 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 pathway
This 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 chain
3rd: N heterocyclic ring

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151
Q

Name 3 2nd generation bisphosphonates?

A

Alendronate
Ibrandronate
Pamidronate

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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 
Genetics
Disease
Age
Obesity
Alcohol
Steroid therapy
Tobacco
Sex
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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

Microtrauma
Inflamm disease
Oral surgery
Oral implantology

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157
Q

What is the pathogenesis of MRONJ?

A 
Inflamm/infection
Microtrauma
Altered bone remodelling or over suppression of bone resorption
ANgiogenesis inhibition
Soft tissue BPs toxicity
Peculiar biofilm of the oral cavity
terminal vascularisation of the mandible
Suppression of immunity
Vit D deficiency
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158
Q

Risk assessment for MRONJ?

A

No risk - if no meds
Low risk - if on meds but not previous diagnosis
Higher 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 drinks
Excellent oral hygiene
Fl toothpaste and mouthwash
Stop smoking
Limit alcohol
Regular dental check ups
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160
Q

What symptoms should an MRONJ patient report to the dentist?

A 
Exposed bone
Loose teeth
Non-healing sores or lesions
Pus
Tingling
Numbness or altered sensations
Pain
Swelling
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161
Q

What are the treatments for established MRONJ?

A

Surgical
Gentle debridement (best)
Avoid resection
Remove 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 patients
A link between oral health and risk of stroke
OH 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 24hrs
Most 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 limbs
Sensory: loss of feeling
Speech: dysarthria/dysphagia
Neglect/visuospatial problems
Vision: loss in one eye or hemianopia
Haze palsy
Ataxia/vertigo
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195
Q

What does the posterior circulation supply?

A

Pons
Midbrain
Hindbrain
Cerebellum

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196
Q

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

A 
Ataxia
Vertigo
Nystagmus
Loss 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 
Migraine
Epilepsy
Structural brain lesions
Metabolic disorders
vestibular disorder
Psychological disorders
Demyelination
Mononeuropathy
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198
Q

Name 4 causes for a stroke?

A

Carotid stenosis
Carotid disease
Atrial fibrillation
Lacunar 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 stroke
Age
Male
Family history

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201
Q

What is the most important modifiable risk factor for stroke?

A

Hypertension

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202
Q

Name 5 other modifiable risk factors for stroke?

A 
Diabetes (3x)
Smoking (2x)
Lipids
Alcohol
Obesity
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203
Q

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

A

1.9 million neurons
13.8 billion synapses
12km of axonal fibres

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204
Q

What is the acronym of FAST?

A

Facial weakness
Arm weakness
Speech problems
Time to call 999

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205
Q

What the the immediate management for stroke?

A

Thrombolysis for patients if they present within 4.5 hours

Thrombectomy

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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)
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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

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208
Q

What is the definition of clot retrieval?

A

Enter the artery in the arm

Tip penetrates clot and suctions it out

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209
Q

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

A 
CT or MRI scan:
- exclude haemorrhage
- exclude tumour
- define lesion
Carotid doppler if anterior circulation signs
Echo:
- to exclude cardiac cause
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210
Q

Why is secondary prevention essential for stroke survivers?

A

7% of patient having a TIA with have another within 1 month
20% of stroke survivors will have another within 5 years
Many de of cardiovascular events

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211
Q

Name 5 secondary prevention techniques for stroke survivors and TIAs?

A 
Anti-hypertensives
Anti-platelets
Lipid lowering drugs
warfarin or DOACS
Carotid endarterectomy
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212
Q

Why do stroke patients have more oral problems?

A

Nil by mouth

Unable to brush teeth due to physical and swallowing problems

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213
Q

Name 6 types of cardiovascular diseases?

A 
Angina
MI
Heart failure
Transient ischaemic attack
Thrombotic stroke
Atrial fibrillation
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214
Q

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

A

Damage to the vessel wall
Activation of platelets and inflammatory cells for abnormal healing
Incorporation of cholesterol forming a fibrous cap

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215
Q

What can cause damage to the vessel walls?

A

Diabetes
Hypertension
Smoking

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216
Q

What drug groups can be used to reduce wall stress?

A

Beta blockers
Renin-angiotensin system
Ca blockers

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217
Q

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

A

Reduces mortality in IHD and HF
Reduces symptoms in angina, AF and SVT
Anti-hypertensive

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218
Q

Name 3 examples of beta blockers?

A

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

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219
Q

Where are Beta 1 receptors found?

A

Aim for beta blockers
Heart
Kidneys: reduce renin release

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220
Q

What is the function of beta 1 receptors when activated?

A

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

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221
Q

Where are beta 2 receptors found?

A

SM

Skeletal muscle

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222
Q

What is the function of beta 2 receptors when activated?

A

Reduces tremor

Lethal bronchospasms for asthmatics, vasoconstriction and PVD

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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

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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 proteinuria
Prevent aberrant remodeling following MI (reduce aneurysm formation)
Reduction in HF symptoms

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225
Q

Explain the renin-angiotensin system?

A

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

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226
Q

What is the function of ANG II?

A

Potent vasoconstrictor:

  • peripheral vasc
  • efferent arteriole of the glomerulus
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227
Q

What is the function of aldosterone?

A

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

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228
Q

Name 3 examples of ACE inhibitors?

A

Ramipril
Captopril
Lisinopril

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229
Q

What are the positive effects of ACE inhibitors?

A

Reduce BP
Reduce afterload on heart
Prevents aberrant remodelling after MI
Reduces proteinuria

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230
Q

What are the negative effects of ACE inhibitors?

A

Reduces perfusion pressure in glom

Cough

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231
Q

Name 2 examples of Angiotensin II receptor blockers?

A

Losartan

Candesartan

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232
Q

What are the positive effects for Angiotensin II receptor blockers?

A

Reduce BP
Reduce afterload on heart
Prevents aberrant remodelling after MI
Reduces proteinuria

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233
Q

What are the negative effects for Angiotensin II receptor blockers?

A

Reduces perfusion pressure in glom

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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

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235
Q

Name 2 examples of aldosterone anatgonists?

A

Spironolactone and eplerenone

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236
Q

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

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

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238
Q

Name the 2 types of Ca channel blockers?

A

Dihydropyridine

Non-dihydropyridine

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239
Q

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

A

Block Ca entry into SM
Less effect in myocardial pacemaking tissues

Amlodipine
Felodipine

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240
Q

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

A

Block CA entry into SM
Blocks Ca entry into myocardial pacemaking tissue slow SA and AV conduction

Verapamil
Diltiazem

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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)
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242
Q

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

A

Clopidogrel
Prasugrel
Ticagrelor

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243
Q

What drug targets phosphodiesterase (as an inhibitor?)

A

Dipyridamole

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244
Q

What drug targets fibrinogen receptor (as a blocker?)

A

Abeximab

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245
Q

What drugs target COX I?

A

Aspirin

NSAIDs

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246
Q

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

A

Vorapaxxar

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247
Q

What are dental implications anti-platelet drugs?

A

Interactions with NSAIDs:

  • potent COX inhibitors
  • increased bleeding risk (GI)
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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

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249
Q

What is the chemical name for a statin?

A

Hydroxy-methyl-glutaryl CoA reductase inhibitor (HMGCoA)

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250
Q

Name 3 examples of statins?

A

Simvastatin
Rosuvastatin
Atorvastatin

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251
Q

What are dental implications for statins?

A

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

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252
Q

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

A

Antihypertensive effect
Promote Na and water loss in kidney
Reduce total content
Reduce BP

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253
Q

Name 2 examples of thiazide diuretics?

A

Indapamide

Bendroflumethizide

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254
Q

Name 2 examples of loop diuretics and their indication?

A

Furosemide
Bumetanide
For HF

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255
Q

What are dental implications for diuretics?

