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3rd Year - Module 5 > Human diseases 2 > Flashcards

Human diseases 2 Flashcards

1
Q

Name four types of malabsorption/small bowel disease

A

1) pernicious anaemia
2) coeliac disease
3) crohn’s disease
4) small bowel infections

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2
Q

Name two types of large bowel disease

A

inflammatory bowel disease (IBS) - Crohn’s and ulcerative colitis
Colonic cancer

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3
Q

What medication used in upper GI disease eliminates formed acids?

A

Antacids

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4
Q

How do antacids work?

A

alkalis that form a salt with gastric acid and neutralise the effects on the tissues e.g. gaviscon, Rennies

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5
Q

What medications used in upper GI disease reduce acid secretion?

A

H2 receptor blockers
proton pump inhibitors

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6
Q

What are the three main triggers for stomach acid production?

A

acetylcholine
gastrin
histamine

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7
Q

What are stomach acids produced by?

A

parietal cells in the stomach wall

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8
Q

How do H2 receptor antagonists work?

A

reduce acid production by preventing histamine activation of acid production

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9
Q

Why are H2 receptor antagonists not as effective as proton pump inhibitors?

A

limited effect as they only interrupt histamine pathway, gastrin and acetylcholine still active whereas PPIs block acid production whether there is a trigger or not

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10
Q

Name two H2 receptor antagonists

A

cimetidine
ranitidine - available over the counter

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11
Q

Name three proton pump inhibitors

A

omeprazole, lanzoprazole, pantoprazole

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12
Q

Which medications end in -prazole?

A

Proton pump inhibitors
anti-ulcer drugs that reduce gastric acid production.

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13
Q

What are proton pump inhibitors used for?

A

profound and prolonged reduction of stomach acid production

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14
Q

What is dysphagia?

A

difficulty swallowing

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15
Q

What are the three main causes of gastro-oesophageal reflux disease?

A

defective lower oesophageal sphincter
impaired lower clearing (oesophagus not emptied properly)
impaired gastric emptying (stomach full so contents re-enter oesophagus)

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16
Q

What are the effects of GORD?

A

Ulceration, inflammation, metaplasia (gastric)
Barrett’s oesophagitis - precancerous adenocarcinoma

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17
Q

What is Barrett’s oesophagitis?

A

lining of the oesophagus damaged by acid reflux, which causes the lining to thicken and become red

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18
Q

What are the signs and symptoms of GORD?

A

epigastric burning - worse lying down, bending, pregnancy
dysphagia
GI bleeding
severe pain - mimics MI, oesophageal muscle spasm

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19
Q

What is a hiatus hernia?

A

when part of the stomach squeezes up into the chest through an opening (“hiatus”) in the diaphragm

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20
Q

How is GORD managed?

A

smoking cessation (improves sphincter)
weightloss
antacids
H2 blockers and PPIs - ranitidine and omeprazole

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21
Q

Where does peptic ulcer disease occur?

A

any acid affected site
oesophagus, stomach, duodenum

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22
Q

What can cause peptic ulcer disease?

A

normal acid secretion - stomach
high acid secretion - duodenal
drugs - NSAIDs, steroids

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23
Q

What bacterium causes peptic ulcer disease?

A

helicobacter pylori

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24
Q

How does helicobacter pylori cause peptic ulcer disease?

A

infects lower part of stomach (antrum), causes loss of mucous barrier and allows stomach acid to cause ulceration to stomach lining

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25
Q

What are the effects of peptic ulcer disease?

A

gastric ulcers
chronic gastric wall inflammation
mucosa assoc lymphoid tumour (MALT)

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26
Q

How is peptic ulcer disease managed?

A

Triple therapy
2 antibiotics, 1 proton pump inhibitor

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27
Q

What are the signs and symptoms of peptic ulcer disease?

A

asymptomatic
epigastric burning pain - worse at night, before/after meals, relieved by food, alkali and vomiting
usually NO physical signs unless complications

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28
Q

How is peptic ulcer disease investigated?

A

endoscopy
radiology - barium meal
anaemia - FBC and faecal occult tests
Helicobacter pylori - breath, antibodies, mucosa

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29
Q

What are the possible complications of peptic ulcer disease? local and systemic

A

local - perforation, haemorrhage, stricture, malignancy
systemic - anaemia

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30
Q

What does coffee ground vomit indicate?

A

large peptic ulcer bleed

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31
Q

How can you improve the mucosal barrier in upper GI disease?

A

eliminate helicobacter pylori
inhibit prostaglandin removal - so reduce/avoid NSAIDs and steroids

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32
Q

What medications are used in triple therapy for peptic ulcer disease?

A

2 antibiotics - amoxycillin, metronidazole
1 proton pump inhibitor - omeprazole

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33
Q

Describe the three surgeries that can be used in management of PUD

A

1) Bilroth 1 - part of stomach removed and duodenum reattached to top half of stomach
2) Bilroth 2 - part of stomach removed and top half reattached to small bowel and duodenum sewn up
3) highly selective vagotomy - dividing vagus nerve supply to stomach to reduce neurological trigger for acid secretion

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34
Q

What is coeliac disease?

A

sensitivity to alpha-gliaden component of gluten

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35
Q

Name some examples of gluten in the diet

A

wheat, barley, spelt, rye, kamut (cereals, breads)

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36
Q

What happens in the body in coeliac disease?

A

genetic susceptibility, environmental trigger (consumption of gluten)
T lymphocytes damage mucosal tissue
villous atrophy - loss of jejunal projections and surface area of jejunum so impaired absorption

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37
Q

What are the effects of coeliac disease?

A

weightloss, lassitude, weakness, abdominal pain and swelling, diarrhoea, oral ulcers, tongue papillary loss, steatorrhoea, dysphagia

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38
Q

What are the typical malabsorption issues associated with coeliac disease?

A

iron
folate
vitamin B12
fat

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39
Q

What is steatorrhoea and what condition can it sometimes occur with?

A

excess fat in stool
coeliac disease

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40
Q

How is coeliac disease investigated?

A

autoantibody test
jejunal biopsy
faecal fat
haematinics - B12, folate, ferritin

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41
Q

What is the effect of a gluten free diet in people with coeliacs disease?

A

reversal of jejunal atrophy, improved wellbeing, reduced risk of lymphoma

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42
Q

What is coeliac disease skin disease and what are the symptoms?

A

coeliac disease associated with dermatitis herpetiformis
oral disease - ulceration and blisters
granular IgA deposit in skin and mucosa - itch and blisters (usually shoulders)

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43
Q

All oral aphthous ulcer patients are screened by what?

A

haematinic assays to detect deficiency
TTG test usually done too - detects IgA

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44
Q

What is pernicious anaemia?

A

disease caused by vitamin B12 deficiency

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45
Q

Where is the absorption site for vitamin B12?

A

discrete area of the terminal ileum - only absorption site in the bowel

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46
Q

What causes pernicious anaemia?

A

lack of B12 in diet - vegans
disease of gastric parietal cells (autoimmune disease)
IBS of terminal ileum - Crohn’s disease
bowel cancer at ileo-coecal junction - resection removes absorptive tissue

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47
Q

What does vitamin B12 need for production?

A

intrinsic factor from gastric parietal cells

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48
Q

How is vitamin B12 deficiency treated?

A

diet with adequate B12
vit B12 supplements if prescribed
IM injections of B12 if GI absorption not possible

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49
Q

What has Crohn’s disease been linked to?

A

infection with myobacteria (paratuberculosis)
Johne’s disease in cattle - milk transmission?

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50
Q

What is a common site for Crohn’s disease?

A

any site along GI tract plus mouth
ileocoecal region popular site, causes malabsorption of vitamin B12 (pernicious anaemia)

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51
Q

Where does ulcerative colitis occur?

A

starts in distal part of bowel and moves forward through large intestine (always present in rectum)

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52
Q

What are two key characteristics of ulcerative colitis?

A

continuous
ulcers in the colon

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53
Q

What are the main differences between ulcerative colitis and Crohn’s disease?

A

UC continuous, C discontinuous
UC rectum always involved, C rectum involved 50%
UC anal fissures 25%, C anal fissures 75%
UC mucosa gran. & ulcers, C mucosa cobbled & fissures
UC vascular, C non-vascular
UC serosa normal, C serosa inflamed

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54
Q

What are the microscopic features of ulcerative colitis?

