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CSP1 YR5 > Human Disease YR3 #2 > Flashcards

Human Disease YR3 #2 Flashcards

1
Q

Name 5 causes of normocytic anaemia?

A 
CancerRAIBSRenal problemsTB
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2
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

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3
Q

What is the definition of macrocytic?

A

Reflects an increased MCV but with reduced Hb level

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4
Q

What is the definition of normocytic?

A

The Hb is low but the MCV is within normal limits

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5
Q

Name 4 causes of microcytic anaemia?

A

Iron deficiencyAnaemia of chronic diseaseSideroblastic anaemiaThalasseamia

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6
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

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7
Q

Name 5 common causes of iron deficiency anaemia?

A 
PeriodGI blood lossIncreased demandSmall bowel diseasePoor diet
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8
Q

What is the FBC diagnosis for iron deficiency anaemia?

A

Low Hb and low MCVLow ferritinTotal iron binding capacity is increased

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9
Q

What is the management for iron deficiency anaemia?

A

Treat causeOral iron (Ferrous sulphate)IM

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10
Q

Name the 2 types of Thalassaemia?

A

Alpha| Beta

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11
Q

Name the 3 types of Beta Thalassaemia?

A

MajorIntermediaMinor

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12
Q

What causes megaloblastic anaemia?

A

Vit b12 deficiency| Folate deficiency

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13
Q

Name the 6 main reasons for B12 deficiency?

A 
Pernicious anaemiaGastrectomyVeganIleal resectionCoeliac diseaseBacterial overgrowth
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14
Q

Name the 4 main reasons for folate deficiency?

A

DietMalabsorptionHigh demandDrugs

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15
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

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16
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)

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17
Q

Blood group O - serum abs and info?

A

Anti A and B| Universal donor

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18
Q

Blood group A - serum abs and info?

A

Anti B

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19
Q

Blood group B - serum abs?

A

Anti A

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20
Q

Blood group AB - serum abs and info?

A

None| Universal recipients

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21
Q

Name 6 respiratory symptoms?

A 
BreathlessnessCoughSputumHaemoptysisChest painWheeze
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22
Q

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

A

Pulse oximetryPulse rateRespiratory ratePeak flow meter

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23
Q

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

A

Low PO2Normal or low PCO2Acute asthmaPneumonia

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24
Q

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

A

Low PO2High PCO2COPDObesity hypoventilation syndrome

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25
Q

Signs and symptoms for asthma and COPD?

A

BreathlessnessWheezeCough

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26
Q

What is the difference between COPD and asthma?

A

COPD:- irreversible airflow obstructionAsthma:- reversible airflow obstruction

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27
Q

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

A

HistoryPeak flow recordingLung function

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28
Q

Name the 5 treatment options for Asthma and COPD?

A 
Inhaled bronchodilators (salbutamol)Inhaled corticosteroids (beclomethasone)Oral theophyllineOral leukotriene receptor antagonist (montelukast)Oral prednisolone
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29
Q

What is the definition of pneuomina?

A

Infection of the lower respiratory tract

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30
Q

What are the signs and symptoms of pneumonia?

A 
FeverMyalgiaHeadacheCoughChest painSputumDyspnoea
Can proceed to TI respiratory failure
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31
Q

What are the treatment for pneumonia?

A

AntibioticsOxygenintravenous fluids

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32
Q

What is the definition of obstructive sleep apnoea?

A

Loud snoring and cessation of breathingDaytime sleepinessPoor concentration

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33
Q

How to treat obstructive sleep apnoea?

A

Weight lossCPAPMandibular repositioning splint

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34
Q

What is the definition of a pulmonary embolism?

A

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

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35
Q

Name 4 risk factors for pulmonary embolism?

A

Recent major operationRecent major traumaImmobilityMajor chronic disease

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36
Q

What are the signs and symptoms of pulmonary embolism?

A

BreathlessnessChest painHaemoptysis

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37
Q

What is the treatment for pulmonary embolism?

A

Anticoagulation

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38
Q

What is the definition of a pneumothorax?

A

Collapsed lung

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39
Q

Name the 2 types of pneumothorax?

A

Primary| Secondary

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40
Q

Signs and symptoms for a pneumothorax?

A

Chest pain| Dyspnoea

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41
Q

How to treat a patient with pneumothorax?

A

Aspiration of air around collapsed lungObservationChest drain

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42
Q

Signs and symptoms for lung cancer?

A

CoughHaemoptysisWeight loss

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43
Q

What is the definition of a chronic cough?

A

Cough lasting longer than 8 weeks

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44
Q

Name 3 common causes of chronic cough?

A

AsthmaGastro-oesophageal refluxPostnasal drip

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45
Q

What is the definition of bronchiectasis?

A

Dilated and damaged airways

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46
Q

Signs and symptoms of bronchiectasis?

A

CoughLarge amount of sputumHaemoptysis

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47
Q

What are the treatment options for chronic cough/

A

Inhaled corticosteroidsgastric acid suppression (omeprazole)Intranasal steroid spray (beconase)

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48
Q

How to diagnose sleep apnoea?

A

Sleep study

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49
Q

How to diagnose lung cancer?

A

CT scan| Bronchoscopy

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50
Q

How to diagnose chronic coughing?

A

Lung function test

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51
Q

How to diagnose bronchiectasis?

A

CT thorax

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52
Q

What is the definition of interstitial lung disease?

A

Thickening, inflammation of interstitium of the lung

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53
Q

Signs and symptoms of interstitial lung disease?

A

Dyspnoea| Dry cough

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54
Q

How to diagnose interstitial lung disease?

A

CT scan

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55
Q

Treatment options for interstitial lung disease?

A

CorticosteroidsOxygenPulmonary rehabPirfenidone

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56
Q

Explain the process of the platelet plug?

A

Vessel damage leads to platelet adhesion to the VWfPlatelets then aggregate to other platelets to form a plug + some fibrinogenFibrinogen is hen broken down to form fibrin forming the clot

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57
Q

What is the intrinsic pathway for clotting?

A 
IX --> IXaIXa --> X via VIIIaX --> XaProthrombin --> Thrombin via XaFibrinogen --> Fibrin by thrombin
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58
Q

What is the extrinsic pathway for clotting?

A 
VII + Tissue factorVIIIa/TF --> XaX --> XaProthrombin --> Thrombin via XaFibrinogen --> Fibrin by thrombin
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59
Q

Name 4 pathological causes for bleeding disorders?

A

Decreased number of plateletsAbnormal platelet functionVon Willebrand diseaseCoagulation factor (deficiency or inhibition)

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60
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 bleedingCongenital or acquiredMode of inheritance
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61
Q

Name 6 times history of bleeding can give information?

A 
BruisingEpistaxisPost-surgical bleedingMenorrhagiaPost-partum haemorrhagePost-trauma
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62
Q

Name 5 types of platelet type of pattern of bleeding?

A 
MucosalEpistaxisPurpuraMenorrhagiaGI
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63
Q

Name 3 types of coagulation factor for pattern of bleeding?

A

ArticularMuscle haematomaCNS

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64
Q

How to determine the difference between acquired and congenital?

A

Previous episodesAge at first eventPrevious surgical challengesAssociated history

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65
Q

What is the definition of Haemophilia A and B?

A

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

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66
Q

What are the clinical features of haemophilia?

A 
HaemarthrosisMuscle haematomaCNS bleedingRetroperitoneal bleedingPost surgical bleeding
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67
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?

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68
Q

What advice is given for severe haemophilia for dental procedures?

