Human diseases Flashcards
1
Q
When would you adopt the ABCDE approach?
A
For a deteriorating patient
2
Q
What approach would you adopt for an unconscious patient?
A
DR ABCDE
3
Q
Asthma attack: A
A
A - wheezing on expiration
4
Q
Asthma attack: B
A
Respiratory rate: >25 (increased)
SpO2: <96% (decreased)
Rapid shallow breaths
5
Q
Asthma attack: C
A
Heart rate: increased (>100)
Pallor (pale)
Hypertension (not always)
6
Q
Asthma attack: D
A
ACVPU scale: ALERT (but anxious)
blood glucose N/A
7
Q
Asthma attack: E
A
Pale, distressed, use of accessory muscles for breathing, inability to complete sentence in one breath
8
Q
Worsening asthma attack: how would the ABCDE signs worsen?
A
“patient is giving up and organs are shutting down”
A - wheeze would become severe
B - RR now decreasing (<12), SpO2 still decreasing, laboured breathing
C - HR decreasing (<60), cyanosis in lips and nose
D - ACVPU: confused due to hypoxia
E - blue/gray in colour exhausted and sleepy
main difference is HR and RR have decreased and patient is slowing down in general… giving up…
9
Q
First stage of management for an asthma attack?
A
Oxygen (15l/min through non-breather mask)
10
Q
Asthma attack in an adult: after oxygen, what would the management follow?
A
Large volume spacer used to administer patients own inhaler/salbutamol (100mg per squeeze) - 4 puffs, repeat as needed.
11
Q
Asthma attack in an children (2-17yrs): after oxygen, what would the management follow?
A
Using a spacer, take one puff of your reliever inhaler every 15 seconds up to 10 puffs.
12
Q
Asthma management: after oxygen and inhalers, the patient isn’t improving - how long before an ambulance should be called?
A
> 5 minutes call 999.
five to survive !!! - after five mins seizure or asthma attack call 999
Sit patient upright and lean forward to open accessory muscle and aid breathing.
13
Q
Absence seizure signs and symptoms
A
Blank state
zoning out
usually short lasting
14
Q
Tonic-clonic seizure: A
A
Difficult to assess but often patent
15
Q
Tonic-clonic seizure: B
A
Respiratory rate: >25 (increased usually but hard to assess)
SpO2: <96% (decreased)
Apnoea (pauses in breathing)
16
Q
Tonic-clonic seizure: C
A
Heart rate: >100
17
Q
Tonic-clonic seizure: D
A
ACVPU: unresponsive
Blood glucose N/A
18
Q
Tonic-clonic seizure: E
A
Convulsions, flushed complexion, rigidity, urinary incontinence, frothing of mouth.
19
Q
What are the four stages of a Tonic-clonic seizure?
A
Aura stage
Tonic stage - back arched and stiff
Clonic stage - frothy saliva, jerky movements
Postictal stage
20
Q
First line management for an Tonic-clonic seizure?
A
Move objects that may harm patient during seizure, do not attempt to restrain patient of put anything in their mouth.
21
Q
When would a seizure become classed as “status epilepticus”?
A
Over 5 minutes of seizing or if it continues in cycles.
five to survive !!! - after five mins seizure or asthma attack call 999
22
Q
What is the management for a status epilepticus in an adult?
A
10mg Midazolam buccally and phone 999.
Oxygen 15l/min through non re-breather mask.
Monitor until help arrives
23
Q
How much midazolam could you administer for a status epilepticus for a baby 6-11months?
A
2.5mg
24
Q
How much midazolam could you administer for a status epilepticus for a young child 1-4 years?
A
5mg
25
How much midazolam could you administer for a status epilepticus for a young child 5-9 years?
7.5mg
26
How much midazolam could you administer for a status epilepticus for a young child 10-17 years?
10mg
27
What is the effect of midazolam and why should it be dosed cautiously?
Muscle relaxant and anticonvulsant effect – be cautious as muscle relaxant effect could cause respiratory muscles
28
Hypoglycaemia: A
Patent
29
Hypoglycaemia: B
Respiratory rate: >25 (increased)
SpO2: <94% (decreased)
30
Hypoglycaemia: C
Heart rate: tachycardia (fast)
BP: hypertension
Pallor and clammy
31
Hypoglycaemia: D
ACVPU: confused
Blood glucose <4mmols "four to the floor"
32
Hypoglycaemia: E
Slurred speech, shaking, aggressive, appears drunk
33
Hypoglycaemia: first line management
Oxygen (if patient allows)
34
Hypoglycaemia: if pt is conscious
Administer 10-20g of oral glucose (repeat every 10-15mins if requires).
Can be in the form of dextrose tablets or a tube of the glucose gel.
35
Hypoglycaemia: if pt is unconscious
Administer 1mg of glucagon IM
Oxygen
CALL 999.
36
Hypoglycaemia: pt has regained conciousness?
give oral glucose to replenish them.
37
Angina/MI signs
Crushing central chest pain radiating to the left arm, neck and jaw.
38
Angina/MI: A
Usually patent but potential for some sounds such as wheezing
39
Angina/MI: B
Respiratory rate: >25 (increased/rapid)
SpO2: <96% decreased
40
Angina/MI: C
Heart rate: can increase or decrease (nit likely to be abnormal either way)
Blood pressure: can increase or decrease (nit likely to be abnormal either way)
Capillary refill time (CRT) - >2 seconds (increases)
Pallor
41
Angina/MI: D
ACVPU; ALERT (but anxious)
Glucose N/A
42
Angina/MI: E
Clammy, grey in colour, sweaty, nauseous, potential evidence of cyanosis
43
Angina/MI: first line management?
oxygen - 15l/min
44
Suspected angina, after oxygen management?
Administer 2 puffs of GTN (400 mg) sublingually.
Repeat after 3 minutes if pain remains.
If worsens --> follow MI protocol
45
Suspected MI, after oxygen management?
Call 999.
Administer aspirin 300mg (chewed and swallowed asap).
Administer 2 puffs of GTN (400 mg) sublingually (repeat after 3 minutes if pain remains).
Monitor and reassure pt until ambulance arrives.
“MI 1,2,3,4
1 = oxygen
2 = call 999
3 = 300mg of aspirin
4 = 400mg of GTN (2 puffs)”
46
What is diabetic ketoacidosis and management?
When your body doesn't have enough insulin to allow blood sugar into your cells for use as energy.
Give fluid replacement and then IV insulin.
