Shock! Flashcards

1
Q

Shock is defined as a state of systemic tissue ________ due to ____________________ and/or _________________________

A

hypoperfusion

reduced cardiac output

reduced effective circulating blood volume.

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2
Q

Types of shock

__________ shock
__________ shock
_______ shock
________ shock
____________ shock

A

cardiogenic

hypovolaemic

septic

neurogenic

anaphylactic

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3
Q

Cardiogenic shock

Acute ______ failure with sudden fall in ________ without actual _________

A

circulatory

cardiac output

reduction of blood volume.

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4
Q

Cardiogenic shock

This results from ___________ failure.

A

myocardial pump

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5
Q

Cardiogenic shock

The causes include
A. Deficient emptying

_________________ is the most obvious cause of pump failure.

_____________ rupture

_________ rupture

acute myocarditis

cardiac _______

Cardiomyopathies

A

Myocardial infarction

papillary muscle

ventricular

arrhythmias

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6
Q

Cardiogenic shock

The causes include
B. Deficient filling

Cardiac _______ [extrinsic ____] from ________

A

tamponade; compression

haemopericardium

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7
Q

Cardiogenic shock

The causes include

C. obstruction to outflow

_______________
Tension __________
Dissecting _____________

A

Pulmonary embolism

pneumothorax

aortic aneurysm

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8
Q

Hypovolaemic shock

This results from ____________ or _______

Causes include

Severe ________,

Fluid loss :severe ____, diarrhoea, vomiting, extensive ____, uncontrolled ________,__________, ______ over _____.

A

loss of blood or plasma volume

haemorrhage

burns; injury; diabetes mellitus

diabetes insipidus

diuretic over dose

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9
Q

Shock associated with systemic inflammation

It is caused by a variety of ______,

Like : _________________

A

insults

Microbial infections, burns, trauma, and or pancreatitis

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10
Q

Shock associated with systemic inflammation

The common pathogenic feature is a massive _________ that produce arterial _______, vascular _____, and venous _______

A

outpouring of inflammatory mediators

vasodilation

leakage
blood pooling

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11
Q

Neurogenic and anaphylactic shock

Less commonly, shock can occur in the setting of an anesthetic accident (accidental high spinal anesthesia) or a _______ injury ( _______ shock), or an ___–mediated hypersensitivity reaction ( _________ shock).

A

spinal cord; neurogenic

IgE; anaphylactic

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12
Q

Neurogenic and anaphylactic shock

In both of these forms of shock, acute _________ leads to ________ and tissue _______

A

vasodilation

hypotension

hypoperfusion

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13
Q

Septic shock

Sepsis is defined as ________________________ due to a dysregulated ______________.

A

life-threatening organ dysfunction

host response to infection.

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14
Q

Sepsis accompanies infection either ____________________, or associated with the _________________________

A

confined to a local site from which toxins are absorbed

invasion of organisms into the blood stream (septicaemia).

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15
Q

Septic shock is defined as a subset of _______ in which particularly profound _____,______, and _______ abnormalities substantially increase mortality.

A

sepsis

circulatory, cellular, and metabolic

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16
Q

Pathogenesis of septic shock

It is associated with systemic ______ and peripheral _______ leading to _______

It is caused by ________ and ______

A

vasodilation

pooling of blood

tissue hypoperfusion

bacterial and fungal infection .

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17
Q

Septic shock is Commonly triggered by _______________ infections followed by _______ organisms and then systemic _______ infections.

A

gram positive bacterial

gram negative

fungal

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18
Q

In septic shock

There is widespread _____________ often leading to a _______ state that can manifest as ____________

A

endothelial cell activation and injury

hypercoagulable

DIC (Disseminated Intravascular Coagulation)

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19
Q

Several microbial constituents can initiate the process of septic shock

T/F

A

T

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20
Q

Septic shock has a ___ to ___% mortality rate depending on centres.

A

20

75

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21
Q

Factors that play major roles in Pathophysiology of septic shock

Inflammatory and counter inflammatory responses
– –
Microbial cell constituents engage _________ of _____ immune system to activate pro inflammatory responses

A

receptors on cells

innate

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22
Q

Factors that play major roles in Pathophysiology of septic shock

Inflammatory and counter inflammatory responses
– –
________________________ + _________________
G-protein coupled receptors that detect bacterial peptides

A

TLRs [Toll-like receptors]+ Pathogen associated molecular patterns[PAMP]

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23
Q

Factors that play major roles in Pathophysiology of septic shock

Activated immune cells (monocytes/macrophages) produce

_____ ,_____,———,______, reactive oxygen species and lipid mediators such as _______ and _________

A

TNF, IL-1, IFN-γ, IL-12, and IL-18

Prostaglandins; platelet activating factor (PAF)