A

Enhanced preventive GDP| All treatments except prosthetics in specialist hospital setting

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69
Q

What advice is given for moderate haemophilia for dental procedures?

A

Enhanced preventive GDP| All treatments except prosthetics specialist hospital setting

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70
Q

What advice is given for mild haemophilia for dental procedures?

A

Enhanced preventive advice and treatment GDPMany procedures at GDP2 yearly review specialist dental centre

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71
Q

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

A 
Prevention as normalMild Haem A:- DDA VP/tranexamic acidMod/Severe Haem A:- coagulation factor replacement for VIIIAll Haem B:- coagulation factor replacement
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72
Q

What dental LA procedures require factor elevations?

A

IAN| Lingual infiltration

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73
Q

What dental LA procedures DO NOT require factor elevations?

A

Buccal infiltrationIntrapapillary injectionIntraligamentary injections

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74
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

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75
Q

Name 8 local haemostatic agents?

A 
Oxidized celluloseSurgicelAbsorbable gelatine spongeGelfoamCyanoacrylate tissue adhesivesSurgical splintsLyostyptAnkaferd blood stopper
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76
Q

Hwat complications can occur with haemophilia treatment?

A 
Viral infections:- HIV, HBV and HCVInhibitors- DDAVPFlushing Rare arterial eventsHyponatremia in babies
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77
Q

What is the definition of Von Willebrand disease?

A 
CommonVariable severityAutosomalMucosal platelet bleeding typeQuantitative and qualitative abnormalities of vWF
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78
Q

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

A

vWF concentrate or DDAVPTranexamic acidTopical applications

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79
Q

Name the 4 valves of the heart?

A

PulmonicAorticBicuspidTricuspid

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80
Q

Name the 3 types of valvular heart disease?

A

Valvular stenosisValvular regurgitationAortic coarctationCHD

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81
Q

What does the aortic valve look like?

A

Inverted Merc badge

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82
Q

Name the 2 types of aortic stenosis?

A

Degenerative| Bicuspid

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83
Q

What is the aetiology of degenerative aortic stenosis?

A

Becomes thick and calcified| Can fuse in the future

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84
Q

What is the aetiology of bicuspid aortic stenosis?

A

2 leaflets rather than 3 leaflets

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85
Q

Name 3 symptoms of aortic stenosis?

A

Chest painBreathlessness on exertionSyncope/Dizziness

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86
Q

Name the 2 types of causes of aortic regurgitation

A

Aortic defects| Leaflet defects

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87
Q

How can the aorta cause aortic regurgitation?

A

Dilated aorta

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88
Q

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

A

BicuspidRheumatic heart diseaseEndocarditis

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89
Q

Explain how Rheumatic heart disease occurs?

A

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

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90
Q

Name the 2 symptoms of aortic regurgitation?

A

Dyspnoea:- orthopnoea- paroxysmal nocturnal dyspnoeaChest pain

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91
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 diseaseInfectious endocarditis
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92
Q

Name the 3 symptoms for mitral valve disease?

A

BreathlessnessPalpitations due to AFEmbolisation

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93
Q

What is the definition of mitral stenosis?

A

Thickening and scarring of the leaflets| Fusion of the commissures

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94
Q

WHat is the definition of mitral regurgitation?

A

Leaflet abnormality| Mitral annular dilatation

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95
Q

Name the 2 right sided valves?

A

Tricuspid| Pulmonary

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96
Q

Name 2 types of congenital heart disease?

A

Ventricular septal defects| Compex CHD

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97
Q

Name 2 types of material for prosthetic heart valves?

A

Mechanical| Tissue

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98
Q

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

A

Warfarin

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99
Q

How often should a blood INR be carried out?

A

Every 6 weeks

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100
Q

What is the INR for AF?

A

2-3

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101
Q

What is the INF for metallic heart valves?

A

2.5-4

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102
Q

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

A

3 months

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103
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 inhibitorsEnsure proper local haemostasis

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104
Q

What are the risks of stopping oral anticoagulation?

A

Small, but fatal

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105
Q

What is the definition of infective endocarditis?

A

Infection on the cardiac or vascular endotheliumForms vegetationContains platelets, fibrin, microorganisms and inflammatory cell

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106
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 valvesBacteremia:- IV drug users- dental procedures- surgical procedures at infected sites
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107
Q

Name the 6 aetiologies for infective endocarditits?

A 
Bacteria:- streptococcus- staphylococcus- enterococcus- pneumococcus- gram -ve bacilliFungiMycobacteriaRickettsiaeChlamydiaMycoplasma
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108
Q

Name the 7 signs and symptoms for infective endocarditis?

A 
FeverMalaiseAnorexiaWeight lossHF due to acute valvular destructionSystemic embolisationAcute renal failure
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109
Q

What are the NICE guidelines for antibiotic prescription?

A

High risk patients when a high risk procedure is performed

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110
Q

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

A

Good oral hygiene| Regular dental review 2 yearly

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111
Q

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

A

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

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112
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)

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113
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 childAllergy to penicillin: single dose 30-60 mins before procedure- clindamycin- 600 mg po/IV adult- 20 mg/kg po/IV
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114
Q

Which procedures do not need antibiotic prophylaxis for infective endocarditis/

A

LA injections in non-infected tissue (superficial caries)Removal of suturesDental x-raysPlacement or adjustment of removable orthodontic appliances or bracesShedding of deciduous teeth or trauma to the lips or oral mucosa

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115
Q

Name 11 invasive dental procedures?

A

Placement of matrix bands• Placement of sub-gingival rubber damclamps• Sub-gingival restorations including fixedprosthodontics• Endodontic treatment before apical stophas been established• Preformed metal crowns (PMC/SSCs)• Full periodontal examinations (includingpocket 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 includingtemporary anchorage devices, mini implants• Uncovering implant sub-structures

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116
Q

Name 8 non-invasive dental procedures?

A 
Infiltration or block local anaestheticinjections in non-infected soft tissues• BPE screening• Supra-gingival scale and polish• Supra-gingival restorations• Supra-gingival orthodontic bands andseparators• Removal of sutures• Radiographs• Placement or adjustment of orthodonticor removable prosthodontic appliances
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117
Q

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

A

3g 60 mins before procedure

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118
Q

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

A

Max dose 3g50 mg/kgOral suspension

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119
Q

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

A

600mg 60 minutes before procedure

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120
Q

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

A

20 mg/kg| 600 mg max dose

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121
Q

What is consisted of the lower GI tract?

A 
JejunumIleumAscedning ColonDescedning colonSigmoid colonRectumCaecum
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122
Q

What is the function of the small bowel?

A

Enzymatic digestionabsorptionGut hormone secretionImmune

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123
Q

What is the function of the large bowel?

A

Storage and elimination of waste| FLuid and electrolyte reabsorption

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124
Q

What are the symptoms for colorectal cancer?

A

Change in bowel habitRectal blood lossAbdominal painWeight lossCo-incidental anaemia

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125
Q

When does bowel cancer screening occur?

A 
50-74 YOEvery 2 yearsFaecal occult bloodImmunochemical test+ve result referral for colonoscopy2% require colonoscopy
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126
Q

Explain how the adenoma can develop into a carcinoma?

A

Normal epitheliumSmall adenomaLarge adenomaInvasive adenocarcinoma

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127
Q

What are the stages of colorectal cancer?

A

Dukes A-D

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128
Q

Dukes A?

A

Tumour confined to mucosa| 93% survival

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129
Q

Dukes B?

