Human diseases 2 Flashcards
(476 cards)
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
2
Q
Name two types of large bowel disease
A
inflammatory bowel disease (IBS) - Crohn’s and ulcerative colitis
Colonic cancer
3
Q
What medication used in upper GI disease eliminates formed acids?
A
Antacids
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
5
Q
What medications used in upper GI disease reduce acid secretion?
A
H2 receptor blockers
proton pump inhibitors
6
Q
What are the three main triggers for stomach acid production?
A
acetylcholine
gastrin
histamine
7
Q
What are stomach acids produced by?
A
parietal cells in the stomach wall
8
Q
How do H2 receptor antagonists work?
A
reduce acid production by preventing histamine activation of acid production
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
10
Q
Name two H2 receptor antagonists
A
cimetidine
ranitidine - available over the counter
11
Q
Name three proton pump inhibitors
A
omeprazole, lanzoprazole, pantoprazole
12
Q
Which medications end in -prazole?
A
Proton pump inhibitors
anti-ulcer drugs that reduce gastric acid production.
13
Q
What are proton pump inhibitors used for?
A
profound and prolonged reduction of stomach acid production
14
Q
What is dysphagia?
A
difficulty swallowing
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)
16
Q
What are the effects of GORD?
A
Ulceration, inflammation, metaplasia (gastric)
Barrett’s oesophagitis - precancerous adenocarcinoma
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
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
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
20
Q
How is GORD managed?
A
smoking cessation (improves sphincter)
weightloss
antacids
H2 blockers and PPIs - ranitidine and omeprazole
21
Q
Where does peptic ulcer disease occur?
A
any acid affected site
oesophagus, stomach, duodenum
22
Q
What can cause peptic ulcer disease?
A
normal acid secretion - stomach
high acid secretion - duodenal
drugs - NSAIDs, steroids
23
Q
What bacterium causes peptic ulcer disease?
A
helicobacter pylori
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
25
What are the effects of peptic ulcer disease?
gastric ulcers
chronic gastric wall inflammation
mucosa assoc lymphoid tumour (MALT)
26
How is peptic ulcer disease managed?
Triple therapy
2 antibiotics, 1 proton pump inhibitor
27
What are the signs and symptoms of peptic ulcer disease?
asymptomatic
epigastric burning pain - worse at night, before/after meals, relieved by food, alkali and vomiting
usually NO physical signs unless complications
28
How is peptic ulcer disease investigated?
endoscopy
radiology - barium meal
anaemia - FBC and faecal occult tests
Helicobacter pylori - breath, antibodies, mucosa
29
What are the possible complications of peptic ulcer disease? local and systemic
local - perforation, haemorrhage, stricture, malignancy
systemic - anaemia
30
What does coffee ground vomit indicate?
large peptic ulcer bleed
31
How can you improve the mucosal barrier in upper GI disease?
eliminate helicobacter pylori
inhibit prostaglandin removal - so reduce/avoid NSAIDs and steroids
32
What medications are used in triple therapy for peptic ulcer disease?
2 antibiotics - amoxycillin, metronidazole
1 proton pump inhibitor - omeprazole
33
Describe the three surgeries that can be used in management of PUD
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
34
What is coeliac disease?
sensitivity to alpha-gliaden component of gluten
35
Name some examples of gluten in the diet
wheat, barley, spelt, rye, kamut (cereals, breads)
36
What happens in the body in coeliac disease?
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
37
What are the effects of coeliac disease?
weightloss, lassitude, weakness, abdominal pain and swelling, diarrhoea, oral ulcers, tongue papillary loss, steatorrhoea, dysphagia
38
What are the typical malabsorption issues associated with coeliac disease?
iron
folate
vitamin B12
fat
39
What is steatorrhoea and what condition can it sometimes occur with?
excess fat in stool
coeliac disease
40
How is coeliac disease investigated?
autoantibody test
jejunal biopsy
faecal fat
haematinics - B12, folate, ferritin
41
What is the effect of a gluten free diet in people with coeliacs disease?
reversal of jejunal atrophy, improved wellbeing, reduced risk of lymphoma
42
What is coeliac disease skin disease and what are the symptoms?
coeliac disease associated with dermatitis herpetiformis
oral disease - ulceration and blisters
granular IgA deposit in skin and mucosa - itch and blisters (usually shoulders)
43
All oral aphthous ulcer patients are screened by what?
haematinic assays to detect deficiency
TTG test usually done too - detects IgA
44
What is pernicious anaemia?
disease caused by vitamin B12 deficiency
45
Where is the absorption site for vitamin B12?
discrete area of the terminal ileum - only absorption site in the bowel
46
What causes pernicious anaemia?
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
47
What does vitamin B12 need for production?
intrinsic factor from gastric parietal cells
48
How is vitamin B12 deficiency treated?
diet with adequate B12
vit B12 supplements if prescribed
IM injections of B12 if GI absorption not possible
49
What has Crohn's disease been linked to?
infection with myobacteria (paratuberculosis)
Johne's disease in cattle - milk transmission?
50
What is a common site for Crohn's disease?
any site along GI tract plus mouth
ileocoecal region popular site, causes malabsorption of vitamin B12 (pernicious anaemia)
51
Where does ulcerative colitis occur?
starts in distal part of bowel and moves forward through large intestine (always present in rectum)
52
What are two key characteristics of ulcerative colitis?
continuous
ulcers in the colon
53
What are the main differences between ulcerative colitis and Crohn's disease?
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
54
What are the microscopic features of ulcerative colitis?
mucosal, vascular, mucosal abscesses
55
What are the microscopic features of Crohn's disease?
transmural (all layers inflamed), oedematous (blockage of lymphatics, granulomas (giant cells occupying lymphatic drainage systems)
56
How much of the bowel wall is involved/inflamed in Crohn's disease?
full thickness
57
What form between the layers of the bowel in Crohn's disease?
abscesses and fistulae
58
What is the appearance of the mucosa in Crohn's disease like?
cobblestone pattern, areas of oedema between fibrous bands
59
What is an issue caused by the thickening/inflammation of the intestinal wall in Crohn's disease?
narrowed lumen can cause issues passing food, obstruction of the bowel
60
What layers of the intestine does ulcerative colitis affect?
only the mucosal layer
61
What are the four names of ulcerative colitis which indicate the site of inflammation?