A

mucosal, vascular, mucosal abscesses

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55
Q

What are the microscopic features of Crohn’s disease?

A

transmural (all layers inflamed), oedematous (blockage of lymphatics, granulomas (giant cells occupying lymphatic drainage systems)

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56
Q

How much of the bowel wall is involved/inflamed in Crohn’s disease?

A

full thickness

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57
Q

What form between the layers of the bowel in Crohn’s disease?

A

abscesses and fistulae

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58
Q

What is the appearance of the mucosa in Crohn’s disease like?

A

cobblestone pattern, areas of oedema between fibrous bands

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59
Q

What is an issue caused by the thickening/inflammation of the intestinal wall in Crohn’s disease?

A

narrowed lumen can cause issues passing food, obstruction of the bowel

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60
Q

What layers of the intestine does ulcerative colitis affect?

A

only the mucosal layer

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61
Q

What are the four names of ulcerative colitis which indicate the site of inflammation?

A

Proctitis - only the rectum
proctosigmoiditis - rectum and sigmoid colon
distal colitis - left side of colon
pancolitis - entire colon

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62
Q

What investigations can be done for inflammatory bowel diseases?

A

blood tests - anaemia, CRP (C-reactive protein), ESR (erythrocyte sedimentation rate) detect inflammatory process
faecal calprotectin - inflammatory protein
endoscopy, barium studies, leukocyte scan

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63
Q

What is a complication of inflammatory bowel disease?

A

ulcerative colitis develops carcinoma - risk increases with time

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64
Q

What are the drug treatment options for inflammatory bowel diseases?

A

immunosuppressive treatment - systemic steroids (prednisolone), local steroids, anti-inflammatories, non-steroid immunosuppressants, biologics (infliximab)

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65
Q

What are the surgical treatment options for inflammatory bowel diseases?

A

colectomy - cures ulcerative colitis
Crohn’s disease - removal of obstructed bowel segments, drain abscesses, close fistulae (palliate symptoms) - usually results in stoma bag

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66
Q

What is orofacial granulomatosis?

A

granuloma formation blocks lymphatics
oedema of mouth and/or face, cobblestone appearance

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67
Q

What is the difference between orofacial granulomatosis and oral Crohn’s disease?

A

Orofacial crohn’s disease when GI tract also involved.
Orofacial granulomatosis when no symptoms further in GI tract

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68
Q

What does “bowel cancer” usually mean?

A

colonic cancer/colonic adenocarcinoma

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69
Q

Who qualifies for bowel cancer screening in the UK?

A

anyone from age 50

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70
Q

What are the symptoms of colonic carcinoma?

A

none
anaemia
rectal blood loss
often no symptoms until tumour causes blockage

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71
Q

What do most colonic carcinomas arise in?

A

polyps

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72
Q

What does bowel cancer screening aim to detect?

A

polyps within the surface of the lumen before they progress to malignancy

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73
Q

What kind of polyps form in colonic carcinoma and how long does it take for them to progress to malignancy?

A

pedunculated or flat
most will bleed due to irritation and trauma
most take 5 years to progress to malignancy

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74
Q

If a colonic carcinoma is removed at the polyp stage what happens?

A

cancer will not develop and patient no longer has lesion

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75
Q

What patient related factors can increase risk of colonic cancer?

A

diet - low fibre, high fat, high meat, low veg
smoking, alcohol missuse, lack of exercise

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76
Q

What is Peutz-Jehgers syndrome and how can it manifest orally?

A

a rare disorder in which growths called polyps form in the intestines
peri-oral melanosis

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77
Q

What are two examples of large intestine conditions that are high risk for progression to carcinoma?

A

Gardner’s syndrome
Cowden’s syndrome - polyps present in mouth too

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78
Q

What are the surgical options for treating colonic cancer?

A

resection of colon with anastomosis
bowel brought to surface as stoma

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79
Q

What are three examples of urinary tract obstructions?

A

renal stones
tumours
prostatic hypertrophy

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80
Q

What does the presence of any bacteria in urine imply?

A

urine should be STERILE. any bacteria present implies infection

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81
Q

What is the most common bacteria found in UTIs?

A

E.coli
Staph, fungi, virus and TB also possible

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82
Q

What is cystitis?

A

bladder inflammation

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83
Q

What can UTIs proceed to cause?

A

cystitis

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84
Q

What are predisposing factors for UTIs?

A

poor bladder emptying
low urinary flow rates (in heat or dehydration)

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85
Q

What are the symptoms of a UTI?

A

dysuria (painful urination)
urinary frequency
cloudy urine
offensive smelling urine
supra-pubic pain

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86
Q

What puts you at risk of a UTI?

A

people of any age can get a UTI
women>men
people with catheters
diabetes or immunosuppressed
spinal cord injuries or other nerve damage
UT abnormalities blocking flow of urine

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87
Q

Urine, if infected can cause what three infections?

A

cystitis
renal infection
prostate infection

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88
Q

What UTI can occur in isolation (does not need to have infected urine)?

A

urethritis - gonococcal infection

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89
Q

What are the symptoms of cystitis?

A

dark cloudy smelly urine
blood in urine
pain in lower stomach and on urination
peeing often
pain during sex
sick and tired

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90
Q

How are UTIs treated?

A

MSSU - Mid-stream sample of urine (less contamination) sent for microscopy, culture and sensitivity
increase fluid intake
frequent urination
occasionally ABx required - amoxicillin

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91
Q

What are four examples of conditions that could cause urinary tract obstruction?

A

1) renal calculi
2) prostatic disease - hypertrophy, malignancy
3) urinary tract strictures
4) external compression

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92
Q

How does prostatic disease cause urinary tract obstruction?

A

urethra passes through the prostate gland, so any enlargement compresses the urethra

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93
Q

What is prostatitis?

A

inflammation of prostate

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94
Q

What is benign prostatic hypertrophy?

A

benign condition in which an overgrowth of prostate tissue pushes against the urethra and the bladder, blocking the flow of urine.

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95
Q

How common is benign prostatic hypertrophy?

A

almost normal, 80% over 80 have BPH
100% if people live long enough

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96
Q

What are the symptoms of urinary outflow obstruction?

A

slow stream
urgency
nocturia
hesitancy
frequency
incomplete voiding - increases UTI risk

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97
Q

What is the treatment for a benign prostatic hypertrophy?

A

Initially drug based - alpha blocking drugs, anticholinergic (both to shrink gland size) and diuretics to flush system
Surgery - prostatectomy

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98
Q

Prostatic malignancy starts after what age?

A

45

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99
Q

What is used for early detection of prostate cancer?

A

mpMRI (multiparametric MRI)

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100
Q

How is prostatic malignancy treated?

A

surgery - radical prostatectomy
radiotherapy
hormone treatment - anti-androgens and LHRH analogues, block hormone dependent tumour growth

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101
Q

What are the two types of renal calculi (stone)?

A

1) calcium and oxalate (radiopaque)
2) uric acid (not radiopaque)

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102
Q

How are renal calculi treated?

A

Lithotrypsy - ultrasound shock waves break ‘simple’ stones which are too large to pass into smaller pieces

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103
Q

What is polyuria?

A

passing large volume of urine

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104
Q

what is haematuria?

A

blood present in urine (frank or microscopic)

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105
Q

What is proteinuria?

A

not normal, protein passing into urine suggests glomerular disease

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106
Q

What is uraemia?

A

increased concentration of urea in blood

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107
Q

What does serum urea rise with?

A

dehydration

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108
Q

What is considered the best measure of renal function?

A

serum creatinine - kidneys should filter creatinine out of the blood. If kidney function is not normal, serum creatinine is increased and urine creatinine is decreased

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109
Q

What is renal failure?

A

loss of renal excretory function
loss of water and electrolyte balance
loss of acid base balance
loss of renal endocrine function

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110
Q

What hormonal impacts does the loss of renal endocrine function in renal failure have?

A

less erythropoietin - so less RBCs produced
calcium metabolism - high serum calcium levels
renin secretion - cause salt and water imbalance

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111
Q

What are the characteristics of acute renal failure?

A

rapid loss of renal function
usually over hours or days

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112
Q

What are the characteristics of chronic renal failure?

A

gradual loss of renal function
usually over many years

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113
Q

What are the causes of renal failure categorised into?

A

pre-renal (in circulation before kidney)
renal (kidney)
post renal (after kidney)

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114
Q

What is a pre-renal cause of renal failure?