A

Extension through mucosa to muscle layer| 77%

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130
Q

Dukes C?

A

Extension through mucosa to muscle layerInvolvement of lymph nodes48%

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131
Q

Dukes D?

A

Distant spread| 7%

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132
Q

What is the surgical management for Dukes A?

A

Endoscopic resection possible for polypsPossible need for stoma if low rectal tumours or perforated or obstructed tumours

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133
Q

What is the genetic and environmental contribution for colorectal cancer?

A

Mainly sporadicCan be geneticIncreased risk with IBD

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134
Q

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

A

Autosomal dominantMutation of APC geneHigh risk cancerAnnual colonoscopySupernumerary teethUnerupted teethMultiple osteomas of mandible (cotton wool like appearances)

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135
Q

What is the definition of Inflammatory bowel disease?

A

Chronic relapsing inflammatory conditions of the bowelUC and Crohn’sPeak incidence in 20s

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136
Q

What is the aetiology for IBD?

A

EnvironmentalGeneticCandidate genes identified

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137
Q

What are the triggering factors for IBD?

A

Bacterial infectionDietVaccination historySocial factors - smoking

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138
Q

Where does UC effect?

A 
Continuous mucosal inflammationAffects the colonRectum - proctitisLeft sided hemiExtensive pan
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139
Q

What are the symptoms for UC?

A

Bloody diarrhoeaAbdominal crampingWeight lossMalaise

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140
Q

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

A 
DiarrhoeaBleedingWeight lossVomitingPerianal symptoms
FistulaAbscessesFissures
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141
Q

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

A 
DiarrhoeaBleedingWeight lossVomitingPerianal symptoms:- fistula- abscesses- fissures
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142
Q

What are the extra-intestinal manifestations for IBD?

A

Eyes: uveitis and conjunctivitisJoint: sacroiliitis, monoarticular arthritis and ankylosing spondylitisLiver: fatty, gallstones, pericholangitis and sclerosing cholangitisSkin: vasculitis, pyoderma gangrenosum and erythema nodosum

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143
Q

What is the definition of toxic megacolon?

A

Colonic dilatation and systemic toxicity due to severe flare of colitis

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144
Q

What is the definition of toxic megacolon?

A

Colonic dilatation and systemic toxicity due to severe flare of colitis

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145
Q

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

A

ImmunosuppressionCorticosteroids for acute flare upsThiopurines (BM suppression)Biologics - infliximab (anti-TNF)Ensure no dental infection ongoing prior to administration

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146
Q

What is the definition of Coeliac disease?

A

Intolerance to gluten| Loss of microscopic villi in the SI, resulting in malabsorption

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147
Q

What are the symptoms for Coeliac disease?

A

DiarrhoeaWeight lossBloatingAnaemia

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148
Q

Diet changes for coeliac +ve patient?

A

No:- bread- pasta- cake- cereals- sauces- pre-prepared meals- beer

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149
Q

What is the definition of small bowel infarction?

A

Acute mesenteric ischaemiaUsually due to arterial thrombus or embolism blocking blood flowRapid onsetEmergency resection required

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150
Q

Name 2 eating disorders?

A

Anorexia nervosa| Bulimia nervosa

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151
Q

What is the definition of anorexia nervosa?

A

Refusal to maintain normal wightFear of weight gainDistorted perception of body image

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152
Q

What’s the definition of bulimia nervosa?

A

Binge eating followed by attempts to restrict weight gain| Purging

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153
Q

Oral manifestations for vomiting?

A 
Palatal erosionOcclusal erosion of maxillary teeth:- incisal edges of incisors thin and knife-edged- cupped out appearanceSwollen parotid glands
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154
Q

What is the definition of hereditary hemorrhagic telangiectasia?

A

Autosomal dominantPerioral telangiectasiaSmall bowel lesions can bleedPhotocoagulation/embolisation/surgery

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155
Q

What is the definition of Peutz-Jeghers syndrome?

A

Autosomal dominantMucocutaneous pigmented maculesMultiple polyps throughout bowel (block or bleed)GI cancers risk hight

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156
Q

Oral manifestations for Crohn’s disease?

A 
Orofacial granulomatosis:- inflammatory condition affect the oral mucosa- found before Crohn diagnosis- non-caseating granulomasRecurrent mouth ulcers
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157
Q

Treatment for oral manifestations for Crohns?

A

Local/systemic corticosteroids| Cinnamon-free diet

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158
Q

What is the definition of diverticular disease?

A

Asymptomatic| Bulging sac of tissue protruding from colonic wall

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159
Q

Complications for diverticular disease?

A

BleedingPerforationInfection + abscessesRequire surgeryHigh fibre diet good

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160
Q

Name 3 types of small bowel diseases?

A

Crohn’sCoeliac diseaseIschaemia/infarction

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161
Q

What are the symptoms of hereditary hemorrhagic telangiectasia?

A

Epistaxis| Pulmonary and cerebral lesions

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162
Q

Oral manifestation for iron-deficiency anaemia?

A

Angular cheilitis

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163
Q

What are the functions of the digestive system?

A

DigestionSecretionAbsorptionMotility

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164
Q

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

A 
MouthOesophagusStomachSIColonRectumAnus
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165
Q

What organ is responsible for digestion?

A

Stomach

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166
Q

Which organ is responsible for absorption and secretion?

A 
Absorption:- upper SI- colonSecretion:- lower SI- colon
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167
Q

Name the 2 forms of digestion?

A

Chemical| Enzymatic

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168
Q

Name each organ/tissue present in the GI tract?

A 
MouthSalivary glandsPharynxTracheaOesophagusLiverGallbladderStomachPancreasLISIRectumAnus
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169
Q

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

A 
SerosaLongitudinal muscularis externaMyenteric plexusCircular muscularis externaSubmucous plexusSubmucosa (BVs and nerves)Mucosa (epithelium)Lumen
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170
Q

Name the 2 autonomic controls of the GI system?

A

Long (para)| Short (ENS) reflexes

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171
Q

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

A 
Vagus nerve mainlyExcept salivation (VII and IX)Stimulatory:- increased secretion- increased motility
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172
Q

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

A

Splanchnic nerveInhibitor (except salviation):- reduced secretion- reduced motility

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173
Q

Where does the blood from the GI system drain to?

A

Hepatic portal vein

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174
Q

What 2 main vessels enter the Liver?

A

Hepatic portal vein| Hepatic artery

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175
Q

Why do we chew?

A

Prolong taste experience| Defence against respiratory failure

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176
Q

Explain the voluntary system in which chewing is controlled?

A

Somatic nerves innervate the skeletal muscles of the mouth and jaw

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177
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

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178
Q

Name the main organs for swallowing?

A 
Hard palateSoft palateTongueEpiglottisGlottisLarynx
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179
Q

Explain the oral phase (voluntary) during swallowing?

A

Bolus pushed to back of the mouth by tongue

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180
Q

Explain the pharyngeal phase during swallowing?

A

On presence of bolus it activates the sequence of reflex contractions of the pharyngeal musclesThis is coordinated y the swallowing centre in the medullaThe 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 tracheaOnce bolus has entered the oesophagus the sphincter contracts (preventing reflux)

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181
Q

Explain the oesophageal phase during swallowing?

A

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

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182
Q

How does the size of the stomach change?

A

50mL –> 1500mL with no Pa change

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183
Q

Name the 3 main parts of the stomach?

A

FundusBodyAntrum

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184
Q

What allows the receptive relaxation of the stomach?

A

Rugae in the stomach

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185
Q

What is the function of the fundus?

