Cardiovascular System Flashcards

0
Q

Name the 3 causes of anaemia

A

Reduced production of Hb
Increased losses of Hb
Increased demand of Hb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Define anaemia

A

Reduction in haemoglobin in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define aplastic anaemia

A

Reduced normal RBCs as a result of bone marrow failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is thalassaemia?

Give the two types

A

Normal haem production

Genetic mutation of globin chains

  • Alpha chains: Asians
  • Beta chains: Mediterraneans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 5 clinical effects thalassaemia?

A
Chronic anaemia
Marrow hyperplasia (skeletal deformities)
Splenomegaly
Cirrhosis
Gallstones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What 2 ways can you manage thalassaemia?

A

Blood transfusions

Prevent iron overload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What 2 reasons are there for an increased demand of Hb resulting in anaemia?

A

Pregnancy

Malignant disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What ethnic group is sickle cell anaemia predominantly seen in?

A

Afro-caribbeans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Define sickle cell anaemia

A

Inherited Hb defect due to defect in structure of beta chain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Define HCT

A

Haematocrit: a measure of the total volume of RBC relative to the total volume of the whole blood in sample

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Define microcytic anaemia and give its 2 causes

A

Small RBCs often hypochromic (pale) due to low Hb concentration

Caused by Fe deficiency and thalassaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Define macrocyclic anaemia and give its 2 causes

A

Large RBC; associated with maturation problems

Caused by vitamin B12/folate deficiency and retics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Define normacytic RBC and give its 3 causes

A

Normal RBCs

Caused by bleeding/renal/chronic disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Define reticulocytes

A

Immature RBCs which are larger than RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How can you detect anaemia using reticulocytes?

A

A reticulocyte percentage that is higher than normal is a sign of anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What differences are there between reticulocytes and RBCs?

A

Reticulocytes are stained purple due to organelles/RNA

Reticulocytes are larger than RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the 7 signs of anaemia?

A
Pale mucosa
Smooth tongue (Fe deficiency)
'Beefy' tongue (Vit B12 deficiency)
Pale
Tachycardia (fast heart rate, due to lower O2 carrying capacity)
Enlarged liver
Enlarged spleen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are 4 symptoms of anaemia?

A

Tired/weak
Dizzy
SOB (shortness of breath)
Palpitations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What 6 things can be investigated for anaemia?

A

Medical history
FBC (full blood count)
FOB (faecal occult blood)- blood in patients stool
Endoscopy/ colonoscopy
Renal function- patients with chronic renal disease will often become anaemic
Bone marrow examination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Name 3 ways anaemia can be treated

A

Replace haematinics (general term for nutrients required to make RBCs) e.g. Iron, folic acid, Vit b12

Blood transfusions

Erythropoietin- hormone; increases rate of RBC production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What 3 functions does blood have?

A

Transport of nutrients
Removal of waste
Transport of host defences

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the 5 components of blood?

A
Cell component
Plasma proteins: albumin
                            globulin
Lipids
Nutrients
Water
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Define leukopenia

A

Low white cell count

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Define thrombocytopenia

A

Low platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Define pancytopenia

A

All cells reduced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Define polycythaemia

A

Raised Hb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Define leukocytosis

A

Raised WCC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Define thrombocythaemia

A

Raised platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Define leukaemia

A
Neoplastic (abnormal) proliferation of white cells
Usually disseminated (wide spread)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Define lymphoma

A

Neoplastic proliferation of white cells

Usually a solid tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

In what 2 cases would someone receive a blood transfusion?

A

When one or more components of the blood has to be replaced quickly e.g. RBCs, platelets, clotting factors

When bone marrow cannot produce blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What 3 complications can result from a blood transfusion and what can they cause?

A
  1. Incompatible blood
    - Cell lysis: fever, jaundice, death
  2. Fluid overload
    - Heart failure
  3. Transmission of infection
    - Blood borne viruses e.g. Hep B, HIV
    - Prion disease
    - Bacterial infections e.g. Syphilis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Describe the transfusion protocol (3 steps)

A

Blood is filtered to remove any clots
The patients temperature, pulse and BP are monitored every 15 minutes during transfusion
Transfusion is stopped if there is any significant change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Define haemostasis

A

The arrest of bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What 3 components can result in a haemostatic disorder?

A

Vascular component- retraction of vessel (collagen disorder)
Cellular component- platelets number and function
Coagulation component- adequate clotting
- adequate clot lysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

How would you investigate the platelet number and platelet function for haemostatic disorders?

A

Full blood count

‘Bleeding time’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How long does it take to make new platelets?

A

7-10 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are 3 visual signs of haemostatic disorders?

A

Purpura- skin rash from bleeding into skin from capillaries
Ecchymosis- bruise from release of blood into tissues either from injury or spontaneous leaking from vessels
Petechiae- small round flat dark red spots caused by bleeding into skin or beneath mucous membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the 3 types of inherited bleeding disorders?

A

Haemophilia A
Haemophilia B
Von Willebrands disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are 2 ways to develop an acquired bleeding disorder?

A

Warfarin

Liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Define porphyria
How many does it affect
What are the 2 types

A

Abnormality of haem metabolism
1 in 10000 population affected
1. Hepatic porphyria
2. Erythropoietic porphyria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the clinical effects of porphyria?

A

Photosensitive rash
Neuropsychiatric disturbance in acute attacks (motor and sensory changes, seizures)
Hypertension
Tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Name 5 triggers of porphyria

A
Many drugs
Pregnancy
Acute infections
Alcohol
Fasting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What name is given to low Hb

A

Anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What name is given to low WCC?