A

hypoperfusion of the kidney - sudden and severe drop in BP (shock) or interruption of blood flow to kidneys from trauma or illness (renal artery or aorta disease)

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115
Q

What are the intrarenal causes of renal failure?

A

direct damage to kidneys by inflammation, toxins, drugs, infection or reduced blood supply

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116
Q

What are some post-renal causes of renal failure?

A

renal outflow obstruction due to enlarged prostate, kidney stones, bladder tumour, injury

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117
Q

What are the signs of acute renal failure?

A

creatinine level >200micromol/L
no urine initially with volume overload - oedema, breathlessness, raised venous pressure
progresses to polyuria
development of hyperkalemia (high potassium) can lead to cardiac arrest
development of uraemia and acidosis

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118
Q

What are the characteristics of the causes of acute renal failure and its management?

A

usually a pre-renal cause
usually reversible with time, renal support until recovery - dialysis, nutrition

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119
Q

What is glomerulonephritis?

A

damage to the tiny filters inside your kidneys (the glomeruli) allowing cells and protein to leak into urine.

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120
Q

What can glomerulonephritis progress to?

A

hypertension
chronic renal failure

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121
Q

What are the symptoms of glomerulonephritis?

A

haematuria and proteinuria
otherwise a healthy individual

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122
Q

What is nephrotic syndrome?

A

condition in which kidneys leak large amounts of protein into the urine, complication of glomerulonephritis.

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123
Q

What are the features of nephrotic syndrome?

A

excessive loss of protein in the urine, >3g in 24hrs
loss of plasma oncotic pressure
tissue swelling (oedema)
hypercoagulable state

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124
Q

What drugs should be avoided in renal disease and why?

A

NSAIDs - inhibit glomerular blood flow causing interstitial nephritis.

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125
Q

What drug is known to be nephrotoxic and what is it used for?

A

cyclosporin - steroid-sparing immunosuppressant used in organ and bone marrow transplants as well as inflammatory conditions such as ulcerative colitis, rheumatoid arthritis

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126
Q

What is renal vascular disease and what can cause it?

A

reduced blood flow to the kidney
atheroma of renal artery/aorta, hypertension causing narrowing of renal artery
microangiopathy - immune reaction causing small blood vessel damage, RBC damage and thrombosis

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127
Q

What are three conditions which can cause immune mediated renal damage?

A

1) multiple myeloma - plasma cell tumour, clogs kidney causing tubular nephritis
2) Good pasture’s syndrome
3) Vasculitis

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128
Q

What is polycystic kidney disease?

A

spontaneous or inherited disorder in which clusters of cysts develop in renal parenchyma of kidneys, causing your kidneys to enlarge and lose function over time.
Gene mutation (PK1, 2 or 3)

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129
Q

What defines when someone has reached end stage renal disease?

A

eGFR <15ml/min
serum creatinine 800-1000micromol/L

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130
Q

How is chronic renal failure managed?

A

reduce the rate of decline
eliminate nephrotoxic drugs
control hypertension, diabetes, vasculitic disease
correct fluid balance - restrict fluid intake, restrict salt, potassium, protein
correct deficiencies - anaemia, calcium
remove outflow obstruction
treat any infection

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131
Q

What are the signs of chronic renal failure?

A

anaemia
hypertension
renal bone disease - low Ca, high phosphate, hyperparathyroidism, osteomalacia

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132
Q

What are the symptoms of chronic renal failure?

A

insidious - may be few
polyuria, nocturia, tired and weak, nausea

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133
Q

What are the dental aspects of renal disease?

A

careful prescribing
avoid NSAIDs, some tetracyclines

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134
Q

What are the dental aspects of renal failure?

A

growth may be slow in children - tooth eruption may be delayed
secondary effects of anaemia - oral ulceration, dysaesthesias
white patches - uraemic stomatitis
oral opportunistic infections - fungal, viral
dry mouth and taste disturbance - fluid restriction and electrolyte imbalance
bleeding tendency - platelet dysfunction
renal osteodystrophy - lamina dura lost, bony radiolucencies

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135
Q

What causes dry mouth and taste disturbance in renal failure?

A

fluid restriction and electrolyte imbalance

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136
Q

What radiographic changes can be seen orally with renal failure?

A

renal osteodystrophy - complication of chronic kidney disease that weakens your bones, lamina dura lost and bony radiolucencies present

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137
Q

What are the renal functions?

A

excretory function
water and electrolyte balance
acid base balance
renal endocrine function - calcium, renin, erythropoietin

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138
Q

What is renal dialysis?

A

a passive process where there is diffusion across concentration gradients. Allows intermittent correction of plasma concentration of small molecules

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139
Q

What are the two types of dialysis?

A

1) haemodialysis - blood extracted, put through unit and returned
2) peritoneal dialysis - catheter through abdominal wall, dialysing solution introduced to peritoneal cavity and inner lining of peritoneum used as dialysis membrane

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140
Q

What anticoagulant is often added into blood during haemodialysis?

A

heparin

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141
Q

How are the endocrine functions of the renal system replaced in renal failure?

A

erythropoietin - replaced by EPO injections to maintain RBC mass
calcium/bone mass maintained by vitamin D supplementation
hypertension control

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142
Q

What is the optimal treatment for end stage renal disease?

A

renal transplantation

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143
Q

Where is a transplanted kidney placed?

A

lower than original for easier access

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144
Q

What are the problems with renal transplantation?

A

rejection - acute or chronic
immunosuppression
high cardiovascular mortality
osteoporosis risk

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145
Q

Is the survival rate better with a renal transplant or dialysis treatment?

A

renal transplant

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146
Q

What are the important factors to remember when treating a patient that undergoes dialysis?

A

treat AFTER haemodialysis sessions
normal renal function at first but may reduce with time so check creatinine levels
complications are those of immune suppressants

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147
Q

Can DMARDs be prescribed alongside corticosteroids?

A

yes

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148
Q

How quickly should DMARDs be escalated to therapeutic dose?

A

as quickly as possible

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149
Q

Name 5 conditions treated by DMARDs in oral medicine

A
  • lichen planus
  • mucous membrane pemphigoid
  • pemphigus vulgaris
  • Behcet’s disease
  • erythema multiforme
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150
Q

What is the difference between DMARDs and NSAIDs?

A

NSAIDs and corticosteroids have a short onset of action while DMARDs can take several weeks or months to demonstrate a clinical effect.

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151
Q

What are the side effects of the DMARD azathioprine?

A

bone marrow suppression, red cell aplasia, neutropenia, thrombocytopenia, increased susceptibility to infections

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152
Q

What are the side effects of the DMARD methotrexate?

A

bone marrow suppression, mouth ulcers, neutropenia, thrombocytopenia, liver toxicity, pneumonitis

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153
Q

What are DMARDs used to treat?

A

stop or slow the disease process in inflammatory forms of arthritis. DMARDs help preserve joints by blocking inflammation

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154
Q

What are the side effects of the DMARD hydroxychloroquine?

A

retinopathy, hepatic failure, bone marrow suppression, anaemia, thrombocytopenia, leucopenia

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155
Q

What are the main dental considerations regarding DMARDs?

A

increased susceptibility to infection
oral ulceration with methotrexate

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156
Q

What are biologics?

A

subset of DMARDs that may slow or stop inflammation that can damage joints and organs in arthritis and other inflammatory diseases. they are proteins produced by living organisms or by bioengineering

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157
Q

What do Biologics target?

A

one aspect of the immune system rather than the entire system like conventional DMARDs

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158
Q

How are biologics administered?

A

IV infusions (would be digested if swallowed)

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159
Q

How do biologics evade the immune system?

A

they do not carry antigenic segments that may elicit an immune response so they are undetected

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160
Q

What are the four categories of monoclonal antibody and what qualifies them as each category?

A

Murine - mouse derived
Chimeric - part mouse
Humanized - part human
Human - human derived

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161
Q

When is monoclonal antibody therapy used?

A

when patients have ‘failed’ therapy with at least two DMARDs

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162
Q

What is etanercept and what is it used to treat?

A

a fusion protein, Anti-TNF drug which blocks TNF (tumour necrosis factor) and reduces inflammation. used to treat psoriasis, psoriatic arthritis, RA, ankylosing spondylitis

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163
Q

What do monoclonal antibodies end in?

