CMS Flashcards
anaemia
reduced haemoglobin level
signs & symptoms of anaemia
symptoms - tiredness, weakness, dizziness, SoB, angina
signs - paleness, ankle swelling, tachycardia
3 types of anaemia
- microcytic
- macrocytic
- normocytic
microcytic anaemia (2)
caused by:
- Fe deficiency; 3 main causes = menstruation, GI bleed, poor intake; ferratin tested, angular cheilitis, spooned nails & smooth tongue may be seen clinically
- thalassemia; normal haem but globin chain production is modified, 2 types = alpha in Asian & beta in Mediterranean, clinically = chronic anaemia, bone marrow hyperplasia, cirrhosis, gall stones, can only be managed by blood transfusion
macrocytic anaemia (3)
caused by:
- vit B12 deficiency ;occurs in pernicious anaemia where autoimmune reaction against parietal cells which should release intrinsic factor which aids absorption of B12 in terminal ileum, can also occur in Chron’s
tx = supplementation via injection
clinically = beefy tongue, dysaesthesia, recurrent oral ulceration, mucosal atrophy
- folic acid deficiency; e.g. in pregnancy / chron’s (absorbed in jejenum)
- reticulocytes; increased bleeding leads to anaemia itself so immature blood cells added to blood & are larger as they still contain organelles so make blood macrocytic
normocytic anaemia (3)
RBCs of normal size but too few, caused by:
- renal disease; glomerulonephritis (glomerulus doesn’t filter properly & blood lost in urine) or renal failure (no endocrine function of kidneys so erythropoietin no produced so kidneys not stimulated to make RBCs)
- sickle cell anaemia; rbcs change shape under certain concentrations of oxygen so they cannot pass through capillaries
- excessive bleeding
to diagnose cause of anaemia (4)
MCV - normal = 75-90Fl/red cell
haemoglobin - normal = <50m 14-18gm/DL, <50f 12-16gm/DL, >50m 12.4-14.9gm/DL, >50f 11.7-13.8gm/DL
RBC count - normal = M 4-5.9x10to12/L, F 3.8-5.2x10 to 12/L
haematocrit - normal = m 41-50%, f 36-44%
GA & anaemia
under GA general oxygen capacity will be lower so dangerous for those with anaemia especially sickle cell
haematological malignancies
haematological cell line can turn neoplastic but earlier in the line the more aggressive the malignancy
cause unknown
leukaemia
cancer of bone marrow which prevents normal blood manufacture leading to
- anaemia; due to insufficient blood production
- infection; neutropenia
- increased bleeding; thrombocytopenia
neutropenia
lack of neutrophils in the blood so disease related to portals of entry
ptx can present with oral candidosis / tonsillitis
thrombocytopenia
decrease in platelet count causing increased bleeding time & increased frequency of bruising
signs & symptoms of leukaemia (6)
anaemia
neutropenia
thrombocytopenia
bone pain
lymphadenopathy
spleno/hepatomegaly (increased size)
acute lymphoblastic anaemia
body in catabolic state so loss of body weight, high heart rate so fever, sweat, malaise , lymphadenopathy & tissue infiltration
prognosis in young is better
acute myeloid leukaemia
affects non lymphocytes
presentation = same as acute lymphoblastic
chronic lymphocytic leukaemia
mostly affects elderly
B cell lymphoproliferative disease i.e. causes out of control B cell growth
slow progression & asymptomatic
only detected on routine blood tests
chronic myeloid leukaemia
least common
generally hereditary
increase in neutrophils & their precursors
lymphoma
clonal proliferation of lymphocytes in a lymph node or associated lymphoid tissue
solid tumour but some cells may leak into blood
2 types = hodgkin’s & non hodgkin’s
non hodgkin’s more common & more aggressive
hodgkin’s lymphoma
painless lymphadenopathy which will fluctuate in size, often cervical & pain on drinking alcohol
fever, night sweats, weight loss, itching, increase in unusual infections
high cure rate
non hodgkins lymphoma
generally affects B lymphocytes
caused by microbial disease / autoimmune disease / immunosuppression
prognosis not great and 50% relapse
lymphadenopathy widely disseminated & extra nodal disease more common, if waldeyer’s ring affected sore throat & noisy breathing, symptoms of bone marrow failure i.e. fatigue, anaemia, neutropenia & thrombocytopenia
multiple myeloma
malignant proliferation of plasma cells causing increased protein in blood & urine, lytic bone lesions leading to fracture & excess plasma cells in bone marrow leading to bone marrow failure
main symptoms = increased infection, bone pain, renal failure (glomerulus clogged with protein) & amyloidosis
tx of haematological malignancies
chemo/radiotherapy, monoclonal antibodies, haemopoietic stem cell treatment & supportive therapy
what is needed & where is production of clotting factors 2, 7, 9, 10
produced in liver & required vitamin K
fibrinolysis factors
antithrombin III will affect intrinsic pathway by inactivating coagulation factors in pathway, protein S will be a cofactor for protein C and they both have anticoagulant effects as they inactivate factor V & VIII
liver will produce all these factors & vitamin K important for proteins C & S
if patient in shock i.e. lost excessive amounts of blood
immediate - stop bleeding via vascular, platelet & plasma responses i.e. smooth muscle constriction & platelet adhesion & aggregation by endothelium
short term - BP restored by vasoconstriction produced by thromboxane A2 & ADP
medium term - restore volume of fluid by activating RA system so kidney absorbs more water & salt to keep blood volume up, ADH has similar effect as well as vasopressin effects constricting blood vessels
long term - replace constituents of blood
2 types of haemophilia
haemophilia A - factor VIII deficiency
haemophilia B - factor IX deficiency
haemophilia A
sex linked recessive
factor VIII deficiency
