Lecture 11- 15 overview Flashcards

1
Q

What do neutrophils do when recognise PAMPs

what are 2 cells that recognise this

A

-they phagocytose the material with Pamps

neutrophils and dendritic cells

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2
Q

What are 3 things phagocytosis is promoted by?

A

neutrophils have receptors for …

  • PAMPS
  • C3b complement component
  • Fc region of antibodies
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3
Q

What do actue phase proteins do?

A
  • promote resolution and repair of inflammatory lesions
  • limit tissue injury (e.g inhibit bacterial enzymes)
  • enhance host resistance
  • can also activate complement cascade
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4
Q

What is involved in innate immunity?

A

Physical barriers to infection - e.g skin
Microbial factors - lysozymes, complement
Phagocytic cells - neutrophils, macrophages

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5
Q

How is material digested endogenously and exogenously

A

Exogenous - phagocytosed material, acidification then protease degradation

Proteosome chops it up into peptide fragments and thes go onto cell surface, then it buds off and fuses with cell membrane

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6
Q

what are the 2 antigen presenting cells?

A
  • dendritic cells

- b cells

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7
Q

Lecture 12 - go over al cue cards again

A

Lecture 12 - go over al cue cards again

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8
Q

Blood vessel injury

Flow of blood - changes

A

-trauma, surgical manipulation, prior thrombosis, atherosclerosis

immobility - post op, plane
Pressure - (blockages) catheter, tumour obstruction
Increased viscosity - polycthaemia, dehydration, EPO

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9
Q

Diagnosis of PE

A

classic symptom triad - pleuritic pain, shortness of breath, haemoptysis (blood in cough)

Signs - tachycardia, tacypnoea, hypoxia

Can do a CT scan
V/Q scan

  • can die, or can get hypotension - need thormbolysis to break down the clot
  • also can get see severe right heart strain due to back pressure from pulmonary arteries
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10
Q

Thrombophilia
-KEY LEARNING POINT - she said it was a hint

  • what is it?
  • what are the main causes?
A
  • Tendency to develop thrombosis
  • Can be acquired or inherited
  • manifested as venous thromboembolism
  • some spontaneous -have genetic increased risk
  • some are provoked events - surgery or trauma, immobility, hospitalisation, malignancy, pregnancy
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11
Q

Inherited Thrombophilia

A

-abnormal inhibitor function - resistance to activated protein C (factor 5 leiden)
-Deficeincey of inhibitors - antithrombin , protien C, protien S
Increased factor levels - prothrobin gene mutation, elveated factor VIII

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12
Q

Factor V leiden

A

Factor 5a enhances factor 10 activation

  • activated protein C cleaves normal factor Va
  • slows Xa production
  • so if have bad protein C then cannot get inactive factor 5 and keep getting the clot
  • if factor V has this mutation then cannot get interaction with protein C as good, so results in it being increased - increased coagulation (cannot inactivate factor 5)
  • may have helped survival in oldern days e.g not bleeding to death with pregnancy

APCr gene
-if have both carriers - then get a huge increase in risk of thrombosis

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13
Q

Treatment PE and DVT

A

Initially - heparin (IV)
Immediate effect
-heparin prolongs the APPT, antithrombin deficiency does not.??!

  • heparin binds to antithrombin, and activates it
  • antithrombin then inactivates thrombin, factor 10a

-causes APPT 1 + 1 and tct to be increasde
reversed with protmine (harder to reverse low molecular weight heparin)

low molecular weight heparin

  • inhibits 10a (dont test with APPT)
  • subcutaneous better bioavailability
  • come in prepackaged vials
  • Enoxaparin 1mg/kg twice daily
  • dont use appt to measure low molecular weight heparin

-basically are changing the bodys mechanisms around so can get clotting

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14
Q

Treatment plan VTE

A

-low molecular weight heaprin
-wafarin (7,9,10)
-

-inhibits coagulation, allows own fibrilitc mechanims to operate unhindered by further clotting

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15
Q

Wafarin

A
  • interacts with a lot of things e.g antibiotics,
  • higher INR increases bleeding risk further
  • takes a days to work as there will still be active clotting factors in the blood
  • keep giving low molecular weight heparin till this works
  • want an INR of 2-3
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16
Q

Bleeding on warfarin

A

vit K IV
-however takes 12-24 hours for the clotting factors to be made

-if need immediate reversal - have prothrombinex which contains 2, 9, 10

17
Q

Direct acting oral anticoagulants

A
  • same as warfarin for treatment of VTE
  • superior for anticoagulation in atrial fibrillation - better stroke prevention with similar rates of bleeding
  • people with kidney failure can accumulate high levels of this

Rivaroxaban works on 10a and dabigatran works on thrombin

Advantages - no monitoring needed, fixed dose
-less intracrainal haemorrhage compared to warfarin
DIsadvantages- renal exrection retained with renal imparimed

18
Q

Clotting tests and DOACs

A
  • Dabigatran - TCT extremely sensitive
  • Rivaroxaban - PR prolonged, APPT less so, wont effect TCT at all
  • idarucizumab - is an antidote for dabigatran - it binds to it, almost immediately reverses this
19
Q

Side effects after DVT

A
  • 30% of DVT patients develop post thrombotic syndrome - pain, swelling/odema, redness, venous eczema, ulceration
  • graduated compression stockings may help manage the symptoms of PTS
  • 2% of PE patients may develop chronic thromboembolic pulmona hypertension
20
Q

Inflammation response to bacterial infection

  • what type of cells
  • how are clots formned?

innate immune responses

A

-bacteria gets past skin barrier
-produces toxins, these damage tissues
-mast cells and macrophages become activated and send of further pro inflammatory cytokines and chemokines
(mast cells - release heparin and histamine) (macrophages can recognise PAMPs)
-vasodilation and increased permeability of blood vessels results
-nuertrophils can squeeze out of blood to site of infection
-platelets produce blood clots around bacteria to stop it getting into blood
-neutrophils fight the bacteria

PAMPS - can trigger proinflammatory cytokines

  • Complement system activated in response to cell wall components on bacteria
  • nuetrophils squeeze out of blood
21
Q

Inflammation response to bacterial infection

  • what type of cells
  • how are clots formed?

innate immune responses

A

-bacteria gets past skin barrier
-produces toxins, these damage tissues
-mast cells and macrophages become activated and send of further pro inflammatory cytokines and chemokines
(mast cells - release heparin and histamine) (macrophages can recognise PAMPs)
-vasodilation and increased permeability of blood vessels results
-nuertrophils can squeeze out of blood to site of infection
-platelets produce blood clots around bacteria to stop it getting into blood
-neutrophils fight the bacteria

PAMPS - can trigger proinflammatory cytokines

  • Complement system activated in response to cell wall components on bacteria
  • nuetrophils squeeze out of blood
22
Q

where is cellulitis found?

A

-Often seen around injury site or deep abscess

23
Q

what is Necrotising fasciitis (flesh eating disease)

A
  • Deep infection of skin, destruction of tissue and fascia
  • development into severe systemic disease
  • high mortality
24
Q

treatment for SSTI
S.pyogenes

s,aureus

A

Penicilin , amyoxicilin

beta lactamase resistant penicilin - flucloxacillin (except for MRSA strains)

25
Q

treatment for SSTI
S.pyogenes

s,aureus

A

Penicilin e.g amyoxicilin

beta lactamase resistant penicilin - flucloxacillin (except for MRSA strains)