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Mod 5 exam > Human diseases > Flashcards

Human diseases Flashcards

1
Q

When would you adopt the ABCDE approach?

A

For a deteriorating patient

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2
Q

What approach would you adopt for an unconscious patient?

A

DR ABCDE

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3
Q

Asthma attack: A

A

A - wheezing on expiration

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4
Q

Asthma attack: B

A

Respiratory rate: >25 (increased)

SpO2: <96% (decreased)

Rapid shallow breaths

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5
Q

Asthma attack: C

A

Heart rate: increased (>100)

Pallor (pale)

Hypertension (not always)

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6
Q

Asthma attack: D

A

ACVPU scale: ALERT (but anxious)

blood glucose N/A

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7
Q

Asthma attack: E

A

Pale, distressed, use of accessory muscles for breathing, inability to complete sentence in one breath

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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…

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9
Q

First stage of management for an asthma attack?

A

Oxygen (15l/min through non-breather mask)

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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.

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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.

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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.

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13
Q

Absence seizure signs and symptoms

A

Blank state
zoning out
usually short lasting

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14
Q

Tonic-clonic seizure: A

A

Difficult to assess but often patent

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15
Q

Tonic-clonic seizure: B

A

Respiratory rate: >25 (increased usually but hard to assess)

SpO2: <96% (decreased)

Apnoea (pauses in breathing)

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16
Q

Tonic-clonic seizure: C

A

Heart rate: >100

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17
Q

Tonic-clonic seizure: D

A

ACVPU: unresponsive

Blood glucose N/A

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18
Q

Tonic-clonic seizure: E

A

Convulsions, flushed complexion, rigidity, urinary incontinence, frothing of mouth.

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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

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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.

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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

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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

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23
Q

How much midazolam could you administer for a status epilepticus for a baby 6-11months?

A

2.5mg

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24
Q

How much midazolam could you administer for a status epilepticus for a young child 1-4 years?

A

5mg

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25
Q

How much midazolam could you administer for a status epilepticus for a young child 5-9 years?

A

7.5mg

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26
Q

How much midazolam could you administer for a status epilepticus for a young child 10-17 years?

A

10mg

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27
Q

What is the effect of midazolam and why should it be dosed cautiously?

A

Muscle relaxant and anticonvulsant effect – be cautious as muscle relaxant effect could cause respiratory muscles

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28
Q

Hypoglycaemia: A

A

Patent

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29
Q

Hypoglycaemia: B

A

Respiratory rate: >25 (increased)
SpO2: <94% (decreased)

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30
Q

Hypoglycaemia: C

A

Heart rate: tachycardia (fast)
BP: hypertension
Pallor and clammy

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31
Q

Hypoglycaemia: D

A

ACVPU: confused

Blood glucose <4mmols “four to the floor”

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32
Q

Hypoglycaemia: E

A

Slurred speech, shaking, aggressive, appears drunk

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33
Q

Hypoglycaemia: first line management

A

Oxygen (if patient allows)

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34
Q

Hypoglycaemia: if pt is conscious

A

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.

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35
Q

Hypoglycaemia: if pt is unconscious

A

Administer 1mg of glucagon IM

Oxygen

CALL 999.

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36
Q

Hypoglycaemia: pt has regained conciousness?

A

give oral glucose to replenish them.

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37
Q

Angina/MI signs

A

Crushing central chest pain radiating to the left arm, neck and jaw.

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38
Q

Angina/MI: A

A

Usually patent but potential for some sounds such as wheezing

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39
Q

Angina/MI: B

A

Respiratory rate: >25 (increased/rapid)
SpO2: <96% decreased

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40
Q

Angina/MI: C

A

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

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41
Q

Angina/MI: D

A

ACVPU; ALERT (but anxious)

Glucose N/A

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42
Q

Angina/MI: E

A

Clammy, grey in colour, sweaty, nauseous, potential evidence of cyanosis

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43
Q

Angina/MI: first line management?

A

oxygen - 15l/min

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44
Q

Suspected angina, after oxygen management?

A

Administer 2 puffs of GTN (400 mg) sublingually.

Repeat after 3 minutes if pain remains.

If worsens –> follow MI protocol

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45
Q

Suspected MI, after oxygen management?

A

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)”

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46
Q

What is diabetic ketoacidosis and management?

A

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.

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47
Q

Diabetic ketoacidosis signs and symptoms

A

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

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48
Q

Type 1 diabetes

A

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.

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49
Q

Most common type of diabetes

A

type 2 (85%)

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50
Q

Difference between diabetes mellitus and insipidus?

A

Mellitus –> glucose regulation
Insipidus –> renal function (water)

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51
Q

HbA1C of a diabetic

A

HbA1C >48mmol/l (6.5%)

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52
Q

Acute presentation of type one diabetes and why?

A

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.

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53
Q

How could a type 1 diabetic have a hypo attack?

A

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.

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54
Q

What is HbA1c?

A

HbA1c is your average blood glucose (sugar) levels for the last two to three months.

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55
Q

What is ketoacidosis?

A

Body cells cannot access glucose for metabolism so the start to metabolise fat which results in Ketones as end product.

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56
Q

What is type 2 diabetes?

A

Cells develop resistance to insulin,

Pancreas works in overdrive to produce more insulin to counter this, eventually it becomes exhausted and dies off.

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57
Q

What medications could cause diabetes?