A

Nephrotoxic effect in combo with NSAIDs

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256
Q

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

A

Primary or secondary prevention in CVD associated AF

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257
Q

Name 2 examples of Vit K antagonists?

A

Warfarin

DOACs

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258
Q

What are dental implications for anticoagulants?

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

Name 1 antianginal? and its implication for dentistry?

A

Nicorandil

Can cause ulceration

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260
Q

Name 2 antiarrhythmics? and its implication for dentistry?

A

Digoxin

Amiodarone - theoretically reduces toxic dose of lignocaine

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261
Q

What occurs during immediate response to injury?

A

Attempts to maintain tissue structure/function
Minimise deleterious effects of injury
Overlaps with the inflammatory process

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262
Q

What is the definition of regeneration?

A

Replaces damaged cells with new cells
Leaves no trace of injury
Tissue requires ongoing mitotic activity

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263
Q

What is the definition of repair?

A

Replaces damaged cells with fibrous CT
Leaves permanent scar
Occurs in non-mitotic tissues and with more severe injuries

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264
Q

What is the definition of stromal regions?

A

Support tissue:
- CT, ECM, BVs and nerves
Non-mitotic

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265
Q

What is the definition of parenchymal tissues?

A

Functional cells of organs
Highly specialised
Hepatocytes and kidney tubular cells
Mitotic cells

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266
Q

What is the definition of a labile cell?

A

Continuous division

Often exposed to damage/abrasion and need constant replacement

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267
Q

Name 4 examples of labile cells?

A

Skin
Oral cavity
GI tract
Uterus

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268
Q

What is the definition of stable cells?

A

Division stops when growth is complete

Still has potential for division (regen)

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269
Q

Name 3 examples of stable cells?

A

Hepatocytes
Kidney tubular cells
SM cells

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270
Q

What is the definition of fixed cells?

A

Incapable of mitotic division
If damaged they are replaced by fibrous scar tissues
Scar lacks any functional capacity

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271
Q

Name 3 examples of fixed cells?

A

Nerve cells
Skeletal muscles cells
Cardiac muscle cells

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272
Q

What is the definition of inflammatory mediators?

A

Released by WBCs such as monocytes and macrophages

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273
Q

Name 6 examples of inflammatory mediators?

A 
TNF-a
IL
Interferons
Arachidonic acid
Leukotrienes
Prostaglandins
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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
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275
Q

What is the definition of growth factors?

A

Released by fibroblasts, macrophages and endothelial cells

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276
Q

Name 5 examples of GFs?

A 
PDGF
FGF
EGF
VEGF
TGF
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277
Q

What is the function of GFs?

A

Coordinate:

  • inflammatory response
  • chemotaxis
  • proliferation and differentiation
  • generation of ECM
  • angiogenesis
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278
Q

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

A

Chemotaxis
Proliferation
Differentiation
Produce ECM

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279
Q

What is the definition of the ECM?

A

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

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280
Q

Name the 3 different types of ECM composition?

A

Structural
Water-hydrated gels
Adhesive glycoproteins

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281
Q

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

A

Scaffolding of ECM provides framework and tensile strength

Collagen
Elastin

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282
Q

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

A

Provides lubrication, resilience and flexibility

Proteoglycans
hyaluronic acid

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283
Q

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

A

Provide cohesion between matrix components and cells

Fibronectin
Laminin

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284
Q

What are the 2 different forms of ECM?

A

Basement membrane

Interstitial matrix

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285
Q

What is the definition of basememnt membrane?

A

ECM sheet that epithelial, endothelial and SM cells lie on
Physical/chemical barrier
Giving structural support and strength

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286
Q

What is the definition of interstitial matrix?

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

How does the ECM aid in tissue repair?

A

Help regulate cell prolif, diff and movement
Contains regulatory molecules for repair
Prived a tissue framework for repair/regen
However, repairing damaged tissue needs largely intact ECM

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288
Q

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

A

Impaired control
Disorganisation
Causing delayed or dysregulated repair

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289
Q

What are the 3 key phases for wound healing?

A

Inflammatory
Proliferative
Remodelling

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290
Q

What is the initial phase of wound healing?

A

Injury
Stop bleeding via vasoconstriction
Platelet activation and aggregation forming a fibrin clot

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291
Q

What occurs during the inflammatory phase of wound healing?

A

Vasodilation and increased vessel permeability
This recruits plasma and WBCs to the wound site
Neutrophils and macrophages ingest debris and fibrin
Neutro secrete GFs to attract other immune cells
Macrophages secrete GFs and stimulate angiogenesis
0-2 days

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292
Q

What occurs during the proliferative phase of wound healing?

A 
Macrophage GFs stimulate:
- continued angiogenesis
- influx and activation of fibroblasts
Fibroblasts:
- variety of ECM components
- secrete GFs to activate angiogenesis or further fibroblasts recruitment
- this forms the granulation tissue
2-21 days duration
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293
Q

What is the defintion of granulation tissue?

A

Precursor to scar tissue
Moist, red CT and develops into a mature scar
Provides a framework for scar formation

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294
Q

What is the process of angiogenesis during granulation tissue formation?

A

Growth of new capillary buds from existing vessels
Visible at wound surface
eventually from new vasculature
Provide blood supply

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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)
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296
Q

What occurs during the late proliferative phase?

A

Inflammation no longer apparent
Fibroblasts persit producing collagen and strength the ECM
Granulation tissue migrates upwards leaving scar behind (scar avascular)
Upper epithelial layer proliferates, using granulation tissue as matrix
Seals wound with new epithelial
Some cell division replaces keratinocytes and epiderma strata

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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 scar
Scar contracts inwards (contractile fibroblasts)

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298
Q

What are the characteristics of mature scar tissue?

A 
Forms from granulation tissue
Formed during late proliferative phase
Pale (few BVs)
Quiescent, spindle fibroblasts
Dense collagen
Elastic fibres
Wound site filled in
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299
Q

How does regeneration differ to repair?

A 
May show different profile of GFs
Fewer fibroblasts and less ECM fill in
Greater emphasis on division of regenerating cells
Minor scar
More function
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300
Q

What factors influence healing?

A

Infection
Separation
Foreign bodies
Affected by extent of injury and tissue loss

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301
Q

What factors are required for healing?

A 
Nutrition
O2
Blood flow
Immune function
Inflammatory function
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302
Q

Difference between primary intention and secondary intention?

A

Primary is minor damage

Second is major damage

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303
Q

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

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

How to send a FBC?

A

EDTA sample to haematology lab

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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 loss
Increased destruction
Lack of production
Defective production

316
Q

Describe the signs and symptoms of anaemia?

A

Tiredness/Fatigue
Dizziness/Lightheadedness
Breathlessness (on exertion)
Chest pains

Pale
Glossitis
Angular stomatitis
Koilonychia (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 microcytic

Test for Serum ferritin (low)

320
Q

Diagnosis for Raised MCV and a further test?

A

Macrocytic

Test for B12/Folate and bone marrow (low)

321
Q

Name 4 causes of hypochromic microcytic anaemia?

A 
Blood loss
Increased requirements
Reduced intake
Normal 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 disease
Folate:
- dietary
- malabsorption
- increased requirements
Myelodysplasia
Liver disease
Drugs
Alcohol
Thyroid 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 replacement
Hypoplasia
(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 destruction
Compensation 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?

A

120 days

328
Q

How are RBCs broken down?

A

By the reticuloendothelial system

329
Q

What are RBCs broken down into?

A

Globin
Iron
Protoporphyrin

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

Bilirubin
Transported to liver
Bound to glucuronides
Excreted 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 infection
PET/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 antagonist
Reduces functional factors II, VII, IX and X
Monitored by INR

338
Q

Indications for Warfarin?

A

Atrial fibrillation
Prosthetic heart valves
Other arterial thromboembolism
Venous thromboembolism

339
Q

What are the disadvantages for warfarin?

