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Semester 3 > General Pathology 300 (Shock, & intro to infectious diseases) > Flashcards

General Pathology 300 (Shock, & intro to infectious diseases) Flashcards

1
Q

define shock

A

state of hypoperfusion to tissues (blood)

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2
Q

what are 3 possible mechanisms of shock

A
  1. Pump failure of heart
  2. Loss of circulating fluid
  3. Loss of peripheral vascular tone
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3
Q

features

A

collapse of circulation

disproportion of circulating blood volume & vascular space

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4
Q

result?

A

Tissue anoxia

multi-organ failure

cardiorespiratory failure

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5
Q

categories of shock (not including

A
  1. Cardiogenic shock = pump failure of heart
  2. Hypovolemic shock = not enough volume (blood)
  3. Hypotonic shock = not enough tone
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6
Q

how do categories of shock correspond to mechanisms of shock?

A
  1. # Pump failure of heartCARDIOGENIC SHOCK
  2. # Loss of circulating fluidHYPOVOLEMIC SHOCK
  3. # Loss of peripheral vascular toneHYPOTONIC SHOCK
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7
Q

what 3 categories of shock are sub-categories instead of main categories (in contrast to AP300 notes)

A

Obstructive shock
(categorized under cardiogenic shock?)

Septic shock
(under Hypotonic shock?)

Neurogenic shock
(hypotonic or cardiogenic??)

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8
Q

note about septic shock

A

“Septic shock is a mixed form of a variety of pathologies (hypovolemia, vasodilation, impaired cardiac function, and mitochondrial dysfunction)”

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9
Q
  1. Cardiogenic shock
A

via heart pump failure

via infarction (MI)

via destruction of large portion of myocardium

=
loss of contractile tissue
—> inability to pump

may also be via
—> myocarditis
—> valve disease
—> Arrythmias
—> conduction block (Obstructive shock?)

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10
Q
  1. Hypovolemic shock
A

Loss of circulatory volume

via
—> massive hemorrahge

via fluid loss
—> burns
—> vomiting
—> diarrhea

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11
Q
  1. Hypotonic shock
A

loss of vascular tone

blood pooling in peripheral vessels (note varicose veins?)

via
—> anaphylactic shock (allergy)

—> neurogenic
(trauma, pain, spinal cord injury)

—> bacterial infection (SEPTIC SHOCK)

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12
Q

anaphylaxis vs sepsis (anaphylactic shock vs septic shock)

A

Septic shock (from a bacterial infection).
Example: A serious infection complication called sepsis that gets so bad it leads to septic shock.

Anaphylactic shock (from an allergic reaction or asthma attack).
Example: An allergic reaction to peanuts that leads to anaphylactic shock.

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13
Q

Events of shock

A

series of events – act synergistically

cause viscious cycles

result in death if not treated

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14
Q

early vs late stages of shock

A

early stages are treatable and reversible

late stage
—> serious organ failure
—> @ this stage shock can be irreversible
(nervous tissue, myocardium = no regeneration

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15
Q

what can shock (late?) lead to

A

Acute Respiratory Distress Syndrome (ARDS)

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16
Q

Acute Respiratory Distress Syndrome

A

AKA “Shock Lung”

result of shock

lungs cannot function properly

pump failure, vasodilation —-> LOW BP
(cardiogenic/hypotonic)

LEADS TO
—> STAGNATION OF BLOOD IN PULMONARY CIRCUIT
—-> PULMONARY EDEMA

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17
Q

What can ARDS lead to?

A

COR PULMONALE

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18
Q

recall cor pulmonale

A

The definition of cor pulmonale (pulmonary heart) is when a lung issue causes your right ventricle (heart chamber) to get so big that your heart starts to fail.

It’s a type of right-sided heart failure. Normally, your right ventricle sends blood to your pulmonary artery to get oxygen from your lungs.

