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Block 2 > Week 3 > Flashcards

Week 3 Flashcards

1
Q

Define the Yerkes-Dodson Law and describe the relationships between stress, performance, and learning

A

Performance adn adaptive learning areoptimal under moderate rather than either high or low stress

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2
Q

Describe the roles of the amygdala and hippocampus in the fight or flight response

A

Modeate stress conditions activate the limbic system, facilitating the coordinated ability of the amygdala, hippocampus, and prefrontal cortex to analyze, respond to , and learn from the challenge.

amygdala coordinates an emergent reaction arousing and mobilizing the organism bia the sympatho-adrenomedullary (SAM)

hypothalamus leads to release of catecholamines and glucocorticoids

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3
Q

Summarize the role of glucocorticoids play in the regulation of the stress response

A

Glucocorticoids

CRH -> ACTH & Beta endorphin -> Glucocorticoids

Can inhibit protein synthesis

Accelerate protein catabloism

Increase lipolysis

Decrease peripheral glucose utilization

Bone loss

Muscle wasting

Immune system suppression

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4
Q

Describe what evolutionary objective most illnesses seen in primary care are the by-product of

A

Surivival of the organism and the survival of the species

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5
Q

Summarize the ways in which chronic stress affects metabolic processes, growth processes, and reproductive processes

A

Shunting of stored nutrients to muscle

Shutting down of digestion and other non-essential functions

Inability to respond to insulin (metabolic syndrome)

Impairs normal growth and development via sympathic NS, inhibited growth hormone, and shortening of telomeres

High levels of stress may result in glucocorticoid inhibiton of hypothalamic release of lutenizing hormone (LH) and follicle stimulating hormone (FSH). Sperm and egg production inhibition.

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6
Q

Explain the bio-behavioral mechanisms by which stress contributes to immune system disorders

A

Acute/moderate stress generally activates the genetically programmed immune system

Excess of glucocorticoids (chronic stress) may impair production of B cells and T cells. Premature migration of T cells to thymus resulting in its shrikage

Impari NK

Heighten immune system response when body is attacked and can lead to autoimmune disorders

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7
Q

Explain the bio-behavioral mechanisms by which stress contributes to cardiovascular disorders

A

High stress diminishes arterial flow increasing blood pressure

Decrease urine

Artheriosclerosis

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8
Q

List the disorders associated with chronic stress-induced system failures

A

anticipatory anxiety (fear)

depression

learned helplessness

PTSD due to helplessness and powerlessness

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9
Q

Define the Holmes and Rahe scale and describe the relationship between life units and illness

A

Attemptes to quantify the relative importance of life changes in terms of distress of the individual

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10
Q

Exercise and stress

Mindfullness and stress

A

Moderate exercise -> Longer telomeres (too much shortens)

Mindfullness -> genes associated with telomeres, insluin, and metabloism

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11
Q

Distinguish between adaptive and maladaptive strategies for coping with stress and research

A

Direct action (preparation, assertive, practive, mastery)

Avoidance (withdrawal/sleeping, denial, rationalization, substance abuse)

Palliation (exercise)

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12
Q

Summarize the role of the unconscious in motivation, according to psychodynamic theory

A

Behavior is motivated by unconscious biological urges, instincts, or drives

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13
Q

Where is the blood flowing the most?

Where is the blood flowing the most if normalized per mass?

At rest where is 50% of blood flowing?

Which organtake up 5% of CO, but accounts for 10% of oxygen conusumption

A

Liver / kidney muscle

Kideny / heart

Liver / kideny

heart

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14
Q

“Ohm’s Law” - blood flow

Puiseulle’s Law

A

Q = dP/R

R=8nl / (PI*r4)

Q = dP r4 PI / 8 n l

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15
Q

Relationship between metabolsi and blood flow

A

Proportional

Blood flow regulated to satisfy minimum requirements of tissue

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16
Q

When blood flow is regulated what variables can be altered?

A

CO

Resistance

Capacitance of veins

Extracellular fluid volume and osmolality

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17
Q

Where can the control of blood flow come from?

A

Local (intrinsic) mechanisms

Systemic (extrinsic) mechanisms

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18
Q

Types of local control of blood flow and examples

Types of systemic control of blood flow and examples

A

Intrinsic

Metabolic: release of vasodilators, nutrient deficiency for vascular smooth muscle

Myogenic: sudden strech, reduced strech

Systemic

Humoral: adrenal hormones, Renin-angiotensin-aldosterone system (RAAS), endothelins, kinins, natriuretic peptides

Neural: Sympathetic, parasympathetic

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19
Q

Pressure Flow Autoregulation

Local or systemic?

When fails?

A

Local control

Constant flow under varying pressures (strech activated Ca2+ channels)

At high pressures resistance cannot be appreciable further decresed.

The changes in blood flow in response to overall homeostasisare not classified as autoregulatory processes.

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20
Q

Hyperemia (increased blood flow)

What is active active hyperemia?

What is reactive hyperemia?

Possible causes?

A

Active hyperemia is increased blood flow caused by increased tissue activity

Reactive Hyperemia is blood flow above control level upon release of an arterial occlusion

Causes:

Deficiency of O2 (vasodilator release / inhibition of contraction)

Increased metabolism (vasodilator release / inhibition of contraction)

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21
Q

Endothelium-derived relaxing factor (EDRF)

A

It is produced and released by the endothelium to promote smooth muscle relaxation.

