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VTS(ECC) Preparation > Clinical pathology, SIRS, sepsis & MODS > Flashcards

Clinical pathology, SIRS, sepsis & MODS Flashcards

1
Q

How many days worth of neutrophil reserves are held within the bone marrow?

A

Approximately 5-days

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2
Q

What are examples of Type A hyperlactataemia?

A

Hypoperfusion
Severe hypoxaemia
Severe, acute anaemia
Carbon monoxide toxicity
Extreme muscle activity

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3
Q

What are examples of Type B1 hyperlactataemia?

A

Underlying disease: DM, neoplasia, liver disease, sepsis, pheochromocytoma, thiamine deficiency

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4
Q

What are examples of Type B2 hyperlactataemia?

A

Drugs/toxins: ethanol, methanol, acetominophen, cyanide, epinephrine, sorbitol, ethylene glycol, xylitol, salicylate, terbutaline

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5
Q

How much ATP is produced during aerobic metabolism per 1 glucose?

A

32

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6
Q

How is lactate used in anaerobic metabolism?

A
  • transported out of the cell
  • oxidised to produce energy
  • converted back to glucose via gluconeogenesis
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7
Q

1mmol/L of lactate is equivalent to ____ of H+ ions released and ____ BE difference

A

1mmol/L, 1mmol/L

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8
Q

What is lactic acidosis?

A

Combination of hyperlactataemia and metabolic acidosis

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9
Q

The liver consumes/processes _____ lactate.

A

50-70%

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10
Q

The renal system consumes/processes _____ lactate.

A

25-30%

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11
Q

Hyperlactataemia is classified as mild, moderate and severe. What are the ranges for each class?

A

Mild 2-4mmol/L
Moderate 4-6mmol/L
Severe >6mmol/L

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12
Q

Puppies generally have _____ lactate compared to adults due to _______.

A

Higher, utilise lactate for energy.

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13
Q

Which isoform of lactate is clinically relevant to mammalian species and commonly measured in-house?

A

L-lactate

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14
Q

How should a sample to be used for lactate measurement be stored if not utilised within 60 minutes and why?

A

Place on ice or collect fresh sample as continued glycolysis of the sample continues after collection.

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15
Q

Lactate is a late indicator of tissue perfusion due to it being produced after tissue oxygen extraction, true or false?

A

True

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16
Q

A lactate level above ____ is shown to be significantly associated with mortality (6-fold) within 3 days in septic peritonitis patients.

A

4mmol/L

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17
Q

Resolution of hyperlactatemia within which time frame has been associated with 79% survival in septic peritonitis patients?

A

6-12 hours

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18
Q

What are some common abdominal fluid ctyology findings in patients with septic peritonitis?

A
  • toxic neutrophils with/without intracellular bacteria
  • high nucleated cell count
  • Micro-organisms
  • pH <7.2
  • pCO2 >55mmHg
  • Glucose <5.0
  • Lactate >5.5
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19
Q

What are the most common micro-organisms found in patients with septic peritonitis?

A

1 Escherichia coli

Enterococcus spp.
Enterobacter spp.
Streptococcus spp.
Clostridium spp.
Klebsiella spp.

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20
Q

What is the gold standard for diagnosis of septic peritonitis? What is the limitation?

A

Bacterial culture and susceptibility but ay take days to weeks to culture and treatment cannot wait to be commenced

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21
Q

What difference in glucose between the peritoneal fluid and blood indicates potential septic peritonitis?

A

BFG >20mg/dL

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22
Q

What difference in lactate between the peritoneal fluid and blood indicates potential septic peritonitis?

A

< -2mmol/L

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23
Q

What are neutrophils?

A

Neutrophils are the most abundant type of WBC and are the hallmark of inflammation due to them being one of the first cells to arrive at an inflamed or injured area during infection or stress.

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24
Q

What are lymphocytes?

A

Help organisms fight infection by producing antibodies and removing foreign invaders. These cells determine the specificity of the immune response.

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25
Q

What are eosinophils?

A

Usually linked to allergic diseases and are made in the bone marrow. They curb infection and boost inflammation.

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26
Q

What are monocytes?

A

Produced in the bone marrow and can turn into macrophagic or dendritic cells which are involved in phagocytosis, antigen presentation, and cytokine production. They are involved in homeostasis, pathogen challenge and clearance, and inflammation.

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27
Q

What are basophils?

A

Attack micro-organisms seen as foreign in the body. Granules store and release enzyme (i.e. histamine, heparin) to fight infection.

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28
Q

What may cause neutrophilia?

A

Increased production of neutrophils (appropriate v. inappropriate)
Demargination
Decreased egress from circulation

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29
Q

What is a ‘left shift’?

