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Applied Pathophysiology > Inflammation & Septic Shock > Flashcards

Inflammation & Septic Shock Flashcards

1
Q

Inflammation:

A

is part of the body’s DEFENSE mechanism/ IMMUNE SYSTEM
* the process of how the immune system RECOGNIZES AND REMOVES HARMFUL AND FOREIGN STIMULI TO BEGIN THE HEALING PROCESS

(imp. to be vague b/c can also be from tissue damage)

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2
Q

Inflammation can be either ___ or ____

A

ACUTE

CHRONIC

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3
Q

Acute inflammation:

A

a short-term response to sudden body damage (injury or a pathogen)
* Redness (erythema), swelling (edema), heat, pain (at site of injury), loss of function
* E.g. cuts, wounds, allergy, muscle tears, microbial infections

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4
Q

Chronic inflammation:

A

a long-term response lasting for prolonged periods (months to years) (result in pain & sing. damage over time due to inflammation)
* Diseases: arthritis, heart disease, Crohn’s/ Colitis, Lupus, etc.

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5
Q

What are the symptoms of Acute inflammation?

A
  • Redness
  • Swelling
  • Heat
  • Pain
  • Loss of function

(freq. at joint but can occur at other places)

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6
Q

What are the symptoms of Chronic inflammation?

A
  • Body pain
  • Constant fatigue & insomnia (b/c of inflammation)
  • Depression, anxiety & mood disorders (affect signals)
  • Problems with digestion (inflammation can occur in intestine)
  • Weight gain
  • Frequent infections (more prone to this)

(systemic feelings therefore all over body)

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7
Q

What are the 3 MOST COMMON CAUSES of inflammation?

A
  • MICROBIAL INFECTIONS→bacteria, viruses, parasites, fungi
  • EXTERNAL INJURIES→cuts, wounds, tears, sprains
  • CHEMICAL OR RADIATION EXPOSURE (can damage tissue)
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8
Q

What does tissue injury trigger?

A

LEUKOCYTE activation

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9
Q

Leukocytes:

A

a.k.a. white blood cells (WBC) immune cells
made in bone marrow and found in the lymphatic system

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10
Q

What falls under Agranular leukocytes?

A

Lymphocytes (20-25% total WBCs)
* T cells
* B cells
* Natural Killer

Monocytes (Macrophages/ Dendritic cells) (3-8% total WBCs)
(small portion - good b/c if they were higher they would be fighting an injury)

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11
Q

What falls under Granular/Granulocytes leukocytes?

A

Basophil (0.5-1%)

Neutrophil (60-70%)
- circulate bloodstream & wait (higher proportion)

Eosinophils (2-4% WBC)

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12
Q

_____ _____ immune cells trigger inflammation

A

SPECIFIC INNATE

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13
Q

What does an inflammatory response involve?

A

An inflammatory response involves a highly coordinated network of many leukocytes of the innate immune system
* Activated MACROPHAGES, GRANULOCYTES, AND NEUTROPHILS mediate local responses to tissue damage and infection (particles/agents)
* INNATE IMMUNITY is body’s 1st line of defense against pathogens
* results in a NON-SPECIFIC IMMUNE RESPONSE, including inflammation (looking for anything diff.)

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14
Q

At sites of tissue injury, damaged epithelial and endothelial cells…

A

release factors that trigger the inflammatory cascade (histamines and prostaglandins) along with CYTOKINES/ CHEMOKINES and growth factors that activate innate immune cells and result in ADAPTIVE IMMUNITY (takes weeks/months & isn’t long lasting)
* ADAPTIVE IMMUNITY develops after infection resulting in WBCs that recognize the infection → *involved in vaccination-mediated immunity

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15
Q

Which immunity is involved in vaccination-mediated immunity?

A

adaptive immunity

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16
Q

Describe the inflammation response

A

Chemical signals released by mast cells and by the invading microorganism(s)

Tissue Injury

Heat: Capillary widening; increased blood flow (more energy)

Redness & swelling: Dilation & leakiness of blood vessels
- increased permeability
- *DIAPEDESIS - fluid release into tissues (WBCs, serum, etc.)

