iii. Diseases of The Blood Flashcards

1
Q

L71: What is sepsis?

A

Life-threatening organ dysfunction due to a dysregulated host immune response to infection

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2
Q

L71: What are the three main stages of sepsis?

A
  • Infection in susceptible patient;
  • Excessive immune response which causes harm;
  • Organ dysfunction.
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3
Q

L71: What differentiates sepsis from any other infection?

A

Progression to organ dysfunction

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4
Q

L71: Diagnosis of sepsis can be based upon ‘infection plus SIRS’, what is SIRS?

A

Systematic Inflammatory Response Syndrome

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5
Q

L71: What are the signs and symptoms of SIRS?

A
  • Elevated HR;
  • Elevated respiratory rate;
  • Elevated wbc count;
  • Altered mentation (glagow coma scale);
  • Fever or chills.
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6
Q

L71: Organ dysfunction can be identified as an acute change in the total SOFA score of how many points?

A

> or = to 2

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7
Q

L71: What is septic shock?

A

Sepsis in which the underlying circulatory and cellular and/ or metabolic abnormalities are marked enough to substantially increase mortality

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8
Q

L71: What type of infection can cause sepsis?

A

Any type of infection and from any site

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9
Q

L71: What microbial factors can cause some infections to progress to sepsis?

A
  • Virulence factors, e.g. LPS, peptidoglycan, pili

these contribute to pathogenicity

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10
Q

L71: What host factors can cause some infections to progress to sepsis?

A
  • Innate immunity;
  • Adaptive immunity;
  • Immunocompromisation (HIV/ AIDs, cancer, autoimmunity, organ transplantation;
  • Pre-existing chronic conditions (diabetes, cirrhosis, CKD);
  • Age;
  • Genetics.
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11
Q

L71: Why are microbes more pathogenic to an immunocompromised host?

A

Microbes have a competitive advantage over the host and can overcome immune response more easily

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12
Q

L71: Who are most prone to sepsis? (based on stats)

A
  • Ageing population (65% of cases in US);

- Immune-compromised patients.

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13
Q

L71: What is the pathophysiology of sepsis?

A
  • Dysregulated, excessive systemic inflammation;
  • Body-wide blood clotting and leaky vessels;
  • One or more organs begin to fail;
  • Persistent hypotension (septic shock).
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14
Q

L71: How does the body usually react to acute infection, in summary?

A
  • Cardinal signs of inflammation, localised to site of infection;
  • Clearance of the source of injury and necrotic tissues;
  • Tissue repair;
  • Homeostasis.
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15
Q

L71: How does the normal immune response become dysregulated in sepsis?

A

Failure to eliminate pathogen, localised acute inflammation progresses to acute systemic inflammation

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16
Q

L71: In a normal immune response to an infection, what inflammatory mediators regulate inflammation?

A

IL-10 and TGF-b

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17
Q

L71: Alongside excessive inflammation, what do patients with sepsis also demonstrate?

A

Immune suppression (apoptosis of T and B cells - adaptive immunity impaired)

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18
Q

L71: Organ dysfunction can lead to hyper-permeability of the gut, how does this further impede sepsis?

A

Further microbial load (from gut) into bloodstream

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19
Q

L71: What are two important factors of the course of tx for a sepsis patient?

A
  • Early IV antibiotics;

- Vasopressors (to contract blood vessels and increase bp), 1-6 hours after onset.

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20
Q

L71: In dentistry, what can cause sepsis?

A
  • Fungal infections;
  • MRSA;
  • Caries (due to high bacterial load);
  • Abscesses.
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21
Q

L71: What two factors make dental abscesses a risk factor for sepsis?

A
  • Can lead to creation of a fistula and drain elsewhere to in head/ neck;
  • High risk of spread of infection
22
Q

L71: What are the ‘red flag’ signs and symptoms of a spreading dental infection?

A
  • Temp < 36 or > 38;
  • Elevated breathing rate (>20 breaths/min);
  • Elevated or reduced HR;
  • Varying degrees of facial swelling;
  • Trismus;
  • Dehydration.
23
Q

L71: What should you do, as a dentist, if you suspect a patient has signs/ symptoms/ risk of sepsis from a dental abscess?