A

Leukopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What name is given to low platelet count?

A

Thrombocytopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What name is given to raised Hb?

A

Polycythaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What name is given to raised WCC?

A

Leukocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What name is given to raised platelet count?

A

Thombocythaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What name is given when all cell types are reduced?

A

Pancytopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What 3 features of cancer cells cause them to be malignant?

A

Uncontrolled proliferation
Loss of apoptosis (cells don’t self destruct)
Loss of normal functions/products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Name 4 causes of leukaemia/lymphoma (aetiology)

A

Inherited DNA mutations (some associated with known syndromes)
Chemicals
Radiation
Viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is a blast?

A

Immature cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What group of cancers does leukaemia refer to?

A

Cancers of the bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What does leukaemia prevent and what 3 things does this result in?

A

Prevents normal manufacture of blood

Anaemia
Infections: neutropenia- decreased WBC so increased susceptibility to disease
Bleeding: thrombocytopenia- decreased platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the pathogenesis (disease process) of leukaemia?

A
  1. Clonal proliferation
  2. Replacement of bone marrow
  3. Increased marginalisation of productive normal marrow resulting in:
    - marrow failure
    - organ infiltration (leading to organ failure)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Name 5 things that can be a clinical presentation of leukaemia

A

Anaemia
Neutropenia- decreased WBCs
Thrombocytopenia- decreased platelets
Lymphadenopathy- neck lumps due to enlarged lymph nodes
Splenomegaly/ Hepatomegaly - swollen abdomen
Bone pain- especially in children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What 3 things can be clinical presentations of neutropenia?

A
  1. Infections associated with portals of entry e.g. Tonsillitis, pneumonia, thrush
  2. Reactivation of latent (dormant) infections
  3. Increased severity and frequency of infections, and can rapidly lead to systemic infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Name 2 symptoms of neutropenia

A

Recurrent infections

Unusual severity of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Name 3 signs of neutropenia

A

Unusual patterns of infection and rapid spread
Will respond to treatment but recur
Signs of systemic involvement e.g. Fever, rigors (shivers), chills

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What investigation can be done for neutropenia?

A

Unusual pathogens, usually bacterial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are 5 symptoms of thrombocytopenia?

A
Bruise easily/spontaneously 
Minor cuts fail to clot
Gingival bleeding
Nose bleeds
Menorrhagia- abnormally heavy menstrual bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Name 4 signs of thrombocytopenia

A

Bruising
Petechiae- small dark bruises cause by bleeding into skin
Bleeding on probing
Bleeding/bruising following procedure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is the peak age for acute lymphoblastic leukaemia?

A

4 y/o

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is the incidence of acute lymphoblastic leukaemia?

A

25 per 1,000,000 per year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is the incidence of acute myeloid leukaemia?

A

25 cases per 1,000,000 per year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

In what age group is acute myeloid leukaemia most prevalent?

A

The elderly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is the most common form of leukaemia?

A

Chronic lymphocytic (lymphoid) leukaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is lymphoma?

A

Clonal proliferation of lymphocytes arising in lymph node or associated tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is the incidence of lymphoma?

A

200 cases per 1,000,000 per year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the ratio of number of suffers of non-hodgkins lymphoma to Hodgkin’s lymphoma?

A

6:1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Define Stage I of lymphoma tumour staging

A

Single lymph node region or single extra lymphatic site involved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Define Stage II of lymphoma tumour staging

A

Two or more sites on same side of diaphragm involved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Define Stage III of lymphoma tumour staging

A

Both sides of diaphragm involved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Define Stage IV of lymphoma staging

A

Diffuse involvement of extra lymphatic (and nodal disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What 3 tests may be used to help stage a tumour?

A

CT
PET
MRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What 3 things does tumour staging take into account?

A

Number of nodes involved and site
Extra nodal involvement
Systemic symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is the peak age of Hodgkin lymphoma?

A

15-40 y/o

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is the clinical presentation of Hodgkin lymphoma?

A

Painless lymphadenopathy- enlargement of lymph nodes
Fever, night sweats, weight loss, itching
Infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are the 2 types of non-Hodgkin lymphoma and how are the divided?

A

B-cell: 85%

T-cell: 15%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is the peak age to develop NHL?

A

Any age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What are 3 possible causes of NHL? (Aetiology)

A
  1. Microbial factors e.g. EBV
  2. Autoimmune disease e.g. Rheumatoid arthritis
  3. Immunosuppression e.g. AIDS, post transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Name 4 aspects of clinical presentation of NHL compared to HL

A
  1. Lymphadenopathy- enlarged lymph nodes (often widely disseminated)
  2. Extra-nodal disease more common- e.g. Oropharyngeal involvement (noisy breathing and sore throat)
  3. Symptoms of marrow failure e.g. Aplastic anaemia
  4. Constitutional symptoms less common e.g. Fever, weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Define Multiple Myeloma

A

The malignant proliferation of plasma cells (WBCs) in bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What are 3 clinical features of Multiple Myelomas?

A
  1. Monoclonal paraprotein released by malignant plasma cells found in the blood and urine
  2. Lytic bone lesions (destruction of bone cells)- pain and fracture likely
  3. Excess plasma cells in bone marrow- leading to marrow failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Name 5 treatment for haematological malignancies

A
Chemotherapy
Radiotherapy
Monoclonal antibodies
Haemopoietic stem cell transplantation
Supportive therapy e.g. Pain control, nutrition, psychological support
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What does chemotherapy target?

A

Targets cells with high turnover rate (e.g. Mucosa) to induce cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is a disadvantage of chemotherapy targeting?