A

Storage of material

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186
Q

What is the function of the body?

A 
StorageMucusHClPepsinogenIntrinsic factor
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187
Q

What is the function of intrinsic factor?

A

Binds B12Aids haemoglobin formationTravels to terminal ileum and transported to the liver

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188
Q

What is the function of HCl and pepsinogen?

A

Digestion

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189
Q

What is the function of the antrum?

A

Mixing/grinding| Gastrin

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190
Q

What is the function of gastrin?

A

Regulates the secretion of HCl and pepsinogen

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191
Q

Name the 4 types of cells of a gastric gland?

A

Surface mucousMucous neckParietalChief

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192
Q

What do mucous neck cells secrete?

A

Mucus

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193
Q

What do chief cells secrete?

A

Pepsinogen

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194
Q

What do parietal cells secrete?

A

HCl| Intrinsic factor

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195
Q

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

A

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

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196
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 cellsGastrin/ACh activate ECL cells which release histamine to further activate Parietal cells

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197
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 cellsPeptides present in the lumen activate G cells secreting gastrin will activate parietal cellsGastrin/ACh will activate ECL cells to release histamine and activate parietal cells

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198
Q

What cells produce pepsiongen?

A

Chief cells

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199
Q

How is pepsinogen activated?

A

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

200
Q

How is pepsinogen packaged?

A

Zymogens to stop cellular digestion

201
Q

How are pepsin and HCl secretion related?

A

Proprotional to one another

202
Q

What secrete gastic mucus?

A

Surface epithelial cells and mucus neck cells

203
Q

What is the function of gastic mucus?

A

Cytoprotective roleProtects mucosal surface from mechanical injuryNeutralise pH as it has a high HCO contentProtects against gastric acid corrosion and pepsin digestion

204
Q

At what pH is pepsin denatured?

A

Neutral pH

205
Q

Explain how acid is neutralised before entering the duodenum?

A

HCO secreted from Brunner’s gland duct cells| H + HCO3 –> H2CO3 -> H20 + CO2

206
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

207
Q

What does secretin activate the release of and from where?

A

HCO3 from pancreas and liver

208
Q

How is secretin release controled?

A

Acid neutralisation leads to the inhibition of secretin release

209
Q

What is the function of the duodenum?

A

To neutralise acid from the stomach

210
Q

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

A

Common bile duct| Sphincter of Oddi

211
Q

Name the 2 types of cells of the exocrine pancreas?

A

Acinar cells| Duct cells

212
Q

What do acinar cells secrete?

A

Digestive enzymes in zymogens

213
Q

What is the function and location of enterokinase?

A

Brush border of duodenal enterocytes| Overt trypsinogen to trypsin

214
Q

What is the function of trypsin?

A

Converts all zymogens to their active forms

215
Q

What stimulates HCO3 secretion in the pancreas?

216
Q

What is secretin secreted in response to?

A

Acid in duodenum

217
Q

What stimulates the release of zymogens from acinar cells?

A

Chlecystokinin

218
Q

What is CCK secerted in response to?

A

Fat/aas in duodenum| Vagal reflex triggered by arrival of organic nutrients in the duodenum

219
Q

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

A

SI increases secretin releaseCausing the pancreas to release HCO3HCO3 flow into SINeutralises the SI acid

220
Q

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

A

Increased CCK release in SICausing enzyme release from pancreasIncreased flow of enzymes into SIIncreased digestion of fast and protein in SI

221
Q

Describe the structure of the liver?

A

Liver lobulePortal triad (hepatic portal veins, hepatic artery and bile canaliculus)HepatocytesHepatic sinusoids

222
Q

What is included in the portal triad?

A

Hepatic portal veinsHepatic arteryBile canaliculus

223
Q

Do the hepatic artery and hepatic protal vein mix?

224
Q

What do the hepatocytes produce?

225
Q

What other fucntions do hepatocytes have?

A

Nutrient storageNutrient interconversionDetoxification

226
Q

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

A

Hepatic portal vein and hepatic artery form the hepatic sinusoidBlood enters the central veins to the hepatic veins back to the heartThe nutrients are taken out by the hepatocytes and stored or convertedHepatocytes also produce bile that pass into canaliculi to the hepatic ducts to aid in digestion

227
Q

What nutrints are stored in the hepatocytes?

A 
GlycogenFatB12A DEKCuFe
228
Q

What is the function of the liver?

A

Bile production and secretion

229
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)
230
Q

What is the function of bile acids, lecithin and cholesterol

A

Solubilse fat

231
Q

What is the function of bile pigments?

A

Bilirubin from ahem

232
Q

What is the function of toxic metals?

A

Detox in liver

233
Q

What is the function of HCO2?

A

Neutralisation of acidic chyme

234
Q

How do we improve the solubility of bile acids?

A

Conjugated with glycine or taurine forming bile salts

235
Q

What is the function of the gallbladder?

A

Overflow area for bile from the common bile duct

236
Q

How are bile salts recyled?

A

enterohepatic circulation

237
Q

What is the pathway for bile?

A 
LiverBile ductDuodenumIleumHepatic portal veinBack to the liver5% lost in the faeces
238
Q

Explain the process of control of bile secretion?

A

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

239
Q

What is the other function of the gallbladder?

A

Concentrates the bile 5-20 times the normal of the liverAbsorbs Na and H2OVia paracellular pathways

240
Q

What is the cross-sectional structure of the SI?

A 
MucosaSubmucosaCircular muscleLongitudinal muscleSerosa
241
Q

What is present on the GI mucosa?

A

Plica:| - have villi increases SA

242
Q

Describe the structure of the epithelium in the SI

A 
VilliCryptsLamina propriaGoblet cellsEndocrine cellsAbsorptive cellsMuscularis mucosae
243
Q

How often os the lining of the gut replaced?

A

Every 5 days

244
Q

Describe the structure of an enterocyte?

A

Microvilli - higher SA| Cuboidal

245
Q

Name 3 disaccharides of glycogen/starch?

A

MaltoseSucroseLactose

246
Q

Which enzymes catalyse maltose, sucrose and lactose to breakdown?

A

MaltaseSucraseLactase

247
Q

What is maltose broken down into?

248
Q

What is sucrose broken down into?

A

1 glucose| 1 fructose

249
Q

What is lactose broken down into?

A

1 glucose| 1 galactose

250
Q

Which enzyme breaks down glycogen/starch?

251
Q

Which enzyme breaks down peptides?

A

Endopeptidases| Forming 2 smaller peptides

252
Q

Which enzyme breaks down the smaller peptides?

A

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

253
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

254
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

255
Q

How are the droplets converted to micelles?

A

Pancreatic lipase| Into FA and monoglycerides

256
Q

How are the FAs absorbed into the cells?

A

Diffuse into the cell

257
Q

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

A

FA and monoglycerides travel to the ERConverted to triacylglycerol via triacylglycerol synthetic enzymes and packed via vesicles to form chylomicronsChylomicron will travel in the lacteal via the lymphatic system to be absorbed into the blood

258
Q

What is the defintion of segementation?

A

Processing the mealSmall sections of the SI constrict and then relax to allow mixingIncreasing Sa of the food to aid absorption

259
Q

What os the defintion of peristalsis?

A

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

260
Q

Name the parts of the LI?

A 
IleumCaecumAsceding colonransverse colonDescedning colonSigmoid colonRectum
261
Q

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

A

Intestinal crypts (very deep) (goblet cells)SubmucosaCircular muscleLongitudinal muscle (tenia coli 3 lines)

262
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)

263
Q

Explain the process of defaecation?

