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General pathology (pathophysiology) > General pathophysiology - hemodynamic disorders, stress/shock > Flashcards

General pathophysiology - hemodynamic disorders, stress/shock Flashcards

1
Q

bradykinin

A

is a potent endothelium-dependent vasodilator and mild diuretic, which may cause a lowering of the blood pressure.

promotes inflammation

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2
Q

Regulation of blood flow is based on

A

the metabolic requirements of the tissues

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3
Q

Blood circulation control centres are located in the

A

diencephalon and cortex.

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4
Q

name 3 Vasoconstrictors

A

adrenalin
noradrenalin
vasopressin, also called antidiuretic hormone

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5
Q

name 6 Vasodilators

A

acetylcholine
bradykinin
histamine

CO2
ATP
lactic acid produced in the muscles

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6
Q

Thrombosis

A

blood clotting at inappropriate sites

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7
Q

Embolism

A

migration of a solid, liquid or gaseous foreign material within the intravascular space, capable of causing occlusion with injurious consequences.

blood clot (thrombus),
a fat globule (fat embolism),
a bubble of air or other (gas embolism),
or foreign material (even bullets, broken off iv catheters can cause embolisms).

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8
Q

Blood hydrostatic pressure is

A

the force exerted by the blood against the wall of a capillary that drives fluid out of capillaries and into the tissues.

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9
Q

Colloid osmotic (oncotic) pressure exerted by plasma proteins tends to

A

pull fluid INTO capillaries.

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10
Q

body fluid makes up what percentage of total body weight

A

60%

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11
Q

body fluids are grossly divided into what two compartments?
what are their percentages?

A

extracellular fluid 20% of all body fluid
&
intracellular fluid 40% of all body fluid

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12
Q

extracellular fluid is further divided into?

A

interstitial fluid
&
intravascular fluid

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13
Q

if extracellular fluid makes up 20% of body fluids, what portion of this is interstitial fluid
& intravascular fluid?

A

interstitial fluid 15%
&
intravascular fluid 5%

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14
Q

Anasarca

A

is a medical condition that leads to general swelling of the whole body. It happens when your body tissues retain too much fluid due to several reasons.

It differs from other types of edema that affect one or two parts of the body. The condition is also known as extreme generalized edema or massive edema.

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15
Q

another word for Noninflammatory oedema

A

transudate

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16
Q

another term for Inflammatory oedema

A

exudate

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17
Q

Hyperemia & congestion

A

increased tissue INflow because of arteriolar dilation/ excess blood builds up

impaired venous OUTflow from a tissue (may include cyanosis)
Arterial inflow to the venous-hyperemic area is impeded due to low blood flow rate.

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18
Q

TYPES OF ARTERIAL HYPEREMIA (2)

A
  1. Physiological or functional arterial hyperemia
  2. Pathological arterial hyperemia
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19
Q

Postischemic hyperemia

A

The rapid reactive hyperemia response to ischemia in a certain region may cause brain ischemia and loss of consciousness.

In case of ruminal dilatation rapid elimination of vascular compression factors; fast removal of transudates from thoracic and abdominal cavities, etc.

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20
Q

What type of heart disease will cause venous hyperemia?

A

right-sided heart failure

When the right side loses pumping power, blood backs up in the body’s veins.

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21
Q

emphysema

A

the alveoli become abnormally inflated, damaging their walls and making it harder to breathe.

causes shortness of breath

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22
Q

Induration

+ name 3 causes

A

hardening of tissue

Induration follows, e.g.:
chronic venous congestion;
impaired cellular nutrition
and cellular atrophy;

the above stimulate proliferation of connective tissue.

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23
Q

Induratio fusca pulmonum

A

chronic pulmonary congestion/edema leading to brown induration

hardening of the pulmonary tissue due to the increase in pulmonary connective tissue.

Diapedesis of RBCs results in the release of pigments and brownish discoloration of the tissue (hemosiderin).