A

Results in many unwanted effects in normal high turn over tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What are 3 side effects of chemotherapy?

A

Hair loss
Nausea and vomiting
Tiredness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What is a long term risk of chemotherapy?

A

Risk of oncogenesis (development of new abnormal growth) in surviving patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Name 3 examples of chemo drugs

A

Methotrexate
Cyclophosphamide
Vincristine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Define radiotherapy

A

Cytotoxic effect of ionising radiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Describe the treatment of monoclonal antibodies

A

Monoclonal antibodies specific to cancer cell antigens are produced artificially in large quantities and given to patient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is a disadvantage of monoclonal antibodies and how are the drugs recognised?

A

Very expensive to produce and deliver

Drug names end in “-mab”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Define allogeneic stem cell transplant

A

Stem cell from live donor, either relative or stranger who has been matched

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Define autologous stem cell transplant

A

Stem cells from patient themselves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Name 6 oral manifestations of haematological malignancies

A
Gingival swelling
Mucosal pallor
Spontaneous bleeding
Petechiae
Oral ulceration
Infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What importance does the mouth have in patients receiving cancer therapy?

A

The mouth is a potential source of infection which can be life threatening in an immunocompromised patient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Pre-cancer treatment, what preventative measures would a dentist take with the patient?

A

OHI
Dietary advice
If gingival disease- alcohol free chlorohexidine
Applicator trays for fluoride gel and tooth mousse
High fluoride toothpaste
High fluoride varnish application

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Define mucositis

A

Acute inflammation of the mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What preventative management can be done to for patients with mucositis?

A

Improve OH of patient so decreased healing time
Ill fitting dentures/sharp restorations adjusted
Mucosal shields (if radiotherapy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Name 6 ways mucositis can be managed

A
  1. Difflam spray
  2. 2% lidocaine mouthwash prior to eating
  3. Gelclair
  4. Chlorohexidine
  5. Ice chips- oral cooking
  6. Cell transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Define xerostomia

A

Thick, acidic and viscous saliva with loss of protective functions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What 2 approaches are there to treat xerostomia?

A

Saliva stimulation

Saliva replacement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Name 4 ways to for stimulate saliva

A

Chewing sugar free gum
Pilocarpine
Acupuncture
Acid pastilles (contraindicated in dentate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Name 4 ways to replace saliva

A

Taking sips of water
Saliva orthana
Biotene
Bio Astra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What 4 things should patients with xerostomia avoid?

A

Hard, spicy, strong flavoured foods
Foaming toothpaste
Alcohol and smoking tobacco
Fizzy drinks and fruit drinks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Name 3 irreversible risk factors of CV disease

A

Age
Sex
Family history

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Name 4 reversible behavioural risk factors for CV disease

A

Smoking
Obesity
Diet
Exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Name 4 reversible medical risk factors for CV disease

A

Hypertension
Hyperlipidaemia (high cholesterol)
Diabetes
Stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Name 8 risk factors for hypertension

A
Age
Race
Obesity
Alcohol
Family history
Pregnancy
Stress
Drugs e.g. non-steroidal, oral contraceptive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Name 6 ways you would test if someone is at high risk of CV disease

A
Family history
Diet
Smoking
Test cholesterol
Test blood pressure
Test for type 2 diabetes
112
Q

Name 4 ways someone can present with CV disease

A

Angina
Myocardial infarction
Stroke
Claudication

113
Q

Name 4 approaches to preventing/controlling CV disease

A
  1. Lifestyle changes
  2. Control total cholesterol- statin treatment
    - reduce cholesterol to
114
Q

Name 2 ways drugs are used in CV system and give examples for each

A
  1. Prevent FURTHER disease
    - anti platelet drugs
    - lipid lowering drugs
    - anti-arrhythmics
  2. To reduce symptoms of current current disease
    - diuretics
    - anti-arrhythmics
    - nitrates
    - calcium channel blockers
    - ACE inhibitors
115
Q

Give three examples of anti-platelet drugs

A

Aspirin
Clopidrogel
Dipyridamole

116
Q

How does aspirin work?

A

It inhibits platelet aggregation
By altering balance between Throboxane A2 and Prostacyclin

It is irreversible for the life of the platelet

117
Q

How does Clopidrogel work?

A

It inhibits ADP induced platelet aggregation

118
Q

How does Dipyridamole work?

A

It inhibits platelet phosphodiesterase (enzyme which breaks phosphodiester bonds)

119
Q

How do Lipid-Lowering drugs work?

A

They inhibit cholesterol synthesis in liver

Therefore reducing both the total cholesterol and LDL cholesterol

120
Q

What side effect can lipid lowering drugs have?

A

Possible myositis (muscle disease) with some drug interactions

121
Q

Give an example of an anti-arrhythmics and 2 types of it

A

Beta-adrenergic blockers (beta blockers)

Atenolol- selective: B1 only
Propranolol- non-selective: B1 and B2

122
Q

What 3 effects so beta blockers have?

A
  1. Prevent increase in HR
    - cause postural hypotension
    - prevent unusual heart rhythms which can lead to a MI
  2. Reduce heart efficiency
    - make heart failure once
  3. Block beta receptors in lungs
    - make asthma worse/difficult to treat
123
Q

How do diuretics work?

A

They increase salt and water loss therefore decreasing plasma volume and decreasing cardiac workload

124
Q

What is a side effect of diuretics?

A

Can lead to Na+/K+ imbalance if not monitored

125
Q

Name 2 types of nitrates

A
Glyceryl trinitrate (GTN)- short acting
Isosorbide Mononitrate- long acting
126
Q

What 3 ways do nitrates work?