A

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

264
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

265
Q

Name 6 pathophysiologies for upper GI disease?

A 
PepticMalignancyAutoimmunityFuncionalInfectiveGenetic
266
Q

What is the definition of helicobacter pylori and how is it transmitted?

A

Flagellate bacteria from spirochete| Transmitted human to human

267
Q

How is helicobacter pylori adapted to survive in the stomach?

A

Adapted to stomach| Converts urea to ammonia to neutralise periplasm

268
Q

What disease does helicobacter pylori cause?

A 
Chronic gastritisAtrophic gastritis (impaired acid prod)Antral gastritis (increased acid production)Pan gastritis (increased prolif of gastric cells)
269
Q

Which precancerous conditions can helicobacter pylori cause?

A

Gastric carcinoma| MALToma

270
Q

How to diagnose for helicobacter pylori infection?

A

Serum Faecal antigen Urease breath testCLO test

271
Q

What is the definition of gastro-oesophageal reflux disease?

A

Reflux acid content into the oesophagus

272
Q

What are the symptoms for Gastro-oesophageal reflux disease?

A

Chronic cough| Hoarse voice

273
Q

What are the predisposing factors for Gastro-oesophageal reflux disease?

A 
Lifestyle ObesityIncreased Intra-abdominal pressureSmokingAlcohol
274
Q

What causes GORD?

A

Lower oesophageal sphincter relaxation| increased or higher frequency

275
Q

What treatment can be prescribed for GORD?

A

Proton pump inhibitorChange lying positionDiet

276
Q

Name the 4 grades for oesophagitis?

277
Q

What is the definition of metaplasia?

A

Where one organ’s lining mutates and becomes the lining of a different organ

278
Q

What is the definition of Barrett’s oesophagus?

A

Metaplasia of the oesophagus from acid exposure| Can be precancerous

279
Q

What is the aetiology for peptic disease for upper GI disease?

A

Helicobacter pyloriNSAIDsZollinger-Ellison disease

280
Q

Name the 2 types of oesophageal cancer?

A

Squamous cell carcinoma| Adenocarcinoma

281
Q

Prognosis of squamous cell carcinoma?

A

1 yr 36%| 5 yrs 12%

282
Q

Prognosis of adenocarcinoma?

A

5 yrs:- localised 45%- nodes 24%- meta 4%

283
Q

What are the risk factors squamous cell carcinoma?

284
Q

How to diagnose and stage oesophageal squamous cell carcinoma?

A 
EndoscopyBiopsyCTUltrasoundPET
285
Q

What is the treatment for oesophageal squamous cell carcinoma?

A

Radiotherapy

286
Q

What are the risk factors adenocarcinoma?

A

SmokingAlcoholHP

287
Q

What are the signs and symptoms for adenocarcinoma?

288
Q

How to diagnose and stage oesophageal adenocarcinoma?

A 
EndoscopyBiopsyCTUltrasoundPET
289
Q

How to treat oesophageal adenocarcinoma?

A

RadiotherapyOesophagectomy Chemotherapy

290
Q

What are the risk factors for gastric adenocarcinoma?

A

HPSmoking Obesity

291
Q

How do patient present when they have a gastric adenocarcinoma?

A

Late stage:- significant invasion of wall- metastasis to nodesLittle symptoms till disease advanced

292
Q

What is a diagnostic aid for a patient with gastric adenocarcinoma

A

Iron-deficiency anaemia

293
Q

How to diagnose and stage gastric adenocarcinoma?

A 
EndoscopyBiopsyCTUltrasoundPET
294
Q

What is the prognosis of gastric adenocarcinoma?

A

Less than 20% after 2 years

295
Q

What is the definition of a MALToma?

A

HP related| Indolent marginal zone b cell lymphoma of the mucosa-associated lymphoid tissue or aggressive large b-cell lymphoma

296
Q

What is the treatment for MALToma?

A

Resolution of HP infection for MALTomaDLBCL more problematicRadiotherapySurgery (bypass)

297
Q

What is the prognosis for MALToma?

A

90% survival at 5 years

298
Q

What is the definition of a neuroendocrine tumour and treatment?

A

Enterochromaffin-like cells of the gastric mucosaIncidental findingTreatment:- treat symptoms

299
Q

What is the definition of a GIST and treatment?

A 
Gastrointestinal stromal tumour:- SM cells- cajal cells tumour- low malignancy rateTreatment:- surgery
300
Q

What is the definition of Crohn’s disease?

A

Full GI tractGeneticEnvironment related to vit D

301
Q

What are the symptoms for Crohn’s disease?

A

Mouth ulcersAbdominal painDiarrhoeaObstruction

302
Q

What are the treatments for prognosis? *****

A

SurgeryMedical managementImmunosuppression

303
Q

What is the definition of coeliac disease?

A

Allergy to glutenMalabsorption of nutrientsAbs made against glutenInflammation of SI

304
Q

What are the symptoms for coeliac disease?

A

DyspepsiaDiarrhoeaAbdominal bloatingWeight loss

305
Q

What is the treatment for Coeliac disease?

A

Diet modification

306
Q

What are the complications for coeliac disease?

A

Refractory| Lymphoma

307
Q

What is the treatment for oesophageal dysmotility?

A

Botox injectionRat tail oesophagusSurgery

308
Q

Name 2 types of infection the upper GI tract can get?

A

Candida| Tropical sprue

309
Q

What are the risk factors for candida infection?

A

Immunocompromised| Steroid inhalers

310
Q

What is the treatment for candida?

A

Fluconazole

311
Q

What are the signs and symptoms for candida?

A

Dysphagia| Odynophagia

312
Q

What causes tropical sprue?

A

BacteriaParasitesViruses

313
Q

How does tropical sprue cause har,?

A

Flattens villi causing malabsorption

314
Q

What are the symptoms for tropical sprue?

A

Nutrient deficiencyDiarrhoeaFatigue

315
Q

What is a form of tropical sprue?

A

Giardiasis

316
Q

What is the definition of small bowel bacterial overgrowth?

A

Bacterial overgrowth in the small bowel?

317
Q

What are the predisposing factors for small bowel bacterial overgrowth?

A

Absence of ileocecal valve Bypass surgeryDiabetesDevelopmental

318
Q

What is the treatment for small bowel bacterial overgrowth?

A

Antibiotics

319
Q

What are the symptoms for small bowel bacterial overgrowth?

A

Malabsorption

320
Q

Name 5 other things that can cause harm to the oesophagus?

A 
Caustic injuryForeign bodyFood bolusStricturesEoE
321
Q

Name 8 rare oesophageal disorders?

A 
VasculitisBehcet (ulcer)Churg-strauss (ulcer)Dermatomyositis (ulcer)CT diseaseScleroderma (dysmobility)Mix CT disease (dysmobility)Crest syndrome (dysmobility)
322
Q

NAme 4 rare gastric diseases?

A

Genetic:- menetrier disease (overgrowth of mucous cells)- HHT- FAP- Peutz-Jegher

323
Q

What are the oral manifestations for Crohn’s?

A

Oral mucosal ulcerationMucogingivitisCobblestoning

324
Q

What are the oral manifestations for Coeliac disease?

A

Enamel hypoplasiaDelayed tooth eruptionGlossitisIDA

325
Q

What are the oral manifestations Pernicious anaemia?

A

Atrophic glossitis

326
Q

What are the oral manifestations Peutz Jegher syndrome?