carriers/mild = DDAVP used to increase levels of factor VIII / oral tranexamic acid (antifibrinolytic agent)
moderate / severe recombinant = factor VIII should be used to replace factor lost
haemophilia B
sex linked recessive
factor IX deficiency
carriers/mild = oral tranexamic acid as DDAVP will not increase factor IX levels
moderate / severe = only use of recombinant factor IX
von willebrands disease
reduced factor VIII levels & reduced platelet aggregation
autosomal dominant disease characterised by deficiency of von willebrands factor
tx = DDAVP to increase factor VIII or oral tranexamic acid
dental relevance of bleeding disorders
depends on severity
carriers / mild can be seen at GDP with review every 2yrs - observed for 2-3hrs following XLA, biopsy etc
moderate / severe should be seen in hospital setting - observed overnight
IBD only undertaken in hospitals
do not give NSAIDs i.e. aspirin so this will inhibit platelet aggregation & increase bleeding
thrombophilia
increases risk of clot development
inherited = protein C/S deficiency, factor V leiden & antithrombin III deficiency
acquired = DVT, OCP, surgery trauma, cancer, pregnancy
where is vitamin k stored
the liver
dental relevance of liver disease
- mild = blood results normal so ptx treated as normal
- moderate = platelet count >100 so shouldn’t be any issue with tx but local measures for haemostasis may need to be accounted for
- severe = lack of many clotting factors, platelet count <100 so XLA & invasive procedures should be undertaken in a hospital setting
warfarin & INR
want consistent INR of 2-4
it will antagonise vit K which is required for synthesis of factors 2 7 9 10, protein C & S
drug interactions with warfarin
potentiating drugs = ACE inhibitors, antibiotics, NSAIDs
inhibiting drugs = epilepsy drugs & alcohol
dental relevance of warfarin
INR must be checked 48hrs before tx, if unstable check 24hrs, avoid IBD if possible, if tx of warfarin is to be stopped for tx wait 72hrs after (12hrs if heparin)
dental relevance of aspirin & clopidogrel
both of these are irreversible for the life of the platelet which is 7 days
if low dose aspirin & clopidogrel used separately there is no effect on post op bleeding but if used together there will so stop 7 days prior to surgery / invasive procedure
risk factors for cardiovascular disease
irreversible - age, sex, family history
behavioural - smoking, alcohol, diet, exercise, obesity
factors managed by drugs - hypertension, hyperlipidaemia, diabetes, stress
drugs that can increase risk - corticosteroids, OCP, sympathomimetrics i.e. adrenaline
drugs that prevent further cardiovascular disease (3)
- anti-platelet
- anti-arrhythmics
- lipid lowering
these help stop build up of atheroma & help keep the rhythm of the heart under control, help to prevent further hypertension, heart arrhythmias & prevent infarction
anti platelet drugs
e.g. aspirin & clopidogrel
widespread atherosclerosis causes more platelet aggregation which can narrow or occlude blood vessels leading to ischaemia / infarction so these drugs are used to decrease total peripheral resistance to decrease BP
lipid lowering drugs
e.g. statins
inhibit cholesterol synthesis in liver reducing blood cholesterol & LDL levels to reduce further build up of atheroma, help to stabilise TPR keeping BP down
these can interact with antifungals & cause myositis
anti arrhythmic drugs
e.g. amiodarone
bock beta receptors in heart preventing increase in heart rate thus reducing cardiac output
these can cause postural hypotension due to decreased heart rate & can worsen heart failure, will also block beta receptors in lungs making asthma more difficult to treat
drugs that reduce current cardiovascular disease (5)
- diuretics
- anti-arrhythmics
- nitrates
- calcium channel blockers
- angiotensin converting enzyme inhibitors
these drugs help reduce BP thus helping to prevent symptoms of disease & prevent further disease occurring
diuretics
e.g. thiazide / loop - furosemide
thiazide; inhibit NaCl cotransporter in DCT of kidney decreasing Na reabsorption so increased fluid passed as urine e.g. chlorothiazide
loop; inhibit NaClK cotransporter in ascending loop of henle
overall reduce blood plasma volume thus reducing cardiac workload & BP helping reduce symptoms of heart failure
side effects are Na/K imbalance if not monitored properly, can cause gout
nitrates
e.g. glyceryl trinitrate
work by releasing nitrous oxide which causes vasodilation throughout the body, veins supplying heart are dilated reducing preload, resistance arteries will dilate reducing workload & oxygen consumption & collateral coronary artery supply will be dilated reducing angina pain
used as a spray sublingually in emergency
calcium channel blockers
e.g. amlodipine
block calcium channels in smooth muscle including the heart slowing conduction (calcium used to lengthen action potentials), causes vasodilation in peripheral blood vessels, both of these decrease BP
side effect - gingival hyperplasia
ACE inhibitors
e.g. prils
inhibit conversion of angiotensin I to angiotensin II which prevents aldosterone release from medulla of adrenal gland meaning that aldosterone will not be used to resorb salt & water leading to reduced salt & water retention which reduces BP
side effects - hypotension & cough
ischaemia & infarction
deficient blood supply to tissue which can lead to hypoxia / necrosis
can be due to atheroma, embolism or thrombosis
ischaemia leads to infarction over time
atheroma
build up of plaque due to accumulation of lipids, smooth muscle proliferation & formation of fibrous tissue
predisposed by hyperlipaemia, smoking, hypertension, diabetes
atheroma leads to arterial narrowing causing angina / intermittent claudication
can cause increased thrombosis which can lead to ischaemia / infarction