Proctitis - only the rectum
proctosigmoiditis - rectum and sigmoid colon
distal colitis - left side of colon
pancolitis - entire colon
62
What investigations can be done for inflammatory bowel diseases?
blood tests - anaemia, CRP (C-reactive protein), ESR (erythrocyte sedimentation rate) detect inflammatory process
faecal calprotectin - inflammatory protein
endoscopy, barium studies, leukocyte scan
63
What is a complication of inflammatory bowel disease?
ulcerative colitis develops carcinoma - risk increases with time
64
What are the drug treatment options for inflammatory bowel diseases?
immunosuppressive treatment - systemic steroids (prednisolone), local steroids, anti-inflammatories, non-steroid immunosuppressants, biologics (infliximab)
65
What are the surgical treatment options for inflammatory bowel diseases?
colectomy - cures ulcerative colitis
Crohn's disease - removal of obstructed bowel segments, drain abscesses, close fistulae (palliate symptoms) - usually results in stoma bag
66
What is orofacial granulomatosis?
granuloma formation blocks lymphatics
oedema of mouth and/or face, cobblestone appearance
67
What is the difference between orofacial granulomatosis and oral Crohn's disease?
Orofacial crohn's disease when GI tract also involved.
Orofacial granulomatosis when no symptoms further in GI tract
68
What does "bowel cancer" usually mean?
colonic cancer/colonic adenocarcinoma
69
Who qualifies for bowel cancer screening in the UK?
anyone from age 50
70
What are the symptoms of colonic carcinoma?
none
anaemia
rectal blood loss
often no symptoms until tumour causes blockage
71
What do most colonic carcinomas arise in?
polyps
72
What does bowel cancer screening aim to detect?
polyps within the surface of the lumen before they progress to malignancy
73
What kind of polyps form in colonic carcinoma and how long does it take for them to progress to malignancy?
pedunculated or flat
most will bleed due to irritation and trauma
most take 5 years to progress to malignancy
74
If a colonic carcinoma is removed at the polyp stage what happens?
cancer will not develop and patient no longer has lesion
75
What patient related factors can increase risk of colonic cancer?
diet - low fibre, high fat, high meat, low veg
smoking, alcohol missuse, lack of exercise
76
What is Peutz-Jehgers syndrome and how can it manifest orally?
a rare disorder in which growths called polyps form in the intestines
peri-oral melanosis
77
What are two examples of large intestine conditions that are high risk for progression to carcinoma?
Gardner's syndrome
Cowden's syndrome - polyps present in mouth too
78
What are the surgical options for treating colonic cancer?
resection of colon with anastomosis
bowel brought to surface as stoma
79
What are three examples of urinary tract obstructions?
renal stones
tumours
prostatic hypertrophy
80
What does the presence of any bacteria in urine imply?
urine should be STERILE. any bacteria present implies infection
81
What is the most common bacteria found in UTIs?
E.coli
Staph, fungi, virus and TB also possible
82
What is cystitis?
bladder inflammation
83
What can UTIs proceed to cause?
cystitis
84
What are predisposing factors for UTIs?
poor bladder emptying
low urinary flow rates (in heat or dehydration)
85
What are the symptoms of a UTI?
dysuria (painful urination)
urinary frequency
cloudy urine
offensive smelling urine
supra-pubic pain
86
What puts you at risk of a UTI?
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
87
Urine, if infected can cause what three infections?
cystitis
renal infection
prostate infection
88
What UTI can occur in isolation (does not need to have infected urine)?
urethritis - gonococcal infection
89
What are the symptoms of cystitis?
dark cloudy smelly urine
blood in urine
pain in lower stomach and on urination
peeing often
pain during sex
sick and tired
90
How are UTIs treated?
MSSU - Mid-stream sample of urine (less contamination) sent for microscopy, culture and sensitivity
increase fluid intake
frequent urination
occasionally ABx required - amoxicillin
91
What are four examples of conditions that could cause urinary tract obstruction?
1) renal calculi
2) prostatic disease - hypertrophy, malignancy
3) urinary tract strictures
4) external compression
92
How does prostatic disease cause urinary tract obstruction?
urethra passes through the prostate gland, so any enlargement compresses the urethra
93
What is prostatitis?
inflammation of prostate
94
What is benign prostatic hypertrophy?
benign condition in which an overgrowth of prostate tissue pushes against the urethra and the bladder, blocking the flow of urine.
95
How common is benign prostatic hypertrophy?
almost normal, 80% over 80 have BPH
100% if people live long enough
96
What are the symptoms of urinary outflow obstruction?
slow stream
urgency
nocturia
hesitancy
frequency
incomplete voiding - increases UTI risk
97
What is the treatment for a benign prostatic hypertrophy?
Initially drug based - alpha blocking drugs, anticholinergic (both to shrink gland size) and diuretics to flush system
Surgery - prostatectomy
98
Prostatic malignancy starts after what age?
45
99
What is used for early detection of prostate cancer?
mpMRI (multiparametric MRI)
100
How is prostatic malignancy treated?
surgery - radical prostatectomy
radiotherapy
hormone treatment - anti-androgens and LHRH analogues, block hormone dependent tumour growth
101
What are the two types of renal calculi (stone)?
1) calcium and oxalate (radiopaque)
2) uric acid (not radiopaque)
102
How are renal calculi treated?
Lithotrypsy - ultrasound shock waves break 'simple' stones which are too large to pass into smaller pieces
103
What is polyuria?
passing large volume of urine
104
what is haematuria?
blood present in urine (frank or microscopic)
105
What is proteinuria?
not normal, protein passing into urine suggests glomerular disease
106
What is uraemia?
increased concentration of urea in blood
107
What does serum urea rise with?
dehydration
108
What is considered the best measure of renal function?
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
109
What is renal failure?
loss of renal excretory function
loss of water and electrolyte balance
loss of acid base balance
loss of renal endocrine function
110
What hormonal impacts does the loss of renal endocrine function in renal failure have?
less erythropoietin - so less RBCs produced
calcium metabolism - high serum calcium levels
renin secretion - cause salt and water imbalance
111
What are the characteristics of acute renal failure?
rapid loss of renal function
usually over hours or days
112
What are the characteristics of chronic renal failure?
gradual loss of renal function
usually over many years
113
What are the causes of renal failure categorised into?
pre-renal (in circulation before kidney)
renal (kidney)
post renal (after kidney)
114
What is a pre-renal cause of renal failure?
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)
115
What are the intrarenal causes of renal failure?
direct damage to kidneys by inflammation, toxins, drugs, infection or reduced blood supply
116
What are some post-renal causes of renal failure?
renal outflow obstruction due to enlarged prostate, kidney stones, bladder tumour, injury
117
What are the signs of acute renal failure?