A

Melanotic macules

327
Q

What are the oral manifestations Plummer vision?

A

Stomatitis

328
Q

What are the oral manifestations HP and PUD?

A

Dental erosionBad taste in mouthHalitosisMucositis

329
Q

What are the oral manifestations Gardner’s syndrome?

A

Osteomas| Supernumerary teeth

330
Q

What are the functions of the liver?

A

SynthesisExcretoryMetabolicStorage

331
Q

Name 2 types of liver disease?

A

Acute| Chronic (inflammation, fibrosis and cirrhosis)

332
Q

Name 5 features of liver disease?

A 
NoneJaundiceSynthetic dysfunctionMetabolic dysfunctionFeatures of portal hypertension
333
Q

Name 2 types of jaundice for the liver?

A

Hepatic| Cholestatic

334
Q

Name 2 types of synthetic dysfunction for the liver?

A

Oedema| Coagulopathy

335
Q

Name 2 types of metabolic dysfunction for the liver?

A

Hypoglycaemia| Encephalopathy

336
Q

Name 2 features of portal hypertension for the liver?

A

GI bleedingAscitesHernia

337
Q

What are the risk factors for liver disease?

A 
Alcohol*Blood-borne virusesObesityDiabetesHyperlipidemiaAutommunityMedicationFamily historyUCChronic biliary tract disease/hepatobiliary surgery
338
Q

What is the mechanism for alcoholic liver disease?

A 
Liver excretes the alcoholAlcohol causes fat accumulation in liverAlcohol is a toxin to the liverSteatosisContinued for a while causes fibrosis and cirrhosis
339
Q

What is the treatment for alcoholic liver disease?

A

Stop drinking| Possible liver transplant

340
Q

What is the definition of hepatitis A?

A 
AcuteRNAOro-faecal transmissionLong life diseaseVaccination and avoid contaminated food and water
341
Q

What is the definition of hepatitis B?

A

DNAVertical/parenteral/sexual transmissionChronicCo-infection with hepatitis D

342
Q

What is the definition of hepatitis C and its treatment?

A 
ssRNAParenteralVerticalSexualCombination therapy
343
Q

What is the definition of hepatitis E?

A

Via contaminated food and waterHepatic failure in pregnancyNo chronicNo treatment

344
Q

What is the definition of non-alcoholic fatty liver disease?

A

Fatty liverLeads to steatohepatitisFurther to fibrosis and cirrhosis

345
Q

What are the risk factors for non-alcoholic fatty liver disease?

A 
ObesityDiabetesHyperlipidemiaMalnutritionTPNAlcohol/DrugsGenetical
346
Q

How to diagnose for non-alcoholic liver disease and treatment?

A

Blood testing| No specific treatment

347
Q

What is the definition of autoimmune liver diseases?

A

Inflammatory| Autoantibodies against nuclear and cytosolic microsomal

348
Q

Name 3 types of autoimmune liver disease?

349
Q

How to diagnose autoimmune liver disease?

A

Abs test| Histology

350
Q

What is the definition of drug and toxin-related liver disease?

A

Zonal necrosis leads to hepatitis leads to cholestasis leads to steatosis leads to fibrosis leads to cirrhosis

351
Q

Name 4 heritable liver diseases?

A

Hereditary haemochromatosis (Fe overload)Wilson’s disease (Cu overlaod)Alpha-1 antitrypsin deficiencyGilbert’s disease (more unconjugated bilirubin)

352
Q

Name the most common liver cancer?

A

Hepatocellular carcinoma:- cirrhosis, hep B and C- scans and detect alpha-fetoprotein

353
Q

Name 4 rare causes of liver disease?

A

CryptogenicInfections (bac or parasite)Vascular insultsSystemic diseases

354
Q

Name 3 biliary diseases?

A

GallstonesAutoimmune diseaseCancer:

355
Q

How to monitor liver function test?

A 
BilirubinAlbumin EnzymesClotting profileFBV
356
Q

What are 2 types of autoimmune disease of the biliary tract?

A
  • primary biliary cirrhosis| - primary sclerosing cholangitis
357
Q

What are the 2 types of cancer of the biliary tract?

A

Cholangiocarcinoma| Cancer of the gallbladder

358
Q

Name the 2 most common child cancers?

A

Leukaemia (80 % ALL)| Lymphoma

359
Q

Name the 5 most common adult cancers?

A 
BreastProstateLungColorectalBladder
360
Q

Name the 4 risk factors for breast cancer?

A

Reproductive historyHormone therapyBreast densityBRAC1/2

361
Q

Name the 6 types of breast cancer?

A 
Ductal carcinoma in situLobular carcinoma in situInvasive ductal breast cancerInvasive lobular breast cancerInflammatory breast cancerPaget disease
362
Q

Name the 3 types of treatment for breast cancer?

A

SurgeryRadioChemoCombo of all

363
Q

Name the 4 types of leukemia?

A

Acute myeloidAcute lymphoblasticChronic myeloidChronic lymphocytic

364
Q

What is the definition of a leukaemia?

A

The malignant cell is a bone marrow derived haemopoietic stem cell which grows uncontrollably and invades and takes over the bone marrow.Invade blood cells and enlarge all organs

365
Q

Name the 3 environmental associations for leukemias?

A

BenzeneChlorambucilRadiation treatment

366
Q

Name the 3 clear genetic events that link to leukaemia progression?

A

Down’s syndrome patientsCML and ALL:- philadelphia chromosome- long arm of Ch22 translocated to long arm of chromosome 9- forms bcr-ablAML:- associated with t15:17 preventing the natural maturation of the myeloid cell line

367
Q

What is the definition of acute leukaemia?

A

Acute leukaemia is when the bone marrow is overrun with immature myeloid and lymphoid precursors are unable to mature further.

368
Q

What are the signs for acute leukaemia?

A

AnemiaBleedingInfectionOrgan enlargement

369
Q

What are the treatment options for acute leukaemias?

A

Correction of RBC and platelet problemTreat infectionKeep hydratedGuard against acute tumour lysis syndrome

370
Q

What is the specific treatment for AML?

A

Cytosine arabinoside| Daunorubicin

371
Q

What is the specific treatment for ALL?

A

VincristinePrednisoneDaunorubicinIf involves brain needs methotrexate or radiation therapy

372
Q

What are the signs and symptoms for CML?

A 
Weight loss SweatingAnaemiaBleedingInfectionsEnlarged spleen.
373
Q

What is the treatment for CML?

A

Alpha interferon| Hydroxyurea

374
Q

What can CML progress to?

A

Acute leukemia (blast transformation) can cause rapid death

375
Q

What is the definition of chronic lymphocytic leukaemia?

A

Incurable malignant proliferation of predominantly mature B cells

376
Q

What ae the signs and symptoms for CLL?

A

AnaemiaBleeding InfectionEnlarged lymph nodes and spleen

377
Q

How can a blood test confirm a diagnosis of CLL?

A

Increase in WBC and predominantly lymphocytes, anaemia and thrombocytopenia on blood testingLymphocytes on blood film (smear cells as they rupture)Bone marrow biopsy

378
Q

What is the treatment for CLL?

A

Oral chlorambucil| +/- prednisolone

379
Q

Name the 9 most common side effects of chemotherapy?

A

Anaemia (reduced bone marrow)Thrombocytosis (thrombocytopenia)Mandibular toriMucositis (and ulceration)DysphagiaHair loss (hair follicle turnover - reversible)Sterility (affects high turnover sperm cell. Pre-treatment samples can be saved)CataractsVomiting (there is a direct stimulation of the vomiting centre in brain stem)

380
Q

Name the 2 types of lymphoma?