A 
Wide individual variation in dose to achieve target INR
High drug inters
Dietary 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

2.0-3.0
Can go up to 3.0-4.0
In 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 allowed
Oxidised cellulose, collagen sponges and sutures can be considered
5% tranexamic acid mouthwash for 2 days can be considered
Avoid NSAIDs
IANB - 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), Intravenous
Gradual:
- 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 thrombosis
Treatment of arterial and venous thrombosis
Need interruption of treatment at least 24hrs pre procedure

346
Q

Describe what the ideal antithrombotic drug should do?

A 
Orally active
Predictable dose-response
No monitoring required
Minimal drug inters
minimal 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 thrombin
Metabolised in the liver
Excreted 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 interruption
High:
- 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 COX
reduce platelet aggregability
Impairs 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 thrombosis
Used 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?

A

7 days

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 
Chemotherapy
Bone marrow malignancy/failure
Megaloblastic anaemia
Drug induced
Alcohol 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/L

Increased bleeding after trauma

364
Q

What is the severe thrombocytopenia platelet count?

A

<20 x10^9/L

Severe bleeding after trauma

365
Q

Platelet count threshold for simple elective procedures?

A

> 20

366
Q

Platelet count threshold for simple extraction?

A

> 30

367
Q

Platelet count threshold for complex extraction?

A

> 50

368
Q

Platelet count threshold for LA?

A

> 30

Avoid IAN

369
Q

Platelet count threshold for Minor oral surgery?

A

> 50

370
Q

Platelet count threshold for major oral surgery?

A

> 80

371
Q

Describe Immune thrombocytopenic purpura?

A 
Autoimmune
Against platelets
Triggered by infection or meds
Variable severity
Responsive 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 = ?

A

Bleeding

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 bruising
No previous bleeding disorder history
Isolated prolonged APTT and low levels of VIII
Antibody to VIII

377
Q

Management of acquired haemophilia?

A 
Bypassing agents (Novoseven) to control bleeding episodes
Immunosuppression 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 
Yes
Cofactor in collagen synthesis
Require 40mg daily
Smokers need more
Can lead to scurvy
379
Q

Signs and symptoms of scurvy?

A 
Normocytic anaemia
Bleeding with normal platelets and coagulation
Skin and gum changes
High risk:
- alcoholics 
- malignancy
380
Q

What are the risk factors for essential hypertension?

A 
Obesity
Alcohol
Salt intake
Stress
Genetics
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 loss
Low salt diet
Moderation of alcohol intake

If risk too high pharmacological measures are indicated

383
Q

Blood pressure value to be diagnosed with hypertension?

A

> 160/100 mmHg

Treatment

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

140-159/90-99 mmHg

Treatment

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

140-159/90-99 mmHg

Lifestyle changes

386
Q

What is the definition of postural hypotension?

A

Where one’s BP falls on standing up with subsequent brief loss of consciousness
This is especially seen when a patient gets up from the dentist’s chair
Can 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

Age
Gender
Genetics

Hypertension
High cholesterol
Diabetes
Obesity
Excess 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 cholesterol
Fatty plaques become large enough to occlude vessel
Plaque 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 diet
Smoking cessation
BP control
DIabetes control
Reduction of cholesterol
397
Q

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

A

Aspirin
Statins
ACE 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 angioplasty
Insertion of a stent via a peripheral artery into a stenosed coronary artery
If 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?

A

6 months

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 fluid
ACE 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?

A

<60 bpm

417
Q

Tachycardia?

A

> 100 bpm

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 
Palpitations
Shortness of breath
Collapse
DIzziness
Fatigue
423
Q

Name 5 conditions that can cause AF?

A 
ISH
Rheumatic HD
Hypertension
Mitral valve disease
Cardiomyopathy
424
Q

How to manage a patient withAF?

A

Rhythm control:
- cardioversion with shocking or amiodarone/flecainide
Rate 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 free

Fatigue
Dizziness
Collapse

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?

A

1st
2nd
3rd

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 rate

There 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 patients
Structural heart disorders
Drugs

438
Q

Aetiology of Second degree heart block?

A

Young people
Athletes
Structural abnormalities
Acute myocardial infarction

439
Q

Aetiology of Third degree heart block?

A

Complete heart block
Elderly (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 heart
Left:
- more severe
- from IHD, aortic valve disease or secondary to chronic hypertension

444
Q

Name the 12 complications of hypertension?

A 
Haemorrhage
Stroke
Cognitive decline
Retinopathy
Peripheral vascular disease
Renal failure
Dialysis
Transplantation
Left ventricular hypertrophy
HF
CHD
MI
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 smoking
Diabetes
Renal disease
Male
Hyperlipidemia
Previous MI/Stroke
Left 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

Vasoconstriction
Reflex tachycardia
Increased CO
All increasing the BP

453
Q

When is the Renin-angiotensin-aldosterone system stimulated?

A

Fall in BP
Fall in blood volume
Na depletion

454
Q

What is the aetiology of hypertension?

A

Polygenic:
- major and poly genes
Polyfactorial:
- environment

455
Q

Name 2 theories on hypertension aetiology?

A

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

456
Q

Name 9 risk factors that contribute to hypertension?

A 
Age
Genetics
Environment
Weight
Alcohol intake
Race 
Birth weight
Na 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 disease
Renal disease
Drug induced
Pregnancy (pre-eclampsia)
Endocrine
Vascular (coarctation of aorta)
Sleep Apnoea
459
Q

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

A

Chronic pyelonephritis
Fibromuscular dysplasia
Renal artery stenosis
Polycystic kidneys

460
Q

Name 3 types of drug inducers of 2nd HT?

A

NSAIDs
Oral contraceptive
Corticosteroids

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 pressure
Monitoring
– 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 approach
Low doses of several drugs
Minimises adverse events and maxismises patient compliance

467
Q

BIHS guidelines for young and elderly patient with HT?

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

Step 1 treatment for a HT patient?

A

<55 offer ACE inhibitor/ARB
contraindicated 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

Ramipril
Perindopril
Lisinopril

472
Q

Contraindications of ACE inhibitors?

A

Renal artery stenosis
Renal failure
Hyperkalaemia

473
Q

ADR of ACE inhibitors?

A 
Cough
First dose hypotension
Taste disturbance
Renal impairment
Angioneurotic oedema
474
Q

Name 3 types of ANG II antagonists (ARB)?

A

Valsartan
Candesartan
Irbesartan

Similar sides and nters
No cough

475
Q

Name 4 types of Ca ch blockers?

A 
Vasodilators:
- amlodipine
- felodipine
Rate limiting:
- verapamil
- diltiazem
476
Q

Contraindications of Ca ch blockers?

A

Acute MI
Heart failure
Bradycardia (rate limiting CCBs)

477
Q

ADRs of CA ch blockers?

A 
Flushing
Headache
Ankle oedema
Indigestion
Reflux oesophagitis

Also cause bradycardia and constipation

478
Q

Name 2 thiazide type diuretics?

A 
Indapamide
Chlorthalidone
1st line for afro-caribbean
Can be combo
Help 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?

A

Doxazosin

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 hypotension
Dizziness
Dry mouth
Headache

486
Q

Indications for methyldopa?

A

HT in pregnancy

487
Q

Mechanism of action for methyldopa?

A

Converted to alpha-methylnoradrenaline which acts on
CNS alpha adrenoceptors which decrease central
sympathetic outflow

488
Q

ADRs for methyldopa?

A 
Sedation
Drowsiness
Depression
Dry mouth
Nasal congestion
Orthostatic 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 inhibitor
Childbearing 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 HT
Sometimes BP rises severely from about 20 weeks
BP>140/90 mmHg and proteinuria >300 mg/24h —
Preeclampsia

493
Q

Treatment for HT pre-pregnancy?

A

Nifedipine
Methyldopa
Atenolol
Labetalol

494
Q

Treatment for HT during pregnancy?