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
118
What are the characteristics of the causes of acute renal failure and its management?
usually a pre-renal cause
usually reversible with time, renal support until recovery - dialysis, nutrition
119
What is glomerulonephritis?
damage to the tiny filters inside your kidneys (the glomeruli) allowing cells and protein to leak into urine.
120
What can glomerulonephritis progress to?
hypertension
chronic renal failure
121
What are the symptoms of glomerulonephritis?
haematuria and proteinuria
otherwise a healthy individual
122
What is nephrotic syndrome?
condition in which kidneys leak large amounts of protein into the urine, complication of glomerulonephritis.
123
What are the features of nephrotic syndrome?
excessive loss of protein in the urine, >3g in 24hrs
loss of plasma oncotic pressure
tissue swelling (oedema)
hypercoagulable state
124
What drugs should be avoided in renal disease and why?
NSAIDs - inhibit glomerular blood flow causing interstitial nephritis.
125
What drug is known to be nephrotoxic and what is it used for?
cyclosporin - steroid-sparing immunosuppressant used in organ and bone marrow transplants as well as inflammatory conditions such as ulcerative colitis, rheumatoid arthritis
126
What is renal vascular disease and what can cause it?
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
127
What are three conditions which can cause immune mediated renal damage?
1) multiple myeloma - plasma cell tumour, clogs kidney causing tubular nephritis
2) Good pasture's syndrome
3) Vasculitis
128
What is polycystic kidney disease?
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)
129
What defines when someone has reached end stage renal disease?
eGFR <15ml/min
serum creatinine 800-1000micromol/L
130
How is chronic renal failure managed?
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
131
What are the signs of chronic renal failure?
anaemia
hypertension
renal bone disease - low Ca, high phosphate, hyperparathyroidism, osteomalacia
132
What are the symptoms of chronic renal failure?
insidious - may be few
polyuria, nocturia, tired and weak, nausea
133
What are the dental aspects of renal disease?
careful prescribing
avoid NSAIDs, some tetracyclines
134
What are the dental aspects of renal failure?
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
135
What causes dry mouth and taste disturbance in renal failure?
fluid restriction and electrolyte imbalance
136
What radiographic changes can be seen orally with renal failure?
renal osteodystrophy - complication of chronic kidney disease that weakens your bones, lamina dura lost and bony radiolucencies present
137
What are the renal functions?
excretory function
water and electrolyte balance
acid base balance
renal endocrine function - calcium, renin, erythropoietin
138
What is renal dialysis?
a passive process where there is diffusion across concentration gradients. Allows intermittent correction of plasma concentration of small molecules
139
What are the two types of dialysis?
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
140
What anticoagulant is often added into blood during haemodialysis?
heparin
141
How are the endocrine functions of the renal system replaced in renal failure?
erythropoietin - replaced by EPO injections to maintain RBC mass
calcium/bone mass maintained by vitamin D supplementation
hypertension control
142
What is the optimal treatment for end stage renal disease?
renal transplantation
143
Where is a transplanted kidney placed?
lower than original for easier access
144
What are the problems with renal transplantation?
rejection - acute or chronic
immunosuppression
high cardiovascular mortality
osteoporosis risk
145
Is the survival rate better with a renal transplant or dialysis treatment?
renal transplant
146
What are the important factors to remember when treating a patient that undergoes dialysis?
treat AFTER haemodialysis sessions
normal renal function at first but may reduce with time so check creatinine levels
complications are those of immune suppressants
147
Can DMARDs be prescribed alongside corticosteroids?
yes
148
How quickly should DMARDs be escalated to therapeutic dose?
as quickly as possible
149
Name 5 conditions treated by DMARDs in oral medicine
- lichen planus
- mucous membrane pemphigoid
- pemphigus vulgaris
- Behcet's disease
- erythema multiforme
150
What is the difference between DMARDs and NSAIDs?
NSAIDs and corticosteroids have a short onset of action while DMARDs can take several weeks or months to demonstrate a clinical effect.
151
What are the side effects of the DMARD azathioprine?
bone marrow suppression, red cell aplasia, neutropenia, thrombocytopenia, increased susceptibility to infections
152
What are the side effects of the DMARD methotrexate?
bone marrow suppression, mouth ulcers, neutropenia, thrombocytopenia, liver toxicity, pneumonitis
153
What are DMARDs used to treat?
stop or slow the disease process in inflammatory forms of arthritis. DMARDs help preserve joints by blocking inflammation
154
What are the side effects of the DMARD hydroxychloroquine?
retinopathy, hepatic failure, bone marrow suppression, anaemia, thrombocytopenia, leucopenia
155
What are the main dental considerations regarding DMARDs?
increased susceptibility to infection
oral ulceration with methotrexate
156
What are biologics?
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
157
What do Biologics target?
one aspect of the immune system rather than the entire system like conventional DMARDs
158
How are biologics administered?
IV infusions (would be digested if swallowed)
159
How do biologics evade the immune system?
they do not carry antigenic segments that may elicit an immune response so they are undetected
160
What are the four categories of monoclonal antibody and what qualifies them as each category?
Murine - mouse derived
Chimeric - part mouse
Humanized - part human
Human - human derived
161
When is monoclonal antibody therapy used?
when patients have 'failed' therapy with at least two DMARDs
162
What is etanercept and what is it used to treat?
a fusion protein, Anti-TNF drug which blocks TNF (tumour necrosis factor) and reduces inflammation. used to treat psoriasis, psoriatic arthritis, RA, ankylosing spondylitis
163
What do monoclonal antibodies end in?
-mab
e.g. infliximab, adalimumab, certolizumab
164
What fusion protein drug (biologic) is used to treat metastatic colorectal cancer?
aflibercept
165
What drugs end in -ine? (not all)
anti-histamines
166
What drugs end in -pine?
calcium channel blockers
e.g. amlodipine
lower BP
167
What drugs end in -asone?
corticosteroids
e.g. fluticasone, betamethasone
168
What drugs end in -ital?
sedatives
e.g. butabarbital
169
What drugs end in -caine?
local anaesthetic
e.g. lidocaine, articaine
170
What drugs end in -cillin?
penicillin antibiotic
e.g. amoxicillin, ampicillin
171
What drugs end in -dazole?
antibiotics, antibacterials
e.g. metronidazole, omeprazole
172
What drugs end in -dipine?
calcium channel blockers
e.g. amlodipine
173
What drugs end in -dronate?
bisphosphonates
e.g. alendronate, zolendronate, risedronate
174
What drugs end in -eprazole?
proton pump inhibitors
e.g. omeprazole
175
What drugs end in -fenac?