A

Hodgkin’s| Non-Hodgkin’s

381
Q

What are the signs and symptoms for Hodgkin’s lymphoma?

A 
Sweating (especially at night)FeverWeight lossPruritusFatigueAnorexiaPain in the lymph nodes on drinking alcohol
382
Q

How is Hodgkin’s lymphoma diagnosed and staged?

A

Lymph node biopsyChest x-rayCT BM scan

383
Q

What is the definition of Non-Hodgkin’s lymphoma?

A

highly heterogenous disease of malignant lymphatic cells which can infiltrate a variety of structures.

384
Q

What are the 2 types of Non-Hodgkin’s lymphoma?

A

High grade| Low grade

385
Q

What is the treatment regime for High grade NHL?

A

CHOP:- cyclophosphamide- hydroxyaunrubicin- oncovin- prednisolone.

386
Q

What does CHOP stand for?

A
  • cyclophosphamide- hydroxyaunrubicin- oncovin- prednisolone.
387
Q

What is the treatment for low grade NHL?

A

Not curable and rumbles on for years with symptomatic treatment with chlorambucil or radiotherapy for masses as they arise.

388
Q

What are the signs and symptoms for NHL?

A

Bruising| Anaemia and Infections

389
Q

What tests ca be conducted to confirm a diagnosis of NHL?

A

Reduced RBC and platelet numbers, with raised white cell count on blood testsAbnormal liver function tests if liver involvedA chest x-ray and CT scan will show masses which will require a biopsy to provide sub-type diagnosis.Bone marrow aspirate is needed to determine spread

390
Q

What are the risk factors for lung cancer?

A 
SmokingUrban livingAsbestos exposureCoal burningPassive smokingArsenicFe oxide
391
Q

What are the clinical features of lung cancer?

A 
CoughHaemoptysisChest painBone spread leading to fracturesMetastases to bone and the brainFinger clubbingWeight lossLymphadenopathy
392
Q

What is the definition of Pancoast’s tumour in relation to lung cancer?

A

Invasion of the brachial plexus causing pain (Pancoast’s tumour)

393
Q

What is the definition of Horner’s syndrome in relation to lung cancer?

A

Invasion of the sympathetic ganglions (Horner’s syndrome); involves recurrent laryngeal nerves leading to hoarseness and invasion of the oesophagus, heart and veins

394
Q

What investigations can be conducted to diagnose lung cancer?

A

Chest x-ray for massesSputum cytology for malignant cellsBronchoscopy for biopsyCT scan for peripheral lesions.

395
Q

What investigation to use to stage a lung cancer tumour?

396
Q

Name the 2 types of lung cancers?

A

Non-small cell| Small cell

397
Q

Name 4 types of non-small cell lung cancers?

A

Squamous cell carcinomaLarge cellAdenocarcinomaALveolar

398
Q

Name a type of small cell lung cancer?

A

Endocrine cell

399
Q

How can skin change with lung cancer?

A

Pigmented skin in axillae (acanthosis nigricans)| Herpes zoster Dermatomyositis

400
Q

What are the treatment options for lung cancer?

A 
SurgeryRadiotherapyChemo for small cell casesHaemodialysisHaemofiltrationPeritoneal dialysis
401
Q

What are the risk factors for colorectal cancer?

A

High meat/low fibre dietFamily historyHereditary non-polyposis carcinoma Familial adenomatous polyposis

402
Q

What genetic mutations contribute to colorectal cancer?

A

K-ras| c-myc

403
Q

Dukes stage A?

A

Bowel only

404
Q

Dukes stage B?

A

Through bowel wall

405
Q

Dukes stage C?

A

Spread to regional lymph nodes

406
Q

Dukes stage D?

A

Distant metastases

407
Q

What are the signs and symptoms for lower colorectal cancer

A

descending colon with bleeding, narrowing and obstruction, leading to alternating diarrhoea and constipation, which may be accompanied by bleeding per rectum

408
Q

What are the signs and symptoms for upper colorectal cancer

A

mass on examination or blood loss related anaemia| Liver involvement will present with jaundice

409
Q

What investaigantions can be done to aid diagnosis?

A

Barium enemaEndoscopyUSS of LiverBloods

410
Q

What is the treatment for colorectal cancer?

A

SurgeryChemotherapy for B/C (5-Fluorouracil and levamisole)Radio

411
Q

How to diagnose prostate cancer?

A

Palpation of hard prostateElevated PSABiopsyTransrectal USS

412
Q

What are the signs and symptoms for prostate cancer?

A

Presence of prostatic specific antigen| Obstructive urinary flow

413
Q

What is the treatment for prostate cancer?

A

SurgeryRadiotherapyMetastasis:- androgen ablation therapy

414
Q

Name the 4 risk factors for bladder cancer?

A

SmokingBenzidineCyclophosphamideChronic infection like schistosomiasis

415
Q

What are the signs and symptoms of bladder cancer?

A

Haematuria| Painless

416
Q

What investigations aid diagnosis of bladder cancer?

A

Cytological exam of urineUrographyCystoscopy

417
Q

What is the treatment for bladder cancer?

A

SurgeryRadioChemo

418
Q

What is an oral side effect for radiotherapy?

A

Osteoradionecrosis

419
Q

What is an oral side effect for chemotherapy?

A

Candidiasis

420
Q

What is the 5 Yr survival rate for NSCLC?

421
Q

Name the 4 stages of Hodgkin’s disease?

422
Q

Describe stage I of Hodgkin’s Lymphoma?

A

Single site with radio

423
Q

Describe stage I of Hodgkin’s Lymphoma?

A

2 or more sites on same side of diaphragmRadio+/- chemo if symptomatic

424
Q

Describe stage III of Hodgkin’s Lymphoma?

A

SItes on both sides of diaphragm| Chemo

425
Q

Describe stage IV of Hodgkin’s Lymphoma?

A

Widespread involvement of non-lymphatic tissue| Chemo

426
Q

What is SI 5 Yr survival rate for Hodgkin’s lymphoma?

427
Q

What is the 5 yr survival for colorectal cancer?

A

45%| Dukes A 95%

428
Q

What is the 5 yr survival for prostate cancer after surgery?

429
Q

Which gender is more at risk of haem cancers?

430
Q

What % of all cancers are haem cancers?

431
Q

What is the most common child cancer?

432
Q

What % of all cancers does leukemia comprise of for childhood cancer?

433
Q

Explain the normal hematopoiesis process for the common myeloid progenitor cell?

A

Differentiate to erythromegakaryotic progenitor cells formins erythrocytes and plateletsCommon myeloid progenitor cells differentiation to monocytes that become macrophagesMyeloid progenitor cells can also differentiate into neutro, eosino and basophils

434
Q

What cells does acute lymphocytic leukemia affect?

A

Lymphoid progenitor

435
Q

What cells do Acute myeloid leukaemia affect?

A

Myeloid progenitor

436
Q

What cells fo chronic lymphoid leukemia?

A

B cells/T cells

437
Q

What cells do multiple myeloma?

A

Plasma cells

438
Q

What cells do myeloproliferative disorders affect?

A 
NeutroEosinoBasoMonoPlateletsRed cells
439
Q

Name 2 types of acute leukemias?

A

Acute lymphoblastic leukemia| Acute myeloid leukemia

440
Q

Name 2 types of chronic leukaemias?

A

Chronic myeloid leukaemia| Chronic lymphocytic leukaemia

441
Q

Name 2 types of malignant lymphomas?