47
Diabetic ketoacidosis signs and symptoms
Excessive thirst, frequent urination, nausea and vomiting, stomach pain, weakness or fatigue, shortness of breath, fruity-scented breath, and confusion.
presentation usually of a type 1 diabetic
48
Type 1 diabetes
insulin deficiency as a result from autoimmune disease
Pancreatic islet (b-cells) under attack --> less insulin produced
Insulin is required for moving glucose into cells that need it to function.
49
Most common type of diabetes
type 2 (85%)
50
Difference between diabetes mellitus and insipidus?
Mellitus --> glucose regulation
Insipidus --> renal function (water)
51
HbA1C of a diabetic
HbA1C >48mmol/l (6.5%)
52
Acute presentation of type one diabetes and why?
Hyperglycaemia and ketoacidosis
If a patient doesn't know they have diabetes they will have reduced insulin levels, this will mean glucose is not being moved into the cells and will accumulate in the blood.
53
How could a type 1 diabetic have a hypo attack?
Too much insulin without enough oral glucose being taken could result in all the glucose being transported into cells and therefore the levels drop in the blood. Resulting in a hypoglycaemia attack.
54
What is HbA1c?
HbA1c is your average blood glucose (sugar) levels for the last two to three months.
55
What is ketoacidosis?
Body cells cannot access glucose for metabolism so the start to metabolise fat which results in Ketones as end product.
56
What is type 2 diabetes?
Cells develop resistance to insulin,
Pancreas works in overdrive to produce more insulin to counter this, eventually it becomes exhausted and dies off.
57
What medications could cause diabetes?
- immune suppressants (cyclosporin, calcineurin inhibitors)
- cancer meds (imatinib, nilotinib)
- antipsychotics (clozapine, olanzapine)
- steroids
- antiviral (protease inhibitor)
I CASA
58
Which endocrine diseases are linked to diabetes?
Cushings (>cortisol)
phaechromocytoma (adrenal tumour - high cortisol release)
Acromegaly (anterior pituitary tumour - high release of ACTH stimulating high cortisol release)
59
What women may be effected by diabetes?
Pregnant - gestational diabetes
Will likely already have risk factors i.e. overweight etc.
60
Why type of diabetes would rarely suffer diabetic ketoacidosis?
Type 2 - still have enough insulin to prevent ketone accumulation (but perhaps just not enough for the body’s glucose requirements)
61
Type 1 diabetes: management
Insulin dose (basal-bolus)
Regular checking of blood glucose level
62
Type 2 diabetes: management
Lifestyle
Medication
Surgery
63
Medication for type 2 diabetes
Metformin --> Biguianides (enhances sensitivity to insulin, reduces glucose production from the liver)
DDP-4 inhibitors ---> gliptins (block the enzyme metabolising incretin)
GLP-1 mimetics --> increase incretin (same effect as DDP-4 inhibitors)
Sulphonylureas --> increase pancreatic insulin secretion - NOTE: can cause hypoglycaemia.
64
When would a type 2 diabetic patient get insulin treatment?
Pt is unable to maintain glycemic control
65
Why could a diabetic have a hypoglycaemic attack?
Type 1 --> insulin without food (glucose) - too glucose into the cells = not enough in the blood.
Type 2 --> seen with sulphonylurea (or insulin too)
66
What are the three chronic complications of diabetes?
CVS - atherosclerosis of vessels
Infection risk - pour wound healing, diabetic foot (as a result of neuropathy)
Neuropathy - glove and stocking, muscles weakening from motor neuropathy, autonomic regulation gone.
67
What could this be?
Diabetic foot
68
What patients are at risk of cataracts, maculopathy and proliferative retinopathy?
Diabetic eye diseases
69
Why might surgery be an issue for a diabetic?
You may need to fast before a surgery (to avoid acidosis as glucose production is increased)
Increase insulin in type 1 diabetics (be careful to avoid a hypo)
70
What are some dental considerations of diabetes?
1. Mouth in pain = poor food intake
2. Infection risk
3. Poorer wound healing - extractions etc.
71
What is jaundice?
Yellowing of the skin due to excess bilrubin in the blood (hyperbilrubineamia).
Liver cells are damaged and can't conjugate bilirubin for it to be excreted OR increased production of bilrubin.
>40
72
Signs of someone with liver disease
REMEMBER “LIVERY”
L - lethargy and malaise
I - itchy
V - volume increase in abdomen (fluids leaking from damaged liver)
E - excrements (dark pee, pale poo)
R - rawboned (anorexia - very skinny!)
Y - yellow = jaundice
73
What two genetic conditions could cause excess bilrubin due to unconjucation?
Gilbert's
Crigler - najjar 1/11
74
What is Dublin-johnson
Genetic condition where conjucated bilrubin accumulated in the blood
75
How does viral hepatitis cause jaundice?
76
How does extra-hepatic issues such as tumours and gall stones contribute to jaundice?
Bile flow is blocked from the obstruction causing the pressure to build and it to leak into the blood.
77
In classic haemophilia (A), which factor in the coagulation cascade is deficient? What other disease can cause a reduction in the this factor?
Factor VIII ("eight")
von Willebrand's disease
78
In haemophilia B, which factor in the coagulation cascade is deficient?
Factor IX ("nine") can be referred to as Christmas disease.
On the ninth day of Christmas, nine ladies dancing - Busting a move (B haemophilia).
79
Why might a mother think she's given her son haemophilia but not her daughter?
Haemophillia is X-linked recessive, daughter becomes a carrier and the son is effected.
80
What might be used to manage haemophilia A?
Recombinant factor VIII
Desmopressin (DDAVP) - releases factor VIII
Tranexamic acid (oral)
81
A patient with a bleeding disorder has been given a mouth wash to aid haemostasis after an extraction - what is this and how does it work?
Tranexamic acid mouthwash which inhibits fibrinolysis --> keeps clots formed.
82
Management of haemophilia B ?
Recombinant factor IX
83
What is used to manage von Willibrand's disease (affecting factor VIII / 8)?
DDAVP (desmopressin acetate) - helps release of factor VIII
tranexamic acid
84
Most common bleeding disorder in the UK
von Willebrand's
Haemophillia A
85
What dental procedure requires special care for a bleeding risk that doesn't involved surgery or extracting a tooth?
Administering LA
86
What LA method is more at risk of a bleeding incident?
IANB
lingual infiltration
posterior superior nerve block
87
Thrombophilia
"clot loving"
embolism risk if clot moves/ruptures
88
What platelet disorders could cause increased bleeding?
Thrombocytopenia (reduced number of platelets)
89
Platelet count: treatment would need to be referred on vs done in primary care.
100 - primary care
50 - hospital setting
90
Thrombocythemia
High number of platelets --> clot risk usually on aspirin for this.
91
What conditions may present as dental erosion?