A
  • immune suppressants (cyclosporin, calcineurin inhibitors)
  • cancer meds (imatinib, nilotinib)
  • antipsychotics (clozapine, olanzapine)
  • steroids
  • antiviral (protease inhibitor)

I CASA

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58
Q

Which endocrine diseases are linked to diabetes?

A

Cushings (>cortisol)

phaechromocytoma (adrenal tumour - high cortisol release)

Acromegaly (anterior pituitary tumour - high release of ACTH stimulating high cortisol release)

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59
Q

What women may be effected by diabetes?

A

Pregnant - gestational diabetes

Will likely already have risk factors i.e. overweight etc.

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60
Q

Why type of diabetes would rarely suffer diabetic ketoacidosis?

A

Type 2 - still have enough insulin to prevent ketone accumulation (but perhaps just not enough for the body’s glucose requirements)

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61
Q

Type 1 diabetes: management

A

Insulin dose (basal-bolus)

Regular checking of blood glucose level

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62
Q

Type 2 diabetes: management

A

Lifestyle

Medication

Surgery

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63
Q

Medication for type 2 diabetes

A

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.

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64
Q

When would a type 2 diabetic patient get insulin treatment?

A

Pt is unable to maintain glycemic control

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65
Q

Why could a diabetic have a hypoglycaemic attack?

A

Type 1 –> insulin without food (glucose) - too glucose into the cells = not enough in the blood.

Type 2 –> seen with sulphonylurea (or insulin too)

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66
Q

What are the three chronic complications of diabetes?

A

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.

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67
Q

What could this be?

A

Diabetic foot

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68
Q

What patients are at risk of cataracts, maculopathy and proliferative retinopathy?

A

Diabetic eye diseases

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69
Q

Why might surgery be an issue for a diabetic?

A

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)

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70
Q

What are some dental considerations of diabetes?

A
  1. Mouth in pain = poor food intake
  2. Infection risk
  3. Poorer wound healing - extractions etc.
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71
Q

What is jaundice?

A

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

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72
Q

Signs of someone with liver disease

A

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

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73
Q

What two genetic conditions could cause excess bilrubin due to unconjucation?

A

Gilbert’s

Crigler - najjar 1/11

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74
Q

What is Dublin-johnson

A

Genetic condition where conjucated bilrubin accumulated in the blood

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75
Q

How does viral hepatitis cause jaundice?

A
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76
Q

How does extra-hepatic issues such as tumours and gall stones contribute to jaundice?

A

Bile flow is blocked from the obstruction causing the pressure to build and it to leak into the blood.

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77
Q

In classic haemophilia (A), which factor in the coagulation cascade is deficient? What other disease can cause a reduction in the this factor?

A

Factor VIII (“eight”)

von Willebrand’s disease

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78
Q

In haemophilia B, which factor in the coagulation cascade is deficient?

A

Factor IX (“nine”) can be referred to as Christmas disease.

On the ninth day of Christmas, nine ladies dancing - Busting a move (B haemophilia).

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79
Q

Why might a mother think she’s given her son haemophilia but not her daughter?

A

Haemophillia is X-linked recessive, daughter becomes a carrier and the son is effected.

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80
Q

What might be used to manage haemophilia A?

A

Recombinant factor VIII

Desmopressin (DDAVP) - releases factor VIII

Tranexamic acid (oral)

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81
Q

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?

A

Tranexamic acid mouthwash which inhibits fibrinolysis –> keeps clots formed.

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82
Q

Management of haemophilia B ?

A

Recombinant factor IX

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83
Q

What is used to manage von Willibrand’s disease (affecting factor VIII / 8)?

A

DDAVP (desmopressin acetate) - helps release of factor VIII

tranexamic acid

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84
Q

Most common bleeding disorder in the UK

A

von Willebrand’s

Haemophillia A

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85
Q

What dental procedure requires special care for a bleeding risk that doesn’t involved surgery or extracting a tooth?

A

Administering LA

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86
Q

What LA method is more at risk of a bleeding incident?

A

IANB
lingual infiltration
posterior superior nerve block

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87
Q

Thrombophilia

A

“clot loving”

embolism risk if clot moves/ruptures

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88
Q

What platelet disorders could cause increased bleeding?

A

Thrombocytopenia (reduced number of platelets)

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89
Q

Platelet count: treatment would need to be referred on vs done in primary care.

A

100 - primary care

50 - hospital setting

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90
Q

Thrombocythemia

A

High number of platelets –> clot risk usually on aspirin for this.

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91
Q

What conditions may present as dental erosion?

A

Diet
GORD
excessive vomiting

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92
Q

GI disease: aphthous ulceration, glossitis, angular cheilitis?

A

Coeliac disease - patients have malabsorption and thus deficiencies.

Glossitis (smoothening of the tongue)

Rarely oral can see dermatitis herpetiformis

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93
Q

Crohn’s disease oral manifestations

A

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”

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94
Q

What would a biopsy of a Crohn’s lesion show?

A

non-caseating granulomas

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95
Q

What is OFG and what condition is it linked to?

A

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.

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96
Q

GI disease: rare oral manifestations, can present with aphthous ulcers, lesions related to anaemia, pyostomatitis vegetans.

A

Ulcerative colitis

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97
Q

Adult average paracetamol overdose limit

A

> 4000mg in 24hours

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98
Q

Worst way to overdose on paracetamol

A

Staggered overdose (excess >1 hours period)

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99
Q

Clinical dosage of paracetamol per kg

A

More than or equal to 75mg per kg in 24 hours

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100
Q

What is the key antioxidant that binds to the toxic metabolite of paracetamol allow it to be excreted?