A
  1. Dilate veins- reduce preload to heart
  2. Dilate resistance arteries- reduce cardiac workload (afterload)
    - reduce cardiac oxygen consumption
  3. Dilate collateral coronary artery supply- reduce anginal pain
127
Q

What 3 ways can nitrates be administered and why?

A

Sublingual
Transdermal
Intravenous

Inactivated by first pass metabolism

128
Q

What side effect do nitrates have?

A

Headache

129
Q

What 2 ways do calcium channel blockers work?

A

They block calcium channels in smooth muscle

Some are more active in heart muscle

  • reduces strength of heart contractions
  • e.g. Verapamil

Some are more active on peripheral blood vessels

  • relaxation and vasodilation
  • e.g. Nifedipine, amlodipine
130
Q

Name a side effect of calcium channel blockers

A

Some cause gingival hyperplasia (increased number of cells)

- those acting on peripheral blood vessels

131
Q

How do Angiotensin Converting Enzyme (ACE) inhibitors work and give examples?

A

Inhibit conversion of Angiotensin I to Angiotensin II
Prevents aldosterone dependant reabsorption of salt and water
Therefore decreases BP

E.g. Enalapril, ramapril, lisinopril

132
Q

Name 2 side effects of ACE inhibitors

A

Cough

Hypotension

133
Q

What other drugs have the same effect as ACE inhibitors?

A

Angiotensin II blockers (e.g. Losartan)

Inhibit same system but use different mechanism

134
Q

Define thrombosis

A

The formation of a solid or semi-solid mass from the constituents of the blood within the vascular system during life

135
Q

Name 3 factors predisposing to thrombosis

A
  1. Abnormality of blood vessel wall particularly the endothelium (e.g. Atheroma)
  2. Alterations in blood flow- stasis and/or turbulence
  3. Hypercoagulable blood
136
Q

Name 4 ways blood vessels are damaged

A

Atheroma
Inflammation
Trauma
Bacterial toxins

137
Q

Name 5 occurrences that blood is hypercoagulable

A
Following surgery
In disseminated cancer
During pregnancy
While taking oral contraceptive pill
In genetic deficiency states of blood clotting factors
138
Q

Name 4 locations of thrombi

A

Arterial
Venous
Cardiac
Capillaries

139
Q

Name 4 causes of DVTs

A

Bed ridden following surgery
Heart failure
Severe tissue injury
Pelvic tumours

140
Q

Name the 3 fates of thrombi

A
  1. Removal by fibrinolytic system
  2. Organisation- replacement fibrosis
  3. Embolism
141
Q

Define embolism

A

Movement of solid, liquid or gaseous material through the blood and its impaction in a blood vessel at a site distant from its origin

142
Q

What are the 2 main types of embolism and explain their mechanism

A

Systemic thrombo-embolism
- thrombi form on left side of heart or in arteries, break free and Impact distally in systemic arterial tree causing ischaemia or infarction due to obstruction of blood flow

Pulmonary Thrombo-embolism

  • thrombi arise in deep veins of leg or pelvis
  • if large, emboli obstruct main pulmonary arteries arising from right side of heart (sudden death)
  • if smaller, emboli obstruct smaller, more peripheral pulmonary artery branch (clinically silent)
143
Q

Define atherosclerosis

A

Patches (plaques) of thickening of artery lining

Due mainly to accumulation of plasma lipids, proliferation of smooth muscle and formation of fibrous tissue

144
Q

Site of occurrence of atherosclerosis

A

Any ARTERY

145
Q

Name 4 clinical effects of atherosclerosis

A
  1. Arterial narrowing sufficient to cause ischaemia
  2. Predisposes to throbosis because of lumenal occlusion of artery
  3. Embolism
  4. Weakening of artery wall leading to aneurysm formation (swelling in wall of artery)
146
Q

Name 6 major risk factors of atherosclerosis (aetiology)

A
  1. Age- atheroma progresses slowly throughout adult life
  2. Sex- lower incidence in women until menopause
  3. Plasma lipids- hyperlipidaemia predisposes to atheroma
  4. Hypertension- atheroma risk increases with increasing BP
  5. Cigarette smoking
  6. Diabetes mellitus
147
Q

Define ischaemia

A

Deficient supply of blood to an area such that it becomes hypoxic (deficient 02 to tissues)

148
Q

What is the aetiology of ischaemia?

A

Most commonly due to narrowing or obstruction of arterial supply caused by atheroma, thrombosis or embolism

149
Q

Name the 2 types of ischaemia and their clinical effects

A
  1. Partial ischaemia (blood flow reduced to a level that is adequate while resting, but hypoxia develops at times of increased oxygen demand e.g. Exercise)

a) Angina pectoris- myocardial ischaemia due to narrowed, atheromatous coronary arteries- often induced by exercise and causes sever crushing central chest pain
b) Intermittent claudication- atheromatous narrowing of leg arteries leading to pain in calf muscles induced by exercise

  1. Complete ischaemia- no blood flow leading to tissue infarction (organs supplied by blocked artery dies)
150
Q

Define infarction and give its aetiology

A

Tissue death or necrosis due to reduction or loss of blood supply.

Usually due to arterial narrowing or occlusion which is often atheromatous and/or thrombotic in nature

151
Q

What 2 things is tissue susceptibility to infarction dependant on?

A
  1. Metabolic rate of tissue- brain more susceptible than fibrous tissue
  2. Anatomy of vascular supply e.g. Occlusion of an end artery in brain- infarction
152
Q

What is the fate of infarcts?

