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Infection > week 4 sepsis > Flashcards

week 4 sepsis Flashcards

1
Q

what is the leading cause of sepsis?

A

gram -ve bacteria

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2
Q

what is sepsis?

A

symptoms from systemic infection

life-threatening organ dysfunction due to pathogen and bad response to infection

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3
Q

septic shock

A

severe sepsis

high risk of mortality

due to physiological compensatory mechanisms

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4
Q

sepsis 6 treatment

A

Give 3:
Oxygen
IV fluids
IV antibiotics

Take:
Lactate
blood cultures
urine output

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5
Q

what is SOFA

A

sequential organ failure assessment

suspected inflammation + change in 2< from baselines:

respiratory, haematology, liver, renal, brain, cardiovascular

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6
Q

pathophysiology of sepsis

A

infection of pathogen

inflammatory response

coagulation cascade

physiological compensation

metabolic compensation

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7
Q

compensated shock?

A

normal blood pressure = treat

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8
Q

decompensated shock?

A

low bp = difficult to treat

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9
Q

acute inflammation?

A

response to tissue injury, infection or irritation

rapid and short lived

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10
Q

symptoms of acute inflammation?

A

fever fatigue loss of appetite

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11
Q

features of acute inflammation

A

loss of appetite

redness

heat

swelling

pain

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12
Q

what is blood pressure?

A

pumps blood through the body, tissues, organs

it is proportional

BP= (heart rate x stroke volume) x systemic vascular resistance

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13
Q

what happens during vasodialation?

A

decrease in vascular resistance

skin is well perfused

organs are not

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14
Q

what happens in vasoconstriction?

A

as sepsis occurs

increase in peripheral SVR and maintains vital organ perfusion

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15
Q

what happens if there is a fall in SVR

A

compensatory tachycardia and increase in Stroke volume (SV) to maintain BP

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16
Q

List 3 red flags for sepsis?

A

· Responds only to voice or pain/ unresponsive
· Acute confusional state
· Systolic B.P ≤ 90 mmHg (or drop >40 from normal)
· Heart rate > 130 per minute
· Respiratory rate ≥ 25 per minute
· Needs oxygen to keep SpO2 ≥92%
· Non-blanching rash, mottled/ ashen/ cyanotic
· Not passed urine in last 18 h/ UO

17
Q

what are the 2 common presentations to septic shock

A

Warm and cold shock

18
Q

What are the common infectious causes of sepsis

A

Pneumonia
Urinary tract
Abdomen

19
Q

What are the effects of sepsis on the brain

A

Confusion
raised blood sugar

19
Q

What are the effects of sepsis on the brain

A

Confusion
raised blood sugar

20
Q

What are the effects of sepsis on tissues

A

Increased anaerobic respiration

21
Q

What are the effects on the lungs in sepsis

A

Increased respiratory rate
shortness of breath
difficulty taking breaths

22
Q

What are the principles of management of TSS?

A

Fluids
antibiotics
removal of source of toxins

23
Q

What are the vascular changes that occur in response to sepsis?

A

Vasodilatation
increased vascular permeability
increased adhesion of white blood cells

24
Q

What cellular events occur in sepsis

A

Cellular recruitment and activation of neutrophils

25
Q

what class of antibiotics is gentamicin and what is its MOA

A

Aminoglycoside
Inhibits protein synthesis by binding to 30S ribosome

26
Q

What occurs as a result of anaerobic respiration in sepsis

A

Increased lactate production leading to reduced pH and metabolic acidosis occuring and respiratory rate increases to compensate for the reduced pH

27
Q

What occurs as a result of reduced circulating volume in sepsis

A

reduced venous return

28
Q

What occurs in cold shock

A

low cardiac output
high SVR(systemic vascular resistance)
cool extremities

29
Q

What occurs in septic shock

A

Severe abnormalities of circulation and /or cellular metabolism
Persistent hypotension

30
Q

what occurs in warm shock

A

high cardiacc output
low SVR
Warm extremities

31
Q

What organs are affected in decreased perfusion in sepsis

A

Kidney
lungs
liver
brain
heart

32
Q

Why does anaerobic respiration occur in sepsis

A

Decreased oxygen intake

33
Q

Why does circulating volume decrease in sepsis

A

Capillary leakage

34
Q

Why is coagulation cascade activated in sepsis(3)

A

Tissue mediated thrombin generation
down regulation of physiological anticogulants
inhibitions of fibrinolysis

Infection (8 decks)

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