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19
Q

ARDS facts

A

break-down of alveolar-capillary units of lungs

loss of lung function

hypoxia/anoxia
dyspnea/tachypnea

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20
Q

what can anoxia lead to in tissues

A

anoxia of tissues can lead to release of cytokines
E.g.
—> TNF
—> IL-1

Leads to
—> increase permeability of vessels
—> vasodilation (hypotonic)

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21
Q

why hypoxia/anoxia lead to cytokine release (?)

(Hypoxia induced factor)

A

Hypoxia leads to the activation of HIF-1α, which is involved in several cellular processes (such as apoptosis, vasomotor control, energy metabolism and angiogenesis).

Additionally, hypoxia leads to the activation of HIF-2α, which is involved in the activation of pro-inflammatory cytokines.

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22
Q

Clinical correlations of shock (THREE STAGES)

A
  1. Early, or compensated shock
  2. Decompensated but reversible shock
  3. Irreversible shock
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23
Q
  1. Compensated (early) shock
A

adaptive characteristics to compensate for changes in homeostasis

E.g.
—> Tachycardia

—> Peripheral artery casoconstriction
(send blood to vital organs?)
-NOTE PALLOR (“paleness or a loss of color from your normal skin tone. Pallor affects your skin and mucous membranes”

—> reduced urine production to preserve volume of circulating blood

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24
Q

Compensated shock symptoms

A

BP is normal

no serious signs of organ ischemia

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25
Q
  1. Decompensated shock
A

compensatory mechanisms failing

Hypotension
—> BP & CO drop

Tachypnea
—> shortness of breath, increased respiratory rate

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26
Q

Decompensated shock symptoms

A

Oliguria (renal fluid output decreases)

Acidosis (build up of metabolic wastes, CO2)

—> renal excretory failure / retention of metabolites

—> note also possible congestion in lungs = CO2 build-up

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27
Q
  1. Irreversible shock
A

circulatory collapse

hypoperfusion of vital organs

loss of vital functions

great distress, unconsciousness, death

NOTE ALSO
—> DISSEMINATED INTRAVASCULAR COAGULATION

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28
Q

disseminated intravascular coagulation (irreversible shock)

A

“Disseminated intravascular coagulation, or DIC, is a complicated condition that can occur when someone has severe sepsis or septic shock.”

widespread clot formation
/
in small blood vessels (?)

via
—> hypercoagulability of blood
—> fluid loss
—> hemoconcentration

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29
Q

Infectious diseases

A

..

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30
Q

infection

A

disease caused by microorganisms (including viruses)

—> esp microorganisms that release toxins or invade body tissues

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31
Q

infection is

A

process where organism establishes parasitic relationship with host

can cause cellular damage
—> producing toxins
—> intracellular multiplication
—> competing with host metabolism

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32
Q

INFECTION vs COLONIZATION

A

colonization:
micro-organisms reside harmlessly on/in body,
&
Perform useful functions
—> gut bacteria/digestive health
—> adaptation of immune system
—> reproductive health

Microbes on/in body outnumber cells by 10-1

Colonies not harmful, but can become harmful if become infections

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33
Q

Colonies

A

do not cause detectable Sx /infection

However, they can be transmitted to others

CAN CAUSE INFECTION IF IMMUNE SYSTEM WEAKENED/COMPRIMISED — or if circumstances like going from one place to another (cut/break in skin)

—> some bacteria may thrive in some parts of body, but not in others

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34
Q

Normal flora

A

mix of organisms typically found @ a particular anatomical site

I.e.
In that part of the body, it would be typical to find a particular set of micro-organisms

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35
Q

what are benefits for normal flora

A

nutrients

stable environment

proection/transport from host

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36
Q

what are benefits for host

A

nutrition/digestion benefits

stimulation/development of immune system

protection against colonization/infection of pathogenic microbes

37
Q

relatively, what is the proportion of micro-organisms that can cause infection?

A

only small proportion are capable of causing infection/disease

38
Q

Clinical manifestations (infection)

A

vary based on pathogen type (etiology)

also vary based on system involved

39
Q

clinical manifestations (SYSTEMIC Sx)

A

fever, chills, malaise, enlarged lymph nodes (lymphadenopathy)

consitutional symptoms (?)