can weaken arterial walls causing aneurysm
thrombosis
formation of solid mass from blood constituents in vascular system
predisposed by atheroma, turbulent blood flow, hypercoagulable blood
embolism
vascular transfer of a substance by blood which becomes stuck in a blood vessel distant from the origin
often caused by thromboembolism
thrombus from left side of heart / arteries break off it can cause ischaemia / infarction due to blood flow obstruction
thrombus formed in DVT can cause focal pulmonary infarction / may obstruct main pulmonary arteries from right side of heart causing sudden death
stable v unstable angina
stable = cardiac arteries become ischaemic so not enough oxygen supplied heart under exertion
unstable = randomly occurs with symptoms sometimes mimicking MI, may be rapid deterioration
diagnosing angina
central crushing autonomic nerve pain which is relieved by rest
sometimes a hyperdynamic circulation
angina investigations
ECG - typically normal but on pain often a raised or lowered ST segment, may see raised ST if previous MI
angiography - to view occlusion or narrowing of coronary arteries
echocardiogram
tx for angina
tx required as over time it will lead to infarction
best action is to modify risk factors i.e. stop smoking, improve diet & increase exercise
drug therapy - anti platelet i.e. aspirin to prevent platelet aggregation on atheroma, Ca channel blockers, diuretics, beta blockers, ACE inhibitors to reduce BP, decreasing amount of atherosclerosis forming & reducing load of heart, nitrates e.g. GTN to reduce preload & dilate coronary arteries
surgical therapy - CABG or angioplasty with stenting
PVD
peripheral vascular disease i.e. ischaemia of the tissues named intermittent claudication & affects lower limbs
pain on exertion & relived by rest
MI
complete blockage of 1 of the coronary arteries leading to functional limitation or death
ST segment elevation and after a Q wave will be present
symptoms - pain, nausea, paleness, sweating
signs - increased troponin level
tx of MI
get to hospital as soon as possible
prescribe aspirin to prevent platelet aggregation, beta blockers & Ca channel blockers to slow heart rate reducing O2 demand, ACE inhibitors & diuretics to reduce heart load by reducing BP
angioplasty & stenting preferred to thrombolysis as this is only effective when given early and will cause all clots to break down causing bleeding so contraindicated in liver disease, severe hypertension & pregnancy
again modify risk factors
stroke
infarction to cerebral arteries in the brain caused by embolism from atheroma or cerebral bleed
dental relevance of angina
central crushing chest pain can radiate to jaw
may struggle to get up stairs in dental surgery
LA with adrenaline may cause angina attack due to increased heart rate if accidentally injected into vein
normal sinus rhythm
p wave - atrial depolarisation
qrs complex - ventricular depolarisation
t wave - ventricular repolarisation
during MI ST is raised and in angina it is lowered
atrial fibrillation
no p wave present
high heart rate with irregular beats
same as in MI
ventricular fibrillation
shockable rhythm
irregularly irregular
common causes of bradyarrhythmia
drug induced by beat blockers
heart block
tx of bradyarrhythmia
pacemaker
caution when using ultrasonic scaler as risk of electrical interference
hypertension
normal = 120/80mmHg
hypertension = 140/90mmHg
systolic = pressure when heart pushes blood out
diastolic = pressure when heart rests between beats
if systolic high there is increased stroke risk due to high BP potentially causing aneurysm & rupturing in cerebral veins & arteries
if diastolic high it causes more problems as heart will have to push harder against already high pressure
3 causes of hypertension
- essential hypertension - no specific cause but thought to be due to how endothelial cells react to different stimuli i.e. different genetics cause a different response
- renal artery stenosis (glomerulonephritis) - kidney arteries become blocked / damaged due to atherosclerosis or thromboembolism causing less water to be excreted increasing BP
- endocrine tumour - release different hormones increasing BP e.g. phaeochromocyte tumours cause sudden adrenaline release, conn’s syndrome causes aldosterone release & cushing’s causes cortisol release
diagnosis of hypertension
often go unnoticed
make get TIAs i.e. mini stroke where cerebral arteries will be temporarily blocked by an embolism which is broken down within 24hrs & neurological function returns
outcome of hypertension
can lead to increased atheroma, MI, stroke, PVD & renal failure
as heart will have to work harder against increased BP causing left ventricular hypertrophy which will increase risk of left heart failure especially if heart can no longer pump against increased BP
tx of hypertension
aim to lower BP to <140/90 by modifying risk factors / pharmacological intervention i.e. diuretics, beta blockers, ca channel blockers, ACE inhibitors
heart failure
output of heart not capable of meeting demands of the tissues; can be:
1. low output failure i.e. problem with heart
2. high output failure i.e. problem with the body as a whole
high output failure
heart is pumping correctly & should be supplying tissues but due to issues with the rest of the body the tissues are not receiving enough oxygen to meet their demands. 2 main causes =
1. anaemia - not enough haemoglobin in blood to transport oxygen to tissues
2. thyrotoxicosis - increased thyroxine hormone produced which increases demands of tissues
low output failure
heart is failing as an organ, not pumping enough blood to keep up with demand; defects include; MI & valve disease
have R, L, congestive (both) failure, often it will start with L then lead to R
aetiology of heart failure