Diet
GORD
excessive vomiting
92
GI disease: aphthous ulceration, glossitis, angular cheilitis?
Coeliac disease - patients have malabsorption and thus deficiencies.
Glossitis (smoothening of the tongue)
Rarely oral can see dermatitis herpetiformis
93
Crohn's disease oral manifestations
o Cobblestone mucosa
o Corners of the mouth (angular cheilitis)
o Round the mouth dermatitis (perioral)
o Red gingiva
o OFG
o Hypertrophy of mucosa (tags etc)
o N – normal expected (ulceration)
o Staghorning – leaf like
“CCRROHNS”
94
What would a biopsy of a Crohn's lesion show?
non-caseating granulomas
95
What is OFG and what condition is it linked to?
Oro-facial granulomatosis
OFG and Oro-facial Crohn’s disease are part of the same process or are separate clinical conditions. This is due to the fact they can present similarly and are indistinguishable histologically, with the presence of non-caseating granulomas. OFG patients tend to have absence of GI symptoms and negative bowel screening on investigation. Orofacial Crohn’s is more likely in those patients who present with linear ulceration and corresponding raised inflammatory markers.
96
GI disease: rare oral manifestations, can present with aphthous ulcers, lesions related to anaemia, pyostomatitis vegetans.
Ulcerative colitis
97
Adult average paracetamol overdose limit
>4000mg in 24hours
98
Worst way to overdose on paracetamol
Staggered overdose (excess >1 hours period)
99
Clinical dosage of paracetamol per kg
More than or equal to 75mg per kg in 24 hours
100
What is the key antioxidant that binds to the toxic metabolite of paracetamol allow it to be excreted?
Glutathione
101
High risk patients for paracetamol over dose
“PARAC-L”
P - psychiatric disorders
A - alcohol use disorder
R - retroviral disease (HIV)
A- anorexia (any eating disorders)
C - cystic fibrosis
L - liver disease
102
Medications that induce cytochrome P450 and thus make a patient at higher risk of paracetamol overdose?
St John’s Wort
HIV drugs - Anti-retrovirals (Efavirenz “if a have a rinse”, Nevirapine “never a peen”) - “vir, vir”
EPILEPSY - Antiepileptics (Carbemazepine “Carb-e-mas-e-peen”, Phenytoin “fen-e-toe-in”, Phenobarbital “feeno-barbie-t-doll”, Primidone “premadonn-e”)
ANTIBIOTICS “R” - (Rifampicin, Rifabutin “rif i’m pissin, rif a beautin”) - “Rif, Rif”
SHEA - cytochrome P450 inducing
103
Paracetamol overdose: in first 24 hours signs
Nausea & Vomiting
General abdominal pain
104
Paracetamol overdose: in acute liver injury (2-3 days) signs
RUQ abdominal pain
Jaundice - Sign of acute liver injury
Hepatomegaly
Reduced GCS
Loin Pain/AKI
Abnormal LFTS/Metabolic Acidosis
105
Course of action overdose paracetamol: less than 4g in 24 hours
Continue with dental treatment
Give leaflet
106
Course of action overdose paracetamol: more than 4g in 24 hours
more than 75mg per kg
postpone treatment
Transfer to A&E (SBAR - relevant medical conditions)
107
Drug management of paracetamol overdose
Acetylcysteine IV (NAC, Parvolex) --> increases hepatic glutathione
Ideally give in first 8 hours (still effective up to 24hours)
108
Overdose? --> 40kg: 5 co-codamol, 6 ibuprofen, 5 paracetamol
109
Overdose? --> 90kg: 7 tramadol, 12 anadin extra, 4 panadol.
110
Overdose? --> 73kg: 8 acetaminophen, 4 solpadeine
111
Anaphylaxis: A
Stridor and wheezing
112
Anaphylaxis: B
Respiratory rate: > 25 (increased)
SpO2: <96% decreased
Rapid shallow breaths
113
Anaphylaxis: C
BP: drastically dropped (vasodilation)
Tachycardia
Bounding pulse
Increased CRT
114
Anaphylaxis: D
ACVPU - alert but with impending sense of doom
Glucose N/A
115
Anaphylaxis: E
Flushing, rash (hives), angioedema of lips, vomiting nausea, incontinence
116
Suspected Anaphylaxis?
* Sudden onset and rapid progression of following symptoms.
* Airway and/or Breathing and/or Circulation problems.
* Usually, skin and/or mucosal changes (flushing, urticaria, angioedema)
117
First-line management of anaphylaxis
Call 999 - state problem and remove source
118
After calling 999 - anaphylaxis management
Administer 1:1000 adrenaline IM. 0.5mg. (1mg/1ml) (recommended in the anterolateral thigh)
O2- 15 litres/min via non re-breather mask
If patient has auto injector then use this first before using adrenaline on emergency kit
Repeat after 5 mins if required
119
Adrenaline dosage in anaphylaxis for children 6 months - 5 years
0.15mg
120
Adrenaline dosage in anaphylaxis for children 6 -11 yrs
0.3mg
121
Adrenaline dosage in anaphylaxis for children 12-17 yrs
0.5mg
122
Why is adrenaline used in anaphylaxis?
The main benefit of adrenaline in this scenario is that it is a vaso-constrictor. This means that it squeezes the peripheral vessels to ensure that blood and fluid is forced back towards the heart
123
Choking management
Encourage the patient to cough, if effective cough is present, encourage patient to cough more and gently pat back to help.
If there is an ineffective cough, advise patient to stand and lean them forward, supporting them across their shoulders at the front with one arm and position yourself to the side of the patient.
Give 5 hard back blows between the shoulder blades at the back with the flat of your hand, checking between each blow for signs of change
If back blows are unsuccessful, perform 5 abdominal thrusts by making a fist under the point of the patient’s ribcage at the diaphragm muscle, locate the landmark by finding bellybutton with thumb of one hand and creating a fist, then roll up into position (between umbilicus and xiphisternum) Grab fist with other hand and pull inwards and upwards in a short sharp motion. (J shape) check between each thrust for signs of change.
124
STIs: Syphilis presentation at the dentist
Treponema pallidum
painless
"hard disc" - chancre
Secondary syphilsis --> greyish membrane, snail trail..
Treatment with antibiotics
125
HIV - oral manifestations
Mucosal candidasis
Kaposi's sarcoma (HHV8 - dark purple)
EBV - oral hairy leukoplakia
126
What viral infections could cause oral cancers?
Human papilloma virus
127
Can you give at least two underlying diseases or conditions which might explain the findings?
HIV, diabetes, steroid inhalers
128
Why might haemophilia B and HIV be associated?
significant number of hemophiliacs were infected with HIV due to the use of blood products derived from pooled plasma, which included donations from individuals who were unknowingly carrying the virus.