40
Q

Integumentary system Sx

A

pus, open wound, rash, red streaks, bleeding

41
Q

CV system Sx

A

tachycardia,

hypotension
(RECALL cytokines —> vasodilation/hypotension E.g. TNF, IL-1)

also
increased pulse rate (?)

42
Q

CNS Sx

A

altered consciousness, confusion, seizures, headache, memory loss

photophobia

Stiff neck (MENINGITIS)
I.e.
NUCHAL RIGIDITY

43
Q

GI Sx

A

nausea, vomiting, diarrhea

44
Q

Genitourinary Sx

A

dysuria, flank pain (kidneys?)

hematuria

oluguria

urgency, frequency, nocturia

45
Q

URT Sx

A

tachypnea, dyspnea

cough, hoarseness, sore throat

nasal drainage, sputum production

decreased exercise tolerance

46
Q

TYPE OF (MICRO)ORGANISMS

A

Viruses

BACTERIA

MYCROPLASMAS

RICKETTSIAE

CHLAMYDIAE

PROTOZOA

FUNGI

PRIONS

47
Q

viruses

A

pathogen made of nucleic acid (DNA/RNA) inside protein shell

smallest known organism (only visibly through electron microscope)

depends on host cells for replication

48
Q

how many virus types that infect humans

A

estimated 400 viruses that infect humans

49
Q

how are viruses classified

A

Nucleic Material

Size

Shape

Means of transmission

50
Q

BACTERIA

A

single-celled microorganism

without true nucleus

without membrane bound-organelles

have CELL WALLS

can grow INDEPENDENTLY without other cells

51
Q

bacteria classified via

A

shape:
—> SPHERICAL (cocci)
—> ROD (bacilli)
—> SPIRAL (spirochetes)

response to staining:
—> gram positive
—> gram negative
—> acid fast

motility

capsulation

spore forming

52
Q

MYCOPLASMAS

A

“mykes (fungus) and πλάσμα, plasma (formed)”

self-replicating, very small bacteria

LACK CELL WALL (cell membrane =/= cell wall)

unique/different from other bacteria in lacking cell wall

53
Q

mycoplasmas usually associated with which diseases/systems

A

diseases of repiratory system

diseases of urinary system

E.g.
PNEUMONIA

54
Q

RICKETTSIAE

A

“Obligate” Intracellular Bacteria
—> I.e. require host for replication (LIKE VIRUS)

“animal reservoire”

arthropod vector (insects?)

55
Q

Obligate define

A

Capable of existing only in a particular environment or by assuming a particular role.

E.g.
An obligate aerobe, such as certain bacteria, can live only in the presence of oxygen.

An obligate parasite cannot survive independently of its host.

56
Q

vector

A

BIOLOGY
an organism, typically a biting insect or tick, that transmits a pathogen, disease, or parasite from one animal or plant to another.

57
Q

Example of conditions via RICKETTSIAE

A

ROCK MOUNTAIN SPOTTED FEVER

TYPHUS

58
Q

CHLAMYDIAE

A

small “OBLIGATE” intracellular bacteria

“Obligate”
—> requires host cell for replicaiton

associated with
—> STDs
—> Respiratory infections

59
Q

PROTOZOA

A

single-celled organisms

classification
—> INTRAINTESTINAL parasites
—> EXTRAINTESTINAL parasites

60
Q

E.g. conditions (intraintestinal protozoa)

A

Amebiasis

Giardiasis

61
Q

E.g. conditions (extraintestinal protozoa)

A

Malaria

Toxoplasmosis

62
Q

FUNGI

A

unicellular / filamentous organisms

have hyphae

have CELL WALL
have NUCLEUS

Can occur as YEASTS (single-cell, oval shaped organisms)

Can occur as MOLDS (organisms with branching filaments)

Can be systemic or local
E.g.
Fungal skin infections (ringworm, athlete’s foot),
fungal mucosal infections (candida vaginitis)

63
Q

hyphae

A

each of the branching filaments that make up the mycelium of a fungus.

