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2a. BDS2 BAMS > iii. Diseases of The Blood > Flashcards

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
Q

L71: What is the baseline qSOFA of a patient with no pre-existing health conditions, how does this differ with underlying conditions?

A

0, with conditions it is automatically 2

26
Q

T4: Clotting is a dynamic process (make v break clots), what happens when this becomes out of sync?

A

Bleeding disorder

27
Q

T4: What are the three inheritable bleeding disorders?

A
  • Haemophilia A;
  • Haemophilia B;
  • Von Willebrand’s.
28
Q

T4: Why are males more likely to inherit haemophilia?

A
  • X-linked recessive disease;
  • Males only have one X chromosome;
  • Will inherit disease if mutation present on X chromosome.
29
Q

T4: What is haemophilia A?

A

Factor VIII (8) deficiency

30
Q

T4: What is haemophilia B?

A

Factor IX (9) deficiency

31
Q

T4: What is von Willebrand’s disease?

A
  • Missing or defective von Willebrand factor (VWF), a clotting protein;
  • VWF binds factor 8 and platelets during clotting process.
32
Q

T4: Before treating a patient with MILD haemophilia A, what must be given?

A
  • May require factor 8 cover with extractions;
  • Usually DDAVP;
  • Very mild cases may only require tranexamic acid.

[same for von Willibrand’s disease]

33
Q

T4: Before treating a patient with MODERATE-SEVERE haemophilia A, what must be given?

A

Factor 8 cover

[same for von Willibrand’s disease]

34
Q

T4: How does DDAVP work?

A
  • Vasopressin antidiuretic;

- Helps to release factor 8 from cells into bloodstream and make it available for clotting.

35
Q

T4: How does tranexamic acid work?

A
  • Inhibitor of fibrinolysis;

- Changes rate of equilibrium to return patient to ‘normal’ and stabilise clot.

36
Q

T4: Before treating a patient with haemophilia B, what must be given?

A
  • Do not respond to DDAVP;
  • Factor 9 cover.

[same for Christmas’ disease]

37
Q

T4: What is thrombophilia?

A
  • Inherited or acquired protein deficiency;
  • Protein antithrombin/ C/ S;
  • Tendency to clot;
  • Break down at normal rate.
38
Q

T4: Thrombophilacs are dependent in a certain protein (antithrombin/ C/ S/ factor V Leiden), what do these proteins usually do?

A

Slow down the rate of making clotting factors

39
Q

T4: When does thrombophilia usually present?

A

Late teens - adulthood

40
Q

T4: What can cause problems for thrombophiliacs?

A
  • 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
Q

T4: How should you treat a patient with thrombophilia?

A
  • If on no medication, may require anticoagulants for MOS/ extractions;
  • If on anticoagulants, check INR;
  • Check history of bleeding after extractions/ tx.
42
Q

T4: Warfarin is a cheap drug to prescribe but why is it complicated to use?

A
  • 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
Q

T4: Why are NOACs superior to warfarin?

A

Do not require INR monitoring

44
Q

T4: What is INR?

A
  • International Normalised Ratio;
  • Laboratory measurement of how long it takes blood to form a clot;
  • Based on prothrombin times.
45
Q

T4: What is a normal INR?

A

1

46
Q

T4: What is the typical INR range for patients on anticoagulants?

A

2-4

47
Q

T4: Can you perform ID blocks on warfarin patients?

A

Yes

48
Q

T4: Can you perform ID blocks on haemophiliacs?

A

No, can induce bleeding in tissues

[infiltration anaesthesia ok]

49
Q

T4: What other patients can suffer from bleeding disorders?

A

Liver disease - inefficient at making clotting factors/ platelets

50
Q

T4: What bloods may be necessary to check before treating a patient with a bleeding disorder/ liver disease?

A
  • Coagulation cascade (via INR test);

- FBC (platelets!).

2a. BDS2 BAMS (10 decks)

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