NSAIDs
e.g. diclofenac
176
What drugs end in -mab?
monoclonal antibodies
e.g. denosumab, infliximab
177
What drugs end in -mycin?
antibiotic, antibacterial
e.g. erythromycin, clindamycin
178
What drugs end in -olol?
beta blockers
e.g. propanolol,
179
What drugs end in -olone?
corticosteroids
e.g. triamcinolone, prednisolone
180
What drugs end in -oprazole?
Proton pump inhibitors
e.g. lansoprazole
181
What drugs end in -pril?
ACE inhibitor
e.g. ramipril
182
What drugs end in -semide?
loop diuretics
e.g. furosemide
183
What drugs end in -zepam?
benzodiazepines
e.g. diazepam
184
What drugs end in -zodone?
anti-depressants
e.g. trazodone
185
What are the dental considerations regarding biologics?
increased risk of infection
neutropenia, thrombocytopenia
careful prescribing - liver and renal function
MRONJ
mucosal disease - immunosuppressed
186
What guidance is given for stopping/continuing biologics for dental surgery?
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
187
Are biologics recommended following surgery?
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
188
For patients taking ritixumab (biologic - separate rule for ritixumab), when should treatment be stopped before surgery?
3-6 months prior
189
What is ritixumab used to treat?
targeted cancer drug (monoclonal antibody)
190
What proportion makes up the blood in an anti-coagulated sample?
55% plasma
45% red blood cells
plus WBC and platelets
191
Name two plasma proteins
albumin
globulin
192
What is anaemia?
Low haemoglobin
193
What is leukopenia?
low WCC
194
What is thrombocytopenia?
low platelet count
195
What is pancytopenia?
all blood cells reduced
196
What is polycythaemia?
raised haemoglobin
197
What is leukocytosis?
raised WCC
198
what is thrombocythaemia?
raised platelet count
199
What does one blood change indicate vs multiple blood changes?
one change - reactive change to environment
multiple - bone marrow failure
200
What is leukaemia?
blood malignancy - neoplastic proliferation of white cells
usually disseminated
201
What is lymphoma?
neoplastic proliferation of white cells
usually a solid tumour
202
How does the point of neoplasia in the haematological cell line affect the malignancy?
earlier in the cell line neoplasia occurs, more potentially aggressive the malignancy
203
What are leukaemia and lymphoma further divided into?
lymphoid and myeloid
204
What is porphyria?
abnormal metabolism of the blood pigment haemoglobin. Porphyrins are excreted in the urine, which becomes dark
205
Which porphyria is most clinically relevant and why?
acute intermittent porphyria
photosensitive rash, neuropsychiatric attacks
hypertension, tachycardia
may be fatal
206
What are the two main ways that haemoglobin issues occur?
inability to make HAEM (usually iron deficiency)
inability to make correct GLOBIN chains (thalassemia, sickle cell)
207
What does the number of RBCs mean in terms of anaemia?
nothing
anaemia can happen with too many or too few RBCs
208
What can the size of RBCs in the blood stream help indicate in anaemia?
cause of anaemia
209
What are the three main causes of anaemia?
reduced production
increased losses
increased demand
210
What kind of things can cause a decreased supply/production of haemoglobin?
nutritional deficiency - prematurity, poverty, diet
malabsorption - coeliac disease, post gastric surgery
211
What kind of things can cause an increased demand for haemoglobin?
pregnancy - lactation
growth
212
What kind of things can cause an increased loss of haemoglobin?
blood loss - colon cancer, polyps, PUD
Intravascular haemolysis - destruction of RBCs
213
What are haematinics?
haematinics stimulate blood cell formation or to increase the hemoglobin in the blood
214
Name three haematinics
1) folic acid (folate)
2) iron
3) vitamin B12
215
Name three sources of iron
meat
green leafy vegetables
iron tablets
216
What is iron stored as in the cell?
ferritin
217
Is it simpler for the body to absorb haem-iron or non-haem iron?
haem-iron
218
Name two diseases that reduce iron absorption
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
Name four ways in which iron can be lost
1) gastric erosions and ulcers
2) inflammatory bowel disease - Crohn's, UC
3) bowel cancer
4) haemorrhoids
220
What is vitamin B12 found in?
mainly meat and milk as well as meat and milk alternatives
221
How is vitamin B12 absorbed?
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
Where is folic acid absorbed?
small bowel
223
What can cause vitamin B12 deficiency?
lack of intake (diet) - vegans
lack of intrinsic factor - gastric disease, pernicious anaemia
disease of terminal ileum - Crohn's disease
224
Name five sources of vitamin B12
1) green leafy vegetables
2) papaya and oranges
3) beans, peas, lentils
4) bell peppers
5) avocado
225
What can cause folic acid deficiency?
lack of intake - peculiar diet
absorption failure - jejunal disease (coeliac disease)
226
What can folic acid deficiency during pregnancy lead to?
neural tube defect in foetus e.g. spinabifida
227
When is haemoglobin formed?
during pregnancy
228
Where is haemoglobin formed?
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
What are the three forms of haemoglobin and when are they produced?
alpha haemoglobin - throughout life
beta haemoglobin - mainly after birth
gamma haemoglobin - after birth
230
What is thalassaemia?
normal haem production
genetic mutation of globin chains
231
What are the clinical affects of thalassaemia?
chronic anaemia
splenomegaly
gallstones
marrow hyperplasia - skeletal deformities
cirrhosis
232
How is thalassaemia managed?
blood transfusions
prevent iron overload
233
What is sickle cell anaemia?
abnormal globin chains but function normally at standard oxygen environments
change shape in low oxygen environments
234
What can the change in shape of RBCs in sickle cell anaemia cause?
prevent RBC from passing through capillaries
tissue ischaemia - pain and necrosis
235
What is an increase in red blood cell volume associated with?
deficiencies in vitamin B12 or folic acid
236
What is a decrease in RBC volume (ie small RBCs) associated with?
iron deficiency or thalassaemia
237
What does the level of haemoglobin indicate?
degree of anaemia
238
What are the RCC and HCT?
Red cell count
Haematocrit
239
What is the HCT?
haematocrit - measures the proportion of red blood cells in your blood
240
What is the MCV?