A

Glutathione

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101
Q

High risk patients for paracetamol over dose

A

“PARAC-L”

P - psychiatric disorders
A - alcohol use disorder
R - retroviral disease (HIV)
A- anorexia (any eating disorders)
C - cystic fibrosis
L - liver disease

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102
Q

Medications that induce cytochrome P450 and thus make a patient at higher risk of paracetamol overdose?

A

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

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103
Q

Paracetamol overdose: in first 24 hours signs

A

Nausea & Vomiting
General abdominal pain

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104
Q

Paracetamol overdose: in acute liver injury (2-3 days) signs

A

RUQ abdominal pain
Jaundice - Sign of acute liver injury
Hepatomegaly
Reduced GCS
Loin Pain/AKI
Abnormal LFTS/Metabolic Acidosis

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105
Q

Course of action overdose paracetamol: less than 4g in 24 hours

A

Continue with dental treatment

Give leaflet

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106
Q

Course of action overdose paracetamol: more than 4g in 24 hours

A

more than 75mg per kg

postpone treatment

Transfer to A&E (SBAR - relevant medical conditions)

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107
Q

Drug management of paracetamol overdose

A

Acetylcysteine IV (NAC, Parvolex) –> increases hepatic glutathione

Ideally give in first 8 hours (still effective up to 24hours)

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108
Q

Overdose? –> 40kg: 5 co-codamol, 6 ibuprofen, 5 paracetamol

A
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109
Q

Overdose? –> 90kg: 7 tramadol, 12 anadin extra, 4 panadol.

A
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110
Q

Overdose? –> 73kg: 8 acetaminophen, 4 solpadeine

A
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111
Q

Anaphylaxis: A

A

Stridor and wheezing

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112
Q

Anaphylaxis: B

A

Respiratory rate: > 25 (increased)
SpO2: <96% decreased
Rapid shallow breaths

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113
Q

Anaphylaxis: C

A

BP: drastically dropped (vasodilation)
Tachycardia
Bounding pulse
Increased CRT

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114
Q

Anaphylaxis: D

A

ACVPU - alert but with impending sense of doom

Glucose N/A

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115
Q

Anaphylaxis: E

A

Flushing, rash (hives), angioedema of lips, vomiting nausea, incontinence

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116
Q

Suspected Anaphylaxis?

A
  • 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)
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117
Q

First-line management of anaphylaxis

A

Call 999 - state problem and remove source

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118
Q

After calling 999 - anaphylaxis management

A

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

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119
Q

Adrenaline dosage in anaphylaxis for children 6 months - 5 years

A

0.15mg

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120
Q

Adrenaline dosage in anaphylaxis for children 6 -11 yrs

A

0.3mg

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121
Q

Adrenaline dosage in anaphylaxis for children 12-17 yrs

A

0.5mg

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122
Q

Why is adrenaline used in anaphylaxis?

A

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

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123
Q

Choking management

A

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.

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124
Q

STIs: Syphilis presentation at the dentist

A

Treponema pallidum

painless

“hard disc” - chancre

Secondary syphilsis –> greyish membrane, snail trail..

Treatment with antibiotics

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125
Q

HIV - oral manifestations

A

Mucosal candidasis
Kaposi’s sarcoma (HHV8 - dark purple)
EBV - oral hairy leukoplakia

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126
Q

What viral infections could cause oral cancers?

A

Human papilloma virus

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127
Q

Can you give at least two underlying diseases or conditions which might explain the findings?

A

HIV, diabetes, steroid inhalers

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128
Q

Why might haemophilia B and HIV be associated?

A

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.

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129
Q

Hepatitis C virus meds

A

DDA - Direct-acting antiviral

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130
Q

HIV pathogenesis and meds

A

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

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131
Q

If this has been caused by sexual transmission what is it and how should it be treated?

A

Primary syphilis - “chancre”

Antibiotics –> Benzathine Penicillin G.

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132
Q

Ulcer

A

trauma

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133
Q

Ulcer type

A

Metabolic/GI ect

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134
Q

Ulcer type

A

Syphilis

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135
Q

Ulcer type

A

Herpes (2)

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136
Q

What causes this characteristic unilateral?

A

Varicella zoster - effects a nerve branch!

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137
Q

What eye condition would contra-indicate no inhalation sedation for risk it could cause acute eye pressure and thus permanent sight loss?

A

Retinal detachment

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138
Q

What eye condition could manifest from diabetes?

A

Diabetic retinopathy

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139
Q

Malignant hyperthermia

A

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.

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140
Q

Appendicitis

A

Right iliac fossa pain
Nausea and vomiting
Anorexia
Constipation or diarrhoea
Pyrexia
Tachycardia
Rovsing’s positive

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141
Q

Pancreatitis

A
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142
Q

NSAID contraindicated in CVS medications (ACE inhibitors etc)

A

Diclofenac

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143
Q

Diagnosing sepsis

A

THRWG

Sepsis = known/presumed source of infection + SIRS (2 or more)

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144
Q

Haemorrhaging stage IV

A

> 2000ml of blood lost

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145
Q

What medication is given to DVT risk patients as prophylaxis?

