iii. Diseases of The Blood Flashcards
L71: What is sepsis?
Life-threatening organ dysfunction due to a dysregulated host immune response to infection
L71: What are the three main stages of sepsis?
- Infection in susceptible patient;
- Excessive immune response which causes harm;
- Organ dysfunction.
L71: What differentiates sepsis from any other infection?
Progression to organ dysfunction
L71: Diagnosis of sepsis can be based upon ‘infection plus SIRS’, what is SIRS?
Systematic Inflammatory Response Syndrome
L71: What are the signs and symptoms of SIRS?
- Elevated HR;
- Elevated respiratory rate;
- Elevated wbc count;
- Altered mentation (glagow coma scale);
- Fever or chills.
L71: Organ dysfunction can be identified as an acute change in the total SOFA score of how many points?
> or = to 2
L71: What is septic shock?
Sepsis in which the underlying circulatory and cellular and/ or metabolic abnormalities are marked enough to substantially increase mortality
L71: What type of infection can cause sepsis?
Any type of infection and from any site
L71: What microbial factors can cause some infections to progress to sepsis?
- Virulence factors, e.g. LPS, peptidoglycan, pili
these contribute to pathogenicity
L71: What host factors can cause some infections to progress to sepsis?
- Innate immunity;
- Adaptive immunity;
- Immunocompromisation (HIV/ AIDs, cancer, autoimmunity, organ transplantation;
- Pre-existing chronic conditions (diabetes, cirrhosis, CKD);
- Age;
- Genetics.
L71: Why are microbes more pathogenic to an immunocompromised host?
Microbes have a competitive advantage over the host and can overcome immune response more easily
L71: Who are most prone to sepsis? (based on stats)
- Ageing population (65% of cases in US);
- Immune-compromised patients.
L71: What is the pathophysiology of sepsis?
- Dysregulated, excessive systemic inflammation;
- Body-wide blood clotting and leaky vessels;
- One or more organs begin to fail;
- Persistent hypotension (septic shock).
L71: How does the body usually react to acute infection, in summary?
- Cardinal signs of inflammation, localised to site of infection;
- Clearance of the source of injury and necrotic tissues;
- Tissue repair;
- Homeostasis.
L71: How does the normal immune response become dysregulated in sepsis?
Failure to eliminate pathogen, localised acute inflammation progresses to acute systemic inflammation
L71: In a normal immune response to an infection, what inflammatory mediators regulate inflammation?
IL-10 and TGF-b
L71: Alongside excessive inflammation, what do patients with sepsis also demonstrate?
Immune suppression (apoptosis of T and B cells - adaptive immunity impaired)
L71: Organ dysfunction can lead to hyper-permeability of the gut, how does this further impede sepsis?
Further microbial load (from gut) into bloodstream
L71: What are two important factors of the course of tx for a sepsis patient?
- Early IV antibiotics;
- Vasopressors (to contract blood vessels and increase bp), 1-6 hours after onset.
L71: In dentistry, what can cause sepsis?
- Fungal infections;
- MRSA;
- Caries (due to high bacterial load);
- Abscesses.
L71: What two factors make dental abscesses a risk factor for sepsis?
- Can lead to creation of a fistula and drain elsewhere to in head/ neck;
- High risk of spread of infection
L71: What are the ‘red flag’ signs and symptoms of a spreading dental infection?
- Temp < 36 or > 38;
- Elevated breathing rate (>20 breaths/min);
- Elevated or reduced HR;
- Varying degrees of facial swelling;
- Trismus;
- Dehydration.
L71: What should you do, as a dentist, if you suspect a patient has signs/ symptoms/ risk of sepsis from a dental abscess?
- Refer to oral or maxillofacial surgeon in hospital, without delay;
- qSOFA criteria - medical emergency?
L71: What is qSOFA?
A tool to clinically characterise patients at risk of sepsis (at risk of prolonged ICU or death)
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
T4: Clotting is a dynamic process (make v break clots), what happens when this becomes out of sync?
Bleeding disorder
T4: What are the three inheritable bleeding disorders?
- Haemophilia A;
- Haemophilia B;
- Von Willebrand’s.
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.
T4: What is haemophilia A?
Factor VIII (8) deficiency
T4: What is haemophilia B?
Factor IX (9) deficiency
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.
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]
T4: Before treating a patient with MODERATE-SEVERE haemophilia A, what must be given?
Factor 8 cover
[same for von Willibrand’s disease]
T4: How does DDAVP work?
- Vasopressin antidiuretic;
- Helps to release factor 8 from cells into bloodstream and make it available for clotting.
T4: How does tranexamic acid work?
- Inhibitor of fibrinolysis;
- Changes rate of equilibrium to return patient to ‘normal’ and stabilise clot.
T4: Before treating a patient with haemophilia B, what must be given?
- Do not respond to DDAVP;
- Factor 9 cover.
[same for Christmas’ disease]
T4: What is thrombophilia?
- Inherited or acquired protein deficiency;
- Protein antithrombin/ C/ S;
- Tendency to clot;
- Break down at normal rate.
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
T4: When does thrombophilia usually present?
Late teens - adulthood
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]
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.
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.
T4: Why are NOACs superior to warfarin?
Do not require INR monitoring
T4: What is INR?
- International Normalised Ratio;
- Laboratory measurement of how long it takes blood to form a clot;
- Based on prothrombin times.
T4: What is a normal INR?
1
T4: What is the typical INR range for patients on anticoagulants?
2-4
T4: Can you perform ID blocks on warfarin patients?
Yes
T4: Can you perform ID blocks on haemophiliacs?
No, can induce bleeding in tissues
[infiltration anaesthesia ok]
T4: What other patients can suffer from bleeding disorders?
Liver disease - inefficient at making clotting factors/ platelets
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!).