A

-mab
e.g. infliximab, adalimumab, certolizumab

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164
Q

What fusion protein drug (biologic) is used to treat metastatic colorectal cancer?

A

aflibercept

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165
Q

What drugs end in -ine? (not all)

A

anti-histamines

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166
Q

What drugs end in -pine?

A

calcium channel blockers
e.g. amlodipine
lower BP

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167
Q

What drugs end in -asone?

A

corticosteroids
e.g. fluticasone, betamethasone

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168
Q

What drugs end in -ital?

A

sedatives
e.g. butabarbital

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169
Q

What drugs end in -caine?

A

local anaesthetic
e.g. lidocaine, articaine

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170
Q

What drugs end in -cillin?

A

penicillin antibiotic
e.g. amoxicillin, ampicillin

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171
Q

What drugs end in -dazole?

A

antibiotics, antibacterials
e.g. metronidazole, omeprazole

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172
Q

What drugs end in -dipine?

A

calcium channel blockers
e.g. amlodipine

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173
Q

What drugs end in -dronate?

A

bisphosphonates
e.g. alendronate, zolendronate, risedronate

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174
Q

What drugs end in -eprazole?

A

proton pump inhibitors
e.g. omeprazole

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175
Q

What drugs end in -fenac?

A

NSAIDs
e.g. diclofenac

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176
Q

What drugs end in -mab?

A

monoclonal antibodies
e.g. denosumab, infliximab

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177
Q

What drugs end in -mycin?

A

antibiotic, antibacterial
e.g. erythromycin, clindamycin

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178
Q

What drugs end in -olol?

A

beta blockers
e.g. propanolol,

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179
Q

What drugs end in -olone?

A

corticosteroids
e.g. triamcinolone, prednisolone

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180
Q

What drugs end in -oprazole?

A

Proton pump inhibitors
e.g. lansoprazole

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181
Q

What drugs end in -pril?

A

ACE inhibitor
e.g. ramipril

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182
Q

What drugs end in -semide?

A

loop diuretics
e.g. furosemide

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183
Q

What drugs end in -zepam?

A

benzodiazepines
e.g. diazepam

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184
Q

What drugs end in -zodone?

A

anti-depressants
e.g. trazodone

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185
Q

What are the dental considerations regarding biologics?

A

increased risk of infection
neutropenia, thrombocytopenia
careful prescribing - liver and renal function
MRONJ
mucosal disease - immunosuppressed

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186
Q

What guidance is given for stopping/continuing biologics for dental surgery?

A

for most biologics consideration should be given to planning surgery when at least one dosing interval has elapsed for that specific drug.
For higher risk procedures consider stopping 3-5 half-lives before surgery

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187
Q

Are biologics recommended following surgery?

A

may be recommended post surgery when there is good wound healing (typically around 14 days), all sutures and staples are out and there is no evidence of infection

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188
Q

For patients taking ritixumab (biologic - separate rule for ritixumab), when should treatment be stopped before surgery?

A

3-6 months prior

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189
Q

What is ritixumab used to treat?

A

targeted cancer drug (monoclonal antibody)

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190
Q

What proportion makes up the blood in an anti-coagulated sample?

A

55% plasma
45% red blood cells
plus WBC and platelets

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191
Q

Name two plasma proteins

A

albumin
globulin

192
Q

What is anaemia?

A

Low haemoglobin

193
Q

What is leukopenia?

A

low WCC

194
Q

What is thrombocytopenia?

A

low platelet count

195
Q

What is pancytopenia?

A

all blood cells reduced

196
Q

What is polycythaemia?

A

raised haemoglobin

197
Q

What is leukocytosis?

A

raised WCC

198
Q

what is thrombocythaemia?

A

raised platelet count

199
Q

What does one blood change indicate vs multiple blood changes?

A

one change - reactive change to environment
multiple - bone marrow failure

200
Q

What is leukaemia?

A

blood malignancy - neoplastic proliferation of white cells
usually disseminated

201
Q

What is lymphoma?

A

neoplastic proliferation of white cells
usually a solid tumour

202
Q

How does the point of neoplasia in the haematological cell line affect the malignancy?

A

earlier in the cell line neoplasia occurs, more potentially aggressive the malignancy

203
Q

What are leukaemia and lymphoma further divided into?

A

lymphoid and myeloid

204
Q

What is porphyria?

A

abnormal metabolism of the blood pigment haemoglobin. Porphyrins are excreted in the urine, which becomes dark

205
Q

Which porphyria is most clinically relevant and why?

A

acute intermittent porphyria
photosensitive rash, neuropsychiatric attacks
hypertension, tachycardia
may be fatal

206
Q

What are the two main ways that haemoglobin issues occur?

A

inability to make HAEM (usually iron deficiency)
inability to make correct GLOBIN chains (thalassemia, sickle cell)

207
Q

What does the number of RBCs mean in terms of anaemia?

A

nothing
anaemia can happen with too many or too few RBCs

208
Q

What can the size of RBCs in the blood stream help indicate in anaemia?

A

cause of anaemia

209
Q

What are the three main causes of anaemia?

A

reduced production
increased losses
increased demand

210
Q

What kind of things can cause a decreased supply/production of haemoglobin?

A

nutritional deficiency - prematurity, poverty, diet
malabsorption - coeliac disease, post gastric surgery

211
Q

What kind of things can cause an increased demand for haemoglobin?

A

pregnancy - lactation
growth

212
Q

What kind of things can cause an increased loss of haemoglobin?

A

blood loss - colon cancer, polyps, PUD
Intravascular haemolysis - destruction of RBCs

213
Q

What are haematinics?

A

haematinics stimulate blood cell formation or to increase the hemoglobin in the blood

214
Q

Name three haematinics

A

1) folic acid (folate)
2) iron
3) vitamin B12

215
Q

Name three sources of iron

A

meat
green leafy vegetables
iron tablets

216
Q

What is iron stored as in the cell?

A

ferritin

217
Q

Is it simpler for the body to absorb haem-iron or non-haem iron?

A

haem-iron

218
Q

Name two diseases that reduce iron absorption

A

1) achlorhydria - lack of stomach acid (no conversion of non-haem iron i.e. Fe3+ to Fe2+)
2) coeliac disease - affects intestinal villi and absorption

219
Q

Name four ways in which iron can be lost

A

1) gastric erosions and ulcers
2) inflammatory bowel disease - Crohn’s, UC
3) bowel cancer
4) haemorrhoids

220
Q

What is vitamin B12 found in?

A

mainly meat and milk as well as meat and milk alternatives

221
Q

How is vitamin B12 absorbed?

A

secretion of intrinsic factor by gastric parietal cells, binding of intrinsic factor to vitamin B12 taken in through diet. Complex passes through terminal ileum and is absorbed

222
Q

Where is folic acid absorbed?

A

small bowel

223
Q

What can cause vitamin B12 deficiency?

A

lack of intake (diet) - vegans
lack of intrinsic factor - gastric disease, pernicious anaemia
disease of terminal ileum - Crohn’s disease

224
Q

Name five sources of vitamin B12

A

1) green leafy vegetables
2) papaya and oranges
3) beans, peas, lentils
4) bell peppers
5) avocado

225
Q

What can cause folic acid deficiency?

A

lack of intake - peculiar diet
absorption failure - jejunal disease (coeliac disease)

226
Q

What can folic acid deficiency during pregnancy lead to?

A

neural tube defect in foetus e.g. spinabifida

227
Q

When is haemoglobin formed?

A

during pregnancy

228
Q

Where is haemoglobin formed?

A

in different tissues at different stages of pregnancy
liver and spleen in very early stages
through birth and beyond it is in the bone marrow

229
Q

What are the three forms of haemoglobin and when are they produced?

A

alpha haemoglobin - throughout life
beta haemoglobin - mainly after birth
gamma haemoglobin - after birth

230
Q

What is thalassaemia?

A

normal haem production
genetic mutation of globin chains

231
Q

What are the clinical affects of thalassaemia?

A

chronic anaemia
splenomegaly
gallstones
marrow hyperplasia - skeletal deformities
cirrhosis

232
Q

How is thalassaemia managed?

A

blood transfusions
prevent iron overload

233
Q

What is sickle cell anaemia?

A

abnormal globin chains but function normally at standard oxygen environments
change shape in low oxygen environments

234
Q

What can the change in shape of RBCs in sickle cell anaemia cause?