A

Heparin SC

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146
Q

Delirium vs dementia

A

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

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147
Q

Blood definitions: anaemia

A

Low Hb (haemoglobin)

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148
Q

Blood definitions: leukopenia

A

low white blood cells count (WCC)

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149
Q

Blood definitions: thrombocytopenia

A

low platelets (PLT)

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150
Q

Blood definitions: pancytopenia

A

all cells reduced

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151
Q

blood definitions: polycythaemia

A

raised Hb (haemoglobin) and hemocrit

Poly = “many”
Cyth = “cells”
emia = “blood”

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152
Q

blood definitions: leukocytosis

A

raised WCC (white blood cell count)

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153
Q

blood definitions: throbocythaemia

A

raised platelets

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154
Q

What is leukaemia?

A

Neoplastic proliferation of white cells - usually disseminated (uncontrolled growth spread around the body).

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155
Q

What is lymphoma?

A

Neoplastic proliferation of white cells - as a solid tumour (uncontrolled growth confined to a certain area).

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156
Q

What is porphyria?

A

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.

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157
Q

Why is porphyria clinically relevant to the dentist?

A

LA interferes with haemoglobin synthesis and can exacerbate the accumulation of porphyrias resulting in an acute attack.

158
Q

What would happen during an acute porphyria attack?

A

o R – rash (photosensitive)
o P – psychiatric attack (seizing/autonomic disturbances)
o H – hypertension and tachycardia

poRPHyria

159
Q

What is the sepsis six?

A
  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
Q

Two causes of anaemia

A
  1. issue making haemoglobin (iron deficiency)
  2. issue folding global chain (thalassemia, sickle cell etc)
161
Q

What is the cause of anaemia, and why is this often confused?

A

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
Q

What autoimmune disease could be linked to anaemia?

A

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
Q

What GI conditions could result in not enough iron being absorbed?

A

Gastric erosions and ulcers
Inflammatory Bowel disease
Crohn’s disease
Ulecerative colitis
Bowel Cancer
Colonic cancer
Rectal Cancer
Haemorrhoids

164
Q

Why might people with Crohn’s be deficient in Vitamin B12?

A

Crohn’s disease –> disease of terminal Ilium

165
Q

Which two disorders cause improper folding of the haemoglobin chains and thus anaemia?

A

Sickle cell and thalassaemia

166
Q

What can be used to give a clue as to the cause of anaemia?

A

Mean corpuscular volume (MCV) is a laboratory value that measures the average size and volume of a red blood cell.

167
Q

Clinical signs of anaemia

A

Pale
Tachycardia
tired and weak
dizzy
palpitations

168
Q

TONGUE DEFICENCIES - iron

A

smooth tongue

169
Q

TONGUE DEFICENCIES - vitamin B12

A

beefy tongue

170
Q

Treatment of anaemia

A

Replace deficiencies ( vit B12, folic acid and ferrious sulphate)

Maybe transfusions if necessary

171
Q

How could anaemia present orally?

A

mucosal atrophy
candidiasis
recurrent oral ulceration
sensory changes

172
Q

HCT (haematocrit) count

A

Hematocrit is the percentage of red cells in your blood.

173
Q

What is the most common reason for excess blood loss causing anaemia?

A

GI bleeding - chronic loss

174
Q

How could hereditary issues such as sickle cell disease be apparent from a RCC or HCT?

A

Cells are abnormal and thus have a reduced life span = less RBCs.

175
Q

How could MCV suggest thalassaemia?

A

MCV (mean corpuscular volume) showing smaller RBCs (microcytic cells).

176
Q

How could MCV suggest B12/folate deficiency?

A

MCV (mean corpuscular volume) showing larger RBCs (macrocytic cells).

177
Q

What if the MCV showed the RBC size to be normal, what might be the cause of the anaemia?

A

Chronic bleeding loss (GI etc)

178
Q

Warfarin

Apixaban
Edoxaban
Rivaroxaban
Dabigatran

A

Examples of anticoagulants

179
Q

Clopidogrel
Dipyridamole
Prasugrel + Aspirin
Abciximab
Eptifibate + Aspirin
Ticagrelor
Tirofaban
Low dose Aspirin

A

antiplatelet drugs

180
Q

Treatment flowchart for bleeding risk: vitamin K antagonist (warfarin)

A

Check INR no more than 24-72 hours before procedure.

If INR is <4 treat as normal.

181
Q

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?

A

NOACs - dabigatran, apixaban, rivaroxaban.

182
Q

Treatment flowchart for bleeding risk: anti platelet drugs

A

treat as normal!

183
Q

Treatment flowchart for bleeding risk: injectable anticoagulant

A
  • consult with GP
184
Q

Treatment flowchart for bleeding risk: high risk treatment

A

Extractions
Minor oral surgery
Implants
Periodontal surgery
Biopsies - sometimes

185
Q

WARFARIN - interactions

A

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
Q

NOACs: Direct thrombin (IIa) inhibitors

A

D for Direct and Dabigatran

187
Q

NOACs: Factor Xa inhibitors

A

Apixaban (2 tablets), Rivaroxiban, Edoxaban

ban = 10

188
Q

Difference between anticoagulants and antiplatelets

A
189
Q

What blood type is most common?

A

O

190
Q

2 types of lymphoma

A

Hodgkin’s lymphoma
Non-Hodgkin lymphoma

191
Q

Symptoms of lymphoma

A

PL-I-NS-W-I-F

plinswif !