129
Hepatitis C virus meds
DDA - Direct-acting antiviral
130
HIV pathogenesis and meds
Destruction of CD4 T cells (attacks immune system)
ART meds ( antiretroviral therapy)
Antiretrovirals (efavirenz, nivirapine) Destruction of CD4 T cell = “Seen that D before” = sexually transmitted
131
If this has been caused by sexual transmission what is it and how should it be treated?
Primary syphilis - "chancre"
Antibiotics --> Benzathine Penicillin G.
132
Ulcer
trauma
133
Ulcer type
Metabolic/GI ect
134
Ulcer type
Syphilis
135
Ulcer type
Herpes (2)
136
What causes this characteristic unilateral?
Varicella zoster - effects a nerve branch!
137
What eye condition would contra-indicate no inhalation sedation for risk it could cause acute eye pressure and thus permanent sight loss?
Retinal detachment
138
What eye condition could manifest from diabetes?
Diabetic retinopathy
139
Malignant hyperthermia
anaesthetic drug induced = ABNORMAL ACCUMULATION OF CALCIUM IN MUSCLE CELLS
This severe reaction typically includes a dangerously high body temperature, rigid muscles or spasms, a rapid heart rate, and other symptoms.
140
Appendicitis
Right iliac fossa pain
Nausea and vomiting
Anorexia
Constipation or diarrhoea
Pyrexia
Tachycardia
Rovsing’s positive
141
Pancreatitis
142
NSAID contraindicated in CVS medications (ACE inhibitors etc)
Diclofenac
143
Diagnosing sepsis
THRWG
Sepsis = known/presumed source of infection + SIRS (2 or more)
144
Haemorrhaging stage IV
>2000ml of blood lost
145
What medication is given to DVT risk patients as prophylaxis?
Heparin SC
146
Delirium vs dementia
Delirium: attention and awareness affected (can be due to chemical imbalances etc) - ACUTE and RAPID
Dementia: memory and cognitive function affected (neurological pathology) - PROGRESSIVE and CHRONIC
147
Blood definitions: anaemia
Low Hb (haemoglobin)
148
Blood definitions: leukopenia
low white blood cells count (WCC)
149
Blood definitions: thrombocytopenia
low platelets (PLT)
150
Blood definitions: pancytopenia
all cells reduced
151
blood definitions: polycythaemia
raised Hb (haemoglobin) and hemocrit
Poly = “many”
Cyth = “cells”
emia = “blood”
152
blood definitions: leukocytosis
raised WCC (white blood cell count)
153
blood definitions: throbocythaemia
raised platelets
154
What is leukaemia?
Neoplastic proliferation of white cells - usually disseminated (uncontrolled growth spread around the body).
155
What is lymphoma?
Neoplastic proliferation of white cells - as a solid tumour (uncontrolled growth confined to a certain area).
156
What is porphyria?
The production of haemoglobin has a series of stages controlled by enzymes. If any of these enzymes are deficient, harmful precursors (different types of porphyrias) will accumulate and result in some side effects.
157
Why is porphyria clinically relevant to the dentist?
LA interferes with haemoglobin synthesis and can exacerbate the accumulation of porphyrias resulting in an acute attack.
158
What would happen during an acute porphyria attack?
o R – rash (photosensitive)
o P – psychiatric attack (seizing/autonomic disturbances)
o H – hypertension and tachycardia
poRPHyria
159
What is the sepsis six?
1. high flow oxygen
2. blood cultures (s. aureus, s. pyogenes etc)
3. give IV antibiotics
4. give a fluid challenge
5. measure lactate (high)
6. measure urine output (decreased)
“U-FOCAL”
160
Two causes of anaemia
1. issue making haemoglobin (iron deficiency)
2. issue folding global chain (thalassemia, sickle cell etc)
161
What is the cause of anaemia, and why is this often confused?
Having too little or too many RBCs (has nothing to do with this).
The only times this is correct is when anaemia is due to marrow failure which does cause reduced RBCs which subsequently results in the anaemia.
162
What autoimmune disease could be linked to anaemia?
Coeliac - malabsorption and thus resulting in a deficiency in Fe, Folate, Vitamin B12.
This is the same reason why vegans can become anaemic - because a lot of iron comes from red meat!
163
What GI conditions could result in not enough iron being absorbed?
Gastric erosions and ulcers
Inflammatory Bowel disease
Crohn’s disease
Ulecerative colitis
Bowel Cancer
Colonic cancer
Rectal Cancer
Haemorrhoids
164
Why might people with Crohn's be deficient in Vitamin B12?
Crohn's disease --> disease of terminal Ilium
165
Which two disorders cause improper folding of the haemoglobin chains and thus anaemia?
Sickle cell and thalassaemia
166
What can be used to give a clue as to the cause of anaemia?
Mean corpuscular volume (MCV) is a laboratory value that measures the average size and volume of a red blood cell.
167
Clinical signs of anaemia
Pale
Tachycardia
tired and weak
dizzy
palpitations
168
TONGUE DEFICENCIES - iron
smooth tongue
169
TONGUE DEFICENCIES - vitamin B12
beefy tongue
170
Treatment of anaemia
Replace deficiencies ( vit B12, folic acid and ferrious sulphate)
Maybe transfusions if necessary
171
How could anaemia present orally?
mucosal atrophy
candidiasis
recurrent oral ulceration
sensory changes
172
HCT (haematocrit) count
Hematocrit is the percentage of red cells in your blood.
173
What is the most common reason for excess blood loss causing anaemia?
GI bleeding - chronic loss
174
How could hereditary issues such as sickle cell disease be apparent from a RCC or HCT?
Cells are abnormal and thus have a reduced life span = less RBCs.
175
How could MCV suggest thalassaemia?
MCV (mean corpuscular volume) showing smaller RBCs (microcytic cells).
176
How could MCV suggest B12/folate deficiency?
MCV (mean corpuscular volume) showing larger RBCs (macrocytic cells).
177
What if the MCV showed the RBC size to be normal, what might be the cause of the anaemia?
Chronic bleeding loss (GI etc)
178
Warfarin
Apixaban
Edoxaban
Rivaroxaban
Dabigatran
Examples of anticoagulants
179
Clopidogrel
Dipyridamole
Prasugrel + Aspirin
Abciximab
Eptifibate + Aspirin
Ticagrelor
Tirofaban
Low dose Aspirin
antiplatelet drugs
180
Treatment flowchart for bleeding risk: vitamin K antagonist (warfarin)
Check INR no more than 24-72 hours before procedure.
If INR is <4 treat as normal.