A

prevent RBC from passing through capillaries
tissue ischaemia - pain and necrosis

235
Q

What is an increase in red blood cell volume associated with?

A

deficiencies in vitamin B12 or folic acid

236
Q

What is a decrease in RBC volume (ie small RBCs) associated with?

A

iron deficiency or thalassaemia

237
Q

What does the level of haemoglobin indicate?

A

degree of anaemia

238
Q

What are the RCC and HCT?

A

Red cell count
Haematocrit

239
Q

What is the HCT?

A

haematocrit - measures the proportion of red blood cells in your blood

240
Q

What is the MCV?

A

Mean cell volume

241
Q

What is a microcytic RBC and when are they found?

A

small RBC - iron deficiency, thalassaemia

242
Q

What is a macrocytic RBC and when are they found?

A

large RBC - B12/folate deficiency

243
Q

What is a hypochromic RBC?

A

microscopically appear pale
less haemoglobin
can be microcytic, normocytic or macrocytic - usually microcytic

244
Q

What do the RBCs look like in a person with anisocytosis?

A

very big cells and very small cells in the same sample

245
Q

What are reticulocytes and how do they affect MCV?

A

almost mature RBCs - due to not being fully mature they are larger than RBCs (shrink on maturation) so increase MCV. released to replace losses

246
Q

What are the signs and symptoms of anaemia?

A

pale, tachycardia rarely, enlarged liver, enlarged spleen
pale mucosa under eye

247
Q

What are the symptoms of anaemia?

A

tired and weak, dizzy, shortness of breath, palpitations

248
Q

What appearances can anaemia present with orally?

A

smooth tongue (glossitis) - iron deficiency anaemia
beefy tongue - vitamin B12 deficiency

249
Q

What investigations are done for anaemia?

A

History
FBC
GI blood loss (faecal occult test, endoscopy)
renal function
bone marrow examination

250
Q

How is anaemia treated?

A

treat cause
replace haematinics - vit B12, Fe, folic acid
transfusions

251
Q

What are the dental aspects of anaemia?

A

GA - oxygen capacity
deficiency states (Fe usually) - mucosal atrophy (thinning), candidiasis, recurrent ulceration, sensory changes

252
Q

What are the names of two injectable anticoagulants and how do they differ?

A

unfractioned Heparin - infusion, only active for. afew minutes
low molecular weight heparin - SC injection

253
Q

Name five anticoagulants

A

1) warfarin
2) apixaban
3) edoxaban
4) rivaroxaban
5) dagibatran

254
Q

How do antiplatelets work?

A

interfere with platelet number or function

255
Q

Name 4 anti-platelet drugs

A

1) low dose aspirin
2) clopidogrel
3) dipyridamole
4) prasugrel and aspirin

256
Q

What dental procedures are considered to require a level of caution regarding anti-platelets and anti-coagulant medication?

A

extractions
minor oral surgery
implants
periodontal surgery
biopsies - sometimes

257
Q

What are the indications for anticoagulation?

A

conditions where blood clots will form too readily on or in the circulation
atrial fibrillation, DVT, heart valve disease, mechanical heart valves, thrombophilia

258
Q

Name two common anticoagulants

A

apixaban
warfarin

259
Q

How long is the onset of warfarin?

A

slow onset - 3 days
initial hypercoagulability

260
Q

How does warfarin work and how is the response to warfarin measured?

A

inhibits production of vitamin K dependent clotting factors.
Response measured by INR - normal 2-3 in warfarin users

261
Q

What is a normal INR?

A

1.1 or below

262
Q

What is the INR of someone taking warfarin?

A

2-3

263
Q

What is the INR of someone with prosthetic valves and higher risk of DVT?

A

3-4

264
Q

How often should INR be checked in someone taking warfarin?

A

every 4-8 weeks

265
Q

What are the appointment requirements for a patient on warfarin?

A

INR and FBC within 72hrs of treatment within 24hrs preferred
apptmt early in day, early in the week
Proceed with caution if INR <4
local haemostatic measures to be applied - cellulose sponge, sutures, LA infiltration around socket to decrease blood flow
post op instructions with contact number

266
Q

What 3 local haemostatic measures are used in patients taking warfarin?

A

cellulose sponge
sutures
LA infiltration (vasoconstriction)

267
Q

What 4 drugs can interact with warfarin, increasing INR?

A

amiodarone
antibiotics
alcohol (with liver disease)
NSAIDs

268
Q

What 4 drugs can interact with warfarin, reducing INR?

A

carbamazepine, barbiturates
cholestyramine
griseofulin
alcohol (without liver disease)

269
Q

Which medications should be avoided in dental patients on warfarin?

A

Aspirin (as an analgesic)
NSAIDs including ibuprofen, diclofenac
azole antifungal drugs - fluconazole

270
Q

What are the hazards of taking warfarin?

A

haemorrhage
soft tissue injury causing bleeding into muscles

271
Q

What can be done to reverse anticoagulation in a warfarin patient if haemorrhage occurs?

A

vitamin K injection (hospital setting)

272
Q

What are NOACs?

A

New/novel oral anticoagulants

273
Q

What are some of the benefits of NOACs instead of warfarin?

A

no need to monitor action
rapid onset - within hour
short duration of action - effect lost within day

274
Q

How do NOACs work?

A

preventing the effect of factor X

275
Q

Name four NOACs

A

1) rivaroxiban
2) apixaban
3) edoxaban
4) dabigatran

276
Q

What are the considerations of doing dental treatment in a patient on NOACs?

A
  • treat early in day, early in week
  • do not need to change regimen in low risk procedure
  • high risk procedure - miss/delay morning dose
  • restart immediately after for 1 dose daily pts
  • omit first dose and take second dose for twice daily pts
277
Q

How long should you keep a NOAC patient after extraction to assess bleeding?

A

20 mins

278
Q

What are the NOACs safe to use alongside (drug interactions)?

A

safe with dental antibiotics except macrolides (erythromycin and clarithyromycin)
safe with antifungals, LA, anti-virals

279
Q

What medications should be avoided in patients taking NOACs?

A

erythromycin and clarithromycin
NSAIDs - prolong action and inhibit platelets
avoid carbamazepine

280
Q

Should antiplatelet drugs be stopped for treatment in patients with stents?

A

No

281
Q

How should dental treatment be carried out in a patient taking aspirin alone?

A

treat without interrupting medication
local haemostatic measures
consider limiting initial treatment area

282
Q

How should dental treatment be carried out in a patient on non-aspirin single antiplatelet therapy or dual therapy WITH aspirin?

A

do not interrupt treatment
expect prolonged bleeding - limit initial area
local haemostasis

283
Q

How should dental treatment proceed in a patient if two antiplatelet drugs are taken in combination WITHOUT aspirin?

A

discuss with doctor - stop one drug 7 days before surgery or refer to hospital unit

284
Q

What MUST post operative instructions include?

A

emergecny contact details

285
Q

What is an inherited bleeding disorder?

A

an acquired defect which affects the coagulation of the blood

286
Q

What are the conditions where too LITTLE clot is formed and where too MUCH clot is formed?

A

Too little - haemophilia
Too much - thrombophilia

287
Q

People with haemophilia/haemophilia A are deficient in what?

A

Factor VIII

288
Q

People with Christmas disease/haemophilia B are deficient in what?

A

Factor IX

289
Q

Von Willebrand’s disease is a reduction in what factor causing what?

A

Factor VIII
reduced platelet aggregation

290
Q

What kind of disease is haemophilia A and B?

A

inherited sex linked recessive
defective gene on the X chromosome

291
Q

How are patients with haemophilia A managed?

A

severe & moderate - recombinant factor VIII
mild carriers - DDAVP (desmopressin) releases factor VIII from endothelial cells
very mild - tranexamic acid, inhibition of fibrinolysis

292
Q

How are patients with haemophilia B managed?

A

ALL require recombinant factor IX

293
Q

What do coagulation factor inhibitors develop into?

A

they are antibodies which develop to factor VIII and IX

294
Q

What kind of disease is Von Willebrand’s disease?

A

Autosomal dominant - NOT transmitted by the X chromosome

295
Q

What is Von Willebrand’s disease and what are they deficient in?

A

bleeding disorder where people lack or have defective vW factor on their platelets which interacts badly with factor VIII, causing poor clot activation

296
Q

How are patients with Von Willebrand’s disease managed?

A

DDAVP (desmopressin) for most
Mild cases only require tranexamic acid

297
Q

What is the function of DDAVP (desmopressin)?