A

Dead tissue incites an inflammatory reaction followed by granulation tissue and eventually fibrous scar replacement

153
Q

Define ischaemic heart disease and give its aetiology

A

An imbalance between myocardial oxygen supply and demand

Most commonly due to narrowed atheromatous coronary arteries and/or thrombosis

154
Q

Name 3 clinical effects IHD

A

Angina pectoris- myocardial ischaemia due to narrowed coronary arteries

Sudden cardiac death

Myocardial infarction

155
Q

Name 3 complications of MIs

A

Cardiac arrhythmias
Cardiac failure/ cardiogenic shock
Mural thrombosis and/or thromboembolism

156
Q

Define hypertension

A

Raised systemic arterial pressure with systolic >140mmHg, diastolic >90mmHg

157
Q

What are the two classifications of hypertension?

A

Primary (essential, idiopathic)- no detectable underlying cause

Secondary- resulting from renal diseases or adrenal diseases (e.g. Cushing’s)

158
Q

Name 3 pathological effects of hypertension

A
  1. Risk factor for development of atheroma, cardiac failure, renal failure and cerebral haemorrhage
  2. In heart, can lead to left ventricular hypertrophy
  3. In brain, associated with rupture of micro aneurysms
159
Q

What is the aetiology of both types of hypertension?

A

Primary- inherited defect of sodium handling by cell membranes (e.g. In the kidney)

Secondary- the renin/angiotensin/aldosterone system is often involved

160
Q

Define cardiac failure

A

Cardiac failure occurs when cardiac function (pump) fails to maintain a circulation adequate for metabolic needs of body DESPITE adequate blood volume

161
Q

Name 3 causes of cardiac failure

A
  1. Myocardial injury e.g MI
  2. Increased workload e.g hypertension, valvular heart disease
  3. Abnormal cardiac rhythm
162
Q

Name the 3 manifestations of cardiac failure

A

Left ventricular failure
Right ventricular failure
Biventricular (congestive) cardiac failure

163
Q

Define shock

A

Widespread hypofusion (low flow) of tissues due to inadequate effective circulating blood volume

As a result there is systemic cellular hypoxia, increased anaerobic metabolism and progressive derangement of cellular function

164
Q

Name and explain the 3 types of shock

A
  1. Hypovolaemic shock
    May be due to: haemorrhage or fluid loss
    Overall effect: critical reduction in blood/plasma volume (not enough blood)
  2. Cardiogenic shock
    May be due to: MI, cardiac rupture, massive pulmonary thromboembolism
    Overall effect: failure of myocardial pump due to damage or blood flow obstruction (adequate blood volume, but inadequate circulation)
  3. Septic shock
    Due to: bacterial infection
    Overall effect: loss of vascular tone, pooling of blood in peripheral vessels (normal blood volume, abnormal blood distribution)
165
Q

Name and describe the 3 pathological stages of shock

A
  1. Compensated shock- mildly decreased BP, increased HR, peripheral vasoconstriction so skin cold and clammy
  2. Decompensated shock- if circulatory deficiency persists compensatory mechanisms fail so further decrease in BP, increase in HR, systemic tissue hypoxia and worsening tissue damage
  3. Irreversible shock- if circulatory defects not corrected, cell necrosis occurs in vital organs leading to coma and death
166
Q

Define valve stenosis

A

Decrease in size of valve orifice so increased pressure load in preceding cardiac chamber

167
Q

Define valve incompetence

A

Failure of complete valve closure, causes regurgitation of blood so increased volume load for cardiac chambers on both sides of valve

168
Q

Define infective endocarditis (IE)

A

Colonisation of normal or damaged heart valves by microorganisms with the formation of friable, infected thrombi (vegetations) on the surface of the valve cusps and resultant valve injury

169
Q

Name 3 predisposing factors to infective endocarditis

A
  1. Conditions which cause bacteraemia or septicaemia e.g. Dental procedures
  2. Abnormalities of heart valves whether congenital or acquired
  3. Immunosuppressed host
170
Q

Name 3 clinical effects of bacterial endocarditis

A
  1. Injury to valves (incompetence and/or stenosis) or adjacent myocardium (abscess formation, perforation)
  2. Embolic events
  3. Fever, malaise, weight loss
171
Q

Name the 2 main types of angina

A

‘Classical’ angina

‘Unstable’ angina

172
Q

Name 4 symptoms of ‘classical’ angina

A

No pain at rest
Pain with certain level of exertion
Pain relieved by rest
Gradual deterioration

173
Q

Name signs of ‘classical’ angina

A

Often none

174
Q

Name 5 investigations of angina

A
ECG- resting and exercise
Eliminate other diseases e.g. Thyroid, anaemia, valve
Angiography
Echocardiography 
Isotope studies
175
Q

Name the 2 main treatments of angina and ways they are done (2 each)

A
  1. Reduce oxygen demands of heart
    - reduce afterload (blood pressure)
    - reduce preload (venous pressure)
  2. Increase oxygen delivery to tissues
    - dilate blocked/ narrowed vessels (angioplasty)
    - bypass blocked/narrowed vessels (CABG)
176
Q

Name 2 non-drug therapies for angina

A
  1. Live with limitations

2. Modify risk factors- stop smoking, graded exercise programme, improve diet/ control cholesterol

177
Q

Name 4 situations drug therapy is used to treat angina and give examples of the drugs used

A
  1. To reduce MI risk– aspirin
  2. To treat hypertension- diuretics, Ca channel antagonists
    - ACE inhibitors, Beta blockers
  3. To reduce preload/dilate coronary vessels- nitrates
  4. In emergency treatments- GTN spray/tab
178
Q

Where is peripheral vascular disease usually located and what causes it?