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24
Q

Factors that play major roles in Pathophysiology of septic shock

The effects TNF-α and IL-1cytokines are as under:

a) By altering _________________

B) Promoting _______ synthase

A

endothelial cell adhesiveness

nitric oxide

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25
Factors that play major roles in Pathophysiology of septic shock Activation of other inflammatory responses such as under: 1) Activation of ____ cells: _____ is released which increases capillary permeability. 2) The ———— cascade is also activated by microbial components, resulting in the production of anaphylatoxins (______),chemotactic fragments (___), and opsonins (___), all of which contribute to the pro-inflammatory state
mast; Histamine complement C3a, C5a C5a; C3b
26
In septic shock Microbial components can activate coagulation directly through ____ and indirectly through altered ______ function
factor XII; endothelial
27
The hyperinflammatory state initiated by sepsis also activates counter-regulatory ________ mechanisms, which may involve _____________ cells..
immunosuppressive both innate and adaptive immune
28
Factors that play major roles in Pathophysiology of sepsis Endothelial activation and injury The (anti or pro?) -inflammatory state and endothelial cell activation associated with sepsis leads to widespread vascular _______ and tissue _____. One effect of inflammatory cytokines is to ____________________, making vessels ____ and resulting in the accumulation of __________ throughout the body.
Pro; leakage; edema loosen endothelial cell tight junctions leaky; protein-rich edema
29
Factors that play major roles in Pathophysiology of sepsis Endothelial activation and injury Activated endothelium also upregulates production of ——- and other vasoactive inflammatory mediators (e.g., C3a, C5a, and PAF), which may contribute to vascular smooth muscle _______ and systemic ______
nitric oxide (NO) relaxation hypotension
30
Factors that play major roles in Pathophysiology of sepsis Induction of a procoagulant state Proinflammatory cytokines increase _____ production by ——- and possibly ______ cells as well, and decrease the production of endothelial anti-coagulant factors, such as tissue factor pathway inhibitor, thrombomodulin, and protein C Decreases fibrinolysis by increasing ______________ expression. These effects lead to systemic activation of ______ and the deposition of _________ in small vessels throughout the body.
tissue factor monocytes; endothelial plasminogen activator inhibitor- 1 thrombin; fibrin-rich thrombi
31
Sepsis alters the expression of many factors against coagulation T/F
F to favor
32
In sepsis Metabolic abnormalities Septic patients exhibit _____ resistance and ______ TNF, IL-1, stress induced hormones eg glucagon, GH, glucocorticoids and catecholamines all drive __________
insulin hyperglycaemia gluconeogenesis
33
Proinflammatory cytokines suppress ________ and promote _______ in liver and other tissues
insulin release insulin resistance
34
Organ dysfunction in sepsis Systemic ___tension and small vessel _____ will ___ease delivery of oxygen and nutrients to tissues
hypo; thrombosis; decr
35
Organ dysfunction in sepsis Inflammatory cytokines and other mediators may decrease myocardial _______ and _______, increase vascular _____, and cause endothelial ____ that may lead to ____________ All these may cause ________, particularly the _____,______,_______, and ______ culminating in death.
contractility and Cardiac Output permeability; injury Adult Respiratory Distress Syndrome multiple organ failure kidneys, liver, lungs, and heart,
36
Septic shock pathogenesis The collective actions of bacterial constituents and chemical mediators result in the following: 1)___ and increased synthesis of ________ 2)Systemic vaso_______ (___tension) 3)Diminished myocardial ______ 4) Activation of the coagulation system culminating in ___________ 5)Widespread endothelial injury and activation, causing systemic _____ and ______________ damage (_____) or ______
fever; acute phase proteins dilatation; hypo contractility (DIC) disseminated intravascular coagulopathy leucocyte adhesion; pulmonary alveolar capillary ; ARDS; shock lung
37
Toxic shock syndrome is similar to septic shock T/F
T
38
Toxic shock syndrome It is caused by _____ produced by ______ The syndrome is associated with the use of __________ during ______ because It aids the ________________________________
exotoxins; staph aureus. absorbent tampons; menstruation growth of staph aureus organism in menstrual blood.
39
Neurogenic shock Occurs as a result of ________ and ___________ ________ and ———— are common causes.
loss of vascular tone peripheral pooling of blood Spinal cord injury and anaesthesia
40
Anaphylactic shock This is initiated by generalised ___________________ reaction.
IgE mediated hypersensitivity
41
Anaphylactic shock Mechanism- acute widespread systemic peripheral vaso_____ and increased vascular _______ resulting in tissue ________ and _______
dilatation permeability hypoperfusion and hypoxia.
42
Pathogenesis of anaphylactic shock Two basic features Reduced ___________________ Reduced _______________ with resultant ______
effective circulating blood volume supply of oxygen to cells and tissues; anoxia
43
Stages of shock __________________ phase ___________ stage _______________ stage
Initial non progressive Progressive Irreversible/intractable
44