multifactorial disease:
- heart muscle disease; includes MI & myocarditis, decreased cardiac output as heart has functional limitation
- pressure overload; diastolic hypertension; heart has to pump harder against already high BP to force blood into peripheral tissues, aortic stenosis; narrowing of aorta so heart uses more pressure
- volume overload; mitral / aortic valve incompetence the efficiency of heart as a pump will be greatly reduced
- arrhythmias; irregular heart rhythm will lead to decreased efficiency of heart i.e. atrial fibrillation
- drugs; beta blockers can decrease HR leading to low output failure
diagnosis of heart failure
LHS - problems with lungs & systolic BP affected causing dyspnoea (fluid in lungs causing breathlessness especially lying down), orthopnoea, tachycardia, low BP/volume/pulse
RHS - increase venous pressure and so diastolic BP leading to swollen ankles, ascites, raised JVP, tender enlarged liver & poor GI tract absorption
tends to be left affected first
tx of heart failure
underlying cause must be treated
in chronic failure inotropes e.g. digoxin taken to increase heart function with negative inotropes e.g. beat blockers stopped
diuretics, ACE inhibitors, nitrates can be used to reduce BP & heart load
in acute heart failure send to hospital where it is treated with oxygen, morphine & furosemide
4 valves of heart
mitral (bicuspid) - left
tricuspid - right
LAB RAT
pulmonary - right
aortic - left
cardiac valve disease
issue with valves of heart
left more likely to be affected due to higher pressure needed; these are the aortic & mitral valves
aetiology of cardiac valve disease (4)
- usually stenosis of valve so it has narrowed & less blood flows through it
- congenital bicuspid aortic valve where tricuspid has only 2 cusps not 3
- after an MI there could be papillary muscle rupture leading to valve incompetence
- rheumatic fever - can lead on to rheumatic heart disease which can cause valve damage; these ptx can require antibiotic prophylaxis
tx of cardiac valve disease
valve replacement therapy
endocarditis
infection of the endocardium usually the valves
where there are surface irregularities, microbial colonisation may occur due to turbulence of blood leading to thrombus formation; likely to aggregate bacteria (usually oral bacteria) which enter through bleeding gingivae or invasive procedures
ptx at risk of infective endocarditis (5)
- acquired valvular heart disease
- valve replacement
- congenital heart disease
- hypertrophic cardiomyopathy
- previous endocarditis
common organisms involved in infective endocarditis
40-50% cases oral streptococci
also s.aureus & c.albicans
dental relevance of endocarditis
used to give antibiotic prophylaxis but risk of anaphylaxis high so ptx must maintain excellent OH instead
AB prophylaxis is 3g amoxicillin given orally 1hr before tx
av pulse & respiratory rate
average pulse = 60-100bpm
average respiratory rate = 12-18 breaths/min
signs & symptoms of respiratory disease
symptoms - cough, wheeze (expiratpory noise), stridor (inspiratory noise), dyspnoea (distress on effort breathing)
signs - resp rate increased, air entry to lungs (is it symmetrical?), percussion note, is fluid present
investigations to diagnose respiratory disease
- examine sputum from ptx
- chest radiograph
- PEFR to investigate flow rate
- FEV1 to test expiratory volume
- bronchoscopy
- VQ scan
delivery of respiratory drugs
MDI - meter dose inhaler
must be used with spacer device
spacer device will help prevent c.albicans settling in oral mucosa causing oral candidosis
short acting beta 2 agonists
1st drug used in stepladder against obstructive airway diseases
treat acute bronchial constriction by relaxing smooth muscles in bronchioles
onset is 2-3mins
route of admin = oral, IV, inhalation
e.g. salbutamol / terbutaline
if ptx on beta blockers this will not be an effective drug as beta blockers are non selective so will oppose the action of the beta 2 agonist
corticosteroids
2nd drug used in stepladder against obstructive airway diseases
will counter immune reaction instead of just opening airways i.e. in asthma the mucous production, inflammation & constriction of airways will all be countered
admin = topical / systemically
if dose >800ug spacer must be used
e.g. beclomethasone / fluticasone
long acting beta 2 agonist
used in conjunction with corticosteroids in later stage respiratory failure
slower onset but lasts 12-15hrs so is used to PREVENT acute bronchial constriction, must be inhaled & used with steroid as long acting beta 2 agonists increase the risk of heart attack but steroid will reduce it
e.g. salmeterol / formoterol
anticholinergics
will block muscarinic nerve transmission in autonomic nerves & will reduce basal tone of bronchioles and may be useful in COPD ptx
dental relevance of respiratory disease
GA uses benzodiazepines which are a respiratory depressant so this can make respiratory failure more likely
asthma
bronchial hypersensitivity reaction causing reversible airflow obstruction of smaller airways leading to difficulty breathing; 3 processes:
1. bronchoconstriction
2. inflammation
3. excessive mucous production
tx of asthma
stepladder:
1. short acting B2 agonist
2. low dose inhaled corticosteroid
3. high dose inhaled corticosteroid
4. long acting B2 agonist with inhaled corticosteroid
5. oral steroid
COPD
2 process disease that is irrerversible:
1. emphysema - destroys alveoli forcing adjacent alveoli to enlarge and fill gap which lowers SA for gas exchange, this plus thickened alveolar mucosal barrier, blood becomes less oxygenated & respiratory failure occurs over time
2. bronchitis - cough with sputum production on most days for 3mths of yr for 2 consecutive yrs, will restrict size of airways as increased mucous production with inflamed walls