A

Usually lower limb

Atheroma in femoral vessels

179
Q

Name 5 characteristics of peripheral vascular disease

A
  1. Claudication pain in limb on exercise (cramping)
  2. Limitation of function
  3. Poor wound healing
  4. May lead to tissue necrosis or gangrene
  5. Aggravated by CV risk factors
180
Q

What are the 2 main strategies for infarction and how are these done?

A
  1. Reduce tissue loss from necrosis
    - open blood flow to ischaemic tissues (thrombolysis, angioplasty)
    - bypass obstruction (CABG, femoral bypass)
  2. Prevent further episode
    - risk factor management
    - aspirin
181
Q

Name 3 causes of a brain infarction (stroke)

A

Usually embolism from atheroma
Occasionally cerebral bleed
Rarely vessel thrombosis (good collateral blood supply)

182
Q

Name a stroke that has symptoms lasting less than 24 hours

A

Transient ischaemic attacks (TIAs)

183
Q

What are the symptoms and signs of MIs?

A

Central chest pain, nausea, pale, sweaty

184
Q

Name 2 MI investigations

A
  1. ECG- ST segment elevating/ T wave abnormalities
  2. Cardiac enzymes- troponin
    - creatinine kinase
    - LDH and AST
185
Q

What is the primary care of MIs?

A

Aim to get to hospital
Analgesia (pain killer), aspirin, reassurance
BLS if required (cardiac arrest)

186
Q

What hospital care is given to MIs?

A

Thrombolysis if indicated, or acute angioplasty and stenting
Drug treatment to reduce tissue damage
Prevent reoccurence/complications

187
Q

Name 2 drugs that can be used for thrombolysis

A

Streptokinase

TPA

188
Q

Name 6 contraindications of thrombolysis

A
Injury
Surgery
Severe hypertension
Diabetic eye disease
Liver disease
Pregnancy
189
Q

Name 6 complications of MIs

A
  1. Death
  2. Arrhythmias
  3. Heart failure
  4. Ventricular hypofunction and thrombosis
    • damaged ventricular wall, clots could form on wall due to lack of
      movement
  5. DVT and pulmonary embolism
  6. Complication of thrombolysis
190
Q

Define bacteraemia

A

It is the transient (short lived) presence of bacteria in the bloodstream

191
Q

Define septicaemia

A

It is the persistent presence of bacteria in the blood stream, with attendant signs and symptoms

192
Q

Define sepsis

A

“The host response to infection”

193
Q

What 4 things make up the SIRS criteria?

A

Chills and fevers
High HR
Panting, increased CO2 in blood
High/low WCC

194
Q

What criteria equals sepsis

A

Infection
+
SIRS criteria (at least 2)

195
Q

What criteria equals severe sepsis?

Give its mortality rate

A

Sepsis
+
Organ dysfunction

40% mortality

196
Q

What criteria equals septic shock?

Give its mortality rate

A

Sepsis
+
Shock refractory to fluid resuscitation

60% mortality

197
Q

Name 4 reactions of sepsis

A

Endothelial damage
Micro vascular dysfunction
Impaired tissue oxygenation
Organ injury

198
Q

What results in clinical features of gram negative septicaemia?

A

Result from endotoxin release (poison within bacteria)

199
Q

What 4 events make people most susceptible to gram negative septicaemia?

A

Major GI surgery
Immunosuppressive chemotherapy
Burns
Extremes of age

200
Q

Where are most gram negative septicaemias acquired?

A

Hospital acquired

201
Q

What is the most common isolate of gram negative septicaemia?

A

E. Coli

202
Q

What causes clinical features in gram positive septicaemia?

A

Teichoic acid and peptidoglycan from cell wall of bacteria

203
Q

Name 4 sources of infection of gram positive septicaemia

A
  1. Skin e.g. Indwelling catheters
  2. Respiratory tract e.g. S. Pneumoniae
  3. Bone/joint infections e.g. S. Aureus
  4. Oral cavity
204
Q

Who is susceptible to fungal septicaemia and what is its most common isolate?

A

Immunosuppressed hosts e.g. Haematological malignancy, AIDS

Candida albicans

205
Q

How is septicaemia treated?

A

IV fluids, oxygen and other supportive measures

‘Blind’, empirical IV antibiotics- broad spectrum given as soon as infection suspected

Identify and remove source where possible e.g. Foreign body, catheter

206
Q

Define infective endocarditis

A

Microbial infection of endothelial lining of heart

Usually manifests are vegetations on heart valves

207
Q

What 6 types of patients are ‘at risk’ of infective endocarditis?

A
  1. Acquired valvular heart disease
  2. Prosthetic heart valve
  3. Structural congenital heart disease (abnormalities of heart tissue)
  4. Previous endocarditis
  5. Hypertrophic cardiomyopathy (enlarged heart)
  6. Recurrent bacteraemia
208
Q

Name 3 clinical feature of IE

A

Fever
Heart murmur
Splenomegaly

209
Q

Name 2 common microbial culprits of IE

A

Streptococci – oral streptococci

Staphylococci– staphylococcus aureus

210
Q

Where is the primary habitat of oral streptococci?

A

Oral cavity/ upper respiratory tract

211
Q

Name 4 ways IE is diagnosed

A
  1. Clinical signs
  2. Blood cultures (3 sets over 24hrs)
  3. Echocardiography- visualise lesions
  4. DUKE criteria
212
Q

Name 2 outcomes of hypertension and what they can lead to

A
  1. Accelerated atherosclerosis
    - MI
    - Stroke
    - Peripheral vascular disease
  2. Renal failure
213
Q

What are common causes of hypertension?