192
Q

Painless lymphadenopathy, fever, night sweats, weight loss, itching, infection…

A

Non-hodgkin lymphoma

193
Q

Non-hodgkin lymphoma

A

Often associated with an autoimmune (Sjogrens) or immune suppressing (HIV) disease

194
Q

What is worse; non-hodgkins lymphoma or Hodgkins lymphoma?

A

non-hodgkins lymphoma’s prognosis is worse.

195
Q

What is multiple myeloma?

A

malignant proliferation of plasma cells

196
Q

How are haematological malignancies managed?

A

Chemotherapy

Radiotherapy

Monoclonal antibodies

Haemopoietic stem cell transplantation

197
Q

Three key manifestations of leukaemia patients

A

Anaemia
Infection (neutropenia)
Bleeding (thrombocytopenia)

198
Q

Four leukaemia types and patients most commonly effected

A

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
Q

INR

A

international normalised ratio (INR) blood test tells you how long it takes for your blood to clot.

200
Q

INR level meaning?

A
201
Q

Bipolar disorders: mood stabiliser meds

A

Lithium, sodium valproate, lamotrigine

202
Q

Bipolar disorders: antipsychotic meds

A

quetiapine, aripiprazole, olanzapine, haloperidol

203
Q

Schizophrenia meds

A

Antipsychotics - chlorpromazine, haloperidol etc

204
Q

MMSE

A

Mini mental state exam (psychiatry)

205
Q

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

A

Somatoform Disorders (Somatisation) - physical manifestation of psychological

206
Q

Frailty –> 2 or more of the following

A

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
Q

Medications most commonly associated with xerostomia

A

anti-depressants
anti-hypertensives
anxiolytics

208
Q

Medications commonly associated with gingival hyperplasia

A

CCBs, anti-epileptic drugs, cyclosporin (immunosuppressant)

209
Q

Most at risk of vitamin D deficiency

A

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
Q

Osteomalacia and management

A

During bone formation = “rickets”
Poorly mineralised osteoid matrix
Poorly mineralised cartilage growth plate
VIT D DEFICIENCY

211
Q

Osteoporosis and management

A

Loss of mineral and matrix
Reduced bone mass

212
Q

Gout on the toe causes

A

Thiazide diuretics
Aspirin

213
Q

Treatment of gout

A

NSAIDs (NOT aspirin, this stops the secretion of uric acid)

214
Q

PAIN
improves with rest
worse with activity
BRIEF morning stiffness
SLOWLY progressive over years
–?

A

Osteoarthritis

Treatment: increase muscle strength, NSAIDs, prosthesis

215
Q

slow onset
initally hands and feet
proximal spread
potentially ALL synovial structures
SYMMETRICAL polyarthritis
Occ. onset with SYSTEMIC symptoms
fever, weight loss, anaemia

A

rheumatoid arthritis

216
Q

Treatment of RA

A

in more severe cases would be –> immune modulators and oral prednisone.

217
Q

Vessel disease: polyarteritis nodosa and Kawasaki

A

medium vessel disease

218
Q

Vessel disease: Wegener’s granulomatosis

A

small vessel disease

219
Q

Vessel disease: giant cell (temporal) arteritis

A

large vessel disease

220
Q

Connective tissue disease general management

A

NSAIDs

Immune modulators:
Hydroxychloroquine
Methotrexate
Azathioprine
Mycophenolate

Systemic steroids - prednisolone

221
Q

Systemic Lypus Erythematosis (SLE)

A

“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
Q

circulating immune complexes - SLE

A

ANA, dsDNA, Ro antibodies

“ROANADNA”

223
Q

What CTD would you definitely NOT stop anti-coagulant therapy for and why?

A

Antiphospholipid Antibody Syndrom (APS) - high risk of arterial thrombosis or pulmonary embolism (heart or lungs stopping! = death)

224
Q

circulating immune complexes - Sjögren’s syndrome

A

ANA, Ro and La

“LAROANA”
think LA for lacrimal gland effected!

225
Q

Sjögren’s syndrome - sicca syndrome type

A

dry mouth or eyes

226
Q

Primary vs secondary sjogrens

A
227
Q

Systemic sclerosis CREST

A

Anti Scl-70 antibodies

228
Q

Dental considerations - Systemic sclerosis

A

can’t open mouth and difficulty swallowing etc. PDL may appear wider radiographically but there will be no associated mobility.

229
Q

How could giant cell arteritis present to the dentist?

A

Carotid branches effected - chewing claudication (pain).

230
Q

Kawasaki disease presentation to the dentist?

A

CHILDREN EFFECTED
“turning into a strawberry”
Fever & lymphadenopathy
Crusting/cracked tongue
Strawberry tongue & erythematous mucosa
Peeling rash on hands and feet

231
Q

Which vasculitis disease causes this presentation?

A

Wegner’s Granulomatosis

232
Q

Sjogren’s syndrome: first line therapy

A

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
Q

Management of xerostomia

A

Artificial saliva - orthana, glandosane etc

Salivary stimulants - gums and sweets

234
Q

Sjogrens oral manifestations

A
  • Opportunistic oral infections
  • Periodontal disease
  • Caries, particularly at the cervical margin
235
Q

Recurrent acute pseudomembranous candidiasis with no obvious cause?

A

Diabetes type II

236
Q

Treatment of burning mouth syndrome

A
237
Q
A

Acne rosacea

238
Q
A

Acne vulgaris

239
Q

What is this? How could it be worsened?