A

+ thiazide diuretic

+ amlodipine

495
Q

Potential complications for hypertensive pregnant women?

A 
Postural hypertension
Renally impaired
Bradycardia
Collapse
Drug 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 
Fatigue
Headaches
Loss of appetite
Weight loss
Breathlessness
Pale skin
Increased HR
Nausea
498
Q

What are the oral symptoms of anaemia?

A 
Angular cheilitis
Glossitis
Burning mouth/tongue
Aphthous ulcer
Oral candidiasis
Delayed wound healing
499
Q

Name 5 causes of normocytic anaemia?

A 
Cancer
RA
IBS
Renal problems
TB
500
Q

What is the definition of microcytic?

A

Red cell is <80 fl in size and is usually associated with reduced intra-cellular haemoglobin (Hb), which creates a hypochromic appearance

501
Q

What is the definition of macrocytic?

A

Reflects an increased MCV but with reduced Hb level

502
Q

What is the definition of normocytic?

A

The Hb is low but the MCV is within normal limits

503
Q

Name 4 causes of microcytic anaemia?

A

Iron deficiency
Anaemia of chronic disease
Sideroblastic anaemia
Thalasseamia

504
Q

How is iron absorbed via the GI?

A

Absorbed in the duodenum in acidic conditions and carried in the blood as transferrin but stored in the marrow, liver and muscle as ferritin

505
Q

Name 5 common causes of iron deficiency anaemia?

A 
Period
GI blood loss
Increased demand
Small bowel disease
Poor diet
506
Q

What is the FBC diagnosis for iron deficiency anaemia?

A

Low Hb and low MCV
Low ferritin
Total iron binding capacity is increased

507
Q

What is the management for iron deficiency anaemia?

A

Treat cause
Oral iron (Ferrous sulphate)
IM

508
Q

Name the 2 types of Thalassaemia?

A

Alpha

Beta

509
Q

Name the 3 types of Beta Thalassaemia?

A

Major
Intermedia
Minor

510
Q

What causes megaloblastic anaemia?

A

Vit b12 deficiency

Folate deficiency

511
Q

Name the 6 main reasons for B12 deficiency?

A 
Pernicious anaemia
Gastrectomy
Vegan
Ileal resection
Coeliac disease
Bacterial overgrowth
512
Q

Name the 4 main reasons for folate deficiency?

A

Diet
Malabsorption
High demand
Drugs

513
Q

What is the definition of sickle cell anaemia?

A

Inheritance of a gene for HbS, sickle haemoglobin. This is needed for the exchange of valine for glutamic acid in position 6 of the Hb beta chain

514
Q

What is the role of G6P dehydrogenase?

A

Glucose-6-phosphate dehydrogenase deficiency is vital to maintain glutathione in a reduced state to help the movement of electrons (H) through the metabolic pathways (oxidation)

515
Q

Blood group O - serum abs and info?

A

Anti A and B

Universal donor

516
Q

Blood group A - serum abs and info?

A

Anti B

517
Q

Blood group B - serum abs?

A

Anti A

518
Q

Blood group AB - serum abs and info?

A

None

Universal recipients

519
Q

Name 6 respiratory symptoms?

A 
Breathlessness
Cough
Sputum
Haemoptysis
Chest pain
Wheeze
520
Q

What assessments would a dentist carry out to assess respiratory disease?

A

Pulse oximetry
Pulse rate
Respiratory rate
Peak flow meter

521
Q

What is the definition of TI respiratory failure and give 2 examples?

A

Low PO2
Normal or low PCO2
Acute asthma
Pneumonia

522
Q

What is the definition of TII respiratory failure and give 2 examples?

A

Low PO2
High PCO2
COPD
Obesity hypoventilation syndrome

523
Q

Signs and symptoms for asthma and COPD?

A

Breathlessness
Wheeze
Cough

524
Q

What is the difference between COPD and asthma?

A

COPD:
- irreversible airflow obstruction
Asthma:
- reversible airflow obstruction

525
Q

What tests can be carried out to help diagnose asthma and COPD?

A

History
Peak flow recording
Lung function

526
Q

Name the 5 treatment options for Asthma and COPD?

A 
Inhaled bronchodilators (salbutamol)
Inhaled corticosteroids (beclomethasone)
Oral theophylline
Oral leukotriene receptor antagonist (montelukast)
Oral prednisolone
527
Q

What is the definition of pneuomina?

A

Infection of the lower respiratory tract

528
Q

What are the signs and symptoms of pneumonia?

A 
Fever
Myalgia
Headache
Cough
Chest pain
Sputum
Dyspnoea

Can proceed to TI respiratory failure

529
Q

What are the treatment for pneumonia?

A

Antibiotics
Oxygen
intravenous fluids

530
Q

What is the definition of obstructive sleep apnoea?

A

Loud snoring and cessation of breathing
Daytime sleepiness
Poor concentration

531
Q

How to treat obstructive sleep apnoea?

A

Weight loss
CPAP
Mandibular repositioning splint

532
Q

What is the definition of a pulmonary embolism?

A

Blood clot in the lungs, that typically arises in the leg veins

533
Q

Name 4 risk factors for pulmonary embolism?

A

Recent major operation
Recent major trauma
Immobility
Major chronic disease

534
Q

What are the signs and symptoms of pulmonary embolism?

A

Breathlessness
Chest pain
Haemoptysis

535
Q

What is the treatment for pulmonary embolism?

A

Anticoagulation

536
Q

What is the definition of a pneumothorax?

A

Collapsed lung

537
Q

Name the 2 types of pneumothorax?

A

Primary

Secondary

538
Q

Signs and symptoms for a pneumothorax?

A

Chest pain

Dyspnoea

539
Q

How to treat a patient with pneumothorax?

A

Aspiration of air around collapsed lung
Observation
Chest drain

540
Q

Signs and symptoms for lung cancer?

A

Cough
Haemoptysis
Weight loss

541
Q

What is the definition of a chronic cough?

A

Cough lasting longer than 8 weeks

542
Q

Name 3 common causes of chronic cough?

A

Asthma
Gastro-oesophageal reflux
Postnasal drip

543
Q

What is the definition of bronchiectasis?

A

Dilated and damaged airways

544
Q

Signs and symptoms of bronchiectasis?

A

Cough
Large amount of sputum
Haemoptysis

545
Q

What are the treatment options for chronic cough/

A

Inhaled corticosteroids
gastric acid suppression (omeprazole)
Intranasal steroid spray (beconase)

546
Q

How to diagnose sleep apnoea?

A

Sleep study

547
Q

How to diagnose lung cancer?

A

CT scan

Bronchoscopy

548
Q

How to diagnose chronic coughing?

A

Lung function test

549
Q

How to diagnose bronchiectasis?

A

CT thorax

550
Q

What is the definition of interstitial lung disease?

A

Thickening, inflammation of interstitium of the lung

551
Q

Signs and symptoms of interstitial lung disease?

A

Dyspnoea

Dry cough

552
Q

How to diagnose interstitial lung disease?

A

CT scan

553
Q

Treatment options for interstitial lung disease?

A

Corticosteroids
Oxygen
Pulmonary rehab
Pirfenidone

554
Q

Explain the process of the platelet plug?

A

Vessel damage leads to platelet adhesion to the VWf
Platelets then aggregate to other platelets to form a plug + some fibrinogen
Fibrinogen is hen broken down to form fibrin forming the clot

555
Q

What is the intrinsic pathway for clotting?

A 
IX --> IXa
IXa --> X via VIIIa
X --> Xa
Prothrombin --> Thrombin via Xa
Fibrinogen --> Fibrin by thrombin
556
Q

What is the extrinsic pathway for clotting?

A 
VII + Tissue factor
VIIIa/TF --> Xa
X --> Xa
Prothrombin --> Thrombin via Xa
Fibrinogen --> Fibrin by thrombin
557
Q

Name 4 pathological causes for bleeding disorders?