A

releases factor VIII that has been bound to the endothelial cells therefore giving a temporary boost of factor VII levels and clotting ability

298
Q

What is tranexamic acid and what does it do?

A

inhibitor of fibrinolysis - prevents or reduces bleeding by impairing fibrin dissolution

299
Q

What is the most common disease - haemophilia A, haemophilia B, Von Willebrand’s disease or Factor XI deficiency?

A

Von Willebrand’s disease

300
Q

Where can severe or moderate haemophilia patients be treated?

A

unit attached to haemophilia centre
pros and other no-risk treatments in primary care

301
Q

Where are mild and carrier haemophilia patients treated?

A

treatment shared with GDP
pt reviewed at haemophilia dental unit every 2 years

302
Q

What are considered bleeding risk procedures in haemophilia?

A
  • administration of LA
  • extractions
  • MOS
  • periodontal surgery
  • biopsies
303
Q

What LA is considered safe in patients with haemophilia?

A

buccal infiltration
intraligamentary injection
intra-papillary injection

304
Q

What LA is considered dangerous in patients with haemophilia?

A

IANB
Lingual infiltration
posterior superior nerve block

305
Q

How long should haemophilia patients be observed following surgery?

A

severe & moderate - overnight
mild & carriers - 2-3hours post surgery

306
Q

What is thrombophilia?

A

increased risk of blood clotting
clot formation ability greater than clot breakdown ability

307
Q

Is thrombophilia acquired?

A

often acquired condition superimposed on a genetic tendency

308
Q

What can cause acquired hypercoagulation?

A

antiphospholipid syndrome - lupus anticoagulants
oral contraceptives
surgery, trauma, cancer, pregnancy, immobilisation

309
Q

What can cause inherited hypercoagulation?

A

protein C deficiency
Protein S deficiency
Factor V leiden
Antithrombin III deficiency

310
Q

What platelet disorder increasing bleeding occurs with reduced platelet numbers?

A

thrombocytopenia

311
Q

What platelet disorder increasing bleeding occurs with increased platelet numbers?

A

thrombocythemia

312
Q

What is thrombocytopenia?

A

low number of normal platelets

313
Q

What are the possible causes of thrombocytopenia?

A

idiopathic (unknown cause)
drug related - alcohol, penicillin based drugs, heparin
secondary to lymphoproliferative disorder - leukaemia

314
Q

What is thrombocythemia?

A

high numbers of (often poor) functioning platelets

315
Q

What are qualitative platelet disorders?

A

normal platelet count but abnormal function

316
Q

What are three examples of inherited qualitative platelet disorders?

A

Bernard Soulier syndrome
Hermansky Pudlak
Glanzmann’s thrombasthenia

317
Q

What are four things associated with acquired qualitative platelet disorders?

A

cirrhosis
drugs
alcohol
cardiopulmonary bypass

318
Q

No additional precautions are required for treating a patient with a platelet disorder when their platelet count is at what level?

A

> 100 x 10⁹/L and no functional issues

319
Q

What treatment can be carried out in a platelet disorder patient with a platelt count of >100 x 10⁹/L?

A

hygiene therapy
removable pros
restorative dentistry, crowns and bridges
endo
ortho

320
Q

At what platelet counts should patients be treated in the hospital?

A

<50 x 10⁹/L
above 500 x 10⁹/L

321
Q

Special care is required for patients with platelet disorders for which procedures?

A

extractions
MOS
periodontal surgery
biopsies

322
Q

What are the four blood types?

A

A
B
O
AB

323
Q

What does the D system regarding blood cell antigens assess?

A

Rhesus positive or negative

324
Q

When are blood transfusions indicated?

A

blood loss
specific production problems - RBC, platelets, plasma proteins

325
Q

Which blood group can donate to groups O, A, B and AB?

A

group O

326
Q

What are three examples of transfusion complications?

A

transmission. ofinfection
fluid overload - heart failure
incompatible blood - RBC lysis (burst), fever, jaundice, death

327
Q

What is lymphoma?

A

cloncal proliferation of lymphocytes in a lymph node or associated tissue
solid tumour but some cells in blood

328
Q

What are the two types of lymphoma and which is most common?

A

Non-hodgkins - most common, 6:1
Hodgkins

329
Q

What are the symptoms of lymphoma?

A

fever
swelling of face and neck
lump in neck, armpits or groin
breathlessness, itchiness
excessive sweating at night
unexpected weightloss
loss of appetite
weakness

330
Q

What factors are considered when staging lymphoma?

A

1) no. of nodes involved and site
2) extra-nodal involvement
3) systemic symptoms

331
Q

What is stage 1 lymphoma?

A

single lymph node region or single extra-lymphatic site

332
Q

What is stage II lymphoma?

A

two or more sites, same side. ofdiaphragm or contagious extralymphatic site

333
Q

What is stage III lymphoma?

A

both sides of diaphragm or spleen or contagious extralymphatic site

334
Q

What is stage IV lymphoma?

A

diffuse involvement of extralymphatic sites with or without nodal disease

335
Q

At what age does the peak incidence of Hodgkin’s lymphoma occur?

A

15-40yrs

336
Q

What is the clinical presentation of Hodgkins lymphoma?

A

painless lymphadenopathy - typically cervical, fluctuate in size, pain with alcohol
fever, night sweats, weightloss, itching
infection

337
Q

What is the aetiology of non-hodgkins lymphoma?

A

microbial factors associated - EBV, HIV, H pylori
autoimmune disease associated - chronic immune activation, RA, PUD, Sjorgren’s
immunosuppression - AIDS, post-transplant

338
Q

What is the presentation of non-hodgkins lymphoma?

A

lymphadenopathy - widely disseminated
extra-nodal disease more common - oropharyngeal, Waldeyer’s ring
symptoms of marrow failure

339
Q

What is multiple myeloma?

A

malignant proliferation of plasma cells, bone marrow cancer

340
Q

What are the features of multiple myeloma? 3

A

1) monoclonal paraprotein in blood and urine
2) lytic bone lesions - pain and fracture
3) excess plasma cells in marrow - marrow failure

341
Q

What are the treatment options for haematological malignancies?

A

chemotherapy
radiotherapy
monoclonal antibodies
haemopoietic stem cell transplantation

342
Q

What kind of cells are targeted by chemotherapy?

A

those with high turnover rate e.g. hair follicles

343
Q

What is radiotherapy?

A

cytotoxic effect of ionising radiation

344
Q

What does allogeneic mean?

A

from a live donor

345
Q

What does autologous mean?

A

obtained from the patient

346
Q

What does haemopoietic stem cell transplantation require?

A

total body irradiation to eradicate malignant cells and host marrow - “clean sheet”

347
Q

What kind of DNA mutation is a haematological malignancy normally and what does it do?

A

translocation - switches off. atumour suppressor gene or on an oncogene

348
Q

What is a “blast” cell?

A

immature cell

349
Q

What does leukaemia cause? 3

A

1) anaemia
2) infection (neutropenia)
3) bleeding (thrombocytopenia)

350
Q

What is the clinical presentation of leukaemia?

A

anaemia
neutropenia
thrombocytopenia
lymphadenopathy - neck lumps
splenomegaly/hepatomegaly
bone pain

351
Q

What age group is acute myeloid leukaemia more common in?

A

elderly

352
Q

What are the symptoms of anaemia?

A

breathlessness
tiredness
easily fatigued
chest pain/angina

353
Q

What are the signs of anaemia?

A

pallor
signs of cardiac failure (ankle swelling, breathlessness)
nail changes e.g. brittle nails, koilonychia

354
Q

What is the clinical presentation of neutropenia?

A

infection assoc with portal of entry - mouth, throat (pharyngitis, tonsilitis), chest (bronchitis, onerumonia), skin (impetigo, cellulitis), perianal (thrush, abscess)
reactivation of latent infection e.g. herpes
increased severity
increased frequency
systemic infection

355
Q

What are the symptoms of neutropenia?

A

recurrent infection
unusual severity of infection

356
Q

What are the signs of neutropenia?

A

unusual patterns of infection and rapid spread
respond to treatment but recur
systemic involvement - fever, rigor, chills

357
Q

What is the peak age of acute lymphoblastic leukaemia?