181
Treatment flowchart for bleeding risk: the only medications that for a high bleeding risk procedure you would need to miss the morning dose and treat early in the day?
NOACs - dabigatran, apixaban, rivaroxaban.
182
Treatment flowchart for bleeding risk: anti platelet drugs
treat as normal!
183
Treatment flowchart for bleeding risk: injectable anticoagulant
- consult with GP
184
Treatment flowchart for bleeding risk: high risk treatment
Extractions
Minor oral surgery
Implants
Periodontal surgery
Biopsies - sometimes
185
WARFARIN - interactions
W - watch for...
A - "-azole" antifungals (fluconazole)
R - replicas (other anti clot drugs - antiplatlets such as aspirin or clopidogrel)
F - fat reducers (atorvastatin, simvastatin)
A - arrhythmic meds (amiodarone)
R - relaxants for seizures (phenytoin and carbamazepine)
I - infection fighters (antibiotics)
N - NSAIDs
186
NOACs: Direct thrombin (IIa) inhibitors
D for Direct and Dabigatran
187
NOACs: Factor Xa inhibitors
Apixaban (2 tablets), Rivaroxiban, Edoxaban
ban = 10
188
Difference between anticoagulants and antiplatelets
189
What blood type is most common?
O
190
2 types of lymphoma
Hodgkin's lymphoma
Non-Hodgkin lymphoma
191
Symptoms of lymphoma
PL-I-NS-W-I-F
plinswif !
192
Painless lymphadenopathy, fever, night sweats, weight loss, itching, infection...
Non-hodgkin lymphoma
193
Non-hodgkin lymphoma
Often associated with an autoimmune (Sjogrens) or immune suppressing (HIV) disease
194
What is worse; non-hodgkins lymphoma or Hodgkins lymphoma?
non-hodgkins lymphoma's prognosis is worse.
195
What is multiple myeloma?
malignant proliferation of plasma cells
196
How are haematological malignancies managed?
Chemotherapy
Radiotherapy
Monoclonal antibodies
Haemopoietic stem cell transplantation
197
Three key manifestations of leukaemia patients
Anaemia
Infection (neutropenia)
Bleeding (thrombocytopenia)
198
Four leukaemia types and patients most commonly effected
Acute lymphoblastic leukaemia - children (ALL = “even kiddies”)
Acute myeloid leukaemia - elderly (AML = aged, mature, late)
Chronic lymphocytic leukaemia - older adults (CLL = cool but late)
Chronic myeloid leukaemia - male 50-70yrs (CML = concerns men)
199
INR
international normalised ratio (INR) blood test tells you how long it takes for your blood to clot.
200
INR level meaning?
201
Bipolar disorders: mood stabiliser meds
Lithium, sodium valproate, lamotrigine
202
Bipolar disorders: antipsychotic meds
quetiapine, aripiprazole, olanzapine, haloperidol
203
Schizophrenia meds
Antipsychotics - chlorpromazine, haloperidol etc
204
MMSE
Mini mental state exam (psychiatry)
205
Can present as:
inexplicable dental symptoms (e.g. atypical facial pain, autonomic symptoms),
frequent attendance at a dental surgery
inexplicably high treatment use
unreasonable requests with regard to treatment
Somatoform Disorders (Somatisation) - physical manifestation of psychological
206
Frailty --> 2 or more of the following
F - four or more days bedbound
R – reliant on walking aid
A - ADLs inability (activities of daily life i.e. eating)
I - incontinence (urine/faeces)
L – low moods/lack of memory (dementia/depression)
T – tumbles (history of falling)
T – Three months has had 1 or more unplanned admissions
- “FRAILTT”
207
Medications most commonly associated with xerostomia
anti-depressants
anti-hypertensives
anxiolytics
208
Medications commonly associated with gingival hyperplasia
CCBs, anti-epileptic drugs, cyclosporin (immunosuppressant)
209
Most at risk of vitamin D deficiency
V - Vaulted away (inside all day)
I - Intestinal malabsorption (poor nutrition or GI disease)
T - tanned (dark skinned in northern countries)
D - drugs (antiepileptics - think light causes epilepsy so lack of it causes vit d deficiency)
210
Osteomalacia and management
During bone formation = "rickets"
Poorly mineralised osteoid matrix
Poorly mineralised cartilage growth plate
VIT D DEFICIENCY
211
Osteoporosis and management
Loss of mineral and matrix
Reduced bone mass
212
Gout on the toe causes
Thiazide diuretics
Aspirin
213
Treatment of gout
NSAIDs (NOT aspirin, this stops the secretion of uric acid)
214
PAIN
improves with rest
worse with activity
BRIEF morning stiffness
SLOWLY progressive over years
--?
Osteoarthritis
Treatment: increase muscle strength, NSAIDs, prosthesis
215
slow onset
initally hands and feet
proximal spread
potentially ALL synovial structures
SYMMETRICAL polyarthritis
Occ. onset with SYSTEMIC symptoms
fever, weight loss, anaemia
rheumatoid arthritis
216
Treatment of RA
in more severe cases would be --> immune modulators and oral prednisone.
217
Vessel disease: polyarteritis nodosa and Kawasaki
medium vessel disease
218
Vessel disease: Wegener's granulomatosis
small vessel disease
219
Vessel disease: giant cell (temporal) arteritis
large vessel disease
220
Connective tissue disease general management
NSAIDs
Immune modulators:
Hydroxychloroquine
Methotrexate
Azathioprine
Mycophenolate
Systemic steroids - prednisolone
221
Systemic Lypus Erythematosis (SLE)
“SABTH”
S - Selena Gomez = effects females of child bearing age, renal damage, steroid and immunosuppressive therapy
A - anaemia (oral ulceration)
B - butterfly rash
T - thrombocytopenia (low platelets = bleeding risk)
H - hard palate pigmentation
222
circulating immune complexes - SLE
ANA, dsDNA, Ro antibodies
"ROANADNA"
223
What CTD would you definitely NOT stop anti-coagulant therapy for and why?
Antiphospholipid Antibody Syndrom (APS) - high risk of arterial thrombosis or pulmonary embolism (heart or lungs stopping! = death)
224
circulating immune complexes - Sjögren's syndrome
ANA, Ro and La
"LAROANA"
think LA for lacrimal gland effected!
225
Sjögren's syndrome - sicca syndrome type
dry mouth or eyes
226
Primary vs secondary sjogrens
227
Systemic sclerosis CREST
Anti Scl-70 antibodies
228
Dental considerations - Systemic sclerosis
can't open mouth and difficulty swallowing etc. PDL may appear wider radiographically but there will be no associated mobility.