Mean cell volume
241
What is a microcytic RBC and when are they found?
small RBC - iron deficiency, thalassaemia
242
What is a macrocytic RBC and when are they found?
large RBC - B12/folate deficiency
243
What is a hypochromic RBC?
microscopically appear pale
less haemoglobin
can be microcytic, normocytic or macrocytic - usually microcytic
244
What do the RBCs look like in a person with anisocytosis?
very big cells and very small cells in the same sample
245
What are reticulocytes and how do they affect MCV?
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
What are the signs and symptoms of anaemia?
pale, tachycardia rarely, enlarged liver, enlarged spleen
pale mucosa under eye
247
What are the symptoms of anaemia?
tired and weak, dizzy, shortness of breath, palpitations
248
What appearances can anaemia present with orally?
smooth tongue (glossitis) - iron deficiency anaemia
beefy tongue - vitamin B12 deficiency
249
What investigations are done for anaemia?
History
FBC
GI blood loss (faecal occult test, endoscopy)
renal function
bone marrow examination
250
How is anaemia treated?
treat cause
replace haematinics - vit B12, Fe, folic acid
transfusions
251
What are the dental aspects of anaemia?
GA - oxygen capacity
deficiency states (Fe usually) - mucosal atrophy (thinning), candidiasis, recurrent ulceration, sensory changes
252
What are the names of two injectable anticoagulants and how do they differ?
unfractioned Heparin - infusion, only active for. afew minutes
low molecular weight heparin - SC injection
253
Name five anticoagulants
1) warfarin
2) apixaban
3) edoxaban
4) rivaroxaban
5) dagibatran
254
How do antiplatelets work?
interfere with platelet number or function
255
Name 4 anti-platelet drugs
1) low dose aspirin
2) clopidogrel
3) dipyridamole
4) prasugrel and aspirin
256
What dental procedures are considered to require a level of caution regarding anti-platelets and anti-coagulant medication?
extractions
minor oral surgery
implants
periodontal surgery
biopsies - sometimes
257
What are the indications for anticoagulation?
conditions where blood clots will form too readily on or in the circulation
atrial fibrillation, DVT, heart valve disease, mechanical heart valves, thrombophilia
258
Name two common anticoagulants
apixaban
warfarin
259
How long is the onset of warfarin?
slow onset - 3 days
initial hypercoagulability
260
How does warfarin work and how is the response to warfarin measured?
inhibits production of vitamin K dependent clotting factors.
Response measured by INR - normal 2-3 in warfarin users
261
What is a normal INR?
1.1 or below
262
What is the INR of someone taking warfarin?
2-3
263
What is the INR of someone with prosthetic valves and higher risk of DVT?
3-4
264
How often should INR be checked in someone taking warfarin?
every 4-8 weeks
265
What are the appointment requirements for a patient on warfarin?
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
What 3 local haemostatic measures are used in patients taking warfarin?
cellulose sponge
sutures
LA infiltration (vasoconstriction)
267
What 4 drugs can interact with warfarin, increasing INR?
amiodarone
antibiotics
alcohol (with liver disease)
NSAIDs
268
What 4 drugs can interact with warfarin, reducing INR?
carbamazepine, barbiturates
cholestyramine
griseofulin
alcohol (without liver disease)
269
Which medications should be avoided in dental patients on warfarin?
Aspirin (as an analgesic)
NSAIDs including ibuprofen, diclofenac
azole antifungal drugs - fluconazole
270
What are the hazards of taking warfarin?
haemorrhage
soft tissue injury causing bleeding into muscles
271
What can be done to reverse anticoagulation in a warfarin patient if haemorrhage occurs?
vitamin K injection (hospital setting)
272
What are NOACs?
New/novel oral anticoagulants
273
What are some of the benefits of NOACs instead of warfarin?
no need to monitor action
rapid onset - within hour
short duration of action - effect lost within day
274
How do NOACs work?
preventing the effect of factor X
275
Name four NOACs
1) rivaroxiban
2) apixaban
3) edoxaban
4) dabigatran
276
What are the considerations of doing dental treatment in a patient on NOACs?
- 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
How long should you keep a NOAC patient after extraction to assess bleeding?
20 mins
278
What are the NOACs safe to use alongside (drug interactions)?
safe with dental antibiotics except macrolides (erythromycin and clarithyromycin)
safe with antifungals, LA, anti-virals
279
What medications should be avoided in patients taking NOACs?
erythromycin and clarithromycin
NSAIDs - prolong action and inhibit platelets
avoid carbamazepine
280
Should antiplatelet drugs be stopped for treatment in patients with stents?
No
281
How should dental treatment be carried out in a patient taking aspirin alone?
treat without interrupting medication
local haemostatic measures
consider limiting initial treatment area
282
How should dental treatment be carried out in a patient on non-aspirin single antiplatelet therapy or dual therapy WITH aspirin?
do not interrupt treatment
expect prolonged bleeding - limit initial area
local haemostasis
283
How should dental treatment proceed in a patient if two antiplatelet drugs are taken in combination WITHOUT aspirin?
discuss with doctor - stop one drug 7 days before surgery or refer to hospital unit
284
What MUST post operative instructions include?
emergecny contact details
285
What is an inherited bleeding disorder?
an acquired defect which affects the coagulation of the blood
286
What are the conditions where too LITTLE clot is formed and where too MUCH clot is formed?
Too little - haemophilia
Too much - thrombophilia
287
People with haemophilia/haemophilia A are deficient in what?
Factor VIII
288
People with Christmas disease/haemophilia B are deficient in what?
Factor IX
289
Von Willebrand's disease is a reduction in what factor causing what?
Factor VIII
reduced platelet aggregation
290
What kind of disease is haemophilia A and B?
inherited sex linked recessive
defective gene on the X chromosome
291
How are patients with haemophilia A managed?
severe & moderate - recombinant factor VIII
mild carriers - DDAVP (desmopressin) releases factor VIII from endothelial cells
very mild - tranexamic acid, inhibition of fibrinolysis
292
How are patients with haemophilia B managed?
ALL require recombinant factor IX
293
What do coagulation factor inhibitors develop into?
they are antibodies which develop to factor VIII and IX
294
What kind of disease is Von Willebrand's disease?
Autosomal dominant - NOT transmitted by the X chromosome
295
What is Von Willebrand's disease and what are they deficient in?
bleeding disorder where people lack or have defective vW factor on their platelets which interacts badly with factor VIII, causing poor clot activation
296
How are patients with Von Willebrand's disease managed?