A

Increased immature neutrophil production

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30
Q

What is the difference between a regenerative and a non-regenerative left shift?

A

Regenerative: production of immature neutrophils with adequate number of mature neutrophils. Production = utilisation and the body is coping.

Degenerative: production of immature neutrophils with low number of mature neutrophils indicating utilisation>production. The body is not coping.

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31
Q

Demargination of neutrophils can occur due to..

A

Corticosteroid administration or epinephrine release/administration

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32
Q

Neutropaenia can result from?

A

Increased utilisation of neutrophils
Increase destruction of neutrophils
Decreased neutrophil production in bone marrow

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33
Q

How is neutropaenia treated?

A

Broad-spectrum antimicrobials
Recombinant G-CSF
Aggressive resuscitation if sepsis/septic shock present
Reduced exposure to infection
Consider home management to reduce nosocomial infection risk
+- antifungals

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34
Q

What are characteristics that may be found in toxic changes of neutrophils?

A
  • foamy basophilic cytoplasm
  • dohle bodies
  • giant neutrophils
  • abberant nuclear shapes
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35
Q

What is the normal platelet count?

A

8-15/hpf or 200,000-800,000 cells/uL

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36
Q

At what platelet count does spontaneous bleeding occur?

A

20,000-50,000 cells/uL

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37
Q

What are the signs of clinical bleeding associated with a low PLT count?

A

Petechiae & ecchymoses
Haematuria
Mucosal bleeding
Anaemia

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38
Q

What are the four broad causes of thrombocytopaenia?

A

Sequestration
Consumption
Increased destruction
Reduced production

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39
Q

All of the following are mechanisms for cellular energy production except:
A. glycolysis
B. gluconeogenesis
C. oxidative phosphorylation
D. the citric acid cycle

A

B.

40
Q

Anaerobic glycolysis will produce a net ___ moles of ATP for each mole of
glucose metabolized.
A. 2
B. 4
C. 6
D. 32

A

A.

41
Q
  1. Lactate is used primarily by the
    a. muscle
    b. red blood cells
    c. liver
    d. brain
A

C.

42
Q

All of the following would cause an increased lactate level except
a. Pregnancy
b. Shock
c. Anemia
d. Seizures

A

A.

43
Q

The main determinant of lactate levels in the blood is
a. Respiratory rate
b. Cellular perfusion
c. Muscle activity
d. Oxygen extraction from the blood

A

B

44
Q

Lactate levels cannot be measured in
a. Whole blood
b. Abdominal effusions
c. Serum
d. Tissues

A

D.

45
Q

A lactate value of 3.0 mmol/L is suggestive of
a. Severe dehydration
b. Prolonged seizure activity
c. Prolonged venous occlusion
d. Septic shock

A

C

46
Q

The dog with the best prognosis is one that has an initial lactate level of
___mmol/L and a level of ____ mmol/L following treatment.
a. 2.0; 1.0
b. 2.0; 3.5
c. 5.5; 3.5
d. 5.5; 7.0

A

A

47
Q

The most important thing when treating an animal with a high lactate blood level
is to
a. Give a large amount of IV fluids
b. Council the owners about the poor prognosis
c. Find and treat the underlying problem
d. Administer bolus sodium bicarbonate immediately

A

C.

48
Q

Which of the following is a possible cause of hypersegmentation in neutrophils?
a. Chronic infection
b. The use of steroids
c. Pernicious anemia
d. a, b, and c
e. None of the above

A

C
(Check)

49
Q

The youngest leukocytes that normally occur in the peripheral circulation are
a. Lymphocytes
b. Monoblasts
c. Neutrophilic band cells
d. Metamyelocytes
e. Metarubicytes

A

C

50
Q

Platelets are formed from
a. Myelocytes
b. Megakaryocytes
c. Erythrocytes
d. Plasma cells
e. Myeloblasts

A

B

51
Q

Which of the following can be produced as an artifact in an improperly handled blood
sample?
a. hypersegmentation
b. karyolysis
c. vacuolation of cells
d. smudge cells
e. all of the above

A

E

52
Q

The largest cells present in the peripheral circulation
a. depend on the age of the patient
b. are lymphocytes
c. depend on the species involved
d. eosinophils
e. are monocytes

A

E

53
Q

The primary function of most leukocytes is
a. antibody production
b. inflammation
c. phagocytosis
d. coagulation
e. hemostasis

A

A

54
Q

The Pelger-Huet anomaly involves cells that are
a. pyknotic
b. hyposegmented
c. giant forms
d.hypersegmented
e. lysed

A

B
(Neutrophil nuclei appear hyposegmented – can appear as a single round nucleus (unilobed, homozygous Pelger-Huet Anomaly) or dumbbell shaped (bilobed, heterozygous Pelger-Huet Anomaly). Anomaly is differentiated from a left shift by displaying mature chromatin pattern, abundant cytoplasm (low nuclear:cytoplasmic ratio), mature granulation, and an absence of toxic changes.)