A
  • Refer to oral or maxillofacial surgeon in hospital, without delay;
  • qSOFA criteria - medical emergency?
24
Q

L71: What is qSOFA?

A

A tool to clinically characterise patients at risk of sepsis (at risk of prolonged ICU or death)

25
L71: What is the baseline qSOFA of a patient with no pre-existing health conditions, how does this differ with underlying conditions?
0, with conditions it is automatically 2
26
T4: Clotting is a dynamic process (make v break clots), what happens when this becomes out of sync?
Bleeding disorder
27
T4: What are the three inheritable bleeding disorders?
- Haemophilia A; - Haemophilia B; - Von Willebrand's.
28
T4: Why are males more likely to inherit haemophilia?
- X-linked recessive disease; - Males only have one X chromosome; - Will inherit disease if mutation present on X chromosome.
29
T4: What is haemophilia A?
Factor VIII (8) deficiency
30
T4: What is haemophilia B?
Factor IX (9) deficiency
31
T4: What is von Willebrand's disease?
- Missing or defective von Willebrand factor (VWF), a clotting protein; - VWF binds factor 8 and platelets during clotting process.
32
T4: Before treating a patient with MILD haemophilia A, what must be given?
- May require factor 8 cover with extractions; - Usually DDAVP; - Very mild cases may only require tranexamic acid. [same for von Willibrand's disease]
33
T4: Before treating a patient with MODERATE-SEVERE haemophilia A, what must be given?
Factor 8 cover [same for von Willibrand's disease]
34
T4: How does DDAVP work?
- Vasopressin antidiuretic; | - Helps to release factor 8 from cells into bloodstream and make it available for clotting.
35
T4: How does tranexamic acid work?
- Inhibitor of fibrinolysis; | - Changes rate of equilibrium to return patient to 'normal' and stabilise clot.
36
T4: Before treating a patient with haemophilia B, what must be given?
- Do not respond to DDAVP; - Factor 9 cover. [same for Christmas' disease]
37
T4: What is thrombophilia?
- Inherited or acquired protein deficiency; - Protein antithrombin/ C/ S; - Tendency to clot; - Break down at normal rate.
38
T4: Thrombophilacs are dependent in a certain protein (antithrombin/ C/ S/ factor V Leiden), what do these proteins usually do?
Slow down the rate of making clotting factors
39
T4: When does thrombophilia usually present?
Late teens - adulthood
40
T4: What can cause problems for thrombophiliacs?
- Immobility; - Cancers (surgical/ chemo risk); - Certain drugs (e.g. contraceptive); - Hormonal changes (pregnancy); - Smoking. [all can lead to DVT - can in turn embolise to other organs e.g. lungs]
41
T4: How should you treat a patient with thrombophilia?
- If on no medication, may require anticoagulants for MOS/ extractions; - If on anticoagulants, check INR; - Check history of bleeding after extractions/ tx.
42
T4: Warfarin is a cheap drug to prescribe but why is it complicated to use?
- Patients must be monitored (INR); - Bioavailability is unpredictable; - Interacts with many (most) drugs; - Takes a few days to work; - Initially inhibits proteins C and C; - Must be on IV heparin over this time.
43
T4: Why are NOACs superior to warfarin?
Do not require INR monitoring
44
T4: What is INR?
- International Normalised Ratio; - Laboratory measurement of how long it takes blood to form a clot; - Based on prothrombin times.
45
T4: What is a normal INR?
1
46
T4: What is the typical INR range for patients on anticoagulants?
2-4
47
T4: Can you perform ID blocks on warfarin patients?
Yes
48
T4: Can you perform ID blocks on haemophiliacs?
No, can induce bleeding in tissues [infiltration anaesthesia ok]
49
T4: What other patients can suffer from bleeding disorders?
Liver disease - inefficient at making clotting factors/ platelets
50
T4: What bloods may be necessary to check before treating a patient with a bleeding disorder/ liver disease?
- Coagulation cascade (via INR test); | - FBC (platelets!).