DDAVP (desmopressin) for most
Mild cases only require tranexamic acid
297
What is the function of DDAVP (desmopressin)?
releases factor VIII that has been bound to the endothelial cells therefore giving a temporary boost of factor VII levels and clotting ability
298
What is tranexamic acid and what does it do?
inhibitor of fibrinolysis - prevents or reduces bleeding by impairing fibrin dissolution
299
What is the most common disease - haemophilia A, haemophilia B, Von Willebrand's disease or Factor XI deficiency?
Von Willebrand's disease
300
Where can severe or moderate haemophilia patients be treated?
unit attached to haemophilia centre
pros and other no-risk treatments in primary care
301
Where are mild and carrier haemophilia patients treated?
treatment shared with GDP
pt reviewed at haemophilia dental unit every 2 years
302
What are considered bleeding risk procedures in haemophilia?
- administration of LA
- extractions
- MOS
- periodontal surgery
- biopsies
303
What LA is considered safe in patients with haemophilia?
buccal infiltration
intraligamentary injection
intra-papillary injection
304
What LA is considered dangerous in patients with haemophilia?
IANB
Lingual infiltration
posterior superior nerve block
305
How long should haemophilia patients be observed following surgery?
severe & moderate - overnight
mild & carriers - 2-3hours post surgery
306
What is thrombophilia?
increased risk of blood clotting
clot formation ability greater than clot breakdown ability
307
Is thrombophilia acquired?
often acquired condition superimposed on a genetic tendency
308
What can cause acquired hypercoagulation?
antiphospholipid syndrome - lupus anticoagulants
oral contraceptives
surgery, trauma, cancer, pregnancy, immobilisation
309
What can cause inherited hypercoagulation?
protein C deficiency
Protein S deficiency
Factor V leiden
Antithrombin III deficiency
310
What platelet disorder increasing bleeding occurs with reduced platelet numbers?
thrombocytopenia
311
What platelet disorder increasing bleeding occurs with increased platelet numbers?
thrombocythemia
312
What is thrombocytopenia?
low number of normal platelets
313
What are the possible causes of thrombocytopenia?
idiopathic (unknown cause)
drug related - alcohol, penicillin based drugs, heparin
secondary to lymphoproliferative disorder - leukaemia
314
What is thrombocythemia?
high numbers of (often poor) functioning platelets
315
What are qualitative platelet disorders?
normal platelet count but abnormal function
316
What are three examples of inherited qualitative platelet disorders?
Bernard Soulier syndrome
Hermansky Pudlak
Glanzmann's thrombasthenia
317
What are four things associated with acquired qualitative platelet disorders?
cirrhosis
drugs
alcohol
cardiopulmonary bypass
318
No additional precautions are required for treating a patient with a platelet disorder when their platelet count is at what level?
>100 x 10⁹/L and no functional issues
319
What treatment can be carried out in a platelet disorder patient with a platelt count of >100 x 10⁹/L?
hygiene therapy
removable pros
restorative dentistry, crowns and bridges
endo
ortho
320
At what platelet counts should patients be treated in the hospital?
<50 x 10⁹/L
above 500 x 10⁹/L
321
Special care is required for patients with platelet disorders for which procedures?
extractions
MOS
periodontal surgery
biopsies
322
What are the four blood types?
A
B
O
AB
323
What does the D system regarding blood cell antigens assess?
Rhesus positive or negative
324
When are blood transfusions indicated?
blood loss
specific production problems - RBC, platelets, plasma proteins
325
Which blood group can donate to groups O, A, B and AB?
group O
326
What are three examples of transfusion complications?
transmission. ofinfection
fluid overload - heart failure
incompatible blood - RBC lysis (burst), fever, jaundice, death
327
What is lymphoma?
cloncal proliferation of lymphocytes in a lymph node or associated tissue
solid tumour but some cells in blood
328
What are the two types of lymphoma and which is most common?
Non-hodgkins - most common, 6:1
Hodgkins
329
What are the symptoms of lymphoma?
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
What factors are considered when staging lymphoma?
1) no. of nodes involved and site
2) extra-nodal involvement
3) systemic symptoms
331
What is stage 1 lymphoma?
single lymph node region or single extra-lymphatic site
332
What is stage II lymphoma?
two or more sites, same side. ofdiaphragm or contagious extralymphatic site
333
What is stage III lymphoma?
both sides of diaphragm or spleen or contagious extralymphatic site
334
What is stage IV lymphoma?
diffuse involvement of extralymphatic sites with or without nodal disease
335
At what age does the peak incidence of Hodgkin's lymphoma occur?
15-40yrs
336
What is the clinical presentation of Hodgkins lymphoma?
painless lymphadenopathy - typically cervical, fluctuate in size, pain with alcohol
fever, night sweats, weightloss, itching
infection
337
What is the aetiology of non-hodgkins lymphoma?
microbial factors associated - EBV, HIV, H pylori
autoimmune disease associated - chronic immune activation, RA, PUD, Sjorgren's
immunosuppression - AIDS, post-transplant
338
What is the presentation of non-hodgkins lymphoma?
lymphadenopathy - widely disseminated
extra-nodal disease more common - oropharyngeal, Waldeyer's ring
symptoms of marrow failure
339
What is multiple myeloma?
malignant proliferation of plasma cells, bone marrow cancer
340
What are the features of multiple myeloma? 3
1) monoclonal paraprotein in blood and urine
2) lytic bone lesions - pain and fracture
3) excess plasma cells in marrow - marrow failure
341
What are the treatment options for haematological malignancies?
chemotherapy
radiotherapy
monoclonal antibodies
haemopoietic stem cell transplantation
342
What kind of cells are targeted by chemotherapy?
those with high turnover rate e.g. hair follicles
343
What is radiotherapy?
cytotoxic effect of ionising radiation
344
What does allogeneic mean?
from a live donor
345
What does autologous mean?
obtained from the patient
346
What does haemopoietic stem cell transplantation require?
total body irradiation to eradicate malignant cells and host marrow - "clean sheet"
347
What kind of DNA mutation is a haematological malignancy normally and what does it do?
translocation - switches off. atumour suppressor gene or on an oncogene
348
What is a "blast" cell?
immature cell
349
What does leukaemia cause? 3
1) anaemia
2) infection (neutropenia)
3) bleeding (thrombocytopenia)
350
What is the clinical presentation of leukaemia?
anaemia
neutropenia
thrombocytopenia
lymphadenopathy - neck lumps
splenomegaly/hepatomegaly
bone pain
351
What age group is acute myeloid leukaemia more common in?
elderly
352
What are the symptoms of anaemia?
breathlessness
tiredness
easily fatigued
chest pain/angina
353
What are the signs of anaemia?
pallor
signs of cardiac failure (ankle swelling, breathlessness)
nail changes e.g. brittle nails, koilonychia
354
What is the clinical presentation of neutropenia?