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24
Q

ischaemia

A

interruption in the arterial blood supply to a tissue/organ

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25
Q

Ischemic (hypoxic) injury (name 2 reasons for the cell damage)

A

Inadequate tissue perfusion leads to cell damage for two reasons:

  1. Tissue hypoxia
  2. The absence of blood flow causes the accumulation of cellular metabolic by-products which cause cellular acidosis
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26
Q

what is reperfusion injury

what negatives effects does it involve (5)

A

Cellular damage after restoration of blood flow of previously viable ischemic tissues.

Involves
* Formation of oxygen-derived free radicals
* Excessive intracellular calcium-ion overload
* Worsening of the mitochondrial damage
* Progression of inflammation
* Microvascular damage – decreased or ceased tissue perfusion (a condition referred to as “no-reflow phenomenon”).

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27
Q

name 5 types of ischemia

A
  1. Compressive ischemia – is the result of artery compression by tumour, scar, foreign body, etc.
  2. Endogenous ischemia – narrowing of the arteries caused by a build-up of plaque – atherosclerosis
  3. Hematogenous /Occlusive ischemia – Changes in the blood – thromboses, embolism
  4. Collateral / Redistributive ischemia – Acute hyperemia in some other parts of the body
    or organs, e.g. postprandial intestinal hyperemia
  5. Neurotonic / Neurogenic ischemia - Stimulation of vasomotor centres and vasoconstrictors: temperature, electrical stimulation, drugs, hormones, etc.
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28
Q

differnce between Petechiae and purpura

A

petechiae (1-2 mm)
purpura (slightly larger >3 mm)

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29
Q

Suggillation/Ecchymosis

A

bruises >1-2 cm

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30
Q

Haemorrhagia per rhexin

A

Is a cause of hemorrhage/classification.

It means bleeding due to rupture of a blood vessel
(cuts/incision, stab/puncture wounds, etc.)

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31
Q

Haemorrhagia per diabrosin

A

A cause of hemorrhage
Erosion of vascular walls due to pathological processes

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32
Q

Haemorrhagia per diapedesin

A

A cause of hemorrhage
Bleeding due to increased permeability of the (undamaged) (micro)vessel wall

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33
Q

Cardiac tamponade

A

is pressure on the heart that occurs when blood or fluid builds up in the pericardial sac

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34
Q

Physiological hemostasis broadly involves what (2)

A

a) Reflex vasoconstriction
b) Blood coagulation

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35
Q

Surgical treatment of hemorrhage broadly involves what (2)

A
  1. Vascular compression to promote hemostasis
  2. Ligation of blood vessels; coagulation products
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36
Q

The three factors of Virchow’s triad include

A

intravascular vessel wall damage/endothelial injury,

stasis or turbulence of bloodflow, and

the presence of a hypercoagulable state/blood hypercoagulability

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37
Q

Mural thrombi are

A

thrombi that attach to the wall of a blood vessel and cardiac chamber.

Mural thrombus occurrence in a normal or minimally atherosclerotic vessel is a rare entity in the absence of a hypercoagulative state or inflammatory, infectious, or familial aortic ailments.

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38
Q

Occlusive thrombi can be classified as either (2)

A

– Arterial thrombi,
– Venous thrombi or phlebothrombi

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39
Q

Parietal thrombi are what

A

(arterial) thrombi adhering to one side of the wall of a vessel; restricts blood flow but does not block it entirely

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40
Q

describe central thrombi

A

cause partial obstruction

thrombus adheres to opposite sides of the vessel wall leaving open spaces inside the lumen between the thrombus and the vessel walls

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41
Q

CLASSIFICATION OF THROMBI
ACCORDING TO THE LOCATION IN A
BLOOD VESSEL (3)

A

Parietal thrombi
Central thrombi
Obstructive/Occluding thrombi

42
Q

Obstructive/Occluding thrombi

A

produce luminal obstruction and cessation of blood flow

43
Q

CLASSIFICATION OF THROMBI
ACCORDING TO COLOUR (3)

A

Thrombus albus – White thrombus
Thrombus ruber – Red thrombus
Thrombus combinatus – Mixed thrombus

44
Q

Thrombus albus

A

White thrombus

Thrombi that are of greyish-white colour. First, adhesion and aggregation of platelets occur in the damaged region, followed by a layer of leukocytes.