442
Q

Name 3 other categories of haem cancers?

A

Multiple myelomaMyelodysplastic syndromeChronic myeloproliferative disease

443
Q

When does NHL peak epidemiologically?

A

18-35| 75+

444
Q

Describe the difference between acute and chronic leukemias?

A 
Acute:- leukaemic cells do not differentiate- BM failure- rapidly fatal if untreated- curableChronic:- leukaemic cells can differentiate- prolif without BM failure- survival for a few years- No cure with BM transplant
445
Q

What diseases has been related for NHL?

A

Glandular fever| Also has peak at 18-35

446
Q

Describe the difference between leukaemia vs lymphoma?

A 
Leukemia - BM:- stem cell- lymphoid progenitor- b progenitor- pre B- immature BLymphoma - lymphoid tissue:- Germinal centre B cell- Plasma cell- mature naive b cell- memory b cell
447
Q

What are the clinical features for acute leukaemia?

A

BM failure:- anaemia- thrombocytopenic bleeding- infection because of neutropenia

448
Q

What are the key properties for multipotential hematopoietic stem cells?

A

Self-renewing population| Multi-potent

449
Q

Name 4 myeloid malignancies?

A

RedPlatGranMono

450
Q

Name 2 Lymphoid malignancies?

451
Q

What are the systemic symptoms for a patient with lymphoma?

A 
FeverDrenching sweatWeight lossPruritusFatigue
452
Q

What are the nodal diseases found with lymphoma presentation?

A

Lymphadenopathy:- >90% HL with nodal disease- 60% NHL present with nodal disease

453
Q

What was the most common localisation of cancer for head and neck lymphomas?

A

Waldeyer’s ring 149 hits| Parotid and salivary glands 41

454
Q

What are the different presenastions of lymphadenopathy?

A

Localised and painfulLocalised and painlessGeneralised and painfulGeneralised and painless

455
Q

Give 1 example of a disease present for localised and painful type of lymphadenopathy?

A

Bacterial infection in draining site

456
Q

Name 5 diseases present for localised and painless type of lymphadenopathy?

A 
Rae infectionsCatch scratch feverTBMetastatic carcinoma from draining site (hard)Lymphoma (rubbery)
457
Q

Name 5 disease for generalised and painful type of lymphadenopathy?

A 
Viral infectionsEBVCMVHepatitisHIV
458
Q

Why is ALL/Lymphoblastic lymphoma related?

A

Same disease| Different area

459
Q

Why is CLL/SCLL related?

A

Same disease with different presentation

460
Q

Why is Burkitt’s lymphoma/leukaemia related?

A

Same disease with different presentations

461
Q

Why is HL/DLBLFL related?

A

Same disease with different presentations

462
Q

Name 5 diseases for generalised and painless type of lymphadenopathy?

A 
LymphomaLeukaemiaCT diseasesSarcoidosisDrugs
463
Q

Name the 7 clinical features for multiple myeloma?

A 
Bone pain and lytic lesionsAnaemiaRecurrent infectionsRenal failureAmyloidosisBleeding tendencyHyperviscosity syndrome
464
Q

Name 5 risk factors for oestonecrosis of the jaw?

A 
Dental disease or surgeryoral traumaPeriodontitisChemotherapy or steroidsNitrogen-containing bisphosphonates
465
Q

Describe the structure of the lymph node?

A

CortexParacortexMedullaGerminal centreMantle zoneMarginal zoneForms the B cell follicle

466
Q

Where does osteonecrosis of the jaw normally affect?

A

Mandible 2/3 cases

467
Q

Explain the B cell maturation pathway?

A 
Progenitor  cellPre B cellImmature B cellNaive B cellEnter GCInteracts with antigenSomatic hypermutationForms centrocyteDifferentiates to Memory B cell or plasma cell
468
Q

What is the definition of lymphadenopathy?

A

Swollen lymph nodes

469
Q

What are the extranodal diseases presentation for lymphoma?

A

40% of NHL present with extranodal component

470
Q

How much fluid does a kidney process?

471
Q

Name the 6 functions of the kidney?

A 
Maintain homeostasisRegulate body waterEliminate waste products of metabolismRegulate blood pressureCa and bone metaErythropoiesis
472
Q

Name the 6 ways to assess kidney function?

A 
Serum ureaSerum creatinineEndogenous creatinine clearanceGFRIsotope GFR (GS) - 55 chromium EDTADerived formulae for GFR
473
Q

What is the average GFR?

474
Q

When can the kidneys be considered compromised when judging GFR?

A

Less than 60mL/min

475
Q

What is creatinine and its levels in M/F?

A 
Breakdown of creatine in musclesMr 113Can give info on renal function60-90 F70-116 M
476
Q

What are the 2 formulas to estimate GFR?

A

MDRD| Cockroft-Gault

477
Q

How does estimated GFR equation change for an African patient?

A

Usually have higher muscle mass compared to other ethnicity (less fat)Raised to 1.210

478
Q

How to measure the degree of renal insufficiency?

A 
eGFR = % kidney functionOnly an estimateWide CIUsually underestimatesRemember ethnicity
479
Q

What is a healthy GFR value?

A

> 60 mL/min

480
Q

What is the creatinine difference between blood and urine?

A

Higher in urine, as it is being excreted| Excretion test may give false results

481
Q

Stage 1 kidney disfunction GFR?

A

Kidney damage| >90 GFR

482
Q

Stage 2 kidney disfunction?

A

Mild| 60-89 GFR

483
Q

Stage 3 kidney dysfunction GFR?

A

Moderate| 30-59 GFR

484
Q

Stage 4 kidney disfunction?

A

Severe| 15-29 GFR

485
Q

Stage 5 kidney disfunction GFR?

A

Kidney failure| <15 or RRT GFR

486
Q

What are the levels of kidney disease and their prevalence per 10,000 patients?

A 
At risk 460Initiation 380Progression 60End stage 6per 10,000 at GP practice
487
Q

What are the clinical problems of CKD?

A

Underecognition at earlier stages of kidney dysfunction| Growth of 6-8% per annum of dialysis patients

488
Q

Name the 7 causes of kidney disease?

A 
Diabetes TI/IIHigh BPGlomerular diseaseCongenital diseaseInherited diseases (polycystic)Obstruction to flow of urineUnknown
489
Q

What is the size of a kidney?

490
Q

What type of genetic is polycystic kidney disease?

A

Autosomal dominant disease

491
Q

What to implement to delay progression and reduce CVS risk for CKD?

A

ACEIBP controlGlucose controlSMoking cessation

492
Q

What to implement to prevent uraemic complications for CKD?

A

MalnutritionAnaemiaCaPO4 PTHAcidosis

493
Q

What are the comorbidities of CKD?

A

Cardiac diseasesVascular diseasesDrug intersNeuropathy/Retinopathy

494
Q

How to prepare for RRT?

A

EducationInformed choiceTimely access placement/transplant listingTimely initiation of RRT

495
Q

What are the contraindications for dialysis?

A

BlindnessIHDDementiaNon-english speaker

496
Q

What ae the causes of hypertension in chronic renal failure?

A

Volume/total body Na excessStimulation of renin-angiotensin systemAugmented sympathetic tone

497
Q

What is the rationale for ACE/All inhibition in chronic renal failure?

A

Reduction of proteinuria and BPReduced hyperfiltration and reduced loss of albumin and proteinsLess renal cell growth and fibrosis

CSP1 YR5 (10 decks)

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