Tenderness: Phagocytic WBCs (macrophages & neutrophils) migrate to area
- attraction of leukocytes
- extravasation of leukocytes to site of injury (eat pathogens (pus b/c of increase of BCs)

Pain: Phagocytes consume dead cells & pathogens. Platelets & clotting factor seal the wound
- systemic response
- fever & proliferation of leukocytes (depend on titre & amount of pathogen)
- signals go to brain & say in pain

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17
Q

What are Histamines?

A

are chemicals released by MAST CELLS, which INCREASE BLOOD VESSEL PERMEABILITY and STIMULATE/ facilitate OTHER WBCs to arrive

(like an alarm bell)

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18
Q

Mediators of inflammation

for Injury Recognition

A
  • Pathogen-associated molecular patterns (PAMPs)
  • Damage-associated molecular patterns (DAMPs)
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19
Q

Why does most inflammation happen?

A

b/c of failure to recognize pathogens

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20
Q

Pathogen-associated molecular patterns (PAMPs):

A

are small molecules often conserved on microbial surfaces that trigger innate immune responses (looking for non-self)
* BACTERIAL: lipopolysaccharides, peptidoglycan, flagella, pilus, etc.
* VIRAL: spike proteins, capsid, glycoproteins, DNA/RNA

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21
Q

What are the bacterial PAMPS?

A

lipopolysaccharides, peptidoglycan, flagella, pilus, etc.

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22
Q

What are the viral PAMPS?

A

spike proteins, capsid, glycoproteins, DNA/RNA

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23
Q

Damage-associated molecular patterns (DAMPs):

A

molecules within damage or dying host cells that when released trigger innate immune responses
* E.g. Human cell nucleus has cytokine IL-1a, when a cell is damaged it is released and triggers (inflammation)
* E.g. Release of cell materials that are normally internalized: DNA, ATP, K+ ions uric acid

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24
Q

What are PAMPS & DAMPS recognized by?

A

PAMPs & DAMPs are recognized by MONOCYTE Toll-like receptors (TLRs) and pattern recognition receptors (PRR)
- recognize those responses

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25
Q

Mediators of inflammation

Mediators involved in leukocyte recruitment:

A

In addition to HISTAMINES, the following also drive and regulate LEUKOCYTE RECRUITMENT:
* Prostaglandins
* Platelet activating factor (PAF)
* Thromboxane A2
* Bradykinin

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26
Q

Prostaglandins:

A

host-derived LIPIDS (fatty therefore can cross BBB & tell you that you’re in pain) made at sites of tissue damage or infection that control processes such as inflammation, blood flow, the formation of blood clots

27
Q

Platelet activating factor (PAF):

A

is a potent phospholipid activator that causes platelet aggregation, degranulation and vasoconstrictor (narrowing of blood vessels)
- turn down BP after increasing it lots

28
Q

Thromboxane A2:

A

a vasoconstrictor released by activated platelets that stimulates activation of new platelets as well as increases platelet aggregation

29
Q

Bradykinin:

A

is a peptide that promotes inflammation by causing arterioles to dilate and makes veins constrict (increases capillary bed leakage)
- increase blood while decrease fluids?

30
Q

Describe the Leukocyte activation consequences

A
  • PHAGOCYTOSIS BY LEUKOCYTE CELLS: macrophages, dendritic cells, neutrophils can engulf damaged host cell components as well as invading microbes based on TLR and PRR
  • Phagocytosis (“cell-eating”) destroys engulfed material in leukocyte cells in the lysosome with acids and degrading enzymes (immediately start fighting pathogens)
  • NEUTROPHIL EXTRACELLULAR TRAPS (NETs):
  • Neutrophils lyse to release their DNA for form a mesh that traps pathogens as well as red blood cells (RBCs) and platelets (good & bad thing)
  • LEUKOCYTE WOULD HEALING (HEMOSTASIS): macrophages, neutrophils, and FIBROCYTES repair damaged tissues to form scar tissue (fibrin)
  • Release growth factors to stimulate tissues to regenerate, repair enzymes and recruit fibrocytes for scar formation

(cells take ~days to fix & can be slowed down with co-moralities b/c ability to phagocytize isn’t as good)

31
Q

What is the Acute Inflammation Diagnosis?

