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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
Q

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

A

mast; Histamine

complement

C3a, C5a

C5a; C3b

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26
Q

In septic shock

Microbial components can activate coagulation directly through ____ and indirectly through altered ______ function

A

factor XII; endothelial

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27
Q

The hyperinflammatory state initiated by sepsis also activates counter-regulatory ________ mechanisms, which may involve _____________ cells..

A

immunosuppressive

both innate and adaptive immune

28
Q

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.

A

Pro; leakage; edema

loosen endothelial cell tight junctions

leaky; protein-rich edema

29
Q

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 ______

A

nitric oxide (NO)

relaxation

hypotension

30
Q

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.

A

tissue factor

monocytes; endothelial

plasminogen activator inhibitor- 1

thrombin; fibrin-rich thrombi

31
Q

Sepsis alters the expression of many factors against coagulation

T/F

A

F

to favor

32
Q

In sepsis

Metabolic abnormalities

Septic patients exhibit _____ resistance and ______

TNF, IL-1, stress induced hormones eg glucagon, GH, glucocorticoids and catecholamines all drive __________

A

insulin

hyperglycaemia

gluconeogenesis

33
Q

Proinflammatory cytokines suppress ________ and promote _______ in liver and other tissues

A

insulin release

insulin resistance

34
Q

Organ dysfunction in sepsis

Systemic ___tension and small vessel _____ will ___ease delivery of oxygen and nutrients to tissues

A

hypo; thrombosis; decr

35
Q

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.

A

contractility and Cardiac Output

permeability; injury

Adult Respiratory Distress Syndrome

multiple organ failure

kidneys, liver, lungs, and heart,

36
Q

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 ______

A

fever; acute phase proteins

dilatation; hypo

contractility

(DIC) disseminated intravascular coagulopathy

leucocyte adhesion; pulmonary alveolar capillary ; ARDS; shock lung

37
Q

Toxic shock syndrome is similar to septic shock

T/F

A

T

38
Q

Toxic shock syndrome

It is caused by _____ produced by ______

The syndrome is associated with the use of __________ during ______ because It aids the ________________________________

A

exotoxins; staph aureus.

absorbent tampons; menstruation

growth of staph aureus organism in menstrual blood.

39
Q

Neurogenic shock

Occurs as a result of ________ and ___________

________ and ———— are common causes.

A

loss of vascular tone

peripheral pooling of blood

Spinal cord injury and anaesthesia

40
Q

Anaphylactic shock

This is initiated by generalised ___________________ reaction.

A

IgE mediated hypersensitivity

41
Q

Anaphylactic shock

Mechanism- acute widespread systemic peripheral vaso_____ and increased vascular _______ resulting in tissue ________ and _______

A

dilatation

permeability

hypoperfusion and hypoxia.

42
Q

Pathogenesis of anaphylactic shock

Two basic features

Reduced ___________________

Reduced _______________ with resultant ______

A

effective circulating blood volume

supply of oxygen to cells and tissues; anoxia

43
Q

Stages of shock

__________________ phase
___________ stage
_______________ stage

A

Initial non progressive

Progressive

Irreversible/intractable

44
Q

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 ________________

A

cerebral and coronary

redistribution of blood

adequately perfused and oxygenated

45
Q

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 _______

A

baroreceptor; adrenal medulla

catecholamines; renin angiotensin

ADH

tachycardia; vasoconstriction; renal conservation of fluid.

46
Q

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 _____

A

hypoxia

Anaerobic; lactic acidosis

Lowering; vasomotor; dilatation

pooling of blood

Decr; anoxic

DIC Organ failure, confusion; urinary output.

47
Q

Irreversible / intractable stage

Widespread cell injury with _________

Decreased myocardial ______

Renal _____ as a result of ________

Ischaemia of the bowel may allow __________________ causing ____ shock.

A

lysosomal enzyme leakage.

contractility

shutdown; acute tubular necrosis

the entry of intestinal bacterial flora into the blood; septic

48
Q

Morphology of shock

Basic pathologic changes include ________, tissue _____ and _______ in capillaries, venules and small veins.

A

haemorrhages

necrosis

fibrin thrombi

49
Q

Morphology of shock

Heart:

subendocardial _______ and _____

__________ necrosis.

A

haemorrhages and necrosis

contraction band

50
Q

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 _______

A

ischaemia; hypotension

Soft; swollen; blurred architectural markings

Acute tubular necrosis (ATN)

oliguria, anuria and electrolyte imbalance.

51
Q

Morphology of shock

The lungs:

1)(Light or Heavy?) and (dry or wet?).

2)____________________ damage (_____)

A

Heavy; wet

Pulmonary alveolar capillary

ARDS

52
Q

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

A

congestion

oedema; alveolar septa

53
Q

The lungs are often affected in pure hypovolemic shock

T/F

With reason

A

F

The lungs are seldom affected in pure hypovolemic shock because of it’s dual vascular supply.

54
Q

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

A

haemorrhagic enteropathy

stress ulcers

Curlings ulcer.

multifocal; superficial ulcers

oedematous and haemorrhagic.

haemorrhagic necrosis

55
Q

Morphology of shock

Liver: ______ and central _______.

_________ appearance is seen.

A

Fatty change

haemorrhagic necrosis

Faint nutmeg

56
Q

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.

A

50 ; ischaemic

cortical functions; vegetative state

Distal ; ischaemic necrosis.

57
Q

Neurons particularly _______ are more prone to ischaemia.

The cytoplasm of the affected neuron is intensely ______ and the nucleus is ____ and ____

A

Purkinje cells

eosinophilic

small and pyknotic.

58
Q

Morphology of shock

Adrenals- __________ depletion

A

cortical cell lipid

59
Q

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

A

Hypo

the stage of shock

Weak rapid

Cool, clammy cyanotic

60
Q

Clinical manifestations of shock

in septic shock the skin is _____ and ______ because of ________

A

warm and flushed

peripheral vasodilatation.

61
Q

Clinical manifestations of shock

Phase of ____uria due to ____, later phase of ______ due to _________________ of _______.

A

oliguria; ATN

diuresis

regeneration of tubular epithelium

62
Q

Clinical manifestations of shock

______________ in early oliguric phase while marked __________ occurs in diuretic phase

A

Haemoconcentration

electrolyte imbalance

63
Q

Management of septic shock

Treat _____ with ___________

Set up ______

Fluid Resuscitation/monitor BP
Administer _____
Nutritional Support
Vaso______
______ drugs
_______ therapy for _______

A

infection; broad spectrum antibiotics

IV line; oxygen

constrictors

Inotropic

Insulin; hyperglycaemia

64
Q

Septic shock can be corrected with infusing fluids

T/F

A

F

65
Q

Septic shock

The most common Gram +ve bacteria include: ______,________,_______

A

S. aureus, enterococci, S. pneumonia.

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