A

Periorificial dermatitis - made worse by steroid cream

240
Q
A

Impetigo - cause by staphy or strep

241
Q
A

Furunculosis - hair follicle infected usually by s.aureus

242
Q
A

Erysipelas - A beta haemolytic strep (may have fever etc –> treat w/antibiotic)

243
Q
A

Human papilloma viral warts

244
Q
A

Molluscum contagiosum - DNA pox virus (cryotherapy)

245
Q
A

Herpes-simplex 1

246
Q
A

Herpes-zoster

247
Q
A

Coxsackie A virus - Hand foot and mouth disease (self-resolving = 2 weeks)

248
Q

Atopy triad

A
249
Q
A

Basal cell carcinoma

250
Q
A

Squamous cell carcinoma

251
Q
A

melanoma

252
Q

Ulcerative colitis: symptoms and bloods

A

Diarrhoea with BLEEDING
Only colon affected.

CRP (C-reative protein)
Albumin
Platelets (thrombocytosis = too many)

253
Q

Crohn’s: symptoms and bloods

A

Weight loss, abdominal pain, peri-anal disease.
Anywhere along the GI tract

CRP, albumin, platelets, B12 (t.ileum), ferritin, FBC

254
Q

Crohn’s vs Celiac

A

Celiac = no meds

255
Q

Crohn’s aggravators

A

smoking and anything high-fibre (low-fibre is recommended)

256
Q

UC vs Crohn’s - therapy options

A

UC: Steroids, 5-ASA (mesalazine), immunosuppressants, biologics

Crohns: Steroids, immunosuppressants, biologics

257
Q

Corticosteroids for GI issues

A

Methylprednisolone

258
Q

Immunosuppressants for GI issues

A

Thiopurines - azathioprine and 6-mercaptopurine

Methotrexate

259
Q

Why might vitamin B12 malabsorption be common in Crohn’s patients?

A

Terminal ileum is effected which is a key absorber for Vitamin B12 and bile acids.

260
Q

Key medications for upper GI disorders

A

Antacids (reduce acid there)

H2 receptor blockers
Proton pump inhibitors
(these reduce acid secretion)

261
Q

Cimetidine and ranitidine

A

H2 receptor blocker

262
Q

Omeprazole, lansoprazole, pantoprazole…

A

PPIs

263
Q

GORD presentation

A

“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
Q

Lifestyle advice for GORD patients

A

Stop smoking and lose weight

265
Q

Two most common causes of peptic ulcer disease (PUD)

A
  1. NSAIDs - too much acid
  2. Helicobacter pylori infection
266
Q

Coeliac disease and sensitivity

A

Small intestine affected
Sensitivity to α-gliaden component of Gluten

267
Q

Colonic carcinoma

A

Lifestyle poor
Genetics; p53

Treatment:
Surgery
Hepatic Metastases
Radiotherapy
Chemotherapy

Screening through FiT test

268
Q

How much bacteria is in a healthy urine?

A

NONE - it is sterile.

269
Q

UTI - bacteria

A

E.coli

270
Q

What is a VERY common issue men in their willies? What is treatment for this?

A

Benign prostatic hypertrophy

⍺-blocking drugs
Anticholinergic
Diuretics

271
Q

LITHOTRIPSY

A

high level shock- waves used to break up renal stones so they can be passed out in the urine easier.

272
Q

Renal disease analgesics?

A

avoid NSAIDs

273
Q

When’s the best time to treat a patient doing dialysis?

A

After sessions of dialysis

274
Q

Addisons disease

A

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
Q

Adrenal cortex - hormones

A

G - salt (aldosterone -

F - sugar (cortisol -

R - sex (androgens)

276
Q

Posterior pituitary hormones

A

ADH - anti-diuretic hormone

Oxytocin

277
Q

Anterior pituitary hormones

A

TSH - Thyroid Stimulating Hormone
ACTH - Adrenocorticotrophic Hormone
GH - Growth Hormone
LH, FSH, Prolactin

278
Q

How could a pituitary tumour resulting in excessive growth hormone production manifest?

A

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
Q

Hyperthyroidism - causes

A
  1. GRAVES disease (70-80%) - primary
  2. Pituitary tumour (uncommon) - secondary
280
Q

Hypothyroidism - causes

A
  1. Hashimoto’s disease (90%) - primary
    (drugs, radioiodine treatment…)
  2. Hypothalamus/pituitary disease
281
Q

Hyperthyroidism - TSH and T3 levels for each kind?

A

Primary cause (graves/adenoma) = low TSH, high T3

Secondary cause (pituitary cause) = high TSH, high T3

282
Q

Hypothyroidism - TSH and T4 levels for each kind?

A

Primary cause (gland failure) = high TSH, low T4

Secondary cause (pituitary cause) = low TSH, low T4

283
Q

Treatment - hyperthyroidism

A

Carbimazole

beta-blockers
radioiodine
surgery

284
Q

Treatment - hypothyroidism

A

Give T4 tablets (thyroxine)

285
Q

What hormone is released from the anterior pituitary to simulate the adrenal cortex and produce salt, sugar and sex hormones?

