Midterms1_Shock Flashcards

(42 cards)

1
Q

The general approach to the management of patients in shock are

A

Assure a secure airway
Control of hemorrhage
Restoration of vascular volume and tissue perfusion

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2
Q

Who suggested that the organism attemtpt to maintain constancy in ythe internal environment against external forces that attempt to disrupt the milleu interieur?

A

Claude Bernard

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3
Q

He introduced tthe term “homeostasis” and emphasized that an rganism’s ability to survive was related to the maintenance of homeostasis

A

Walter B. Cannon

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4
Q

According to Alfred Blalock, shock state in hemorrhage is associated with what factor?

A

Reduced CO due to volume loss

This is in contrary to the previous proposal of Cannon of the toxic factor as caused of shock (secondary shock)

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5
Q

He proposed four categries of shock

A

Alfred Blolock

Hypovolemic, vasogenic, cardiogenic and neurogenic

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6
Q

The most common type of shock; results from loss of circulating bloo volume

A

Hypovolemic shock

Results from loss of whole blood (hemorrhagic shock), plasma, interstitial fluis or a combination

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7
Q

Type of shock that results from decreased resistance within capacitance vessels, usually seen in sepsis.

A

Vasogenic shock

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8
Q

a form of vasogenic shock in which spinal cord injury or spinal anesthesia causes vasodilation due to acute loss of sympathetic vascular tone.

A

Neurogenic shock

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9
Q

A type of shock that results from failure of the heart as a pump, as in arrhythmias or acute myocardial infarction (MI)

A

Cardiogenic shock

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10
Q

a form of cardiogenic shock that results from mechanical impediment to circulation leading to depressed cardiac output rather than primary cardiac failure.

A

Obstructive shock

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11
Q

Soft tissue and bony injury lead to the activation of inflammatory cells and the release of circulating factors, such as cytokines and intracellular molecules that modulate the immune response. This type of shock is

A

Traumatic shock

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12
Q

The phenomenon of fluid redistribution after major trauma involving blood loss is termed as

A

Third spacing

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13
Q

Core principles in the management of patients in hemorrhagic shock include

A
  1. Control of active hemorrhage
  2. Volume resuscitation with blood products
  3. Recognize and adequate hypoprerfusion correction
  4. Controlled fluid resuscitation
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14
Q

Core principles in the management of patients in septic shock include:

A
  1. Treatment/resuscitation should begin ASAP
  2. Identify sopecific anatimic diagnosis of infection and implement any required source control intervention as soon as medically and logistically practical
  3. Initiate antibiotics within 1 hour of diagnosis
  4. Give at least 30 ml/kg of IV crystalloid fluid within 3 hours + additional fluids
  5. Give vassopressors to achieve a MAP of 65 mmHG if fluid resuscitation is inadequate
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15
Q

Initial physiologic responses in shock are driven by

A

Tissue hypoperfusion and developing cellular deficit

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16
Q

In hemorrhagic shock, the body compenstae for the initil loss of blood volume primarily throught the

A

Neuroendocrince responses
## FOOTNOTE
This is the compenstated phase of shock. If cellular death and injury ensues this is called the decompensated phase of shock

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17
Q

This term is used to describe persitent hypoperfusion resulting in further hemodynaic **derangements* and cardiovascular collapse

A

Irreversible phase of shock

18
Q

The goal of the neuroendocrine response to hemorrhage is to

A

Maintain perfusion to the heart and brain

Peripheral vasoconstriction occurs
Fluid excretion is inhibited

19
Q

What stimlates the afferent signals to activate to restore homeostasis?

A

Loss of circulating blood volume

20
Q

Thesee tracts transmit pain sensation from injured tissue which results in the action of the hypothalamic-piituitary-adrenal axis and ANS

A

Spinothalamic tract

Induces direct sympathetic stimulattion of the adrenal medulla to release cateecholamines

21
Q

These receptors are sensitive to changes in both chamber pressure and wall stretch, and are present within the atria of the heart.

A

Volume receptors

22
Q

These receptors are sensitive to changes in O2 tension, H+ ion concentration, and carbon dioxide (CO2) levels.

A

Chemoreceptors (in the aorta and carotid bodies)

23
Q

Effects of chemoreceptors in the aorta and carotd bodies

A

Vasodilation of the coronary arteries
Slows heart rate
Vasoconstriction of the splanchnic and skeletal circ’n

24
Q

It results in diminished venous return to the heart and decreased cardiac output and is compensated by increased cardiac heart rate and contractility, and venous and arterial vasoconstriction

25
These receptors increases heart rate and contractility of the heart to increase cardiac output
Beta 1 adrenergic receptors ## FOOTNOTE These receptors are stiimulated by the sympathetic fibers innervating the heart
26
Sympathetic stimulation of the peripheral circulation activates which receptors?
Alpha-1 adrenergric receptors ## FOOTNOTE These receptors induces vasoconstriction and causes a compensatory increase in systemic vasccular resistance and blood pressure
27
Release of ACTH by the pituitary is mediated by which hormone
Cortiocotropin-releasing hormone
28
ACTH stimulates the adrenal cortex to release which hormone?
Cortisol
29
acts synergistically with epinephrine and glucagon to induce a catabolic state
Cortisol
30
stimulates gluconeogenesis and insulin resistance, resulting in hyperglycemia as well as muscle cell protein breakdown and lipolysis to provide substrates for hepatic gluconeogenesis
Cortisol
31
True or False A. Cortisol causes retention of sodium and water by the nephrons of the kidney. B. In the setting of severe hypovolemia, ACTH secretion occurs independently of cortisol negative feedback inhibition.
Both are true
32
Factors that cause the release of renin from the juxtaglomerular cells
1. Decreased renal artery perfusion 2. β-adrenergic stimulation and 3. Increased renal tubular sodium concentration
33
It catalyzes the conversion of angiotensinogen (produced by the liver) to angiotensin I
Renin
34
A potent vasoconstrictor of both splanchnic and peripheral vascular beds. Ialso stimulates the secretion of aldosterone, ACTH, and antidiuretic hormone (ADH).
Angiotensin II
35
A mineralocorticoid, that acts on the nephron to promote reabsorption of sodium, and as a consequence, water.
Aldosterone
36
A mineralocorticoid, that acts on the nephron to promote reabsorption of sodium, and as a consequence, water.
Aldosterone
37
converted to angiotensin II by angiotensin-converting enzyme (ACE) produced in the lungs; has no functional activity
Angiotensin I
38
What ions are lost in the urine in exchange for sodium?
Potassium and hydrogen ions
39
This hormone is releases by the pituitary in response to hypovolemia, changes in circulating blood volume and increased plasma osmolality
Vasopressin or ADH
40
What factors/hormones increase the production of ADH?
Epinephrine Angiotensin II Pain Hyperglycemia
41
Which part of the nephron does the ADH act upon?
Distal tubule and collecting duct ## FOOTNOTE ADH increase water permeability, decrease water and sodiul losses and preserve intravascular volume
42
Also known as arginine vasopressor, this hoormone acts as a potent mesenteric vasoconstrictor, shunting circulating blood away from the splanchnic organs during hypovolemia
ADH ## FOOTNOTE Also increases hepatic gluconeogenesis annd increase hepatic glycolysis