A

Decreased number of platelets
Abnormal platelet function
Von Willebrand disease
Coagulation factor (deficiency or inhibition)

558
Q

Name 5 points to think about when gauging bleeding history?

A 
Do you have a bleeding disorder?
How severe is the disorder?
Pattern of bleeding
Congenital or acquired
Mode of inheritance
559
Q

Name 6 times history of bleeding can give information?

A 
Bruising
Epistaxis
Post-surgical bleeding
Menorrhagia
Post-partum haemorrhage
Post-trauma
560
Q

Name 5 types of platelet type of pattern of bleeding?

A 
Mucosal
Epistaxis
Purpura
Menorrhagia
GI
561
Q

Name 3 types of coagulation factor for pattern of bleeding?

A

Articular
Muscle haematoma
CNS

562
Q

How to determine the difference between acquired and congenital?

A

Previous episodes
Age at first event
Previous surgical challenges
Associated history

563
Q

What is the definition of Haemophilia A and B?

A

X-linked
Identical phenotypes
Severity of bleeding depends on the residual coagulation factor activity

564
Q

What are the clinical features of haemophilia?

A 
Haemarthrosis
Muscle haematoma
CNS bleeding
Retroperitoneal bleeding
Post surgical bleeding
565
Q

What questions to ask a dental patient with a suspicion of bleeding disorders?

A

Do you have a history of bleeding disorder?
Do you have a family history of bleeding?
Have you had any previous operations?
Are you taking any anticoagulant drugs?

566
Q

What advice is given for severe haemophilia for dental procedures?

A

Enhanced preventive GDP

All treatments except prosthetics in specialist hospital setting

567
Q

What advice is given for moderate haemophilia for dental procedures?

A

Enhanced preventive GDP

All treatments except prosthetics specialist hospital setting

568
Q

What advice is given for mild haemophilia for dental procedures?

A

Enhanced preventive advice and treatment GDP
Many procedures at GDP
2 yearly review specialist dental centre

569
Q

What treatment should a haemophiliac +ve patient have for dental management?

A 
Prevention as normal
Mild Haem A:
- DDA VP/tranexamic acid
Mod/Severe Haem A:
- coagulation factor replacement for VIII
All Haem B:
- coagulation factor replacement
570
Q

What dental LA procedures require factor elevations?

A

IAN

Lingual infiltration

571
Q

What dental LA procedures DO NOT require factor elevations?

A

Buccal infiltration
Intrapapillary injection
Intraligamentary injections

572
Q

What adjunctive to treatment is useful for bleeding disorder patient?

A

Suturing and local haemostatic measure for extractions

Resorbable and non-resorbable sutures acceptable

573
Q

Name 8 local haemostatic agents?

A 
Oxidized cellulose
Surgicel
Absorbable gelatine sponge
Gelfoam
Cyanoacrylate tissue adhesives
Surgical splints
Lyostypt
Ankaferd blood stopper
574
Q

Hwat complications can occur with haemophilia treatment?

A 
Viral infections:
- HIV, HBV and HCV
Inhibitors
- DDAVP
Flushing 
Rare arterial events
Hyponatremia in babies
575
Q

What is the definition of Von Willebrand disease?

A 
Common
Variable severity
Autosomal
Mucosal platelet bleeding type
Quantitative and qualitative abnormalities of vWF
576
Q

What precautions should you advice to a Von willebrand disease patient before treatment?

A

vWF concentrate or DDAVP
Tranexamic acid
Topical applications

577
Q

Name the 4 valves of the heart?

A

Pulmonic
Aortic
Bicuspid
Tricuspid

578
Q

Name the 3 types of valvular heart disease?

A

Valvular stenosis
Valvular regurgitation
Aortic coarctation
CHD

579
Q

What does the aortic valve look like?

A

Inverted Merc badge

580
Q

Name the 2 types of aortic stenosis?

A

Degenerative

Bicuspid

581
Q

What is the aetiology of degenerative aortic stenosis?

A

Becomes thick and calcified

Can fuse in the future

582
Q

What is the aetiology of bicuspid aortic stenosis?

A

2 leaflets rather than 3 leaflets

583
Q

Name 3 symptoms of aortic stenosis?

A

Chest pain
Breathlessness on exertion
Syncope/Dizziness

584
Q

Name the 2 types of causes of aortic regurgitation

A

Aortic defects

Leaflet defects

585
Q

How can the aorta cause aortic regurgitation?

A

Dilated aorta

586
Q

How can the leaflets of the aortic valve cause aortic regurgitation?

A

Bicuspid
Rheumatic heart disease
Endocarditis

587
Q

Explain how Rheumatic heart disease occurs?

A

Occurs from primary infection that leads to cross-abs to heart structure

588
Q

Name the 2 symptoms of aortic regurgitation?

A

Dyspnoea:
- orthopnoea
- paroxysmal nocturnal dyspnoea
Chest pain

589
Q

Name the 4 aetiologies for mitral valve disease?

A 
Myxomatous degeneration (valves become redundant and elongated)
Functional MR (enlarged ventricles, valves don't match up)
Rheumatic heart disease
Infectious endocarditis
590
Q

Name the 3 symptoms for mitral valve disease?

A

Breathlessness
Palpitations due to AF
Embolisation

591
Q

What is the definition of mitral stenosis?

A

Thickening and scarring of the leaflets

Fusion of the commissures

592
Q

WHat is the definition of mitral regurgitation?

A

Leaflet abnormality

Mitral annular dilatation

593
Q

Name the 2 right sided valves?

A

Tricuspid

Pulmonary

594
Q

Name 2 types of congenital heart disease?

A

Ventricular septal defects

Compex CHD

595
Q

Name 2 types of material for prosthetic heart valves?

A

Mechanical

Tissue

596
Q

What medication must you be on if you have a mechanical heart valve?

A

Warfarin

597
Q

How often should a blood INR be carried out?

A

Every 6 weeks

598
Q

What is the INR for AF?

A

2-3

599
Q

What is the INF for metallic heart valves?

A

2.5-4

600
Q

How long should a tissue valve transplantee stay on anticoagulants for?

A

3 months

601
Q

What to ensure about your patient with bleeding disorders before invasive treatments?

A

Ensure INR 2-4 72 hrs prior
Ensure no other antiplatelet therapy (aspirin or clopidogrel)
DO NOT prescribe NSAIDs or COX-2 inhibitors
Ensure proper local haemostasis

602
Q

What are the risks of stopping oral anticoagulation?

A

Small, but fatal

603
Q

What is the definition of infective endocarditis?

A

Infection on the cardiac or vascular endothelium
Forms vegetation
Contains platelets, fibrin, microorganisms and inflammatory cell

604
Q

Name the 2 predisposing factors and their subtypes for infective endocarditis?

A 
Endothelium subjected to turbulent flow:
- any valvaular or cardiac abnormality
- prosthetic heart valves
Bacteremia:
- IV drug users
- dental procedures
- surgical procedures at infected sites
605
Q

Name the 6 aetiologies for infective endocarditits?

A 
Bacteria:
- streptococcus
- staphylococcus
- enterococcus
- pneumococcus
- gram -ve bacilli
Fungi
Mycobacteria
Rickettsiae
Chlamydia
Mycoplasma
606
Q

Name the 7 signs and symptoms for infective endocarditis?

A 
Fever
Malaise
Anorexia
Weight loss
HF due to acute valvular destruction
Systemic embolisation
Acute renal failure
607
Q

What are the NICE guidelines for antibiotic prescription?

A

High risk patients when a high risk procedure is performed

608
Q

What is the emphasis for dentists when treating patients with bleeding disorders?

A

Good oral hygiene

Regular dental review 2 yearly

609
Q

Which patient count as a high risk patient for antibiotic prescription?