229
How could giant cell arteritis present to the dentist?
Carotid branches effected - chewing claudication (pain).
230
Kawasaki disease presentation to the dentist?
CHILDREN EFFECTED
“turning into a strawberry”
Fever & lymphadenopathy
Crusting/cracked tongue
Strawberry tongue & erythematous mucosa
Peeling rash on hands and feet
231
Which vasculitis disease causes this presentation?
Wegner's Granulomatosis
232
Sjogren's syndrome: first line therapy
Pilocarpine (5mg tablets; up to four times daily)
a cholinergic agonist which stimulates salivary secretion both in individuals with normal salivary gland function and in those with impaired salivary flow (xerostomia or oral dryness).
233
Management of xerostomia
Artificial saliva - orthana, glandosane etc
Salivary stimulants - gums and sweets
234
Sjogrens oral manifestations
* Opportunistic oral infections
* Periodontal disease
* Caries, particularly at the cervical margin
235
Recurrent acute pseudomembranous candidiasis with no obvious cause?
Diabetes type II
236
Treatment of burning mouth syndrome
237
Acne rosacea
238
Acne vulgaris
239
What is this? How could it be worsened?
Periorificial dermatitis - made worse by steroid cream
240
Impetigo - cause by staphy or strep
241
Furunculosis - hair follicle infected usually by s.aureus
242
Erysipelas - A beta haemolytic strep (may have fever etc --> treat w/antibiotic)
243
Human papilloma viral warts
244
Molluscum contagiosum - DNA pox virus (cryotherapy)
245
Herpes-simplex 1
246
Herpes-zoster
247
Coxsackie A virus - Hand foot and mouth disease (self-resolving = 2 weeks)
248
Atopy triad
249
Basal cell carcinoma
250
Squamous cell carcinoma
251
melanoma
252
Ulcerative colitis: symptoms and bloods
Diarrhoea with BLEEDING
Only colon affected.
CRP (C-reative protein)
Albumin
Platelets (thrombocytosis = too many)
253
Crohn's: symptoms and bloods
Weight loss, abdominal pain, peri-anal disease.
Anywhere along the GI tract
CRP, albumin, platelets, B12 (t.ileum), ferritin, FBC
254
Crohn's vs Celiac
Celiac = no meds
255
Crohn's aggravators
smoking and anything high-fibre (low-fibre is recommended)
256
UC vs Crohn's - therapy options
UC: Steroids, 5-ASA (mesalazine), immunosuppressants, biologics
Crohns: Steroids, immunosuppressants, biologics
257
Corticosteroids for GI issues
Methylprednisolone
258
Immunosuppressants for GI issues
Thiopurines - azathioprine and 6-mercaptopurine
Methotrexate
259
Why might vitamin B12 malabsorption be common in Crohn's patients?
Terminal ileum is effected which is a key absorber for Vitamin B12 and bile acids.
260
Key medications for upper GI disorders
Antacids (reduce acid there)
H2 receptor blockers
Proton pump inhibitors
(these reduce acid secretion)
261
Cimetidine and ranitidine
H2 receptor blocker
262
Omeprazole, lansoprazole, pantoprazole...
PPIs
263
GORD presentation
“ACIDS”
A - acute burning
C - CVS ? severe pain mimics an MI.
I - internal bleeding
D - dysmotility of GI muscles
S - swallowing issues (dysphasia)/ Sitting back in chair worsening
264
Lifestyle advice for GORD patients
Stop smoking and lose weight
265
Two most common causes of peptic ulcer disease (PUD)
1. NSAIDs - too much acid
2. Helicobacter pylori infection
266
Coeliac disease and sensitivity
Small intestine affected
Sensitivity to α-gliaden component of Gluten
267
Colonic carcinoma
Lifestyle poor
Genetics; p53
Treatment:
Surgery
Hepatic Metastases
Radiotherapy
Chemotherapy
Screening through FiT test
268
How much bacteria is in a healthy urine?
NONE - it is sterile.
269
UTI - bacteria
E.coli
270
What is a VERY common issue men in their willies? What is treatment for this?
Benign prostatic hypertrophy
⍺-blocking drugs
Anticholinergic
Diuretics
271
LITHOTRIPSY
high level shock- waves used to break up renal stones so they can be passed out in the urine easier.
272
Renal disease analgesics?
avoid NSAIDs
273
When's the best time to treat a patient doing dialysis?
After sessions of dialysis
274
Addisons disease
Tired depressed, woman, low sex drive, trying to tan to make herself feel better, trying to lose weight.
Adrenal cortex deterioration - salt (aldosterone), sugar (cortisol), sex hormones (aldosterone) all effected.
Pigmentation due to high ACTH (over produced since it's trying to stimulate cortisol release) - this affects melanocytes = melanin
Low aldosterone = low salt retention = low BP
275
Adrenal cortex - hormones
G - salt (aldosterone -
F - sugar (cortisol -
R - sex (androgens)
276
Posterior pituitary hormones
ADH - anti-diuretic hormone
Oxytocin
277
Anterior pituitary hormones
TSH - Thyroid Stimulating Hormone
ACTH - Adrenocorticotrophic Hormone
GH - Growth Hormone
LH, FSH, Prolactin
278
How could a pituitary tumour resulting in excessive growth hormone production manifest?
Stimulates IGF-1 (insulin-like growth hormone) release from the liver = growth abnormalities
ACROMEGALY
enlarged hands
carpal tunnel syndrome - finger numbness,
Type 2 diabetes mellitus
insulin resistance from increased GH
Cardiovascular disease
Ischaemic heart disease
acromegalic cardiomyopathy
Intraoral changes
enlarged tongue
interdental spacing
‘shrunk’ dentures
Reverse overbite
279
Hyperthyroidism - causes
1. GRAVES disease (70-80%) - primary
2. Pituitary tumour (uncommon) - secondary
280
Hypothyroidism - causes
1. Hashimoto's disease (90%) - primary
(drugs, radioiodine treatment...)
2. Hypothalamus/pituitary disease
281
Hyperthyroidism - TSH and T3 levels for each kind?
Primary cause (graves/adenoma) = low TSH, high T3
Secondary cause (pituitary cause) = high TSH, high T3
282
Hypothyroidism - TSH and T4 levels for each kind?
Primary cause (gland failure) = high TSH, low T4
Secondary cause (pituitary cause) = low TSH, low T4
283
Treatment - hyperthyroidism
Carbimazole
beta-blockers
radioiodine
surgery
284
Treatment - hypothyroidism
Give T4 tablets (thyroxine)
285
What hormone is released from the anterior pituitary to simulate the adrenal cortex and produce salt, sugar and sex hormones?
adrenocorticotropic hormone (ACTH)
286
High aldosterone levels will...