Initial non progressive stage In the early stage of shock an attempt is made to maintain an adequate _____ and ______ blood supply by __________ so that the vital organs (brain, heart) are ________________
cerebral and coronary redistribution of blood adequately perfused and oxygenated
45
Initial non progressive stage Neurohumoral mechanisms that help maintain C.O and blood pressure: ________ reflexes, chemoreceptors, stimulation of _______ with release of ______, activation of _________ system, ____ release, generalised sympathetic stimulation. These mechanisms will have a net effect of ______, peripheral _______, and _______
baroreceptor; adrenal medulla catecholamines; renin angiotensin ADH tachycardia; vasoconstriction; renal conservation of fluid.
46
Progressive shock Widespread tissue ______ ________ glycolysis with ______ _______ of pH, makes the ______ response ineffective- arteriolar _____ and _______ in the microcirculation. ___ease in CO, _____ injury to the endothelium which may progress to _______,_______ and decreased _____
hypoxia Anaerobic; lactic acidosis Lowering; vasomotor; dilatation pooling of blood Decr; anoxic DIC Organ failure, confusion; urinary output.
47
Irreversible / intractable stage Widespread cell injury with _________ Decreased myocardial ______ Renal _____ as a result of ________ Ischaemia of the bowel may allow __________________ causing ____ shock.
lysosomal enzyme leakage. contractility shutdown; acute tubular necrosis the entry of intestinal bacterial flora into the blood; septic
48
Morphology of shock Basic pathologic changes include ________, tissue _____ and _______ in capillaries, venules and small veins.
haemorrhages necrosis fibrin thrombi
49
Morphology of shock Heart: subendocardial _______ and _____ __________ necrosis.
haemorrhages and necrosis contraction band
50
Morphology of shock kidneys: renal ______ following sustained systemic _______ is responsible for the changes Grossly, the kidneys are (soft or hard?) and _____. Sectioned surface shows _______________ Microscopically:__________ leading to _______,________ and _______
ischaemia; hypotension Soft; swollen; blurred architectural markings Acute tubular necrosis (ATN) oliguria, anuria and electrolyte imbalance.
51
Morphology of shock The lungs: 1)(Light or Heavy?) and (dry or wet?). 2)____________________ damage (_____)
Heavy; wet Pulmonary alveolar capillary ARDS
52
Adult Respiratory Distress Syndrome shows ———, interstitial and alveolar _____, interstitial lymphocytic infiltrate, alveolar hyaline membranes, thickening and fibrosis of _______, fibrin and platelet thrombi in the pulmonary microvasculature
congestion oedema; alveolar septa
53
The lungs are often affected in pure hypovolemic shock T/F With reason
F The lungs are seldom affected in pure hypovolemic shock because of it’s dual vascular supply.
54
Morphology of shock GIT: Patchy mucosal haemorrhages and necroses (_____________), acute _______ of the stomach or duodenum may occur and are known as _______. Grossly: lesions are ____ and widely distributed throughout. The lesions are _______. The bowel mucosa is _______ and _______ Microscopically there is ___________ of the mucosa and sometimes submucosa
haemorrhagic enteropathy stress ulcers Curlings ulcer. multifocal; superficial ulcers oedematous and haemorrhagic. haemorrhagic necrosis
55
Morphology of shock Liver: ______ and central _______. _________ appearance is seen.
Fatty change haemorrhagic necrosis Faint nutmeg
56
Morphology of shock Hypoxic encephalopathy: Sustained blood pressure of below __mmHg leads to serious brain tissue ______ damage with loss of _______, coma and _____ state Grossly: The area supplied by the most (distal or proximal?) branches of the cerebral arteries (border zone between the anterior and middle cerebral arteries) suffers from severe ________ Changes are more noticeable in prolonged cerebral ischaemia.
50 ; ischaemic cortical functions; vegetative state Distal ; ischaemic necrosis.
57
Neurons particularly _______ are more prone to ischaemia. The cytoplasm of the affected neuron is intensely ______ and the nucleus is ____ and ____
Purkinje cells eosinophilic small and pyknotic.
58
Morphology of shock Adrenals- __________ depletion
cortical cell lipid
59
Clinical manifestation of shock ___tension Decreased/increased SVR(Systemic vascular resistance also known as TPR) depending on _______ (Weak or strong?) (slow or rapid?) pulse (Cool or warm?) _______ ______ skin
Hypo the stage of shock Weak rapid Cool, clammy cyanotic
60
Clinical manifestations of shock in septic shock the skin is _____ and ______ because of ________
warm and flushed peripheral vasodilatation.
61
Clinical manifestations of shock Phase of ____uria due to ____, later phase of ______ due to _________________ of _______.
oliguria; ATN diuresis regeneration of tubular epithelium
62
Clinical manifestations of shock ______________ in early oliguric phase while marked __________ occurs in diuretic phase
Haemoconcentration electrolyte imbalance
63
Management of septic shock Treat _____ with ___________ Set up ______ Fluid Resuscitation/monitor BP Administer _____ Nutritional Support Vaso______ ______ drugs _______ therapy for _______
infection; broad spectrum antibiotics IV line; oxygen constrictors Inotropic Insulin; hyperglycaemia
64
Septic shock can be corrected with infusing fluids T/F
F
65
Septic shock The most common Gram +ve bacteria include: ______,________,_______
S. aureus, enterococci, S. pneumonia.