A

Prosthetic valve or prosthetic material used for cardiac valve repair
Previous infective endocarditis
CHD:
- unrepaired cyanotic disease
- complete repair up to 6 months after procedure
- residual defects persists at the site of implantation of prosthetic material

610
Q

What is the definition of a invasive dental procedure?

A

Procedures requiring the manipulation of the gingival or peri-apical region of the teeth or perforation of the oral mucosa including scaling and RCT)

611
Q

What are the ESC 2015 guidelines for infective endocarditis prophylaxis?

A 
No allergy: single dose 30-60 mins before procedure
- amoxicillin or ampicillin 
- 2 g po/IV adult
- 50 mg/kg po/IV child
Allergy to penicillin: single dose 30-60 mins before procedure
- clindamycin
- 600 mg po/IV adult
- 20 mg/kg po/IV
612
Q

Which procedures do not need antibiotic prophylaxis for infective endocarditis/

A

LA injections in non-infected tissue (superficial caries)
Removal of sutures
Dental x-rays
Placement or adjustment of removable orthodontic appliances or braces
Shedding of deciduous teeth or trauma to the lips or oral mucosa

613
Q

Name 11 invasive dental procedures?

A

Placement of matrix bands
• Placement of sub-gingival rubber dam
clamps
• Sub-gingival restorations including fixed
prosthodontics
• Endodontic treatment before apical stop
has been established
• Preformed metal crowns (PMC/SSCs)
• Full periodontal examinations (including
pocket charting in diseased tissues)
• Root surface instrumentation/subgingival scaling
• Incision and drainage of abscess
• Dental extractions
• Surgery involving elevation of a mucoperiosteal flap or muco-gingival area
• Placement of dental implants including
temporary anchorage devices, mini implants
• Uncovering implant sub-structures

614
Q

Name 8 non-invasive dental procedures?

A 
Infiltration or block local anaesthetic
injections in non-infected soft tissues
• BPE screening
• Supra-gingival scale and polish
• Supra-gingival restorations
• Supra-gingival orthodontic bands and
separators
• Removal of sutures
• Radiographs
• Placement or adjustment of orthodontic
or removable prosthodontic appliances
615
Q

What dose of amoxicillin is needed for an adult with bleeding disorder patient prophylactically?

A

3g 60 mins before procedure

616
Q

What dose of amoxicillin is needed for a child with bleeding disorder patient prophylactically?

A

Max dose 3g
50 mg/kg
Oral suspension

617
Q

What dose of clindamycin is needed for an adult with bleeding disorder patient prophylactically?

A

600mg 60 minutes before procedure

618
Q

What dose of clindamycin is needed for a child with bleeding disorder patient prophylactically?

A

20 mg/kg

600 mg max dose

619
Q

What is consisted of the lower GI tract?

A 
Jejunum
Ileum
Ascedning Colon
Descedning colon
Sigmoid colon
Rectum
Caecum
620
Q

What is the function of the small bowel?

A

Enzymatic digestion
absorption
Gut hormone secretion
Immune

621
Q

What is the function of the large bowel?

A

Storage and elimination of waste

FLuid and electrolyte reabsorption

622
Q

What are the symptoms for colorectal cancer?

A

Change in bowel habit
Rectal blood loss
Abdominal pain
Weight loss

Co-incidental anaemia

623
Q

When does bowel cancer screening occur?

A 
50-74 YO
Every 2 years
Faecal occult blood
Immunochemical test
\+ve result referral for colonoscopy
2% require colonoscopy
624
Q

Explain how the adenoma can develop into a carcinoma?

A

Normal epithelium
Small adenoma
Large adenoma
Invasive adenocarcinoma

625
Q

What are the stages of colorectal cancer?

A

Dukes A-D

626
Q

Dukes A?

A

Tumour confined to mucosa

93% survival

627
Q

Dukes B?

A

Extension through mucosa to muscle layer

77%

628
Q

Dukes C?

A

Extension through mucosa to muscle layer
Involvement of lymph nodes
48%

629
Q

Dukes D?

A

Distant spread

7%

630
Q

What is the surgical management for Dukes A?

A

Endoscopic resection possible for polyps

Possible need for stoma if low rectal tumours or perforated or obstructed tumours

631
Q

What is the genetic and environmental contribution for colorectal cancer?

A

Mainly sporadic
Can be genetic
Increased risk with IBD

632
Q

What is the definition of familial adenomatous polyposis and its dental significance?

A

Autosomal dominant
Mutation of APC gene
High risk cancer
Annual colonoscopy

Supernumerary teeth
Unerupted teeth
Multiple osteomas of mandible (cotton wool like appearances)

633
Q

What is the definition of Inflammatory bowel disease?

A

Chronic relapsing inflammatory conditions of the bowel
UC and Crohn’s
Peak incidence in 20s

634
Q

What is the aetiology for IBD?

A

Environmental
Genetic
Candidate genes identified

635
Q

What are the triggering factors for IBD?

A

Bacterial infection
Diet
Vaccination history
Social factors - smoking

636
Q

Where does UC effect?

A 
Continuous mucosal inflammation
Affects the colon
Rectum - proctitis
Left sided hemi
Extensive pan
637
Q

What are the symptoms for UC?

A

Bloody diarrhoea
Abdominal cramping
Weight loss
Malaise

638
Q

What are the signs and symptoms of Crohn’s disease?

A 
Diarrhoea
Bleeding
Weight loss
Vomiting
Perianal symptoms

Fistula
Abscesses
Fissures

639
Q

What are the signs and symptoms of Crohn’s disease?

A 
Diarrhoea
Bleeding
Weight loss
Vomiting
Perianal symptoms:
- fistula
- abscesses
- fissures
640
Q

What are the extra-intestinal manifestations for IBD?

A

Eyes: uveitis and conjunctivitis
Joint: sacroiliitis, monoarticular arthritis and ankylosing spondylitis
Liver: fatty, gallstones, pericholangitis and sclerosing cholangitis
Skin: vasculitis, pyoderma gangrenosum and erythema nodosum

641
Q

What is the definition of toxic megacolon?

A

Colonic dilatation and systemic toxicity due to severe flare of colitis

642
Q

What is the definition of toxic megacolon?

A

Colonic dilatation and systemic toxicity due to severe flare of colitis

643
Q

What is the medical treatment for IBD and their dental impact?

A

Immunosuppression
Corticosteroids for acute flare ups
Thiopurines (BM suppression)
Biologics - infliximab (anti-TNF)

Ensure no dental infection ongoing prior to administration

644
Q

What is the definition of Coeliac disease?

A

Intolerance to gluten

Loss of microscopic villi in the SI, resulting in malabsorption

645
Q

What are the symptoms for Coeliac disease?

A

Diarrhoea
Weight loss
Bloating
Anaemia

646
Q

Diet changes for coeliac +ve patient?

A

No:

  • bread
  • pasta
  • cake
  • cereals
  • sauces
  • pre-prepared meals
  • beer
647
Q

What is the definition of small bowel infarction?

A

Acute mesenteric ischaemia
Usually due to arterial thrombus or embolism blocking blood flow
Rapid onset
Emergency resection required

648
Q

Name 2 eating disorders?

A

Anorexia nervosa

Bulimia nervosa

649
Q

What is the definition of anorexia nervosa?

A

Refusal to maintain normal wight
Fear of weight gain
Distorted perception of body image

650
Q

What’s the definition of bulimia nervosa?

A

Binge eating followed by attempts to restrict weight gain

Purging

651
Q

Oral manifestations for vomiting?

A 
Palatal erosion
Occlusal erosion of maxillary teeth:
- incisal edges of incisors thin and knife-edged
- cupped out appearance
Swollen parotid glands
652
Q

What is the definition of hereditary hemorrhagic telangiectasia?