Increase sodium and water RETENTION = BP increases
This action is blocked by ACE inhibitors
287
Too much aldosterone
Conn's syndrome
288
Too much cortisol
Cushings syndrome
289
Addison's disease specific test for diagnosis
negative synACTHen test
290
Prophylaxis for patients with adrenal diseases undergoing dental treament
Steroid prophylaxis
291
Oral manifestation of Cushings
Candidiasis
292
Oral manifestation of Addisons/cushings
oral pigmentations
293
What is a stroke?
Death of brain tissue from hypoxia
294
What differentiates a TIA from a stroke?
Pt makes a full recovery within 24 hours
295
What is the most common causes of a stroke?
296
Treatement for preventing a stroke caused by infarction?
Lifestyle changes (i.e. stop smoking)
Antiplatelet + anticoagulant therapy
297
Epilepsy causes
issues with the neurotransmitters in the brain
298
Febrile seizure
CHILDREN WITH FEVERS
but presents the same as a tonic-clonic
299
Generalised seizures examples
Tonic clinic
Absent seizure (petit mal) - childhood usually
300
Preventative anticonvulsant drugs - tonic clonic
Valproate, carbamazepine, phenytoin, gabapentine, lamotrigine
301
Absent seizures medication
levitiracetam
302
Parkinsons treatment
Dopaminergic drugs; Direct replacement and
Agonists
303
Salbutamol and terbutaline
Intermittent short acting Beta-adrenergic Agonists
304
Fluticasone,
Budesonide,
Mometasone
Inhaled Corticosteroids – low dose
305
Salmeterol
Regular long acting Beta-adrenergic agonist
306
Spacer vs nebuliser (in asthma)
307
Respiratory failure type 1 and type 2
Type 1 is pink, Type 1 normal CO2, ventilation is maintained because of overzealous breaths, trying to catch a breath quickly pink cheeks --> emphysema
Type 2 is Blue, Type 2 high CO2, breaths aren’t adequate, failure of ventilation--> chronic bronchitis.
308
Oral manifestations of inhaled steroids
Candida
309
Cystic fibrosis
Genetic disease
Sticky mucous
CFTR gene - chromosome 7
Shaking physiotherapy
310
Lung tumours most common cell type
non-small cell
311
83% of lung cancers is a result of ...
SMOKING
312
Drugs that could cause impaired breathing
beta-blockers (chronic cough)
Respiratory depressants
Benzodiazepines
opioids
313
Ipratropium
Anticholinergic - for asthma
314
Other less common asthma drugs
315
3 drug cocktail for acute coronary syndromes
Antiplatelets - aspirin
Anti-hypertensives - diuretics, CCBS, ACE inhibitors, beta-blockers
Vasodilators - nitrates
316
MI treatment options - after 3 hours
Primary PCI
317
MI treatment options - after 6 hours
Thrombolysis
318
Common cause of bradyarrhythmia
too much beta-blocker
319
Features of atrial fibrillation on ECG
narrow QRS on ECG
Atrial fibrillation - rapid atrial impulses conducted to ventricles giving high heart rate. No p waves as disorganized atrial activity. Irregular pulse
320
Features of Ventricular tachyarrhthmias on ECG
broad QRS on ECG
Dangerous as it can lead to ventricular fibrillation and death
321
Cardiac pacemakers
For bradyarrhythmias --> keeps it above 50bpm and senses if this drops.
AVOID ULTRASONIC SCALERS interferes with the electrical field
322
Sinus rhythm
the normal ECG
323
Ventricular fibrillation
Use defibrillators
324
Asystole
Don't use defibrillators
325
When should you use a defibrillator?
Asystole isn't a shockable rhythm, and defibrillation may actually make it harder to restart the heart. Defibrillation is only an option if your heart goes from asystole to a shockable rhythm, which is possible when someone with asystole receives effective CPR.
326
Finger clubbing causes
327
When would someone display cyanosis?
5g/dl or more of deoxygenated Hb in the blood
(50g/l of blood)
328
Which congenital septal defects are at higher risk of IE?
Ventricular
329
Which congenital septal defects are at higher risk of long term heart failure?
ventricular
330
Congenital issue effecting the aorta
Co-arctation of the aorta
331
Patient ductus arteriosus
Congenital heart defect - an extra blood vessel found in babies before birth and just after birth.
332
Cardiac valves order...
Tricuspid
Pulmonic
Mitral
Aortic
333
Which valves most commonly fail?
Aortic and mitral
334
This is bicuspid aortic valve, a congenital abnormality.
335
Valve replacements
Mechanical usually - anticoagulant therapy!
Occasionally porcine
336
Targets for cholesterol in CVS patients
Below 5mmol/L or 25%
337
high output failure heart disease
– demands of the system have increased beyond the capacity of the pump
anaemia, thyrotoxicosis (HYPERTHYROIDISM)
“Despite the heart working harder to pump more blood, the tissues and organs may still not receive enough oxygen and nutrients.”
338
low output failure heart disease
– pump is failing and not strong enough to force liquid around the body
cardiac defect e.g. MI, valve disease
339
Side of heart effected? dyspnoea, tachycardia, low BP, low vol. Pulse
LEFT
340
Side of heart effected? swollen ankles, ascites, raised JVP, tender enlarged liver, poor GI absorption
RIGHT
“the right side of my heart still swells like your foooooot” - Dr. Faye Webster
341
Key difference in management of heart failure cf. with IHD?
STOP negative inotropes - NO beta-blockers!
342
Hypertension treatment
343
Symptoms of IE
fever, heart murmur, sepsis, nail splintering
344
Treatment of IE
345
Cardiac conditions at risk of IE
1. Congential heart structural defect (valve, or chambers etc effected)
2. Previous IE diagnosis
3. Valve prosthesis
NOT - atrial septal defects (less risky compared to ventricular) OR ventricular septal defects that have been fully repaired OR patent ductus arteriosus that has been fully repaired)
346
What are the drugs that end in -pril? (i.e. Enalapril)
ACE inhibitors
347
How do ACE inhibitors work?
1. Inhibit the conversion of angiotensin I to angiotensin II and prevent aldosterone dependent reabsorption of salt and water.
2. Basically they reduce blood pressure by reducing excess salt and water retention
348
What are some side effects of taking ACE inhibitors?
ACE
A - allergic (lichenoid reaction)
C - chronic cough
E - elevation from chair causing hypotension
349
WHat should you be mindful of when prescribing NSAIDs (i.e ibuprofen, aspirin..) to someone on ACE inhibitors?