55
Q

Plasma cells are derived from
a. Leukocytes
b. B lymphocytes
c. T lymphocytes
d. megakaryocytes
e. b or c

A

B
(CHECK NOT E)

56
Q

The nucleus of a mature neutrophil characteristically has
a. three to five lobes
b. twin lobes
c. pale pink granules
d. lysomes
e. 6 to 10 lobes

A

A

57
Q

One of the most common bacteria involved in septic peritonitis is:
a. staphylococcus aureus
b. Streptococcus intermedius
c. Pseudomonas aeruginosa
d. Escherichia coli

A

D

All may be found but E. coli is #1

58
Q

Criteria for SIRS

A
  1. hypothermia or hyperthermia
  2. Tachypnoea
  3. Tachycardia
  4. Leukocytosis or leukopaenia
59
Q

CARS

A

Compensatory anti-inflammatory response syndrome
Releases anti-inflammtory mediators in response to an inflammatory state but when excessive can result in immunoparalysis putting the patient at risk for infection.

60
Q

Consequences of SIRS

A

Loss of vascular tone (drop in vasopressin and cortisol; nitric oxide release)
Disruption of endothelial permeability layer
Stimulation of coagulation layer

61
Q

C-reactive protein

A

CRP
Produced by hepatocytes in response to inflammatory cytokine release
* Not an ideal marker of sepsis

62
Q

Procalcitonin (PCT)

A

Precursor to calcitonin and released when endotoxin released and persists <24h.
* good marker for sepsis

63
Q

MODS

A

“development of potentially reversible physiologic derangement involving 2 or more organ systems that aren’t involved in the disorder that resulting in ICU admission, and arising in the wake of potentially life-threatening physiologic insult

64
Q

Simple MODS pathophysiology

A

Immune dysregulation that causes disordered systemic inflammatory processes (proinflammatory and anti-inflammatory).
- Excessive pro-inflammatory = SIRS
- Excessive anti-inflammatory = CARS
Primary insult > PAMPS & DAMPS > cytokine release > immune response > dysfunction > reduced organ perfusion, tissue hypoxia, ROS, RNS, Autophagy, apoptosis, necrotic cell death > sustained & secondary insult.

65
Q

GIT and MODS

A

Commensal bacteria overgrowth coupled with loss of mucosal barrier function permits bacterial translocation from GIT to systemic circulation. After insult the GIT can generate pro-inflammatory cytokines that drive SIRS & MODS

66
Q

Lung - specific organ dysfunction in MODS

A

Systemic proinflammatory state > sequestration of primed neutrophils > damage to basement membrane > interrupted tight junctions > increased pulmonary capillary permeability > protein-rich pulmonary oedema > alveolar flooding & surfactant inactivation > alveoli collapse > shunting > hypoxaemia > ALI

67
Q

Sepsis cardiomyopathy

A
  • early contractile dysfunction
  • biventricular dilation
  • reduced ejection fraction & fractional shortening
  • reduced response to preload and catecholamines
68
Q

Liver - specific organ dysfunction in MODS

A

Liver has extensive endogenous macrophage population (Kupffer cells) which would normally prevent systemic endotoxaemia and bacteraemia. Primary or secondary damage can result in:
- impaired gluconeogenesis & glycolysis
- coagulopathy
- reduced metabolic function
- produce cytokines

69
Q

AKI in MODS

A

associated with worse mortality and usually results from renal hypoperfusion from shock

70
Q

Sequential organ failure assessment (SOFA)

A
  1. Cardiovascular
  2. Respiratory
  3. Neurologic
  4. Renal
  5. Hepatic
  6. Haematologic
    Scored 0-4 (0= normal, 4= severe), higher the number the higher the mortality
71
Q

Management of MODS

A

Cardiovascular - optimize preload, restore effective circulating volume, maintain perfusion pressure
Ventilatory - lung protective ventilation
RRT - only if AKI present
Nutrition - early intervention with glycaemic control
Corticosteroids - only if vasopressor-dependent septic shock

72
Q

Above what temperature is considered abnormal

A

39.2

73
Q

Thermoregulation

A

A balance between the heat production & heat loss. This is controlled by the thermoregulatory centre located in the CNS in the preoptic area in the anterior hypothalamus. Thermoreceptors sense changes in temperature and either increase or decrease production; or increase or decrease heat dissipation

