infection and shock Flashcards

(59 cards)

1
Q

What is pericarditis?

A

Typically acute (can be chronic); inflammation of pericardium +/- effusion -pericardium has two layers and innervated by phrenic hence inflammation results in pain

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2
Q

Epidemiology of pericarditis?

A
  • males - 20-50yrs
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3
Q

Causes of pericarditis

A

1) Usually idiopathic 2) Or caused by a virus: - most common cause = coxsackievirus - mumps - EBV - VZV - HIV Less common causes: - bacterial - TB - systemic autoimmune disorders - malignancy - trauma

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4
Q

Pathophysiology of pericarditis

A
  • inflamed pericardial layers rub against each other = more inflammation -cause exudate and adhesions within pericardial sac 1) may stay dry (no extra fluid needed to compensate for friction) 2) develop pericardial effusion (extra fluid) - if it become
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5
Q

Symptoms of pericarditis

A

Sudden onset sharp, pleuritic chest pain which can spread to left shoulder tip (phrenic) - Relieved by sitting up or leaning forward - Worse laying flat *may have signs of rhs failure due to constructive pericarditis -> SOB, peripheral oedema and tachycardia

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6
Q

Sign of pericarditis

A

Pericardial friction rub on auscultation - heard at left sternal edge as patient leans forward - squeaky leather “to and fro” sound

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7
Q

Differential diagnosis of pericarditis

A

Most key to rule out MI - central crushing chest pain not related to lying down - no pericardial rub

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8
Q

What is constructive pericarditis

A
  • granulation tissue formation in pericardium means impaired diastolic filling as it becomes thickened and hardened - late complication of pericarditis - sign of poor prognosis‚Äî> congestive heart failure - commonly associated with TB
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9
Q

Primary investigations to diagnose pericarditis

A

ECG: widespread saddle shaped ST-elevation (sensitive) and PR depression (specific) Eg. CXR: may show “water bottle” heart = pericardial effusion - pneumonia commonly seen in bacterial pericarditis Transthoracic ecg: to exclude pericardial effusion or tamponade ESR and CRP: might increase due to inflammation Troponin will be daisies if there’s an element of concomitant myocarditis

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10
Q

Treatment for idiopathic or viral pericarditis

A

1st line: NSAIDs + Colchine 2nd line: NSAIDs + Colchine + low-dose prednisolone

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11
Q

Treatment for bacterial pericarditis

A

IV antibiotics and pericardiocentesis with washout, culture and sensitivities

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12
Q

Compilcations of pericarditis

A

1) Pericardial effusion—> cardiac tamponade 2) Myocarditis 3) Constrictive pericarditis

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13
Q

What is infective endocarditis

A

Infection of endocardium: - an abnormal endocardium - bacterial source —> vegetation

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14
Q

Two most common causes of infective endocarditis

A

1) S.aureus- most common overall + associated with IV drug use and prosthetic heart valves => increased virulence, Sx onset in days-weeks = ACUTE 2) S.viridans- second most common + usually affects a native valve and associated with poor dental hygiene => decreased virulence, Sx onset in weeks-months = SUBACUTE

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15
Q

Catergorisations of endocarditis

A

1) Acute 2) Subacute 3) Non- bacterial thrombotic ‘marantic’ - non-infective cause of endocarditis secondary to thrombus formation on the valvular surface - associated with malignancy or SLE (Libman-Sacks endocarditis)

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16
Q

Other less common causes of infective endocarditis

A

S. Bovis (associated with colon cancer) S. Epidermis (associated with in dwelling lines and prosthetic valves) HACEK organsisms (usually culture -ve) - Haemophilus - Aggregatibacter - Cardiobacterium - Eikenella - Kingella

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17
Q

Risk factors for infective endocarditis

A

Male 2.5x Elderly with prosthetic valve Young IV drug user Young with congenital heart defect Rheumatic heart disease

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18
Q

Which valves are more commonly affected by Infective endocarditis

A

Mitral valve most commonly affected overall Tricuspid valve is most associated with IV drug use (Mitral valve)

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19
Q

Pathophysiology of infective endocarditis

A
  • any cause of abnormal endocardium ‚Äî> turbulent blood flow and thrombus formation (platelets) - thrombus can get infected due to bacterial source - bacterial colonisation of the thrombus ‚Äî> formation of vegetations ‚Äî> valvular damage -ty
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20
Q

Symptoms of infection endocarditis

A

Rather vague -Fever or chills -headache -SOB -night sweats, fatigue, weight loss -joint pain (might be due to septic emboli)

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21
Q

Signs of infective endocarditis

A

1) Osler nodes (painful nodules on fingers\toes) 2) Janeway lesions (painless placques on palms and soles) 3) splinter haemmorrhages (red plum lines under nails) 4) Roth’s spots: white centred retinal haemorrhages heart murmer +- signs of heart failure

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22
Q

Primary investigations for infective endocarditis

A

-ECG (prolonged PR interval=aortic root abscess) -Blood cultures - 3 sets in 24 hours BEFORE ANTIBIOTICS -Inflammatory markers (CRP) - eg raised ESR\CRP + neutrophillia -FBC -ECHO: TOE more invasive than TTE but much more sensitive and specific = gold st

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23
Q

What is the modified Duke Criteria

A

Requires 2 major criteria, or 1 major and 3 minor, or 5 minor criteria for diagnosis of infective endocarditis