The interaction could reduce the anti-hypertensive effect as well as increase the risk of acute renal injury.
350
What are the drugs that end in -artan? (i.e Losartan, candesartan…)
Angiotensin II blockers
351
What is the mode of action of angiotensin II blockers?
Similar to how ACE inhibitors work EXCEPT; ACE inhibitors inhibit the conversion of angiotensin I to angiotensin II, while the ARBs antagonize receptor binding of angiotensin II to AT1 receptors.
352
What are some side effects of ARBs?
Renal impairment, cough, postural hypotension
A - after sitting down for too long (postural hypotension)
R - renal impairment
B - breathing (cough)
353
What should you be mindful of prescribing for someone taking ARBs?
NSAIDs
354
What drugs (most often but not always) end in -ipine? (i.e Amlodipine, Nifedipine, verapamil, diltiazem..)
Calcium channel blockers
355
What is the mode of action of calcium channel blockers?
Calcium channel blockade affects smooth muscle and results in vasodilation and a reduction in heart rate (useful in treating some arrhythmias).
356
Which of the CCBs are more are more active on peripheral blood vessels compared with ones that are more active on the heart muscle?
Some drugs are more active on peripheral blood vessels (-ipines) and others are more active on the heart muscle (verapamil, diltiazem)
357
What are some dental implications of a patient taking calcium channel blockers?
gingival hyperplasia, postural hypotension
358
What antibiotic should you be cautious of prescribing for a patient on calcium channel blockers?
Macrolides ( azithromycin, clarithromycin and erythromycin XXXXX CCBs)
359
What bendroflumethiazide and furosemides?
Diuretics
360
Bendroflumethiazide
Thiazide diuretic
361
Furosemide
Loop diuretic
362
Thiazide compared with loop diuretics and indications for both
Thiazide:
tHiazide - Hypertension/Heart oedema
Loop:
Loop - Lung oedema/Left ventricular failure
363
Mode of action of diuretics
1. Used in Hypertension and for heart failure.
2. Increase salt and water LOSS leading to reduced plasma volume and therefore reduced cardiac workload
“Dry” uretics —> dry out by increasing salt and water loss —> blood plasma volume decreases.
364
What are some side effects of diuretics use?
SE: can lead to Na+/K+
imbalance if not monitored carefully
Dental: Dry Mouth
365
What are the drugs ending in -olol? (i.e. bisoprolol, propranolol, atenolol…)
Beta-blockers
366
Mode of action for beta-blockers
Beta-blockers work by blocking beta receptors, hindering the effects of adrenaline. This reduces heart rate and blood pressure, making them effective for conditions like hypertension and anxiety. Picture beta-blockers as "stress shields" that calm the heart's response to adrenaline, like a protective barrier against excessive excitement and high blood pressure.
367
Uses of beta blockers
Used in management of IHD, Hypertension AND Arrhythmias.
Stop arrhythmias leading to cardiac arrest (Ventricular fibrillation – VF). They prevent increase in heart rate by reducing heart muscle excitability.
368
Side effects of beta blockers
worsen asthma, postural hypotension
369
Drugs that end in -statin (atorvastatin, rosuvastatin, simvastatin etc)
HMG coA Reductase inhibitors
370
Statins mode of action
“ELF”
Enzyme inhibiton (HMG-CoA)
Liver located
Fluconazole contraindications
HMG-CoA reductase inhibitors, commonly known as statins, act on a key enzyme called 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase in the liver. By inhibiting this enzyme, statins reduce the synthesis of cholesterol, lowering overall cholesterol levels in the blood. Including, LDL cholesterol.
371
LDL cholestrol
Low-density lipoprotein (“bad cholestrol”)
372
Side effects of statins
Myositis (“muscle” + “inflammation”) with some drug interactions - such as dental antifungals.
Fluconazole - stop taking the statin whilst on this anti fungal and then restart when course is over.
373
Examples of anti-anginal drugs
Nitrates:
1. Isosorbide mononitrate - prevents angina
2. Glyceryl trinitrate (GTN spray) - short acting, useful in emergency management of angina symptoms
374
Mode of action of nitrates
Dilate VEINS and reduce preload to the heart
Dilate resistance arteries and reduce cardiac workload (afterload) and cardiac oxygen consumption
Dilate collateral coronary artery supply and reduce anginal pain
375
Side effects of nitrates
Headache, hypotension. No specific dental implications.
376
What are some examples of anti-platelet drugs?
Aspirin, clopidogrel, dipyridamole, new antiplatelet drugs (Prasugrel, Ticagrelor etc.)
377
Mode of action of aspirin
Aspirin = “OAR”
One: Cox-1 inhibition
A2 thromboxane reduced.
Retarded platelets don’t form clots.
Favouring; thromboxane A2 over prostaglandin may result in excessive platelet aggregation and vasoconstriction - aspirin corrects this ratio.
378
Mode of action of clopidogrel
Requires metabolic activation in the liver to become effective. Once activated, clopidogrel inhibits a specific receptor called the P2Y12 receptor (ADP usually acts on this to form clots) on the surface of platelets.
379
Mode of action of Dipyridamole
Inhibits platelet phosphodiesterase
380
When would new antiplatelet drugs be prescribed?
They are only licensed in the management of ACS.
381
Side effects of anti-platelet drugs
Increased bleeding risk. Bleeding implications - local haemostatic measures.
382
Anti-coagulants examples
Warfarin
383
Mode of action of warfarin
Inhibits synthesis of Vitamin K dependent clotting factors.
384
Side effects of warfarin
SE: Multiple drug interactions – Assume ALL drugs interact with Warfarin!
Dental: Bleeding Risk – local haemostatic measures
385
New oral anti-coagulants (NOACs) examples
* Rivaroxiban
* Apixaban
* Edoxaban
* Dabigatran
386
Side effects of NOACs
No significant drug interactions relevant to dentistry
Dental: Bleeding risk
387
What could happen with a patient taking too much prednisolone?
adrenal gland insufficiency —> adrenal crisis
388
How would you treat a patient (dental treatment) with addisons?
Supplemental steroid treatment as prophylaxis “double up tablets” bring emergency hydrocortisone injection kit to all appointments
389
What would the blood glucose of an addisons patient be and why?
Low glucose level <4mmol/l
Deficiency of cortisol increases insulin sensitivity.
390
Cortisol and fat retention/blood glucose
High cortisol levels = higher fat and blood glucose levels
Low cortisol levels = lower fat and lower blood glucose levels
think of cortisol as a chocolate !!
391
A patient has had a hypo and you’ve give IM glucagon - what must happen to the patient now?
Anyone who’s had glucagon needs to go to A&E!!! even if they regain conciousness.