A

Autosomal dominant
Perioral telangiectasia
Small bowel lesions can bleed
Photocoagulation/embolisation/surgery

653
Q

What is the definition of Peutz-Jeghers syndrome?

A

Autosomal dominant
Mucocutaneous pigmented macules
Multiple polyps throughout bowel (block or bleed)
GI cancers risk hight

654
Q

Oral manifestations for Crohn’s disease?

A 
Orofacial granulomatosis:
- inflammatory condition affect the oral mucosa
- found before Crohn diagnosis
- non-caseating granulomas
Recurrent mouth ulcers
655
Q

Treatment for oral manifestations for Crohns?

A

Local/systemic corticosteroids

Cinnamon-free diet

656
Q

What is the definition of diverticular disease?

A

Asymptomatic

Bulging sac of tissue protruding from colonic wall

657
Q

Complications for diverticular disease?

A

Bleeding
Perforation
Infection + abscesses
Require surgery

High fibre diet good

658
Q

Name 3 types of small bowel diseases?

A

Crohn’s
Coeliac disease
Ischaemia/infarction

659
Q

What are the symptoms of hereditary hemorrhagic telangiectasia?

A

Epistaxis

Pulmonary and cerebral lesions

660
Q

Oral manifestation for iron-deficiency anaemia?

A

Angular cheilitis

661
Q

What are the functions of the digestive system?

A

Digestion
Secretion
Absorption
Motility

662
Q

What is the sequence of organs that the food passes through?

A 
Mouth
Oesophagus
Stomach
SI
Colon
Rectum
Anus
663
Q

What organ is responsible for digestion?

A

Stomach

664
Q

Which organ is responsible for absorption and secretion?

A 
Absorption:
- upper SI
- colon
Secretion:
- lower SI
- colon
665
Q

Name the 2 forms of digestion?

A

Chemical

Enzymatic

666
Q

Name each organ/tissue present in the GI tract?

A 
Mouth
Salivary glands
Pharynx
Trachea
Oesophagus
Liver
Gallbladder
Stomach
Pancreas
LI
SI
Rectum
Anus
667
Q

Describe the cross-sectional structure of the GI tract wall? Out to In

A 
Serosa
Longitudinal muscularis externa
Myenteric plexus
Circular muscularis externa
Submucous plexus
Submucosa (BVs and nerves)
Mucosa (epithelium)
Lumen
668
Q

Name the 2 autonomic controls of the GI system?

A

Long (para)

Short (ENS) reflexes

669
Q

Describe how the parasympathetic NS control the GI function during digestion?

A 
Vagus nerve mainly
Except salivation (VII and IX)
Stimulatory:
- increased secretion
- increased motility
670
Q

Describe how the sympathetic NS control the GI function during fight/flight?

A

Splanchnic nerve
Inhibitor (except salviation):
- reduced secretion
- reduced motility

671
Q

Where does the blood from the GI system drain to?

A

Hepatic portal vein

672
Q

What 2 main vessels enter the Liver?

A

Hepatic portal vein

Hepatic artery

673
Q

Why do we chew?

A

Prolong taste experience

Defence against respiratory failure

674
Q

Explain the voluntary system in which chewing is controlled?

A

Somatic nerves innervate the skeletal muscles of the mouth and jaw

675
Q

Explain the reflex pathway for chewing?

A

Contraction of jaw muscles leads to pressure of food against the gums, hard palate and tongue, activating mechanoreceptors that communicate to inhibit jaw muscles thus reduces the pressure causing contraction

676
Q

Name the main organs for swallowing?

A 
Hard palate
Soft palate
Tongue
Epiglottis
Glottis
Larynx
677
Q

Explain the oral phase (voluntary) during swallowing?

A

Bolus pushed to back of the mouth by tongue

678
Q

Explain the pharyngeal phase during swallowing?

A

On presence of bolus it activates the sequence of reflex contractions of the pharyngeal muscles
This is coordinated y the swallowing centre in the medulla
The soft palate is reflected backwards and upwards (closing off the nasopharynx)
As the bolus reaches the oesophagus the upper oesophageal sphincter relaxes and the epiglottis will cover the opening to the larynx stopping food entering the trachea
Once bolus has entered the oesophagus the sphincter contracts (preventing reflux)

679
Q

Explain the oesophageal phase during swallowing?

A

The propulsion of the bolus to the stomach
Peristaltic waves sweep the bolus along the oesophagus and reaches stomach in 10s
As the bolus nears the stomach the lower oesophageal sphincter relaxes allowing the bolus to enter the stomach
Receptive relaxation of the stomach is initiated following relaxation of the sphincter and entry of bolus
Vagal reflexes communicate to that there is relaxation of the thin, elastic SM of the gastric fundus and body

680
Q

How does the size of the stomach change?

A

50mL –> 1500mL with no Pa change

681
Q

Name the 3 main parts of the stomach?

A

Fundus
Body
Antrum

682
Q

What allows the receptive relaxation of the stomach?

A

Rugae in the stomach

683
Q

What is the function of the fundus?

A

Storage of material

684
Q

What is the function of the body?

A 
Storage
Mucus
HCl
Pepsinogen
Intrinsic factor
685
Q

What is the function of intrinsic factor?

A

Binds B12
Aids haemoglobin formation
Travels to terminal ileum and transported to the liver

686
Q

What is the function of HCl and pepsinogen?

A

Digestion

687
Q

What is the function of the antrum?

A

Mixing/grinding

Gastrin

688
Q

What is the function of gastrin?

A

Regulates the secretion of HCl and pepsinogen

689
Q

Name the 4 types of cells of a gastric gland?

A

Surface mucous
Mucous neck
Parietal
Chief

690
Q

What do mucous neck cells secrete?

A

Mucus

691
Q

What do chief cells secrete?

A

Pepsinogen

692
Q

What do parietal cells secrete?

A

HCl

Intrinsic factor

693
Q

Name the 3 ways mechanism in which gastric acid is controlled?

A

Neurocrine (vagus)
Endocrine (gastrin)
Paracrine (histamine)

694
Q

Explain the cepahlic phase of gastric acid secretion?

A

Sight, smell or taste of food witl activate the vagus nerve which activate parietal and g cells which release gastrin to further activate parietal cells
Gastrin/ACh activate ECL cells which release histamine to further activate Parietal cells

695
Q

Explain the gastric phase of gastric acid secretion

A

Distension of stomach after arrival of food stimulates the vagal and enteric reflexes releasing ACh activating the parietal cells
Peptides present in the lumen activate G cells secreting gastrin will activate parietal cells
Gastrin/ACh will activate ECL cells to release histamine and activate parietal cells

696
Q

What cells produce pepsiongen?

A

Chief cells

697
Q

How is pepsinogen activated?

A

pH of lover than 3
Acid hydrolysis and forms pepsin
Pepsin continues to hydrolysis of pepsinogen

698
Q

How is pepsinogen packaged?

A

Zymogens to stop cellular digestion

699
Q

How are pepsin and HCl secretion related?

A

Proprotional to one another

700
Q

What secrete gastic mucus?

A

Surface epithelial cells and mucus neck cells

701
Q

What is the function of gastic mucus?

A

Cytoprotective role
Protects mucosal surface from mechanical injury
Neutralise pH as it has a high HCO content
Protects against gastric acid corrosion and pepsin digestion

702
Q

At what pH is pepsin denatured?

A

Neutral pH

703
Q

Explain how acid is neutralised before entering the duodenum?

A

HCO secreted from Brunner’s gland duct cells

H + HCO3 –> H2CO3 -> H20 + CO2

704
Q

Explain how the duodenum controls the secretion of HCO3?

A

Long and short reflex for HCO3 secretion

Release of secretin from S cells increases HCO3 secretion

705
Q

What does secretin activate the release of and from where?

A

HCO3 from pancreas and liver

706
Q

How is secretin release controled?

A

Acid neutralisation leads to the inhibition of secretin release

707
Q

What is the function of the duodenum?