A

4yrs but does occur in adults

358
Q

Name the six ways in which infections are transmitted during sex

A

1) direct innoculation (e.g. HSV)
2) trauma (e.g. hep C)
3) IVDU Intravenous drug use(e.g. HIV, hep C)
4) fomites (objects) (e.g. gonorrhoea)
5) ingestion (e.g. shigella)
6) sexual/genital secretions (many)

359
Q

What is vertical transmission?

A

to baby through direct contact with the mother’s fluids, usually during delivery

360
Q

What is the general trend of sexual behaviours in recent times?

A

having sex younger with more lifetime partners

361
Q

What are eight risk factors for STIs?

A

1) <25yrs old
2) changing sexual partner
3) past history of STI
4) social deprivation
5) non-condom use
6) men who have sex with men (MSM)
7) large urban areas
8) black ethnicity

362
Q

What six STIs can affect the mouth?

A

1) chlamydia trachomatis
2) treponema pallidum
3) Human papillomavirus
4) Neisseria gonorrhoea
5) herpes simplex virus
6) human immunodeficiency virus

363
Q

Which two STIs are not symptomatic in the mouth but are both carried in the oropharynx and transmitted by oral sex?

A

chlamydia trachomatis
neisseria gonorrhoea

364
Q

What spirocheate causes syphilis?

A

treponema pallidum

365
Q

What are the stages in syphilis?

A

exposure
primary syphilis
secondary syphilis
early latent
late latent
tertiary - neurological, cardiovascular, gummatous effects

366
Q

How long does it take to go from syphilis exposure to primary syphilis?

A

10-90 days

367
Q

What time period is classed as early syphilis?

A

1st 2 years of infection

368
Q

How long does it take to progress from primary to secondary syphilis?

A

less then 2 years, usually 3-6 weeks

369
Q

How long does primary syphilis last?

A

10-90 days

370
Q

What are characteristically seen in primary syphilis and how long do they last?

A

Chancres
Resolves without treatment 3-6 weeks

371
Q

What do chancres look like?

A

1-2cm, indurated with a lot of inflammatory infiltrate, well circumscribed with a raised border and ulcerated

372
Q

Where are chancres commonly found in syphilis?

A

genitals are the most common location for chancres to develop, but these ulcers also can form around the mouth or anus

373
Q

When does secondary syphilis usually develop?

A

<2yrs (usually 3-6 weeks)

374
Q

Where is secondary syphilis found in the body?

A

haematogenous (in blood) and lymphatic dissemination

375
Q

What kind of disease is secondary syphilis?

A

multi-system

376
Q

What are the systemic symptoms of secondary syphilis?

A

low grade fever
sore throat
headache
lymphadenopathy
rash - palms and soles of feet

377
Q

What symptoms are found orally in secondary syphilis?

A

white glistening patches - greyish membrane, hyperaemic halo, coalesce to form “snail trail” ulcers
found on HP, SP, gingivae and buccal mucosa

378
Q

What may patients with syphilis present with?

A

meningitis
iritis
hepatitis
ureitis
periositis
glomerulonephritis
condylomata lata

379
Q

How is syphilis diagnosed?

A

lesion - swab for treponema pallidum by PCR
venous blood - syphilis antibody

380
Q

How is syphilis treated?

A

antibiotic - benzathene penicillin IM or doxycycline
Public health - partner notification, STI testing, sexual abstinence, risk reduction advice

381
Q

What is HIV?

A

Human immunodeficiency virus

382
Q

List 5 key facts about HIV

A

1) remains fatal if untreated
2) remains incurable
3) undiagnosed infection ket to transmission
4) near normal life expectancy with treatment
5) effective treatment renders pt uninfectious

383
Q

What are the modes of transmission of HIV?

A

Sexual transmission
injection drug use
other - vertical transmission (rare)

384
Q

What are the high risk groups for HIV?

A

Everyone is at risk
higher risk - MSM, high prevalence countries, injecting drugs, sexual contact of above

385
Q

What is the average time to death for untreated HIV?

A

9-11yrs

386
Q

What count decreases over time with the increase of HIV RNA copies in the blood?

A

CD4+ count (T helper lymphocyte count) - falls as viral load rises

387
Q

What are the stages of HIV infection?

A

1) primary infection - CD4 count falls, viral load rises (HIV RNA copies per ml plasma)
2) asymptomatic infection - develop antibodies, bring down viral load, can be years with few symptoms, immune system depletes again
3) symptomatic - develop signs of poor immune system, opportunistic infection arises e.g. pneumonia, Kaposi’s sarcoma, cerebral toxiplasmosis
leading to death

388
Q

What are the symptoms of primary HIV infection and when do they occur?

A

fever, myalgia, rash (macropapular), pharyngitis, headache/aseptic meningitis
2-4 weeks after infection

389
Q

What are teh oral lesions seen in primary HIV?

A

Apthous ulcers
candidiasis

390
Q

What does mucosal candidiasis in symptomatic HIV look like and indicate?

A

pseudomembranous
erythematous
angular chelitis
oesophageal extension
predictive of progression to AIDS

391
Q

Name five main oral/facial symptoms in symptomatic HIV

A

1) mucosal candidiasis
2) gingivitis
3) Kaposi’s sarcoma
4) Oral hairy leukoplakia
5) Seborrhoeic dermatitis

392
Q

What are the features of gingivitis in symptomatic HIV?

A

linear gingival erythema
necrotising ulcerative gingivitis
often sudden onset with no plaque or calculus

393
Q

What is Kaposi’s sarcoma?

A

vascular cancerous tumour
caused by human herpes virus 8 (HHV8)
localised or visceral

394
Q

What causes Kaposi’s sarcoma?

A

Human Herpes virus 8

395
Q

what causes oral hairy leukoplakia?

A

EBV infection

396
Q

What two oral symptoms are predictors of progression from HIV to AIDS?

A

mucosal candidiasis
oral hairy leukoplakia

397
Q

In what condition can Kaposi’s sarcoma be seen?

A

HIV

398
Q

Staff with HIV can carry out exposure-prone procedures as long as they are what?

A

on antiretroviral treatment
have undetectable viral load in last 3 months

399
Q

How quickly does PEP (post-exposure prophylaxis) need to begin to be effective following HIV exposure?

A

within 72hrs

400
Q

What is post-exposure prophylaxis?

A

combination anti-retroviral drugs
4 week course
reduce risk of transmission by 80%

401
Q

What are the indications of post-exposure prophylaxis?

A

-high risk injury, source and fluid
-sexual
-occupational

402
Q

What types of HSV are there?

A

Type 1 and type 2

403
Q

What are the oral symptoms of primary infection of HSV?

A

Gingivostomatitis (inflammation of gums and lips)
pharyngitis
with or without symptoms

404
Q

What is the main symptom of recurrent HSV infection (usually HSV-1)?

A

Herpes labialis - a rash of the skin and mucous membranes (in particular, the lips) characterized by erythema and blisters that are preceded and accompanied by burning pain.

405
Q

How is herpes simplex virus transmitted?

A

kissing
oral sex
asymptomatic shedding of virus

406
Q

HSV in HIV may be resistant to what anti-viral?

A

aciclovir - used for cold sores

407
Q

How long do orolabial herpes lesions usually last?

A

self limiting 7-10 days

408
Q

How are orolabial herpes lesions managed?

A

usually no treatment
symptom control
avoid kissing and oral sex
wash hands after touching

409
Q

What is a common route of infection of HPV?

A

Oral sex

410
Q

What is the most common STI?

A

HPV

411
Q

Why are HPV infections dangerous regarding progression?

A

some strains are oncogenic (e.g. HPV16, HPV18)

412
Q

What cancers are commonly associated with HPV?

A

Oropharyngeal cancer

413
Q

What are the main dentally relevant factors regarding liver disease?

A

pts have impaired wound healing
impaired clotting - reduced platelets, deficient clotting factor
risk of BBV

414
Q

Name 7 functions of the liver

A

1) protein metabolism
2) lipid metabolism
3) bilrubin metabolism
4) immunological defence
5) carbohydrate metabolism
6) bile acid metabolism
7) hormone and drug metabolism

415
Q

How do you know it a patient has liver disease?

A

past history
jaundice
stigmata of chronic liver disease

416
Q

What are the symptoms of jaundice?

A

yellowness of eyes
yellow skin colour
look at whites of eyes

417
Q

What causes jaundice?

A

increased production of bilrubin
failure of excretion and conjugation of bilrubin

418
Q

What is bilrubin?