A

Typically, acute Inflammation is often diagnosed on the basis of patient HISTORY and SYMPTOMS as well the *SITE OF INJURY (essential b/c can result in chronic inflammation or septic shock)

32
Q

What is the Acute Inflammation Diagnosis for non-obvious history/symptoms tests?

A

JOINT EXAMINATION for acute inflammation symptoms (to determine arthritis)

BLOOD TESTS: to measure biomarkers→typically, done for higher risk patients
* C-reactive protein (CRP); a liver protein that increases in blood with inflammation
* Erythrocyte sedimentation rate (ESR): measures how quickly red blood cells settle in a test tube (b/c they’re v. heavy ?)

X-RAYS are only used to determine muscle or bone damage (if it is suspected) as local inflammation cannot be confidently assessed on X-ray film
- sprains & bone breaks & damage on surface that doesn’t break skin (ex: broke finger)

33
Q

What is the Acute Inflammation Treatment?

A

Need to REDUCE INFLAMMATORY SYMPTOMS:
* ICE/COLD compresses→reduces heat
* REST and immobilization of the injury→allows damaged area to heal/ clot (can risk more serious/chronic damage)
* WOUND CARE→purulent vs non-purulent care (see SSTI lecture)

Treatment with NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDs)→reduces pain/ swelling (b/c patient will complain about this most - can lead to cellulitis or nerve damage etc.)
* Aspirin (Bayer), Ibuprofen (Advil), Naproxen (Aleve), Celecoxib (Celebrex)
* NSAIDs are inhibitors of cyclooxygenase (COX) enzymes that synthesize PROSTAGLANDINS (tells us we got pain & inflammation)

Corticosteroids (cortisone, prednisone) are reserved for CHRONIC INFLAMMATION treatments
- where it’s systemic/long-term

34
Q

What is Sepsis?

A

SEPSIS is a LIFE-THREATENING SYSTEMIC (BLOODSTREAM) ILLNESS attributed to a DYSREGULATED HOST RESPONSE TO INFECTION
* 2016 Sepsis-3 definition
* It is a RAPIDLY PROGRESSING DISEASE that impacts multiple organ systems causing potentially IRreversible ORGAN SHUTDOWN

35
Q

What is the problem with sepsis?

A

It is a medical emergency (in ICU - not a clinic case) that when left untreated, has HIGH PROBABILITY OF DEATH
* It is a global burden killing ~11 million persons annually*
* Since the pandemic in 2019, sepsis from COVID-19 has increased*
* “Cytokine storms” caused by SARS-Co-V2

36
Q

For sepsis, the HIGHEST MORTALITY (50.7%) for patients with:

A
  • complicated intra-abdominal infections, chronic kidney disease, renal replacement therapy, multiple organ dysfunction, prior infections, and SEPTIC SHOCK
37
Q

Sepsis vs. Septic Shock

A

Sepsis:
- Life-threatening organ dysfunction caused by a DYSREGULATED HOST RESPONSE to infection
- Acute change in total SOFA score greater than or equal (>) 2 points

Septic shock:
- Sepsis + persistent hypotension REQUIRING VASOPRESSOR USE and SERUM LACTATE >2 mmol/L despite adequate fluid resuscitation (or shows with OLIGURIA)

38
Q

Sepsis features

A
  • VASOPRESSORS are drugs or other agents that can cause the CONSTRICTION OF BLOOD VESSELS
  • HYPOTENSION (or low blood pressure) is a blood pressure UNDER: (organs will start to shut down)
  • Systolic <90 mm/Hg
  • mean arterial pressure (MAP) <70 mm Hg
  • OLIGURIA = low urinary output <400 mL/day or <20 mL/hr
  • Sequential Organ Failure Assessment (SOFA) Score (0-4)
39
Q