A

There are none

214
Q

Name 2 rare causes of hypertension

A
  1. Renal artery stenosis (narrowing)
  2. Endocrine tumours
    - phaechromocytoma
    - Cushing’s syndrome
215
Q

What are signs of symptoms of hypertension?

A

Usually none

May get headache
May get TIAs

216
Q

Name 5 ways hypertension can be investigated

A
  1. Urinalysis- look at what kidneys are excreting in urine
  2. Serum biochemistry
  3. Serum lipids
  4. ECG
  5. Renal ultrasound, renal angiography, hormone estimations
217
Q

What is the aim of treating hypertension

A

To get BP to less than 140/90mmHg

218
Q

Name 2 ways hypertension can be treated

A
  1. Modify risk factors- smoking, exercise, weight

2. Single daily drug dose

219
Q

Define heart failure

A

“output of heart incapable of meeting demands of tissues”

220
Q

Give examples of both high and low output cardiac failure

A

High output failure- anaemia, thyrotoxicosis

Low output failure- cardiac defect e.g. MI, valve disease

221
Q

What is the biggest cause of heart failure?

A

Ischaemic heart disease

222
Q

Name 5 things that can cause low output heart failure (aetiology)

A
  1. Heart muscle disease e.g. MI
  2. Pressure overload e.g. Hypertension, aortic stenosis
  3. Volume overload e.g. Mitral/aortic incompetence
  4. Arrhythmias e.g. Atrial fibrillation, heart block
  5. Drugs e.g. Beta blockers, corticosteroids
223
Q

Name 8 symptoms of heart failure

A
SOB
Ankle swelling
Chronic lack of energy
Difficulty sleeping due to breathing
Swollen/tender abdomen
Cough with frothy sputum
Increased urination at night
Confusion and/or impaired memory
224
Q

Name signs of left heart failure

A

LUNGS and systolic effects

- dyspnoea (difficulty breathing), tachycardia, low BP, low volume pulse

225
Q

Name signs of right heart failure

A

Venous pressure elevated
- swollen ankles, ascites (accumulation of fluid- abdominal swelling), raised JVP (jugular venous pressure), tender enlarged liver, poor GI absorption

226
Q

What treatment would be given for acute heart failure

A

Emergency hospital management

- O2, morphine, frusemide (diuretic used to treat fluid retention)

227
Q

What treatment would be given for chronic heart failure?

A

Community based

  • improve myocardial function
  • decrease ‘compensation’ effects (decrease salt and water retention)
  • where possible, treat cause
228
Q

What 4 types of drugs may be used in chronic heart failure and why

A
  1. Diuretics- increase salt and water loss
  2. ACE inhibitors- decrease salt and water retention
  3. Nitrates- decrease venous filling pressure
  4. Inotropes e.g. Digoxin
229
Q

What drugs would be stopped when treating heart failure and why

A

Stop negative inotropes e.g. Beta blockers

- decrease HR and makes heart beat less efficiently

230
Q

Name the 4 heart valves and state what side they are on

A

Left- aortic, mitral (bicuspid)

Right- pulmonary, tricuspid

231
Q

The heart valves on what side of the heart most commonly fail and why?

A

Left side

Valves have to do more work under higher pressure

232
Q

What 4 things cause valve disease?

A
  1. Congenital abnormality e.g bicuspid aortic valve (instead of tricuspid)
  2. MI
  3. Rheumatic fever
    - MAY cause valve damage
    - Patients with history MUST be investigated for RHD
    - If no disease, no antibiotic prophylaxis is required
  4. Dilation of aortic root
233
Q

What 2 types of replacement valves are there?

A
Mechanical
Porcine (pig valve)
234
Q

Give 3 facts about porcine valves

A

Only last 10 years
Do not need anticoagulant
Good for elderly and young

235
Q

Name 4 congenital heart defects and describe them

A
  1. Atrial septal defects- hole in wall between the 2 atria
  2. Ventricular septal defects- hole in wall between 2 ventricles
  3. Patent ductus arteriosus- opening between 2 major blood vessels leading from heart (usually closes after birth)
  4. Great vessel malformations
236
Q

What is cyanosis, give the 2 types and when it occurs

A

Bluish discolouration of skin and mucous membranes resulting from inadequate amounts of O2 in blood

Central- from congenital heart disease
Peripheral- cold environment

Exists when there is 5g/dL or more if DEoxygenated Hb in blood

237
Q

What is the term for a fast heart rate/rhythm and give 2 examples

A

Tachy arrhythmias

  • atrial fibrillation
  • ventricular tachycardia– diastolic time decreases so chambers less filled
238
Q

What is the term for slow heart rates/rhythms and give 2 examples

A

Brady arrhythmias

  • heart block (electrical impulses impaired)
  • drug induced– beta blockers, digoxin
239
Q

What are pace makers used to treat and how do they work?

A

Treat bradyarrhythmias

Senses electrical impulses in heart and stimulates heart beat if one does not occur

240
Q

What is the term for a normal heart rhythm and explain the wave

A

Sinus rhythm

P-wave: atrial depolarisation
QRS complex: ventricular depolarisation
T-wave: ventricular repolarisation

Q wave most seen in patients who’ve suffered MIs

241
Q

What is the term for a heart no longer beating and why is this the case?