major cause of COPD
smoking
2 outcomes of COPD
type 1 = failure of oxygenation as hypoxaemia (<90% O2 saturation in blood) due to poor ventilation or diffusion abnormality caused by thickening of alveoli; causes VQ mismatch & death
type 2 = failure of ventilation as hypercapnia (high CO2), narrowing or blockage of airways & breathing out will be a problem leading to inadequate CO2 removal and so death
dental relevance of COPD
if chronic COPD oxygen given with care as if ptx resp rate driven by hypoxia then high levels of O2 detected from O2 delivery system then it can cause ptx to stop breathing
cystic fibrosis
inherited autosomal recessive disorder of CFTR gene on chromosome 7 that affects the lungs - excess production of sticky mucous & pancreas - malabsorption of nutrients & disorder of Cl - channels
symptoms of CF
cough with repeated chest infections (pseudomonas staphylococci), poor weight gain, prolonged diarrhoea
tx of CF
physio
medication - bronchodilators, steroids to open airway & reduce inflammation / antibiotics to reduce chest infection frequency, replacement of pancreatic enzymes
in final stages heart & lung transplant required
types of lung tumours
difficult to diagnose, main risk is smoking & majority of these will be malignant so metastasise:
1. squamous cell carcinoma
2. large cell
3. small cell
4. adenocarcinoma
sleep apnoea
airway obstructed for about 10s while sleeping as he tone to airway muscles will drop
can cause drowsiness during day, increases risk of MI
2 types = obstructive sleep apnoea - likely to snore & central sleep apnoea
tx = mandibular advancement devices to pull bottom jaw forwards to hopefully eliminate blocking of airway
defences of the respiratory system
secretions of lactoferrin, salivary IgA, cilia, neutrophils, normal flora
pneumonia
consolidation of lung parenchyma meaning it is no longer compressible due to fluid being present in the active areas of the lung i.e. alveoli & there is inflammation of the gas exchange areas with intense inflammatory infiltrate
signs & symptoms of pneumonia
sudden onset, fever, malaise, rigors, SoB, cough with purulent sputum (pus which is green / yellow, consolidation of lungs in chest x ray
3 types of pneumonia & their causes
- community acquired - step pneumoniae, haemophilus influenzae, staph aureus
- atypical - chlamydophilia pneumoniae, mycoplasma pneumoniae
- legionella - inhalation of contaminated aerosols i.e. in the dentist
TB & risk factors
highest worldwide cause of Addison’s disease
risk factors = contact with another person with TB, HIV, IV drug abuse, alcoholism, residency in prison
diagnosing & treating TB
chronic cough with haemoptysis (coughing up blood), weight loss & night sweats plus chest xray, sputum culture & if high risk ptx or not
tx = multiple drug therapy over time
2 different forms of bronchitis
- acute = during winter & is viral
- chronic = productive cough on most days over 3 months in 2 successive years
predisposing factors for bronchitis = smoking, infections, air pollution & allergies, usually viral or bacterial agents involved
streptococcal sore throat
common bacteria in this is strep pyrogenesis group A, complications are:
1. suppurative - retropharyngeal abscesses, sinusitis, otitis media, cervical lymphadenitis
2. non suppurative - scarlet fever, strep toxic shock, glomerulonephritis, rheumatic fever
influenza
highly infectious epidemic RNA virus with type a, b, c but only type a will undergo major changes necessary to form a pandemic
highest mortality in elderly
coeliac disease
genetic disease where there is sensitivity to gluten due to alpha gliadin in it & this protein will react with jejunum causing an inflammatory reaction causing villus atrophy (may be to extent that is clinically visible) & this causes insufficient nutrient absorption
signs & symptoms of coeliac
malabsorption of iron, folate, B12 (anaemia) & fat
weight loss
lassitude (lack of energy)
weakness, abdominal pain
diarrhoea
steatorrhea
dysphagia
tx of coeliac
do jejunal biopsy
check haematinics
check if they respond to gluten free diet
bowel carcinoma
risk factors = smoking, age, obesity, alcohol, ulcerative colitis, intestinal polyps
often no symptoms so usually diagnosed by routine screening i.e. FOB, endoscopy, CT/MRI
if poorly differentiated survival rate is low, if metastasis to liver survival as low as 5%
inflammatory bowel diseases
caused by immunological / psychological factors, smoking
2 main types:
1. crohn’s
2. ulcerative colitis
ulcerative colitis
continuous inflammation, colon always involved, abscesses in mucosa but below the serosa will be normal, may develop into carcinoma over time so must be monitored
crohn’s disease
inflammation discontinuous, will affect whole of GI tract not only the colon, mucosa cobbled & fissured with inflamed serosa, oedema & granulomas i.e. OFG (lip swelling, angular cheilitis, cobblestoning of lips & cheeks, gingivitis, ulceritis)
symptoms of IBD
both diseases will include diarrhoea, abdominal pain, rectal bleeding as they involve the colon
crohns - includes other areas of GI tract so can have small bowel disease causing pain, obstruction & malabsorption, can also lead to anaemia, OFG
tx of IBD
systemic steroids to reduce inflammation - infliximab (stop inflammation), azathioprine (immunosuppression) & sulphasalazine (reduce inflammation), surgery as a last resort
upper GI disease
affects stomach upwards
3 main categories of disease:
1. oral disease
2. oesophageal disease
3. gastric disease
drugs for GI disease
2 categories:
1. eliminating acid formed (antacids)
2. reducing acid secretion
stomach acid produced in parietal cells when there is a trigger for acid production; the 3 triggers are:
1. acetylcholine
2. gastrin (released when food in stomach)