45
Q

Thrombus ruber

A

Red thrombus

A conglomeration of fibrin and the cellular components of blood (the percentage of formed elements is similar to that of the blood). Typically, the formation of white
thrombi that causes the initial formation of the clots precedes the formation of red thrombi.

46
Q

Thrombus combinatus

A

Mixed thrombus (layered thrombus)

Contains both white and red thrombi. After the formation of a white thrombus a layer of
red thrombus will adhere on it. Deposition of several new white and red layers may occur.

47
Q

potential Fate of the Thrombus (4)

A

Propagation
Embolization
Dissolution
Organization and recanalization

48
Q

Propagation of a thrombus

A

The thrombus may accumulate more platelets and fibrin (propagate), eventually leading to vessel obstruction.

49
Q

Embolization of thrombi

A

Thrombi may dislodge and travel to other sites in the vasculature.

50
Q

Dissolution of thrombi

A

Thrombi may be removed by fibrinolytic activity.

51
Q

Organization and recanalization of thrombi

A

Thrombi may induce inflammation and fibrosis (organization) and may
eventually become recanalized;

that is, may reestablish vascular flow, or may be incorporated into a thickened
vascular wall.

52
Q

DIC

A

disseminated intravascular coagulation
* the sudden onset of widespread fibrin thrombi in the microcirculation

  • Although these thrombi are not usually visible on gross inspection, they are readily apparent microscopically and can cause diffuse circulatory insufficiency, particularly in the brain, lungs, heart, and kidneys
  • It should be emphasized that DIC is not a primary disease but rather a potential
    complication of any condition associated with widespread activation of thrombin.
53
Q

another term for a dislodged thrombus

A

thromboembolism

54
Q

infarct

A

An infarct is an area of ischemic necrosis caused by occlusion of either the arterial
supply or the venous drainage in a particular tissue.

55
Q

infarctions can be classified:

A

on the basis of their color
- red (haemorrhagic)
- white (anemic)

presence or absence of microbial infection
- septic
- bland

56
Q

infarction can locally lead to? (3)

A

ischemic coagulative necrosis (most infarcts are ultimately replaced by scar tissue)

liquefactive necrosis

abscess

57
Q

types of stasis (3)

A

ischemic stasis
– Cessation of capillary blood flow caused by arterial occlusions

stagnation
– Cessation of blood flow caused by venous congestion

true capillary stasis
– A distinct disorder of capillary circulation. Pathological changes can be caused by
inflammation.

58
Q

Chronic stasis can cause (3)

A

parenchymal atrophy
proliferation of connective tissue
induration (hardening) of organs

59
Q

Phases of stress (3)

A
  1. ALARM phase
    a. Shock – occurs after the stressor effects, glucocorticoids ↓
    b. Anti-shock – glucocorticoids ↑ sympathetic nervous system ↑
  2. RESISTANCE phase
    Most prevalent– sympathetic nervous system will normalize
  3. EXHAUSTION phase
    Glucocorticoids ↓
60
Q

ACTH

A

adrenocorticotropic hormone

produced by and secreted by the anterior pituitary. ACTH controls the production of cortisol produced by the zona fasciculata layer of the adrenal coretex.

61
Q

Shock (circulatory)

A

is a lifethreatening condition that occurs due to inadequate oxygenated blood supply of tissues by circulatory system resulting in inadequate tissue level of oxygen. Circulatory shock is related to a problem with the circulatory system and is not related to the emotional state of shock (acute stress reaction).

Typical signs of shock are low blood pressure, a tachycardia and poor end organ perfusion – low urine output and loss of consciousness.

62
Q

Rheological properties of blood

A

Rheological behaviour of blood is studied as dominated by plasma viscosity, hematocrit and Red Cell properties, namely aggregability and deformability.

Rheology is the science of deformation of material.