A

To neutralise acid from the stomach

708
Q

What duct enters the duodenum and the name of its sphincter?

A

Common bile duct

Sphincter of Oddi

709
Q

Name the 2 types of cells of the exocrine pancreas?

A

Acinar cells

Duct cells

710
Q

What do acinar cells secrete?

A

Digestive enzymes in zymogens

711
Q

What is the function and location of enterokinase?

A

Brush border of duodenal enterocytes

Overt trypsinogen to trypsin

712
Q

What is the function of trypsin?

A

Converts all zymogens to their active forms

713
Q

What stimulates HCO3 secretion in the pancreas?

A

Secretin

714
Q

What is secretin secreted in response to?

A

Acid in duodenum

715
Q

What stimulates the release of zymogens from acinar cells?

A

Chlecystokinin

716
Q

What is CCK secerted in response to?

A

Fat/aas in duodenum

Vagal reflex triggered by arrival of organic nutrients in the duodenum

717
Q

Explain the process if acid from the stomach reaches the duodenum?

A

SI increases secretin release
Causing the pancreas to release HCO3
HCO3 flow into SI
Neutralises the SI acid

718
Q

Explain the process if there is an increase in FA and aas related to pancreatic function?

A

Increased CCK release in SI
Causing enzyme release from pancreas
Increased flow of enzymes into SI
Increased digestion of fast and protein in SI

719
Q

Describe the structure of the liver?

A

Liver lobule
Portal triad (hepatic portal veins, hepatic artery and bile canaliculus)
Hepatocytes
Hepatic sinusoids

720
Q

What is included in the portal triad?

A

Hepatic portal veins
Hepatic artery
Bile canaliculus

721
Q

Do the hepatic artery and hepatic protal vein mix?

A

Yes

722
Q

What do the hepatocytes produce?

A

Bile

723
Q

What other fucntions do hepatocytes have?

A

Nutrient storage
Nutrient interconversion
Detoxification

724
Q

Describe the pathway for blood and nutrients through the liver system?

A

Hepatic portal vein and hepatic artery form the hepatic sinusoid
Blood enters the central veins to the hepatic veins back to the heart
The nutrients are taken out by the hepatocytes and stored or converted
Hepatocytes also produce bile that pass into canaliculi to the hepatic ducts to aid in digestion

725
Q

What nutrints are stored in the hepatocytes?

A 
Glycogen
Fat
B12
A 
D
E
K
Cu
Fe
726
Q

What is the function of the liver?

A

Bile production and secretion

727
Q

Name the 6 components of bile?

A 
Bile acids (secreted by L)
Lecithin (secreted by L)
Cholesterol (secreted by L)
Bile pigments (secreted by L)
Toxic metals (secreted by L)
Bicarbonate (secreted by pancreas)
728
Q

What is the function of bile acids, lecithin and cholesterol

A

Solubilse fat

729
Q

What is the function of bile pigments?

A

Bilirubin from ahem

730
Q

What is the function of toxic metals?

A

Detox in liver

731
Q

What is the function of HCO2?

A

Neutralisation of acidic chyme

732
Q

How do we improve the solubility of bile acids?

A

Conjugated with glycine or taurine forming bile salts

733
Q

What is the function of the gallbladder?

A

Overflow area for bile from the common bile duct

734
Q

How are bile salts recyled?

A

enterohepatic circulation

735
Q

What is the pathway for bile?

A 
Liver
Bile duct
Duodenum
Ileum
Hepatic portal vein
Back to the liver
5% lost in the faeces
736
Q

Explain the process of control of bile secretion?

A

Sphincter of Oddi controls the release of bile and pancreatic juice into the duodenum
If contracted, stays closed and overflows into gallbladder
If fat is present in the duodenum the response is to release CCK, in turn this relaxes the sphincter and contracts the gallbladder
The bile enters the duodenum and solubilises the fat
CCK activates pancreatic enzyme secretion and bile secretion

737
Q

What is the other function of the gallbladder?

A

Concentrates the bile 5-20 times the normal of the liver
Absorbs Na and H2O
Via paracellular pathways

738
Q

What is the cross-sectional structure of the SI?

A 
Mucosa
Submucosa
Circular muscle
Longitudinal muscle
Serosa
739
Q

What is present on the GI mucosa?

A

Plica:

- have villi increases SA

740
Q

Describe the structure of the epithelium in the SI

A 
Villi
Crypts
Lamina propria
Goblet cells
Endocrine cells
Absorptive cells
Muscularis mucosae
741
Q

How often os the lining of the gut replaced?

A

Every 5 days

742
Q

Describe the structure of an enterocyte?

A

Microvilli - higher SA

Cuboidal

743
Q

Name 3 disaccharides of glycogen/starch?

A

Maltose
Sucrose
Lactose

744
Q

Which enzymes catalyse maltose, sucrose and lactose to breakdown?

A

Maltase
Sucrase
Lactase

745
Q

What is maltose broken down into?

A

2 glucose

746
Q

What is sucrose broken down into?

A

1 glucose

1 fructose

747
Q

What is lactose broken down into?

A

1 glucose

1 galactose

748
Q

Which enzyme breaks down glycogen/starch?

A

Amylase

749
Q

Which enzyme breaks down peptides?

A

Endopeptidases

Forming 2 smaller peptides

750
Q

Which enzyme breaks down the smaller peptides?

A

Exopeptidases called aminopeptidase and carboxypeptidase to produce amino acids and even smaller peptides

751
Q

How do the enterocytes transport nutrients across their membranes?

A

Na-coupled secondary active transport:

  • Na/K pump to bring in K
  • Na coupled with nutrient into cell
  • nutrients enter bloodstream
  • K leaves via K channel
  • also water follow Na
752
Q

Explain the process of emulsification of fat in the stomach?

A

Mechanical breakdown in the antrum

Bile salts to stop the droplets from reforming large fat droplets in the duodenum

753
Q

How are the droplets converted to micelles?

A

Pancreatic lipase

Into FA and monoglycerides

754
Q

How are the FAs absorbed into the cells?

A

Diffuse into the cell

755
Q

How do the enterocytes convert and package the FA for future use?

A

FA and monoglycerides travel to the ER
Converted to triacylglycerol via triacylglycerol synthetic enzymes and packed via vesicles to form chylomicrons
Chylomicron will travel in the lacteal via the lymphatic system to be absorbed into the blood

756
Q

What is the defintion of segementation?

A

Processing the meal
Small sections of the SI constrict and then relax to allow mixing
Increasing Sa of the food to aid absorption

757
Q

What os the defintion of peristalsis?

A

Contraction behind the bolus and relaxation ahead to move the bolus towards the anus

758
Q

Name the parts of the LI?

A 
Ileum
Caecum
Asceding colon
ransverse colon
Descedning colon
Sigmoid colon
Rectum
759
Q

Describe the structure of the cross-sectional wall of the LI?

A

Intestinal crypts (very deep) (goblet cells)
Submucosa
Circular muscle
Longitudinal muscle (tenia coli 3 lines)

760
Q

Name the 2 sphincters in control of defaecation?

A

Anus closed by internal anal sphincter (SM under autonomic control) and external anal sphincter (skeletal muscle and voluntary control)

761
Q

Explain the process of defaecation?

A

Wave of intense contraction (mass movement contraction) from colon to rectum
Distension of rectal wall produced by MM of faeces into rectum activates the mechanoreceptors activating the defaecation reflex giving the urge to defaecate

762
Q

Explain the process of the defaecation reflex?

A

Parasympathetic control via the pelvic splanchnic nerve:

  • contraction of rectum
  • relaxation of internal and contraction of external anal sphincter
  • Increased peristaltic activity in colin increases the PA on the external sphincter
  • relaxation of external sphincter under voluntary control allow expulsion of faeces

3rd Year BDS (21 decks)

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