3. histamine - H2 receptor agonists will block this receptor
H2 receptor agonists
reduce stomach acid production by preventing histamine activation of stomach acid production but there are 2 other pathways present for production of acid so it is not that effective
proton pump inhibitors
will target proton pump at top of parietal cells meaning it will effectively block all acid production in the stomach reducing reflux
manifestation of GI disease in oral cavity
- recurrent oral ulcerations - often idiopathic but can have pathological causes
- OFG - most often if they have crohn’s
- lichen planus - inflammatory disease of skin & mucous membranes
3 main oesophageal disorders
- dysmotility - issues with muscle tissue caused by fibrosis from acid reflux
- dysphagia - difficulty swallowing due to blockage / compression of oesophagus
- GORD - defective lower oesophageal sphincter leading to impaired lower cleaning & gastric emptying causing acid to leak into oesophagus; will cause ulcerations, inflammation & metaplasia (change from oesophageal mucosa to gastric mucosa)
signs & symptoms of oesophageal disorders
burning in epigastric region, worse when laying, bending & birth
may cause dysphagia, stricture, dysmotility, GI bleeding (leading to anaemia)
barrett’s oesophagus
recurrent acid reflux into lower oesophagus causing metaplasia of the lower oesophageal lining into gastric type mucosa
associated with malignant change and may change to adenocarcinoma over time
peptic ulcer disease
name for disease of any acid affected site e.g. increased stomach acid will cause oesophageal / duodenal ulceration; if there is normal acid secretion it may cause ulceration if there is reduced protective barrier, in this situation there is often H.pylori involvement
NSAIDs & steroids can increase risk of PUD
helicobacter pylori
this bacterium will cause inflammation of stomach lining leading to ulcerations, these will break down the wall due to acid secretion & if severe can lead to bleeding & perforation even lymphoma of stomach
tx is via triple therapy - 2 antibiotics (amoxycillin & metronidazole) and a PPI
signs & symptoms of PUD
often asymptomatic
can cause epigastric burning pain just before / after a meal
relieved by alkaline food / vomiting
investigated via endoscopy
tx of PUD
if reversible, disease can be changed by lifestyle i.e. stopping smoking, small regular meals or by drugs
may require surgical intervention i.e. stricture
jaundice
clinical appearance of bilirubin pigmentation in skin & other organs
will cause itching & ptx known to be icteric
bilirubin metabolism process
enterohepatic process:
in this, liver haem is conjugated and made water soluble for excretion. it will initially be secreted into the bile however, some is reabsorbed & released as urobilinogen in the urine & in jaundice this process is disrupted; it can pre hepatic, hepatic or post hepatic
pre hepatic jaundice
jaundice due to problems before the liver i.e.
- increased haem load due to excess RBC or excess breakdown
can be due to haemolytic anaemia, post transfusion if bad match, neonatal due to mother’s blood type not matching baby’s
hepatic jaundice
failure of the hepatic cells themselves due to liver failure so cirrhosis or drug induced liver dysfunction or may even be due to hepatitis
if there is failure of secretion then the urine will be dark as conjugated bilirubin is dark & faeces will be lighter
post hepatic jaundice
problem after the hepatocytes usually caused by an obstruction
- if obstruction in hepatic biliary system it could be due to primary biliary sclerosis
- if extrahepatic it could be due to gall stones or pancreatic carcinoma compressing the common bile duct or due to pancreatitis which will cause inflammation & swelling that will compress ; usually from CF, alcoholism
signs & symptoms of jaundice
yellow discolouration due to deposition of excess unconjugated bilirubin throughout the body
if stool is pale & urine is dark there is post hepatic jaundice as conjugated bilirubin in urine
if due to haemolytic anaemia the stool & urine will be normal
gall stones
formed in gall bladder & may block biliary tree causing obstructive jaundice
stones cause cholecystitis (inflammation of gall bladder itself), inflammation of biliary tree, pain in tip of shoulder (radiation from diaphragm as they are both phrenic nerve)m, right side abdominal pain
management of jaundice
identify cause & treat it
neonatal jaundice
if baby born under high amount of trauma this will cause increased haem breakdown so there is more in blood & due to poor liver function of neonate it will not break down bilirubin correctly causing jaundice
blue light can be used to break it down
can cause kernicterus
liver supply
supplied by hepatic artery & portal vein with connecting bile ducts forming a portal triad which then connects to the hepatic vein output
the further away a hepatocyte is away from the blood vessel, the more likely it will be damaged due to its low oxygen concentration so it will not regenerate easily
acute liver failure
most often caused by paracetamol poisoning
can cause sudden loss of liver function & rapid death due to bleeding & encephalopathy (too much nitrogen in blood)
chronic liver function
occurs over a no of years
causes loss of synthetic function of liver & metabolic function; this means plasma proteins & clotting factors will not be produced
tested via INR (time it takes prothrombin to be converted to thrombin)
dose of drugs must be carefully controlled as no longer adequate FPM
detoxification will not longer occur nor conjugation of RBC breakdown products i.e. jaundice occurs
causes = cirrhosis, primary liver cancer, secondary liver cancer from metastasis or hepatitis
cirrhosis