Sepsis is an _____ _____ caused by the body’s release of _____

A

INFLAMMATORY RESPONSE

CYTOKINES

fill in slide 22

40
Q

Describe the inflammatory response of sepsis

A
  1. Pathogen (PAMPs)
  2. Infection: Viremia/Bacteremia
  3. Activation of:
    - Endothelial cells
    - Macrophage cells
    - Coagulation + inflammation
  4. Inflammatory cytokines
    ↑Pro vs ↓Anti-inflammatory
    Pro: Tumor necrosis factor (TNF), Interleukins (IL)-1, IL-6, IL- 12
    Anti: Interleukin-1 receptor antagonist (IL- 1RA), IL-4, IL- 10
  5. Loss of Homeostasis Organ dysfunction
41
Q

Sepsis induced organ dysfunction occurs most frequently in ___ (40%), then ____ (39%), ____ (24%), liver, and central nervous system

A

HEART

KIDNEYS

LUNGS

(not in order all the time)

42
Q

Where can sepsis also result in?

A
  • CONSUMPTIVE THROMBOCYTOPENIA→low blood platelet counts
  • HAEMOLYTIC ANAEMIA→red blood cells destroyed faster than they are made
  • VASCULAR MICROTHROMBOSIS→a host response that prevents bacteria in the tissues from reaching the systemic circulation via the capillaries (red & puffy, esp. closest to injury)
  • MULTI-ORGAN DYSFUNCTION SYNDROME→progressive physiological dysfunction of two or more organs where homeostasis cannot be maintained
  • COAGULOPATHY→the ability to form blood clots is impaired
  • septic shock
  • respiratory failure
  • fever
  • LEUKOPENIA→decreased leukocytes (WBCs), typically neutrophils (probs won’t have them in places you need them)
  • hypotension
  • LEUKOCYTOSIS→an elevated WBC count, above 11 x109/L on smear
  • high cytokine production
  • high predisposition to opportunistic infections
43
Q

What are Sepsis Risk Factors & Pathogens?

A

Pathogenesis of sepsis is MULTIFACTORIAL (may be more complicated), which begins with the patient’s specific predisposition to infection
* YOUNG <5 yrs and ELDERLY >60 yrs high risk
* PRE-EXISTING CONDITIONS, CO-MORBIDITIES: heart failure, diabetes, chronic obstructive pulmonary disease, cirrhosis, alcohol dependence, and end-stage renal disease
* immunosuppressive diseases (eg. HIV) (leukemia’s or other cancer too)

44
Q

Where do the most common pathogens come from for sepsis?

A

Most common pathogens from hospitalized blood work (bacteremia)

45
Q

What is the pathogen typically that causes sepsis?

A

Gram negative (51%)
- b/c see lots of fecal-oral route of inf. (which is also becoming more antimicrobial resistant)

Gram positive (44%)
- find in skin more (lung, upper & lower respiratory tract, kidney, bladder inf’s)

Fungi (5%)
- seeing a rise, esp. in immunosuppressant/co-morbilities

46
Q

What are the Gram negative bacteria for sepsis?

A

E. coli (50-60%), Klebsiella spp., Proteus, Enterobacter, Pseudomonas aeruginosa, Acinetobacter spp.

47
Q

What are the Gram positive bacteria for sepsis?

A

Staphylococcus aureus (+/- MRSA), Enterococcus, Streptococcus pneumoniae

48
Q

What are the fungi for sepsis?

A

Candida albicans (candidemia) then other Candida spp.

49
Q

What are the initial symptoms for sepsis?

A
  • general malaise or myalgia (muscle pain) and non- specific signs such as fever (or hypothermia), chills, tachycardia (heart rate >100 beats/min), tachypnea (abnormal breathing rate), or change in mental status

(heart working v. fast b/c decrease BP, feeling like not getting enough oxygen despite increase HR & that can lead to heart arrest/heart attack, not as alert; changes in mood/beh.)

50
Q

What are the progressive uncontrolled sepsis (septic shock)?