A

yellowish pigment that is made during the breakdown of red blood cells. Bilirubin passes through the liver and is eventually excreted out of the body

419
Q

Name three main types of liver disease

A

1) acute liver disease - hepatitis, drug induced liver injury
2) chronic liver disease (cirrhosis) - alcohol, chronic viral hepatitis (HBV, HCV), Non-alcoholic fatty liver disease (NAFLD)
3) jaundice secondary to biliary obstruction

420
Q

What are the clinical features of jaundice?

A

yellow skin
dark urine - conjugated bilrubin
lethargy and malaise
pale stools
itch
anorexia

421
Q

What do liver function tests measure and give an example?

A

measure liver damage
ALT/AST
ALP
GGT

422
Q

what do true liver function tests measure?

A

measure how well the liver is working

423
Q

Name three true liver function tests

A

1) bilirubin - biomarker of liver disease
2) albumin - marker of liver synthetic function
3) prothrombin time -how long it takes for a clot to form in a blood sample, prothrombin made by liver, time increases in liver disease

424
Q

What is the most common hepatitis virus?

A

Hep E

425
Q

How is HBV (Hepatitis B) transmitted?

A

blood, sex, vertical transmission, chronic carriage in ethnic groups.

426
Q

What are the dangers of HBV?

A

Highly infectious
progression to cirrhosis in 10yrs
liver failure
hepatoma

427
Q

What is hepatoma?

A

most common type of primary liver cancer

428
Q

How is HBV treated?

A

PEG alpha-interferon
Tenofovir
Entecavir

429
Q

Is the transition from acute HBV to chronic HBV infection “carrier” common?

A

<5% risk if infected as adult

430
Q

How often does infection with HCV result in chronic infection?

A

80% cases

431
Q

Is there a vaccine for Hep C (HCV)?

A

no vaccine

432
Q

What can chronic hepatitis (HCV) progress to?

A

cirrhosis (20-100%)
Hepatocellular carcinoma (1-4%)

433
Q

What occurs with hepatitis A and how is it managed?

A

acute illness only, self limiting
rest, low fat diet, alcohol avoidance

434
Q

How is hepatitis A transmitted?

A

faecal-oral spread
poor hygiene/overcrowding
food and water contamination

435
Q

Is there a vaccine for hepatitis A?

A

yes

436
Q

What disease causes the destruction of adrenal tissue?

A

Addison’s disease

437
Q

What disease causes excess adrenal action?

A

Cushing’s disease

438
Q

What affect do therapeutic corticosteroids have on adrenal tissues?

A

suppression of adrenal action
steroid adverse effects

439
Q

What does the zona glomerulosa of the adrenal gland secrete?

A

aldosterone - renin/angiotensin system

440
Q

What does the zona fasicularis of the adrenal gland secrete?

A

cortisol

441
Q

What does the zona reticularis of the adrenal gland produce?

A

adrenal androgens

442
Q

What are the three zones of the adrenal gland and name them from most superficial to deep

A

zona glomerulosa - between cortx and outside of gland
zona fascicularis - in between
zona reticularis - between cortex and medulla

443
Q

Where is adrenal regulation controlled from?

A

hypothalamus then pituitary

444
Q

Explain the stages in adrenal regulation

A

1) corticotrophic-releasing hormone released from hypothalamus passes to anterior pituitary through venous plexus
2) cells in anterior pituitary secrete ACTH into circulation
3) ACTH (Adrenocorticotropic hormone) passes to adrenal cortex where it stimulates release of hormones including cortisol
4) cortisol feedback to pituitary and hypothalamus reduce secretion (negative feedback)

445
Q

What is the function of aldosterone?

A

steroid hormone made by the adrenal cortex - control the balance of water and salts in the kidney by keeping sodium in and releasing potassium from the body
renin-angiotensin system

446
Q

how does aldosterone indirectly effect blood pressure?

A

Too much aldosterone can cause high blood pressure and a build-up of fluid in body tissues

447
Q

The action of aldosterone is inhibited by which drugs?

A
  • ACE inhibitors
  • AT2 (angiotensin 2 receptor) blockers
448
Q

What is a common side effect of ACE inhibitors?

A

dry cough

449
Q

What is cortisol?

A

natural glucocorticoid, primary stress hormone
enhances your brain’s use of glucose and increases the availability of substances that repair tissues

450
Q

What are the physiological effects of cortisol?

A

antagonist to insulin - gluconeogenesis, fat and protein breakdown, increase the availability of blood glucose to the brain
lowers immune reactivity
raises bp - enhances salt and water reabsorption
inhibits bone synthesis - osteoporosis long term

451
Q

Therapeutic steroids cause an enhanced glucocorticoid effect, what can this cause?

A

immunosuppression
reduced inflammatory response

452
Q

What are the adverse effects of therapeutic steroids?

A

hypertension
Type II diabetes
osteoporosis
increased infection risk
peptic ulceration
thinning of skin
easy bruising
cataracts and glaucoma
hyperlipidaemia (atherosclerosis)
icreased cancer risk
psychiatric disturbance

453
Q

What syndrome occurs with hyperfunction of the adrenal gland producing excess glucocorticoids?

A

Cushings syndrome

454
Q

What syndrome is caused by hyperfunction of the adrenal gland causing excess aldosterone?

A

Conn’s syndrome

455
Q

What causes Cushings syndrome?

A

pituitary tumour affecting ACTH production
adrenal adenoma or hyperplasia
too much cortisol produced as a consequence

456
Q

What are the symptoms of Cushing’s syndrome?

A

DM features
poor resistance to infections
osteoporotic changes
psychiatric disorders
hirsuitism
skin and mucosal pigmentation
amenorrhoea, impotence and infertility

457
Q

What are the signs of Cushings syndrome?

A

centripetal obesity - moon face, buffalo hump
hypertension
think skin and purpura
muscle weakness
osteoporotic changes

458
Q

What do we see in the skin in ACTH excess?

A

pigmentation of skin esp over joints
pigmentation of mucosa

459
Q

What can cause adrenal gland failure and hypofunction?

A

autoimmune gland destruction
infection
infarction

460
Q

What can cause pituitary failure and hypofunction?

A

compression from another adenoma
Sheehan’s syndrome - failure of ALL pituitary hormones

461
Q

What are two causes of Addison’s disease?

A

TB
Autoimmune adrenalitis

462
Q

What are the signs of Addison’s disease?

A

postural hypotension
weightloss and lethargy
hyperpigmentation
vitiligo

463
Q

What are the symptoms of Addison’s disease?

A

weakness
anorexia
loss of body hair (females)

464
Q

What investigations are done for Cushing’s syndrome?

A

high 24hr urinary cortisol excretion
CRH tests - rise in ACTH with CRH

465
Q

What investigations are done for Addison’s disease?

A

high ACTH level
negative synACTHen tests - no cortisol rise in response to ACTH injection

466
Q

What are the key features of adrenal hyperfunction caused by pituitary adenoma or ectopic ACTH production?

A

HIGH ACTH and Cortisol

467
Q

What are the key features of adrenal hyperfunction caused by gland adenoma?

A

LOW ACTH
High cortisol

468
Q

What are the key features of adrenal hypofunction caused by pituitary failure?

A

LOW ACTH
LOW cortisol
positive synACTHen test

469
Q

what are the key features of adrenal hypofunction caused by gland destruction?

A

High ACTH
lOW CORTISOL
Negative synACTHen test (no gland to stimulate)

470
Q

How is adrenal hyperfunction treated?

A

detect cause (adenoma) - pituitary, adrenal, ectopic (lung)
Surgery - pituitary, adrenal (partial/complete adrenalectomy)

471
Q

What is Addison’s disease defined as?

A

autoimmune destruction of adrenal gland

472
Q

What are the features of Addison’s disease crisis?

A

hypotension
vomiting
eventual coma
absence of mineralcorticoid and effect of glucocorticoids

473
Q

What is the management technique for Addison’s disease?

A

hormone replacement - cortisol AND fludrocortisone (replacement for aldosterone)

474
Q

Do patients with Addison’s disease require steroid prophylaxis?

A

require consideration for steroid cover during dental procedures

475
Q

What is the main dental feature seen in Cushings syndrome?

A

Candidiasis

476
Q

What is the main dental feautre seen in Addisons and Cushings?

A

oral pigmentation

3rd Year - Module 5 (12 decks)

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