Shock! Flashcards
Shock is defined as a state of systemic tissue ________ due to ____________________ and/or _________________________
hypoperfusion
reduced cardiac output
reduced effective circulating blood volume.
Types of shock
__________ shock
__________ shock
_______ shock
________ shock
____________ shock
cardiogenic
hypovolaemic
septic
neurogenic
anaphylactic
Cardiogenic shock
Acute ______ failure with sudden fall in ________ without actual _________
circulatory
cardiac output
reduction of blood volume.
Cardiogenic shock
This results from ___________ failure.
myocardial pump
Cardiogenic shock
The causes include
A. Deficient emptying
_________________ is the most obvious cause of pump failure.
_____________ rupture
_________ rupture
acute myocarditis
cardiac _______
Cardiomyopathies
Myocardial infarction
papillary muscle
ventricular
arrhythmias
Cardiogenic shock
The causes include
B. Deficient filling
Cardiac _______ [extrinsic ____] from ________
tamponade; compression
haemopericardium
Cardiogenic shock
The causes include
C. obstruction to outflow
_______________
Tension __________
Dissecting _____________
Pulmonary embolism
pneumothorax
aortic aneurysm
Hypovolaemic shock
This results from ____________ or _______
Causes include
Severe ________,
Fluid loss :severe ____, diarrhoea, vomiting, extensive ____, uncontrolled ________,__________, ______ over _____.
loss of blood or plasma volume
haemorrhage
burns; injury; diabetes mellitus
diabetes insipidus
diuretic over dose
Shock associated with systemic inflammation
It is caused by a variety of ______,
Like : _________________
insults
Microbial infections, burns, trauma, and or pancreatitis
Shock associated with systemic inflammation
The common pathogenic feature is a massive _________ that produce arterial _______, vascular _____, and venous _______
outpouring of inflammatory mediators
vasodilation
leakage
blood pooling
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).
spinal cord; neurogenic
IgE; anaphylactic
Neurogenic and anaphylactic shock
In both of these forms of shock, acute _________ leads to ________ and tissue _______
vasodilation
hypotension
hypoperfusion
Septic shock
Sepsis is defined as ________________________ due to a dysregulated ______________.
life-threatening organ dysfunction
host response to infection.
Sepsis accompanies infection either ____________________, or associated with the _________________________
confined to a local site from which toxins are absorbed
invasion of organisms into the blood stream (septicaemia).
Septic shock is defined as a subset of _______ in which particularly profound _____,______, and _______ abnormalities substantially increase mortality.
sepsis
circulatory, cellular, and metabolic
Pathogenesis of septic shock
It is associated with systemic ______ and peripheral _______ leading to _______
It is caused by ________ and ______
vasodilation
pooling of blood
tissue hypoperfusion
bacterial and fungal infection .
Septic shock is Commonly triggered by _______________ infections followed by _______ organisms and then systemic _______ infections.
gram positive bacterial
gram negative
fungal
In septic shock
There is widespread _____________ often leading to a _______ state that can manifest as ____________
endothelial cell activation and injury
hypercoagulable
DIC (Disseminated Intravascular Coagulation)
Several microbial constituents can initiate the process of septic shock
T/F
T
Septic shock has a ___ to ___% mortality rate depending on centres.
20
75
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
receptors on cells
innate
Factors that play major roles in Pathophysiology of septic shock
Inflammatory and counter inflammatory responses
________________________ + _________________
G-protein coupled receptors that detect bacterial peptides
TLRs [Toll-like receptors]+ Pathogen associated molecular patterns[PAMP]
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 _________
TNF, IL-1, IFN-γ, IL-12, and IL-18
Prostaglandins; platelet activating factor (PAF)
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
endothelial cell adhesiveness
nitric oxide
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
In septic shock
Microbial components can activate coagulation directly through ____ and indirectly through altered ______ function
factor XII; endothelial
The hyperinflammatory state initiated by sepsis also activates counter-regulatory ________ mechanisms, which may involve _____________ cells..
immunosuppressive
both innate and adaptive immune
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
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
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
Sepsis alters the expression of many factors against coagulation
T/F
F
to favor
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
Proinflammatory cytokines suppress ________ and promote _______ in liver and other tissues
insulin release
insulin resistance
Organ dysfunction in sepsis
Systemic ___tension and small vessel _____ will ___ease delivery of oxygen and nutrients to tissues
hypo; thrombosis; decr
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,
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
Toxic shock syndrome is similar to septic shock
T/F
T
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.
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
Anaphylactic shock
This is initiated by generalised ___________________ reaction.
IgE mediated hypersensitivity
Anaphylactic shock
Mechanism- acute widespread systemic peripheral vaso_____ and increased vascular _______ resulting in tissue ________ and _______
dilatation
permeability
hypoperfusion and hypoxia.
Pathogenesis of anaphylactic shock
Two basic features
Reduced ___________________
Reduced _______________ with resultant ______
effective circulating blood volume
supply of oxygen to cells and tissues; anoxia
Stages of shock
__________________ phase
___________ stage
_______________ stage
Initial non progressive
Progressive
Irreversible/intractable
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
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.
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.
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
Morphology of shock
Basic pathologic changes include ________, tissue _____ and _______ in capillaries, venules and small veins.
haemorrhages
necrosis
fibrin thrombi
Morphology of shock
Heart:
subendocardial _______ and _____
__________ necrosis.
haemorrhages and necrosis
contraction band
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.
Morphology of shock
The lungs:
1)(Light or Heavy?) and (dry or wet?).
2)____________________ damage (_____)
Heavy; wet
Pulmonary alveolar capillary
ARDS
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
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.
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
Morphology of shock
Liver: ______ and central _______.
_________ appearance is seen.
Fatty change
haemorrhagic necrosis
Faint nutmeg
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.
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.
Morphology of shock
Adrenals- __________ depletion
cortical cell lipid
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
Clinical manifestations of shock
in septic shock the skin is _____ and ______ because of ________
warm and flushed
peripheral vasodilatation.
Clinical manifestations of shock
Phase of ____uria due to ____, later phase of ______ due to _________________ of _______.
oliguria; ATN
diuresis
regeneration of tubular epithelium
Clinical manifestations of shock
______________ in early oliguric phase while marked __________ occurs in diuretic phase
Haemoconcentration
electrolyte imbalance
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
Septic shock can be corrected with infusing fluids
T/F
F
Septic shock
The most common Gram +ve bacteria include: ______,________,_______
S. aureus, enterococci, S. pneumonia.