A

adrenocorticotropic hormone (ACTH)

286
Q

High aldosterone levels will…

A

Increase sodium and water RETENTION = BP increases

This action is blocked by ACE inhibitors

287
Q

Too much aldosterone

A

Conn’s syndrome

288
Q

Too much cortisol

A

Cushings syndrome

289
Q

Addison’s disease specific test for diagnosis

A

negative synACTHen test

290
Q

Prophylaxis for patients with adrenal diseases undergoing dental treament

A

Steroid prophylaxis

291
Q

Oral manifestation of Cushings

A

Candidiasis

292
Q

Oral manifestation of Addisons/cushings

A

oral pigmentations

293
Q

What is a stroke?

A

Death of brain tissue from hypoxia

294
Q

What differentiates a TIA from a stroke?

A

Pt makes a full recovery within 24 hours

295
Q

What is the most common causes of a stroke?

A
296
Q

Treatement for preventing a stroke caused by infarction?

A

Lifestyle changes (i.e. stop smoking)

Antiplatelet + anticoagulant therapy

297
Q

Epilepsy causes

A

issues with the neurotransmitters in the brain

298
Q

Febrile seizure

A

CHILDREN WITH FEVERS

but presents the same as a tonic-clonic

299
Q

Generalised seizures examples

A

Tonic clinic

Absent seizure (petit mal) - childhood usually

300
Q

Preventative anticonvulsant drugs - tonic clonic

A

Valproate, carbamazepine, phenytoin, gabapentine, lamotrigine

301
Q

Absent seizures medication

A

levitiracetam

302
Q

Parkinsons treatment

A

Dopaminergic drugs; Direct replacement and
Agonists

303
Q

Salbutamol and terbutaline

A

Intermittent short acting Beta-adrenergic Agonists

304
Q

Fluticasone,
Budesonide,
Mometasone

A

Inhaled Corticosteroids – low dose

305
Q

Salmeterol

A

Regular long acting Beta-adrenergic agonist

306
Q

Spacer vs nebuliser (in asthma)

A
307
Q

Respiratory failure type 1 and type 2

A

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
Q

Oral manifestations of inhaled steroids

A

Candida

309
Q

Cystic fibrosis

A

Genetic disease
Sticky mucous
CFTR gene - chromosome 7

Shaking physiotherapy

310
Q

Lung tumours most common cell type

A

non-small cell

311
Q

83% of lung cancers is a result of …

A

SMOKING

312
Q

Drugs that could cause impaired breathing

A

beta-blockers (chronic cough)
Respiratory depressants
Benzodiazepines
opioids

313
Q

Ipratropium

A

Anticholinergic - for asthma

314
Q

Other less common asthma drugs

A
315
Q

3 drug cocktail for acute coronary syndromes

A

Antiplatelets - aspirin
Anti-hypertensives - diuretics, CCBS, ACE inhibitors, beta-blockers
Vasodilators - nitrates

316
Q

MI treatment options - after 3 hours

A

Primary PCI

317
Q

MI treatment options - after 6 hours

A

Thrombolysis

318
Q

Common cause of bradyarrhythmia

A

too much beta-blocker

319
Q

Features of atrial fibrillation on ECG

A

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
Q

Features of Ventricular tachyarrhthmias on ECG

A

broad QRS on ECG
Dangerous as it can lead to ventricular fibrillation and death

321
Q

Cardiac pacemakers

A

For bradyarrhythmias –> keeps it above 50bpm and senses if this drops.

AVOID ULTRASONIC SCALERS interferes with the electrical field

322
Q

Sinus rhythm

A

the normal ECG

323
Q

Ventricular fibrillation

A

Use defibrillators

324
Q

Asystole

A

Don’t use defibrillators

325
Q

When should you use a defibrillator?

A

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
Q

Finger clubbing causes

A
327
Q

When would someone display cyanosis?

A

5g/dl or more of deoxygenated Hb in the blood
(50g/l of blood)

328
Q

Which congenital septal defects are at higher risk of IE?

A

Ventricular

329
Q

Which congenital septal defects are at higher risk of long term heart failure?

A

ventricular

330
Q

Congenital issue effecting the aorta

A

Co-arctation of the aorta

331
Q

Patient ductus arteriosus

A

Congenital heart defect - an extra blood vessel found in babies before birth and just after birth.

332
Q

Cardiac valves order…

A

Tricuspid
Pulmonic
Mitral
Aortic

333
Q

Which valves most commonly fail?

A

Aortic and mitral

334
Q
A

This is bicuspid aortic valve, a congenital abnormality.

335
Q

Valve replacements

A

Mechanical usually - anticoagulant therapy!

Occasionally porcine

336
Q

Targets for cholesterol in CVS patients

A

Below 5mmol/L or 25%

337
Q

high output failure heart disease

A

– 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
Q

low output failure heart disease

A

– pump is failing and not strong enough to force liquid around the body
cardiac defect e.g. MI, valve disease

339
Q

Side of heart effected? dyspnoea, tachycardia, low BP, low vol. Pulse

A

LEFT

340
Q

Side of heart effected? swollen ankles, ascites, raised JVP, tender enlarged liver, poor GI absorption

A

RIGHT

“the right side of my heart still swells like your foooooot” - Dr. Faye Webster

341
Q

Key difference in management of heart failure cf. with IHD?

A

STOP negative inotropes - NO beta-blockers!

342
Q

Hypertension treatment

A
343
Q

Symptoms of IE

A

fever, heart murmur, sepsis, nail splintering

344
Q

Treatment of IE

A
345
Q

Cardiac conditions at risk of IE

A
  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
Q

What are the drugs that end in -pril? (i.e. Enalapril)

A

ACE inhibitors

347
Q

How do ACE inhibitors work?