63
Q

Development and progression of circulatory shock depend on:

A
  1. The cause and duration of the shock
  2. Persistence of compensatory negative homeostatic feedback mechanisms
  3. Positive feedback mechanisms resulting from inadequate tissue perfusion and vicious circle (circulus vitiosus) that lead to inability to maintain homeostasis (cause homeostatic imbalance/failure)
64
Q

Kidney/Renal failure develops in –?– after shock

A

1 to 3 days

65
Q

Lung failure develops in –?– after shock

A

3 to 5 days

66
Q

Liver failure develops in –?– after shock

A

4 to 8 days

67
Q

Name 3 other conditions may develop at different times due to untreated/unresolved shock

A

– Severe respiratory failure
– Sepsis
– Severe hemorrhagic gastroenteritis

68
Q

According to cause circulatory shock can be divided to:

A

– Hypovolemic e.g. hemorrhage
– Cardiogenic e.g. myocardial infarction
– Obstructive eg. pulmonary embolism

– Distributive
* impaired utilization of oxygen by the cell because of vasodilation e.g. septic shock

69
Q

Which arteries are not involved in
vasoconstriction_

A

Coronary and cerebral arteries are not involved in vasoconstriction.

70
Q

Name 5 characteristic features of hypovolemic shock

A
  1. Hypotonic blood pressure values / low
    blood pressure
  2. Tachycardia
  3. Decreased cardiac output
  4. Cold, pale skin and mucous membranes
  5. Thirst (dry mouth) and oligoanuria (diminished urine output)
71
Q

What is neurogenic shock?

A

A condition caused by the loss of signals from the
sympathetic nervous system that maintain the normal vasomotor tone, that results in extensive vasodilation.
Low blood pressure occurs due to decreased
systemic vascular
resistance.

72
Q

Name 3 causes of neurogenic shock.

A

Improper administration of regional spinal
anesthesia – “spinal shock” resulting from
disruption of efferent pathways to spinal
sympathetic neurons.

Deep general anesthesia – vasomotor centre
depression.

  • Severe brain damage – cerebral ischemia.
73
Q

syncope

A

Fainting; a variation of
neurogenic shock, associated with several
neurological disorders caused by surgery or
pharmacological blockade (ganglioblockators).

A ganglionic blocker is a type of medication that inhibits transmission between preganglionic and postganglionic neurons in the autonomic nervous system, often by acting as a nicotinic receptor antagonist.

74
Q

Orthostatic collapse/syncope

A

Results from the increased excitation in the parasympathetic nervous system; bradycardia, vasodilation of skeletal muscles that leads to the reduction in arterial blood pressure; reduction in cerebral blood flow; loss of consciousness (vasovagal
syncope).

The word “orthostasis” means to stand up, so the condition is defined as low blood pressure that occurs upon standing.

75
Q

Septic shock

A

Bacteria and their toxins will stimulate macrophages to produce and release cytokines.
Cytokines have a direct impact on endothelial cells and as a result the coagulation cascade is
activated and agglutination receptors will be activated.

Follows vasodilatation, fluid will leave vessels and blood viscosity will rise causing hypovolemia and intravascular coagulation -> DIC.

76
Q

Stages of septic shock / Progression of sepsis

A
  1. Early stage / Developing phase /vasodilation phase
  2. Late stage or hypovolemic phase / hypoperfusion
77
Q

Name 4 inflammatory mediators contributing to septic shock.

A
  1. The interleukins
  2. Tumor necrosis factor-alfa
  3. Platelet-activating factor
  4. Myocardial depressant factor
78
Q

In the event of septic shock, interleukins are released from where in response to what?

A

Interleukins are
released by macrophages in response to bacterial toxins.

Net effect: produce fever, vasodilation and hypotension, edema and elevated WBC.

79
Q

In the event of septic shock, tumor necrosis factor-alfa is released from where in response to what?

A

Tumor necrosis factor-alfa is produced by macrophages, NK cells & mast cells in response to endotoxins & interleukins.

80
Q

In the event of septic shock, platelet-activating factor is released from where in response to what?

A

Platelet-activating factor released from mononuclear phagocytes, platelets and some endothelial cells in response to endotoxin.

Net effect: generates symptoms of shock as do interleukins and TNF but may also initiate multiple organ failure.

81
Q

In the event of septic shock, myocardial depressant factor is released from where in response to what?