A

Asystole

No electrical activity (defibrillator won’t help)

242
Q

Define ventricular fibrillation

A

Unstable electrical activity (usually during MI)
No cardiac output
Treat with defibrillation

243
Q

Name 5 dental treatments that would require no special care for those with coagulation problems

A
Hygiene therapy
RPDs
Restorative (including crowns and bridges)
Endodontics
Orthodontics
244
Q

Name 4 dental treatments that would require special care for those with coagulation problems

A

Extractions
Minor oral surgery
Periodontal surgery
Biopsies

245
Q

What 5 things need to be considered/done when performing extractions/surgery on patient with coagulation problems

A
  1. Appropriate monitoring prior to treatment
  2. Atraumatic treatment
  3. Consider antibiotics
  4. Observe to ensure haemostasis (arrest in bleeding)
  5. Comprehensive post-op instructions
246
Q

What are the 2 main types of antithrombotic medication

A

Oral anti coagulation

Antiplatelet medications

247
Q

What are 5 indications for the use of oral anticoagulants?

A
Atrial fibrillation
DVT
Heart valve disease
Mechanical heart valves
Thrombophilia
248
Q

Name the 4 main types of oral anticoagulants available and an example of each

A
  1. Coumarins e.g. Warfarin
  2. Indanediones e.g. Phenindione
  3. Direct thrombin (DT) inhibitor e.g. Dabigatian
  4. Factor Xa inhibitor e.g. Apixaban
249
Q

What is the daily dose of warfarin?

A

1-15mg

250
Q

How is warfarin response measured?

A

INR (international normalised ratio)

251
Q

What is INR?

A

Ratio of the patients prothrombin time (PT) to a standardised ‘normal’ PT

INR= patient PT/mean normal PT

252
Q

What is the target INR for

  1. Mechanical heart valves
  2. Recurrent VTE while adequately anti coagulable
  3. Other cases
A
  1. 3.0-4.0
  2. 3.0-4.0
  3. 2.0-3.0
253
Q

Name 4 medications that should be avoided by people with coagulation problems (on warfarin)

A

Aspirin (as an analgesic)
Co-proxamol
Ketorolac
Azole anti-fungal drugs

254
Q

What is major risk for warfarin users

A

Haemorrhage

255
Q

Name 4 characteristics of DT and FXa inhibitors

A

No routine blood tests required
Standard dose for each patient
Tablets take either once or twice a day
No reversal agent available

256
Q

Name 5 anti-platelet medications

A
Low dose aspirin
Clopidogrel 
Dipyridamole 
Tirofaban 
Ticagrelor
257
Q

What 3 effects do antiplatelet drugs have on clotting

A

Inhibit platelet aggregation

Inhibit thrombosis formation

258
Q

Define inherited bleeding disorders

A

A genetic defect which effects the coagulation of blood

259
Q

Name 3 things inherited bleeding disorders may affect

A
  1. Coagulation cascade
    - a reduction in one or more of the coagulation factors
  2. Platelets
    - number
    - function
  3. A combined deficieny
260
Q

Name 4 common inherited bleeding disorders and give the different subtypes for each (where applicable)

A
  1. Factor VIII deficiency
    - haemophilia
    - haemophilia A
  2. Factor IX deficiency
    - Christmas disease
    - Haemophila B
  3. Von Willebrands disease (reduced factor VIII level)
  4. Factor XI deficiency
261
Q

Describe the inheritance of factor VIII and IX deficiencies

A

Sex-linked recessive

Males are affected
Females are carriers

262
Q

How are severe and moderate cases of factor VIII deficiency treated

A

Require use of recombinant factor VIII

263
Q

How are mild sufferers and carriers of factor VIII deficiency treated?

A

Majority respond to DDAVP

Very mild cases may only require oral tranexamic acid

264
Q

How are sufferers of Factor IX deficiency treated?

A

Require recombinant factor IX

Does not respond to DDAVP

265
Q

Describe the inheritance of Von Willebrands disease

A

Autosomal dominant

Sexes affected equally

266
Q

How is Von Willebrands disease treated

A

Majority respond to DDAVP

Very mild cases may only need oral tranexamic acid

267
Q

Name 3 ‘safe’ LA injection sites for patients with bleeding disorders

A

Buccal infiltration
Intraligamentary injections
Intrapapillary injections

268
Q

Name 3 ‘dangerous’ sites for LA injections

A

Inferior alveolar nerve block
Lingual infiltration
Posterior superior nerve block

269
Q

Name 5 steps taken when performing extractions/surgery on patient with bleeding disorder

A
  1. Appropriate care from haemophilia unit
  2. Atraumatic treatment
  3. Consider antibiotics
  4. Observe after surgery
    - 2-3 hours for mild/carriers
    - overnight for severe/moderate
  5. Comprehensive post-op instructions
270
Q

Define thrombophilia

A

Increased risk of developing blood clots

271
Q

Name 4 types of inherited thrombophilia syndromes

A

Protein C deficiency
Protein S deficiency
Factor V Leiden
Antithrombin III deficiency

272
Q

Name 6 ways to acquire thrombophilia

A
Antiphospholipid syndrome
Oral contraceptives
Surgery
Trauma
Cancer
Pregnancy
273
Q

What is the term for decreased platelet numbers

A

Thrombocytopenia

274
Q

What is the term for normal platelet numbers but abnormal function

A

Qualitative disorders

275
Q

What is the term for increased platelet numbers

A

Thrombocythemia

276
Q

At what platelet count can dental treatment be safely done in thrombocytopenia patients

A

Platelet count >50*10x9

277
Q

Name 3 common causes of liver disease

A

Alcohol
Hepatitis
Drug induced

278
Q

What haematological changes occur in those with liver disease in terms of:

  1. Hb
  2. Platelets
  3. PT (prothrombin time)
  4. APTT (activated partial thromboplastin time)
  5. Thrombin time
A
  1. Little change
  2. Decrease
  3. Increase
  4. Increase
  5. Increase