A
  • Arterial hypotension and oliguria, hyperventilation leading to respiratory alkalosis (tissues become more alkaline b/c starting to get disregulated in signalling/ion-flow controlling net ion flow), hyperglycemia or hypoglycemia
  • Hypoperfused (reduced blood flow) liver and kidneys results in elevated lactate levels which then contributes to metabolic acidosis
  • decrease BP, therefore less BF to major organs (ex: liver, kidneys, etc.)
  • pyruvate that builds up in tissues will convert metabolically to lactate
  • see increase b/c lactose is a WA & will get more acidification in these tissues
51
Q

Describe the Sepsis Diagnosis?

A

Sepsis is due to an infection so *IDENTIFYING LOCATION AND PATHOGEN IS CRITICAL
* History: Co-morbidities, injuries, animal exposure, past antibiotic use, etc.
* Complete physical examination to identify the source of infection (esp. if from long-term care facility b/c may have missed it)
* BLOOD WORK and CULTURE SPECIMENS needed
* URINALYSIS can confirm if bladder/kidney function is compromised

SOFA score (from 0-4) where values = >2 increase mortality by 10%

52
Q

Describe the SOFA score

A

SOFA score (from 0-4) where values = >2 increase mortality by 10%

53
Q

What are SOFA concerns?

A

clinicians need laboratory results such as BLOOD PLATELETS, BILIRUBIN, and CREATININE for SOFA→TAKES TIME TO ACQUIRE (bad b/c want to diagnosis ASAP)

54
Q

What is the Quick SOFA (qSOFA)?

A

uses 3 elements (0-3), scores of >2 need urgent care
1. Respiratory rate ≥22 breaths/min, yes = 1
2. Altered mental status, yes = 1
3. Systolic blood pressure ≤ 100 mmHg, yes =1

(*imp. to know this one)

55
Q

What is the Sepsis Treatment?

A

Progressive sepsis requires intensive care hospital (ICU) treatment with IV antimicrobial therapy
* early goal-directed therapy (EGDT) with resuscitation targets (want to meet certain levels to try to pull patients out of sepsis so that if they get full blown septic shock you have some targets to meet in terms of meeting those barriers when defining septic shock)

56
Q

In ICU Sepsis treatment will involve:

A
  • Fluid therapy
  • Antimicrobial therapy
  • Vasopressors
  • Corticosteroids
  • Glucose control
  • Venous thromboembolism prophylaxis
  • Stomach Stress ulcer prophylaxis
57
Q

Fluid therapy (for ICU sepsis treatment):

A

isotonic 30 mL/kg crystalloid fluids (+/- saline) WITHIN the FIRST 3 HOURS

(Mg2+, minalial salts, water soluble molecules etc.)

58
Q

Antimicrobial therapy (for ICU sepsis treatment):

A

broad-spectrum antibiotics IV, reassessed daily to identified pathogen (esp. if unsure of causative organism)

59
Q

Vasopressors (for ICU sepsis treatment):

A

Norepinephrine (1st line), vasopressin or epinephrine to maintain MAP >65 mmHg (bring up BP ASAP)

60
Q

Corticosteroids (for ICU sepsis treatment):

A

IV hydrocortisone (if hemodynamically unstable after fluids and vasopressors)

*unlike acute inflammation

61
Q

Glucose control (for ICU sepsis treatment):

A

insulin if 2 or more blood glucose levels are >180 mg/dL (rise)

(esp. if insulin levels fall)

62
Q

Venous thromboembolism prophylaxis (for ICU sepsis treatment):

A

daily low molecular weight heparin (an anticoagulant) treatment

(trying to prevent coagulation associated with sepsis)

(for preventing dysregulated inflammation caused by net formation, neutrophil activation, to prevent nets from forming to cause stroke, blood clotting, or blockage of arteries due to an overwhelming inflammatory response)

63
Q

Stomach Stress ulcer prophylaxis (for ICU sepsis treatment):

A

patients with ↑bleeding risk

(can cause stress ulcers partic. in stomach)

(adding a proton pump inhibitor for ex to try to prevent acidity of stomach to reduce the stress of tears/breakens & ulcer formation in stomach - done preventally so patient has a better chance of recovery if inf. hasn’t gone irreversible)

Applied Pathophysiology (34 decks)

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