74
Q

Normal thermoregulation for heat loss

A

Panting
Vasodilation
Seeking cool environment
Posture changes
Grooming (cats)
Perspiration

75
Q

Normal thermoregulation for heat gain

A

Shivering
Seeking warm environment
Vasoconstriction
Posture changes
Catecholamines
Thyroxine
Piloerection

76
Q

Hyperthermia

A

Increase in C.B.T where heat is stored more than it is lost

77
Q

Pyrexia

A

Usually due to invasion or injury and is part of the acute-phase response.
- exogenous and endogenous pyrogens

78
Q

Heat stroke

A

Inadequate heat dissipation usually as a result of exposure to high ambient temperature and increased humidity.
- immediate body cooling to 39.4 to prevent MODS (radiation, convection, conduction, evaporation)

  • antipyretics will not be effective
79
Q

Benefits of fever

A

Many viruses and bacteria unable to survive and replicate above physiologic temperature
Has been shown to reduce morbidity & mortality
Part of the acute-phase response and is a normal response to infection

80
Q

Detriments of fever

A

Increased tissue metabolism
Increases caloric and water needs by 7% per 0.6 degree increase above normal
Suppresses the appetite centre
>41.6 increased cellular O2 consumption and loss of cellular functions and integrity

81
Q

Temperature above 41.6

A

Poses a risk of irreversible organ damage and DIC and must be reduced.
- Inhibit PG synthesis (NSAIDS)
- Total body cooling
- Glucocorticoids to block acute-phase response
- phenothiazines work on thermoregulatory centre
- if infectious provide antimicrobials

82
Q

CIRCI

A

Pressor-resistance hypotension in the face of adequate volume
Treated with LD hydrocortisone

83
Q

Neutrophils in response to pathogens

A

Pattern recognition receptors of the surface of neutrophils bind with PAMPs or DAMPs on the cell walls of pathogens which causes activation of neutrophils inducing the neutrophilic response (phagocytosis and/or degranulation)

84
Q

Myelopoeisis

A

Cytokine production > PRR bind to PAMPs/DAMPs > proliferation of progenitor cells > neutrophil production

85
Q

Most common drug to induce neutropaenia

A

Chemotherapy agents as they target rapidly dividing cells (myelotoxicity) and this usually results in severe neutropaenia

86
Q

Signs of febrile neutropaenia

A

Sepsis or septic shock
+- fever
Marked degenerative left shift
Opportunistic infection I.e. catheter sites

87
Q

Diagnostics for neutropaenia patients

A

CBC/Smear
Blood culture
Radiographs
Urinalysis
Bone marrow

88
Q

Gram positive sepsis

A

Usually from GIT and contains LPS and seems to be the most potent stimuli of the host immune response > TNFa and IL’s activated > pro inflammatory and CARS response

89
Q

Gram negative sepsis

A

Usually involves soft tissue, skin etc > production of exotoxins > “superantigens”

90
Q

Key factors in early phase sepsis

A

Macrophage activation and TNFa production (triggered by LPS)

91
Q

Vasomotor tone loss

A

Loss of balance between vasoconstriction and vasodilation > overproduction NO which is a smooth muscle relaxant so causes vasodilation > hyperaemic gums, prolonged CRT, increased heart rate

92
Q

Coagulation in sepsis

A

Bacterial infection and inflammation > cytokines up regulate tissue factor > TF + fVIIa and downstream products > elaboration of inflammatory cytokines and platelet activation.
Normal anticoagulant and fibrinolytic mechanisms deactivated > reduced tPA, anti thrombin, blockade of protein C/S and increased plasminogen leading to a procoagulant state

93
Q

SvO2

A

Measure of oxygen in venous blood and a marker of global O2 debt as measured in the pulmonary artery. Reflects the balance between DO2 and VO2.
ScvO2 similar but 2-3% under as measured from the jugular

94
Q

Treatment of sepsis

A
  1. Fluid resuscitation
  2. Treatment of hypertension
  3. Early empiric antimicrobials
  4. Bundle of care targets
  5. Remove source
95
Q

Options for hypotension in septic patients

A
  1. Crystalloids (avoid synthetic colloids)
  2. Blood components
  3. If adequate volume but still hypotension = vasopressors
96
Q

All RBC and most wbc are produced where by what process

A

Bone marrow via haematopoesis

97
Q

Preferred anaesthetic agents in septic patients and which to avoid

A

Ketamine; supports the cardiovascular system, blunts adverse immune response and may prevent ARDS
Benzo’s
Opioids
Sevo; favours respiratory function, less risk of lung injury, less effect on glycocalyx

Avoid; Propofol and etomidate

VTS(ECC) Preparation (21 decks)

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