A
  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
Q

What are some side effects of taking ACE inhibitors?

A

ACE
A - allergic (lichenoid reaction)
C - chronic cough
E - elevation from chair causing hypotension

349
Q

WHat should you be mindful of when prescribing NSAIDs (i.e ibuprofen, aspirin..) to someone on ACE inhibitors?

A

The interaction could reduce the anti-hypertensive effect as well as increase the risk of acute renal injury.

350
Q

What are the drugs that end in -artan? (i.e Losartan, candesartan…)

A

Angiotensin II blockers

351
Q

What is the mode of action of angiotensin II blockers?

A

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
Q

What are some side effects of ARBs?

A

Renal impairment, cough, postural hypotension

A - after sitting down for too long (postural hypotension)
R - renal impairment
B - breathing (cough)

353
Q

What should you be mindful of prescribing for someone taking ARBs?

A

NSAIDs

354
Q

What drugs (most often but not always) end in -ipine? (i.e Amlodipine, Nifedipine, verapamil, diltiazem..)

A

Calcium channel blockers

355
Q

What is the mode of action of calcium channel blockers?

A

Calcium channel blockade affects smooth muscle and results in vasodilation and a reduction in heart rate (useful in treating some arrhythmias).

356
Q

Which of the CCBs are more are more active on peripheral blood vessels compared with ones that are more active on the heart muscle?

A

Some drugs are more active on peripheral blood vessels (-ipines) and others are more active on the heart muscle (verapamil, diltiazem)

357
Q

What are some dental implications of a patient taking calcium channel blockers?

A

gingival hyperplasia, postural hypotension

358
Q

What antibiotic should you be cautious of prescribing for a patient on calcium channel blockers?

A

Macrolides ( azithromycin, clarithromycin and erythromycin XXXXX CCBs)

359
Q

What bendroflumethiazide and furosemides?

A

Diuretics

360
Q

Bendroflumethiazide

A

Thiazide diuretic

361
Q

Furosemide

A

Loop diuretic

362
Q

Thiazide compared with loop diuretics and indications for both

A

Thiazide:
tHiazide - Hypertension/Heart oedema

Loop:
Loop - Lung oedema/Left ventricular failure

363
Q

Mode of action of diuretics

A
  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
Q

What are some side effects of diuretics use?

A

SE: can lead to Na+/K+
imbalance if not monitored carefully

Dental: Dry Mouth

365
Q

What are the drugs ending in -olol? (i.e. bisoprolol, propranolol, atenolol…)

A

Beta-blockers

366
Q

Mode of action for beta-blockers

A

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
Q

Uses of beta blockers

A

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
Q

Side effects of beta blockers

A

worsen asthma, postural hypotension

369
Q

Drugs that end in -statin (atorvastatin, rosuvastatin, simvastatin etc)

A

HMG coA Reductase inhibitors

370
Q

Statins mode of action

A

“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
Q

LDL cholestrol

A

Low-density lipoprotein (“bad cholestrol”)

372
Q

Side effects of statins

A

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
Q

Examples of anti-anginal drugs

A

Nitrates:
1. Isosorbide mononitrate - prevents angina
2. Glyceryl trinitrate (GTN spray) - short acting, useful in emergency management of angina symptoms

374
Q

Mode of action of nitrates

A

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
Q

Side effects of nitrates

A

Headache, hypotension. No specific dental implications.

376
Q

What are some examples of anti-platelet drugs?

A

Aspirin, clopidogrel, dipyridamole, new antiplatelet drugs (Prasugrel, Ticagrelor etc.)

377
Q

Mode of action of aspirin

A

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
Q

Mode of action of clopidogrel

A

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
Q

Mode of action of Dipyridamole

A

Inhibits platelet phosphodiesterase

380
Q

When would new antiplatelet drugs be prescribed?

A

They are only licensed in the management of ACS.

381
Q

Side effects of anti-platelet drugs

A

Increased bleeding risk. Bleeding implications - local haemostatic measures.

382
Q

Anti-coagulants examples

A

Warfarin

383
Q

Mode of action of warfarin

A

Inhibits synthesis of Vitamin K dependent clotting factors.

384
Q

Side effects of warfarin

A

SE: Multiple drug interactions – Assume ALL drugs interact with Warfarin!
Dental: Bleeding Risk – local haemostatic measures

385
Q

New oral anti-coagulants (NOACs) examples

A
  • Rivaroxiban
  • Apixaban
  • Edoxaban
  • Dabigatran
386
Q

Side effects of NOACs

A

No significant drug interactions relevant to dentistry
Dental: Bleeding risk

387
Q

What could happen with a patient taking too much prednisolone?

A

adrenal gland insufficiency —> adrenal crisis

388
Q

How would you treat a patient (dental treatment) with addisons?

A

Supplemental steroid treatment as prophylaxis “double up tablets” bring emergency hydrocortisone injection kit to all appointments

389
Q

What would the blood glucose of an addisons patient be and why?

A

Low glucose level <4mmol/l

Deficiency of cortisol increases insulin sensitivity.

390
Q

Cortisol and fat retention/blood glucose

A

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
Q

A patient has had a hypo and you’ve give IM glucagon - what must happen to the patient now?

A

Anyone who’s had glucagon needs to go to A&E!!! even if they regain conciousness.

Mod 5 exam (5 decks)

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