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
What are the symptoms of neutropenia?
recurrent infection
unusual severity of infection
356
What are the signs of neutropenia?
unusual patterns of infection and rapid spread
respond to treatment but recur
systemic involvement - fever, rigor, chills
357
What is the peak age of acute lymphoblastic leukaemia?
4yrs but does occur in adults
358
Name the six ways in which infections are transmitted during sex
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
What is vertical transmission?
to baby through direct contact with the mother's fluids, usually during delivery
360
What is the general trend of sexual behaviours in recent times?
having sex younger with more lifetime partners
361
What are eight risk factors for STIs?
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
What six STIs can affect the mouth?
1) chlamydia trachomatis
2) treponema pallidum
3) Human papillomavirus
4) Neisseria gonorrhoea
5) herpes simplex virus
6) human immunodeficiency virus
363
Which two STIs are not symptomatic in the mouth but are both carried in the oropharynx and transmitted by oral sex?
chlamydia trachomatis
neisseria gonorrhoea
364
What spirocheate causes syphilis?
treponema pallidum
365
What are the stages in syphilis?
exposure
primary syphilis
secondary syphilis
early latent
late latent
tertiary - neurological, cardiovascular, gummatous effects
366
How long does it take to go from syphilis exposure to primary syphilis?
10-90 days
367
What time period is classed as early syphilis?
1st 2 years of infection
368
How long does it take to progress from primary to secondary syphilis?
less then 2 years, usually 3-6 weeks
369
How long does primary syphilis last?
10-90 days
370
What are characteristically seen in primary syphilis and how long do they last?
Chancres
Resolves without treatment 3-6 weeks
371
What do chancres look like?
1-2cm, indurated with a lot of inflammatory infiltrate, well circumscribed with a raised border and ulcerated
372
Where are chancres commonly found in syphilis?
genitals are the most common location for chancres to develop, but these ulcers also can form around the mouth or anus
373
When does secondary syphilis usually develop?
<2yrs (usually 3-6 weeks)
374
Where is secondary syphilis found in the body?
haematogenous (in blood) and lymphatic dissemination
375
What kind of disease is secondary syphilis?
multi-system
376
What are the systemic symptoms of secondary syphilis?
low grade fever
sore throat
headache
lymphadenopathy
rash - palms and soles of feet
377
What symptoms are found orally in secondary syphilis?
white glistening patches - greyish membrane, hyperaemic halo, coalesce to form "snail trail" ulcers
found on HP, SP, gingivae and buccal mucosa
378
What may patients with syphilis present with?
meningitis
iritis
hepatitis
ureitis
periositis
glomerulonephritis
condylomata lata
379
How is syphilis diagnosed?
lesion - swab for treponema pallidum by PCR
venous blood - syphilis antibody
380
How is syphilis treated?
antibiotic - benzathene penicillin IM or doxycycline
Public health - partner notification, STI testing, sexual abstinence, risk reduction advice
381
What is HIV?
Human immunodeficiency virus
382
List 5 key facts about HIV
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
What are the modes of transmission of HIV?
Sexual transmission
injection drug use
other - vertical transmission (rare)
384
What are the high risk groups for HIV?
Everyone is at risk
higher risk - MSM, high prevalence countries, injecting drugs, sexual contact of above
385
What is the average time to death for untreated HIV?
9-11yrs
386
What count decreases over time with the increase of HIV RNA copies in the blood?
CD4+ count (T helper lymphocyte count) - falls as viral load rises
387
What are the stages of HIV infection?
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
What are the symptoms of primary HIV infection and when do they occur?
fever, myalgia, rash (macropapular), pharyngitis, headache/aseptic meningitis
2-4 weeks after infection
389
What are teh oral lesions seen in primary HIV?
Apthous ulcers
candidiasis
390
What does mucosal candidiasis in symptomatic HIV look like and indicate?
pseudomembranous
erythematous
angular chelitis
oesophageal extension
predictive of progression to AIDS
391
Name five main oral/facial symptoms in symptomatic HIV
1) mucosal candidiasis
2) gingivitis
3) Kaposi's sarcoma
4) Oral hairy leukoplakia
5) Seborrhoeic dermatitis
392
What are the features of gingivitis in symptomatic HIV?
linear gingival erythema
necrotising ulcerative gingivitis
often sudden onset with no plaque or calculus
393
What is Kaposi's sarcoma?
vascular cancerous tumour
caused by human herpes virus 8 (HHV8)
localised or visceral
394
What causes Kaposi's sarcoma?
Human Herpes virus 8
395
what causes oral hairy leukoplakia?
EBV infection
396
What two oral symptoms are predictors of progression from HIV to AIDS?
mucosal candidiasis
oral hairy leukoplakia
397
In what condition can Kaposi's sarcoma be seen?
HIV
398
Staff with HIV can carry out exposure-prone procedures as long as they are what?
on antiretroviral treatment
have undetectable viral load in last 3 months
399
How quickly does PEP (post-exposure prophylaxis) need to begin to be effective following HIV exposure?
within 72hrs
400
What is post-exposure prophylaxis?
combination anti-retroviral drugs
4 week course
reduce risk of transmission by 80%
401
What are the indications of post-exposure prophylaxis?
-high risk injury, source and fluid
-sexual
-occupational
402
What types of HSV are there?
Type 1 and type 2
403
What are the oral symptoms of primary infection of HSV?
Gingivostomatitis (inflammation of gums and lips)
pharyngitis
with or without symptoms
404
What is the main symptom of recurrent HSV infection (usually HSV-1)?
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
How is herpes simplex virus transmitted?
kissing
oral sex
asymptomatic shedding of virus
406
HSV in HIV may be resistant to what anti-viral?
aciclovir - used for cold sores
407
How long do orolabial herpes lesions usually last?
self limiting 7-10 days
408
How are orolabial herpes lesions managed?
usually no treatment
symptom control
avoid kissing and oral sex
wash hands after touching
409
What is a common route of infection of HPV?
Oral sex
410
What is the most common STI?
HPV
411
Why are HPV infections dangerous regarding progression?
some strains are oncogenic (e.g. HPV16, HPV18)
412
What cancers are commonly associated with HPV?