fibrosis of liver leading to nodule formation
end stage is irreversible
often no symptoms other than larger / smaller liver but may be acute bleeding, hypertension, jaundice, oedema with ascites, encephalopathy, spider naevi
hepatitis
inflammation of liver
1. acute = acute liver failure, non specific symptoms i.e. nausea, malaise, hepatomegaly, jaundice, prolonged bleeding due to not enough clotting factors & elevated bilirubin
2. chronic = diagnosed by inflammation over 6mths as progressive injury with liver cell loss, fibrosis & regeneration over a long period of time; will lead to cirrhosis
main particle in hep B is dane particle
causes of hepatitis
viral infections, drugs, autoimmune disease, alcohol, metabolic disease, biliary disease i.e. gall stones or idiopathic
dental relevance of liver problems
- must liaise with physician
- antifungals avoided
- NSAIDs will increase bleeding risk so paracetamol best analgesic
- sedatives will have prolonged effect so IV sedation must be avoided
- reduced clotting factor synthesis so liaise with haematologist
- reduced plasma transport protein synthesis so drug binding is reduced so need to reduce drug dose
- reduced gamma globulin synthesis so ptx will be more prone to infection
*no issues with LA as LA broken down in plasma, not liver
endocrine diseases
disease associated with dysfunction of a hormone secreting gland
2 different forms of failure:
1. control failure
2. gland failure
hypothalamus & pituitary gland
hormones secreted by hypothalamus & transfer to anterior pituitary to trigger secretion of hormones here
transferred via hypothalamic pituitary portal vessels
hormones released inc: adrenocorticotrophic, thyroid stimulating, growth
these are kept at homeostasis via negative feedback
growth hormone disorders
over secretion - acromegaly
under secretion - growth failure
dental aspect of acromegaly = enlarged tongue with interdental spacing
thyroid gland
produces thyroxine which will act to increase metabolic rate of all cells
hyperthyroidism
excess thyroxine
primary = problem affecting the gland not pituitary
secondary = rare
causes = grave’s disease, toxic multinodular goitre, toxic adenoma, pituitary tumour (rare)
grave’s disease
autoimmune disease - most common cause of hyperthyroidism
caused by autoantibodies stimulating thyroid stimulating hormone receptor on thyroid gland so release thyroxine
specific symptoms = inflamed scleral blood vessels, proptosis, periorbital oedema
signs & symptoms of hyperthyroidism
symptoms - hot sweaty skin, weight loss, diarrhoea, palpitations, muscle weakness, heat intolerance, irritability
signs - tachycardia, atrial fibrillation, increased BP, tremor, eyelid retraction
tx for hyperthyroidism
generally involved blocking thyroid gland / thyroxine
carbimazole will block thyroid gland, thyroxine then must be supplemented as hypothyroidism develops
radioiodine tx can be used; kills off part of thyroid gland
hypothyroidism
lowered amounts of thyroxine produced so basal metabolic rate of cells is reduced
primary = more common i.e. hashimoto’s thyroiditis, radioiodine tx, iodine deficiency
secondary = very rare
if thyroxine not produced this leads to increased amounts of thyroid stimulating hormone to be released from anterior pituitary which leads to hypertrophy of the thyroid gland
hashimoto’s thyroiditis
autoimmune disease
present with goitre
symptoms = tiredness, cold intolerance, weight gain, constipation, goitre, angina
signs = slow pulse, bradycardia, hyperlipidaemia, goitre, delayed reflex response
tx = T4 tablets
blood tests in thyroid disease
3 main molecules tested for = TSH, T3, T4
primary hyperthyroidism (problem with gland itself) = low TSH (not stimulated by pituitary) & high T3
secondary hyperthyroidism = raised TSH, high T3
primary hypothyroidism = problem with the thyroid gland so high TSH but low T4
secondary hypothyroidism = low TSH & T4 due to problems with anterior pituitary itself
action of aldosterone
mineralocorticoid produced in zone glomerulosa of adrenal gland cortex; involved in RAAS
if BP too low it is detected in juxtaglomerular apparatus leading to renin synthesis & release which converts angiotensin to angiotensin I which is converted by ACE to angiotensin II in the lungs; this stimulates the adrenal cortex to produce aldosterone which acts to increase Na+ resorption water retention & increases K+ loss which will act to increase BP
drugs inhibiting aldosterone
ACE inhibitors - inhibit conversion of angiotensin I to angiotensin II lowering BP, has side effects of cough, angiooedema (fat tongue), oral lichenoid drug reactions
cortisol action
natural glucocorticoid that is an antagonist to insulin meaning it causes gluconeogenesis, fat & protein breakdown, lowers immune reactivity of ptx (anti-inflammatory), decreases chemotaxis of neutrophils so less of them involved in inflammatory reactions, inhibits bone synthesis which over time can lead to osteoporosis, will increase BP as it is chemically related to aldosterone. it is controlled by CRH & ACTH
cortisol as therapeutic agent
as anti-inflammatory drug or for immunosuppression
however can cause adrenal gland atrophy because there no longer will be stimulation of it from the anterior pituitary gland so it is no longer needed
adverse effects of therapeutic steroids
hypertension
type 2 diabetes
cataracts
hyperlipidaemia (accelerated atherosclerosis)
decreased chemotaxis of neutrophils so increased infection risk
osteoporosis due to inhibition of bone synthesis
hyperfunction of adrenal gland
increased glucocorticoid & mineralocorticoid synthesis leading to conn’s syndrome and cushing’s syndrome
conn’s syndrome
increased aldosterone production leading to hypertension & hypokalaemia with hypernatremia
cushing’s syndrome