A

Myocardial depressant factor is secreted from WBCs in response to endotoxin.

Net effect: produces myocardial depression and ventricular dilation.

82
Q

Describe the progression of shock using 6 points.

A
  1. Hypotension
  2. Tachycardia
  3. Hypoventilation
  4. Acute renal failure (oliguria = low urine output -> azotemia)
  5. Acidosis and hypoxia
  6. Impaired consciousness
83
Q

What type of shock is typically warm shock?

A

septic

84
Q

What type of shock is typically cold shock?

A

hypovolemic
cardiogenic

85
Q

Anaphylactic reactions (immediate-type reactions) are
caused by

A

IgG and IgE antibodies that have the ability to bind to receptors on basophils and mast cells.

86
Q

Homocytotropic
antibodies are

A

antibodies that have an affinity for mast cells of the same species.

87
Q

Anaphylaxis is an

A

acute systemic hypersensitivity reaction to a sensitizing antigen.

88
Q

Atopy is a

A

genetic disposition to develop an immediate-type allergic reaction and produce elevated levels of IgE upon exposure to an environmental antigen

89
Q

Type I hypersensitivity is also known as an immediate reaction and involves which immunoglobulin…?

A

E (IgE) mediated release of antibodies and mast cell degranulation -> histamine release.

Reaction can be very fast and severe – anaphylaxis.

Note: Some non allergenic factors can cause anaphylactic shock – so called
anaphylactoid (IgE independent) reactions
– Eg. opioids, muscle relaxants, cold and heat.

90
Q

An anaphylactogen is

A

any substance capable of producing a condition of anaphylaxis
(e.g., blood serum, egg
white/albumen, erythrocytes, microbes, etc.)

91
Q

difference between anaphylaxis and anaphylactic shock

A

Anaphylaxis is a severe, life-threatening, generalized or systemic rapid-onset hypersensitivity reaction.

Anaphylactic shock is a severe rapidly progressing anaphylactic reaction (anaphylaxis) resulting in a life-threatening drop in blood pressure.

92
Q

the 4 hypersensitivity reactions’ mediators

A

Type I - immediate type, mediated by IgE-antibodies

Type II - mediated by CD4+ T cells and IgM or IgG antibodies

Type III - mediated by neutrophils & immune complexes

Type IV - delayed-type, mediated by T-lymphocytes

93
Q

What is Arthus phenomenon?

A

Immune complex–mediated hypersensitivity

After local administration (intradermal injection) of the antigen, the local reaction is seen as hyperemia and edema.

Exudative haemorrhagic inflammation will develop at the site of injection that may lead to
necrosis.

94
Q

Immune complex vasculitis

A

In immune complex vasculitis, immune complexes deposit in the vascular endothelium activating the complement, and causing leukotaxis.

Capillaries of the
limbs and renal glomeruli are mostly involved (glomerulonephritis).

membranoproliferative glomerulonephritis
= when immune complexes are deposited in the glomeruli and stimulate basement membrane thickening and glomerular cell proliferation

95
Q

Serum sickness is

A

a special form of immune complex vasculitis. It is a hypersensitivity reaction that results from the single injection of a large dose of heterologous protein or serum, and
is related to the onset of antibody synthesis.

Latent period is 6 – 10 days. Prodromal
symptoms may occur. Serum sickness is characterised by a diversity of symptoms
and multiple organ failure.

96
Q

How do you calculate absolute reticulocyte count?

A

= Reticulocyte percentage × Hematocrit percentage / normal_Hematocrit.

97
Q

How do you calculate the reticulocyte index?

A

You first calculate the corrected reticulocyte count and then using a provided table, divide that sum by the estimated maturation coefficient given in table.

(Hct / 45) * Retic / Maturation

98
Q

How long does the reticulocyte regeneration response take?

A

4-5 days from onset of blood loss or anemia

99
Q

What species do not release reticulocytes?

A

horses

horse spleens have a huge store of mature red blood cells

their regenerative response is not really clinically interpretable like in dogs

100
Q

What is a leukemoid reaction?

A

an excessive increase in WBCs

“leukemia-like”

General pathology (pathophysiology) (16 decks)

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