64
Q

mycelium

A

A mycelium is a network of fungal threads or hyphae. Mycelia often grow underground but can also thrive in other places such as rotting tree trunks. A single spore can develop into a mycelium.

The function of the mycelium is to provide a transportation network to pass nutrients along the fungal body.

65
Q

presence of fungus or yeast in the blood

A

Fungemia

66
Q

Fungal diseases in humans called

A

mycoses

“Fungal infections, or mycosis, are diseases caused by a fungus (yeast or mold).”

“most common on your skin or nails, but fungi can also cause infections in your mouth, throat, lungs, urinary tract and many other parts of your body.”

67
Q

PRIONS

A

infectious particles

consist of proteins, WITHOUT NUCLEUS ACIDS

transmitted from animals to humans

E.g.
Creutzfeldt-Jakob disease

Bovine spongiform encephalopathy (Mad Cow disease)

68
Q

Classification

A

endogenous (from within)
—> microorganism that was previously not pathogenic, but now pathogenic
E.g.
Yeast

exogenous (not from within)
—> from source outside body
E.g. Influenza virus

Nosocomial
—> acquired in health care setting
E.g. staphylococcus

69
Q

nosokomos

A

from Greek nosokomos ‘person who tends the sick’

70
Q

Tranmission

A

invading organism must be transported from the infected source to susceptible host

71
Q

portals of exit from host

A

feces, urine, vomit, tears, semen, open lesions, blood

72
Q

transmission routes

A

via several possible routes

contact
airborne
droplet
vehicle
vector

73
Q

contact

A

direct or indirect

74
Q

airborne

A

float

air currents

remain suspended

small particles

75
Q

droplet

A

“fall out within 3 ft of source” (??)

large particles

76
Q

vehicle

A

E.g.
food, water

77
Q

vector

A

intermediate source
E.g.
insect (usually)

78
Q

pathogen may enter new host via

A

ingestion
inhalation
bites
contact with mucosa

transplacentally

injections

79
Q

other

A

skin to skin contact

contact with blood/fluids

contact with contaminated articles

80
Q

variation (requirement for infection to take place)

A

number of organisms required to start infection

duration of exposure required to start infection (RECALL LYME)

pathogenecity:
“the property of causing disease.”

81
Q

Susceptibility – depends on

A

vary from person to person

—>
Age?
Nutrition
hormonal balance

concurrent disease (immmune comprimised?)

drug use?

hygiene

82
Q

chain of transmission

A

pathogen or agent: virus, mycobacteria, bacteria, fungi, prions

reservoire:
humans

portal of exit: GU, GI, oral cavity, open lesion, semen, tears, blood, feces, urine

Transmission: contact (direct/indirect), airborne, droplet, vehicle, vector

modes of entry: ingestion, inhalation, injeciton, transplacental

susceptible host

83
Q

portal of exit

A

The Portal of Exit refers to any route that the pathogen can leave the reservoir

84
Q

chain of transmission define

A

This describes how microorganisms are transmitted from one person or place to another.

This could be via someone’s hands, on an object, through the air or bodily fluid contact. portal of entry. This is how the infection enters another individual.

85
Q

chain of transmission is

A

mode of transmission

portal of entry

susceptible host?

infectious agent

reservoir

portal of exit

86
Q

defense

A

first, second, third line of defense

first = mechanical barriers

second = inflammation, nonspecific/innate immune response

third = acquired imune response

87
Q

first line of defense e.g.

A

intact skin, mucous membranes

oil, perspiration

cilia (resp tract)

gag/cough

peristalsis (GI)

flushing of tears, saliva, mucus

normal flora

88
Q

2nd/3rd line of defense

A

2
inflammatory process
NK cells, eosinophils, neutrophils, macrophage, basophil

3
lymphatic system
leukocytes/lymphocytes (B/T cells)

cehmical, proteins, enzymes

89
Q
A

Semester 3 (32 decks)

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