main cause is cushing’s disease which is a pituitary tumour
other causes - adrenal adenoma or ectopic ACTH production
symptoms of cushing’s
diabetes features i.e. polyurea & lethargy
poor resistance to infection
hirsutism (bearded ladies)
amenorrhea
increased ACTH leading to increased skin pigmentation
signs of cushing’s
moon face
buffalo hump
thin skin that is easy bruised
hypofunction of adrenal gland
decreased amount of glucocorticoid & mineralocorticoid released from adrenal gland
caused by compression of pituitary from another adenoma or sheehan’s syndrome or hypovolaemic shock
addison’s disease
primary cause of hypofunction being gland failure; due to autoimmune gland destruction, infection or infarction
signs & symptoms of addison’s
signs - postural hypotension due to depletion of water & salt as there is absence of aldosterone, weight loss, lethargy, hyperpigmentation
symptoms - weakness, anorexia, loss of body hair in females
diagnosing adrenal dysfunction
in 2ndary hyperfunction - increased ACTH & cortisol
in primary hyperfunction - low ACTH & high cortisol
in 2ndary hypofunction - low ACTH & low cortisol
in primary hypofunction - high ACTH & low cortisol
diabetes mellitus
type 1 - body does not produce enough insulin
type 2 - cells do not respond to insulin that is produced (insulin resistant)
insulin
produced by beta cells in islets of langerhans in the pancreas
released in response to high blood glucose levels & will act to lower concentration
occurs by facilitating glucose uptake into muscle cells & adipocytes (NOT LIVER CELLS)
here insulin will promote formation of glycogen, triglycerides & proteins
testing for diabetes
glucose tolerance test
if >11.1 = diabetes and <7.8 is normal
type 1 diabetes
insulin deficient
insulin cannot be produced in response to high blood glucose level so hyperglycaemia can result
no stores of glycogen to break down in low blood glucose hypoglycaemia can occur which can lead to ketoacidosis
causes = environmental / genetic
type 2 diabetes
insulin resistant
due to elevated insulin levels due to incorrect beta cell response to hyperglycaemia leading to excessive secretion so basal hepatic glucose output will be increased to compensate for lowered blood glucose levels and insulin stimulated muscle glucose uptake reduced due to resistance of insulin
links with obesity & inactivity
drugs for diabetes
subcutaneous insulin given basal-bolus (injections before meals)
metformin
acute & chronic complications of diabetes
acute - due to hypoglycaemia
chronic - cardiovascular; higher incidence of atherosclerosis & hypertension (which can lead to angina/MI), eye disease; cataracts / maculopathy, diabetic neuropathy; general sensation loss, poor wound healing & increased infection risk
dental aspects of diabetes
- food intake may be disrupted
- poor wound healing
- increased infection risk
glomerulus
has podocytes which act as basement membrane
allows for ultrafiltration which occurs here due to high hydrostatic pressure in kidneys with low osmotic pressure as plasma proteins will oppose filtration; this forces smaller blood constituents out
proximal convoluted tubule
majority of filtrate will be absorbed, dependent on Na+/K+ pump
Na+ moved out of PCT, Cl- follows due to electric gradient produced
water reabsorbed via osmotic forces
substances that cannot be filtered in glomerulus will be secreted here
reabsorption & secretion occurs against concentration gradient so ATP required
loop of henle
concentrates urine & regulated by ADH
ascending limb impermeable to water & here using triporter pumps, Na, Cl & K removed
this produces concentrated hyperosmolar environment in medulla that causes water to be removed from descending limb whilst urea is added
produced counter current multiplier system in which urine is concentrated
vasa recta
blood supply to capillaries
distal convoluted tubule
Na, Cl, K regulated here
Na & H2O reabsorption with H+ & K+ secretion
controlled by aldosterone, AD, ANH
collecting duct
controlled by ADH
water reabsorbed here
ADH
anti diuretic hormone
secreted from posterior pituitary when water is needing to be lost
aldosterone
regulated by RAAS
will cause proximal & distal tubules to reabsorb more water & sodium but secrete more potassium
erythropoietin
secreted by kidney in response to hypoxia - increases release of RBCs in bone marrow
renal failure
pre renal - hypoperfusion of kidney (not enough O2; occurs in hypovolaemic shock or renal vascular disease - reduction in blood flow to kidneys due to atheroma in atheroma in aorta / renal artery)
renal - problem in kidney itself; glomerulonephritis or 2ndary cause i.e. diabetes, hypertension or drug therapy
post renal - renal outflow obstruction i.e. passing kidney stone or tumour compressing urethra
acute renal failure
rapid loss over a few days
creatine in excess of 200umol/L
cause is usually pre renal
chronic renal failure
occurs over a no of yrs
causes = glomerulonephritis / polycystic kidney disease / nephrotic syndrome
drugs in renal disease
NSAIDs - inhibit prostaglandin synthesis which is required for opening & closing of kidney blood vessel valves
cyclosporin - nephrotoxic
tetracyclines
management of chronic renal failure
reduce rate of decline of kidneys by eliminating nephrotoxic drugs & controlling hypertension, diabetes, vasculitis disease
if post renal - removal of i.e. gall stones
replace function via dialysis
only real cure is replacement
renal dialysis
- haemodialysis - outside body, arteriovenous fistula between elbow & wrist placed, heparin also injected as anticoagulant to stop blood clotting in dialyser
- peritoneal dialysis - inside body in peritoneal sack
dialysis & dentistry
peritoneal done in body so no impact but haemodialysis is not so ptx must be treated after session