Oropharyngeal cancer
413
What are the main dentally relevant factors regarding liver disease?
pts have impaired wound healing
impaired clotting - reduced platelets, deficient clotting factor
risk of BBV
414
Name 7 functions of the liver
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
How do you know it a patient has liver disease?
past history
jaundice
stigmata of chronic liver disease
416
What are the symptoms of jaundice?
yellowness of eyes
yellow skin colour
look at whites of eyes
417
What causes jaundice?
increased production of bilrubin
failure of excretion and conjugation of bilrubin
418
What is bilrubin?
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
Name three main types of liver disease
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
What are the clinical features of jaundice?
yellow skin
dark urine - conjugated bilrubin
lethargy and malaise
pale stools
itch
anorexia
421
What do liver function tests measure and give an example?
measure liver damage
ALT/AST
ALP
GGT
422
what do true liver function tests measure?
measure how well the liver is working
423
Name three true liver function tests
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
What is the most common hepatitis virus?
Hep E
425
How is HBV (Hepatitis B) transmitted?
blood, sex, vertical transmission, chronic carriage in ethnic groups.
426
What are the dangers of HBV?
Highly infectious
progression to cirrhosis in 10yrs
liver failure
hepatoma
427
What is hepatoma?
most common type of primary liver cancer
428
How is HBV treated?
PEG alpha-interferon
Tenofovir
Entecavir
429
Is the transition from acute HBV to chronic HBV infection "carrier" common?
<5% risk if infected as adult
430
How often does infection with HCV result in chronic infection?
80% cases
431
Is there a vaccine for Hep C (HCV)?
no vaccine
432
What can chronic hepatitis (HCV) progress to?
cirrhosis (20-100%)
Hepatocellular carcinoma (1-4%)
433
What occurs with hepatitis A and how is it managed?
acute illness only, self limiting
rest, low fat diet, alcohol avoidance
434
How is hepatitis A transmitted?
faecal-oral spread
poor hygiene/overcrowding
food and water contamination
435
Is there a vaccine for hepatitis A?
yes
436
What disease causes the destruction of adrenal tissue?
Addison's disease
437
What disease causes excess adrenal action?
Cushing's disease
438
What affect do therapeutic corticosteroids have on adrenal tissues?
suppression of adrenal action
steroid adverse effects
439
What does the zona glomerulosa of the adrenal gland secrete?
aldosterone - renin/angiotensin system
440
What does the zona fasicularis of the adrenal gland secrete?
cortisol
441
What does the zona reticularis of the adrenal gland produce?
adrenal androgens
442
What are the three zones of the adrenal gland and name them from most superficial to deep
zona glomerulosa - between cortx and outside of gland
zona fascicularis - in between
zona reticularis - between cortex and medulla
443
Where is adrenal regulation controlled from?
hypothalamus then pituitary
444
Explain the stages in adrenal regulation
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
What is the function of aldosterone?
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
how does aldosterone indirectly effect blood pressure?
Too much aldosterone can cause high blood pressure and a build-up of fluid in body tissues
447
The action of aldosterone is inhibited by which drugs?
- ACE inhibitors
- AT2 (angiotensin 2 receptor) blockers
448
What is a common side effect of ACE inhibitors?
dry cough
449
What is cortisol?
natural glucocorticoid, primary stress hormone
enhances your brain's use of glucose and increases the availability of substances that repair tissues
450
What are the physiological effects of cortisol?
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
Therapeutic steroids cause an enhanced glucocorticoid effect, what can this cause?
immunosuppression
reduced inflammatory response
452
What are the adverse effects of therapeutic steroids?
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
What syndrome occurs with hyperfunction of the adrenal gland producing excess glucocorticoids?
Cushings syndrome
454
What syndrome is caused by hyperfunction of the adrenal gland causing excess aldosterone?
Conn's syndrome
455
What causes Cushings syndrome?
pituitary tumour affecting ACTH production
adrenal adenoma or hyperplasia
too much cortisol produced as a consequence
456
What are the symptoms of Cushing's syndrome?
DM features
poor resistance to infections
osteoporotic changes
psychiatric disorders
hirsuitism
skin and mucosal pigmentation
amenorrhoea, impotence and infertility
457
What are the signs of Cushings syndrome?
centripetal obesity - moon face, buffalo hump
hypertension
think skin and purpura
muscle weakness
osteoporotic changes
458
What do we see in the skin in ACTH excess?
pigmentation of skin esp over joints
pigmentation of mucosa
459
What can cause adrenal gland failure and hypofunction?
autoimmune gland destruction
infection
infarction
460
What can cause pituitary failure and hypofunction?
compression from another adenoma
Sheehan's syndrome - failure of ALL pituitary hormones
461
What are two causes of Addison's disease?
TB
Autoimmune adrenalitis
462
What are the signs of Addison's disease?
postural hypotension
weightloss and lethargy
hyperpigmentation
vitiligo
463
What are the symptoms of Addison's disease?
weakness
anorexia
loss of body hair (females)
464
What investigations are done for Cushing's syndrome?
high 24hr urinary cortisol excretion
CRH tests - rise in ACTH with CRH
465
What investigations are done for Addison's disease?
high ACTH level
negative synACTHen tests - no cortisol rise in response to ACTH injection
466
What are the key features of adrenal hyperfunction caused by pituitary adenoma or ectopic ACTH production?
HIGH ACTH and Cortisol
467
What are the key features of adrenal hyperfunction caused by gland adenoma?
LOW ACTH
High cortisol
468
What are the key features of adrenal hypofunction caused by pituitary failure?
LOW ACTH
LOW cortisol
positive synACTHen test
469
what are the key features of adrenal hypofunction caused by gland destruction?
High ACTH
lOW CORTISOL
Negative synACTHen test (no gland to stimulate)
470
How is adrenal hyperfunction treated?
detect cause (adenoma) - pituitary, adrenal, ectopic (lung)
Surgery - pituitary, adrenal (partial/complete adrenalectomy)
471
What is Addison's disease defined as?
autoimmune destruction of adrenal gland
472
What are the features of Addison's disease crisis?
hypotension
vomiting
eventual coma
absence of mineralcorticoid and effect of glucocorticoids
473
What is the management technique for Addison's disease?
hormone replacement - cortisol AND fludrocortisone (replacement for aldosterone)
474
Do patients with Addison's disease require steroid prophylaxis?
require consideration for steroid cover during dental procedures
475
What is the main dental feature seen in Cushings syndrome?
Candidiasis
476
What is the main dental feautre seen in Addisons and Cushings?
oral pigmentation