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24
Q

Major Duke Criteria for infactive endocarditis

A
  • 2 positive blood cultures - ECHO TOE shows endocardia‚Äôs involvement Eg. Vegetations , abscess or regurgitation
25
Minor Duke criteria for infective endocarditis
-predisposing heart condition -IVDU -Fever >38°C -1 +ve blood culture -immunological phenomenon (Osler’a nodes, Roth’s spots or rheumatoid factor) -vascular abnormalities (eg. Septic/arterial emboli, pulmonary infarct)
26
First line treatment for infective endocarditis
IV antibiotics for 4 weeks following nice guidelines, extended to 6 weeks for prosthetic valves -local guidelines should be followed with nice antibiotic guidance below (Idk if you need to know all these but have a rough idea)
27
Second line treatment for infective endocarditis
Surgery: aim to remove infected tissue and repair it replace affected valves
28
Complications of infective endocarditis
Congestive heart failure Septic embolisation Valvular rupture or fistula Aortic root abscess
29
Epidemiology of rheumatic fever
Almost exclusively in developing countries only In young people
30
Cause of rheumatic fever
Systemic response to B haemolytic group A strep (Strep pyogenes) Typically pharyngitis
31
Rheumatic heart disease?
In 50% of cases of rheumatic fever it goes on to affect the heart
32
Histological appearance of rheumatic fever
Valves affected show Aschoff Bodies (Seen on the right)
33
Pathophysiology of rheumatic fever
M protein from S. pyogenes reacts with valve tissue of the heart Antibodies vs this “cross-link” results ins auto-antibody mediated destruction +- inflammation Molecular Mimicry!! * mostly affects the mitral valve (70% just mitral and 25% mitral and aortic) Typically thickens leaflets causing mitral stenosis
34
Symptoms of rheumatic fever
- New murmur (esp mitral stenosis) - Syadenham’s chorea (neurological disorder that results in uncoordinated jerky movements) - arthritis - Erythema nodosum (swollen fat causing red patches\bumps) - pyrexia - evidence of strep A infection
35
Investigations to diagnose rheumatic fever
CXR= cardiomegaly/ heart failure (signs of mitral stenosis) ECHO= details extent of valvular damage
36
Jone’s criteria for diagnosis of rheumatic fever
1) recent S. pyogenes infection AND 2) 2 major signs (new murmur, arthritis, erythema nodosum, syndham chorea) OR 3) 1 major + 2 minor (pyrexia, increased ESR/CRP, arythalgia)
37
Treatment for rheumatic fever
Antibiotics- IV benzyloenicillin STAT, then phenoxypenicillin for 10days
38
Treatment for Sydenham’s chorea
Haloperidol
39
What is shock
A medical emergency- life threatening -hypoperfusion -due to acute circulation failure -leads to tissue hypoxia and risk of organ dysfunction
40
What are the five different types of shock?
- Cardiogenic (heart pump failure) - Distributive (arterial supply to tissues): 1) septic 2) neurogenic 3) anaphylactic - Hypovolemic (affects venous return to heart and therefore preload)
41
Presentation of shock
1) decreased urine output 2) reduced GCS (Glasgow coma scale) 3) Skin - pale , cold, sweaty, vasoconstriction - increased capillary refill time = earliest, most accurate indicator - takes 3+ seconds for hand to turn pink after pressed for 5seconds 4) confusion 5) pulse- weak + rapid 6) prolonged hypotension = can lead to life threatening organ failure AFTER acute emergency recovery
42
Causes of hypovolemic shock
1) Blood loss - trauma, GI bleed 2) Fluid loss- dehydration
43
Symptoms of hypovolemeic shock
Clammy pale skin Confusion Hypotension Tachycardia
44
Treatment of hypovolemic shock
ABCDE Airways Breathing (give O2) Circulation (IV fluids)
45
Cause of anaphylactic shock
Due to IgE mediated Type 1 hypersensitivity vs allergen -Histamine release causes construction -causes excess vasodilation and bronchoconstriction Hypoxic!
46
Symptoms of anaphylactic
Hypotension Tachycardia Urticaria Puffy face flushing of cheeks
47
Treatment of anaphylactic shock
ABCDE IM adrenaline (SNS activation=stress response)
48
Key organs at risk of failure from shock?
Kidneys Lungs Heart Brain
49
Cause of neurogenic shock
Due to spinal cord trauma eg RTA Results in disrupted SNS, but intact PSNS
50
Symptoms of neurogenic shock
Hypotension Bradycardia Confused Hypothermic
51
Treatment for neurogenic shock
ABCDE IV Atropine (Blocks vagal tone: allows more psns inhibition, more chance for SNS to work)
52
Cause of cardiogenic shock
Due to heart pump failure; MI, cardiac tamponade, pulmonary emboli
53
Symptoms of cardiogenic shock
Heart failure signs (oedema) Increased JVP S4
54
Treatment of cardiogenic shock
ABCDE Treat underlying cause
55
Cause of septic shock
Due to uncontrolled bacterial infection
56
Symptoms of septic shock
Pyrexia warm peripheries Tachycardic
57
Treatment for septic shock
ABCDE Broad spectrum antibiotic
58
Prognosis of pericarditis
Majority of cases (viral and Idiopathic) are self limiting, whereas bacterial (purulent) pericarditis can be fatal if untreated.
59
Another name for pericarditis?
Dressler syndrome