The best-characterized is nitric oxide (NO)

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22
Q

Different mechanisms that can activate production of NO in endothelial cells

A

iNOS = inducible nitric oxide synthase

cNOS = constitutive nitric oxide synthase

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23
Q

What hormones and their proportions that are released from Adrenal Medulla?

What is tumor associated with Adrenal medulla?

A

80% epinephrine and 20% norepinephrine

phenochromocytoma

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24
Q

Endothelins

Effect on heart?

Effect on hormones?

Effect on autonimic nervous system?

Effect on lungs?

Effect on kideny?

A

Vasoconstriction

Positive inotropic and chronotropic effect

Increase plasma levels of ANP, renin, aldosterone, and catecholamines

Increase release of sympathetic transmitters

Produce bronchoconstriction

Decrease glomerular filtration rate, renal blood flow, increases Na+ reabsorption

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25
Q

Describe Renin-Angiotensin-Aldosteron system

A
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26
Q

Kinins effect on blood vessels

ACE inhibitors importance?

A

Bradykinin and lysylbradykinin cause vasodilation

Prevent not only inhibition of Angiotensin I conversion to Angiotensin II, but also prevent degradation of bradykinins.

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27
Q

Natiuretic peptides

Examples?

Function?

When released?

Counter-regulation to which system?

A

Human heart breain (ANP); Human heart blood (BNP) * not in brain; Human brain vascular endothelium (CNP)

Vasodilation; Renal effects = natriuresis (increased Na+ excretion) and diuresis

Released in presence of strech, endothelin, sympathetic stimulation, or ANG II stimulation.

RAAS

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28
Q

3 regulatory mechanisms of smooth muscle (vasodilation/vasconstriction)

A

Activation of Receptor (a1, AT, ET, 5HT) => Gq => PLC => IP3/DAG => PKC pathway => Contraction

(a2, A1) => inhibition of Gs pathway => Constriction

(b2, A2) => Gs => AC => cAMP => PKA => Relxation

No => GC => cGMP => PKG => Relaxation

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29
Q

What is the organs the receives the most blood during rest?

What is the organ that receives the most blood during rest (normalized)?

A

Liver then kidney

Kideny then heart

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30
Q

Which organs exhibit autoregulation?

Which organs are the most sensitive to sympathetic innervations?

A

Heart, brain, and kidney

Skin > Muscle > Kideny >>>

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31
Q

What is unique about?

Main regulatory mechanism?

cerebral circulation

coronary circulation

skeletal muscle circulation

cutaneous circulation

A

cerebral circulation

constant large blood supply

Autoregulation / CO2 & hypoxia / local metabolite

coronary circulation

Works 24h/day with high O2 demand

Metabolic intrinsic factors (adenosine/lactate/K+/NO) regulate resistance

skeletal muscle circulation

BP maintenance; flow can change up to 20x

rest / exercise

cutaneous circulation

regulation of temperature

extrinsic control

32
Q

Circle of Willis

and other structures importance?

A

Alternative blood veseels.

Provides high density capillaries.

33
Q

What is the most important vasodilator for cerebral circulation?

A

CO2

CO2 > autoregulation

34
Q

Regulation of blood in brain:

What is cushing reflex?

What types of local controls are present?

A

Increasing cranial pressure leading to high BP (pulmonary edema)

Autoregulation (CO2 and hypoxia) and active hyperemia

35
Q

Adaptation for circulation in:

Brain

Coronary circulation

Skeletal muscle

Cutaneous

A

Brain

High basal flow

Protects its own supply

Autoregulation

Sensitive to carbon dioxide and hypoxia

Local metaboli hyperemia (active hyperemia)

BBB

Coronary

Main regulation by coronary vascular resistance

Weak neural control

Metabolic intrinsic factors are most important

Coronary reserve (can increse flow 3-4 times)

Muscle

Slow (type I) and fast (type II) twich

Regulatory mechanism varies during rest and exercise

Cutaneous

Sympathetic extrinsic control linked to body temperature

Arteriovenous anastomoses in apical skin

SNS and temperature regulation in nonapical skin

36
Q

Challenges in circulation of:

Brain

Coronary circulation

Skeletal muscle

Cutaneous

A

Brain

Effect of gravity (postural hypotension)

Occupies a rigid box

Coronary circulation

Coronary arteries are end arteries (problems with occlusions)

Cardiac hypertrophy (insufficiency)

Reactive hyperemia (during diastole because of blood vessels compresion)

Lack of demand during tachycardia

Coronary reserve and coronary steal during exercise in disease states

Skeletal muscle

Inhibition of blood during isometric exercise

Increased capillary filtration possible edema

Cutaneous

Strenous exercise in hot weather

Hemorrage

37
Q

Difference in pathogenesis in coronary heart disease in men and women

A

**In women: **smaller coronary blood vessels cease to constrict and dilate properly

In men: suffer from plaque build-up in the large arteries around the heart

38
Q

Coronary Microvascular Disease (MVD)

A

It is heart disease that affects the walls and inner lining of tiny coronary artery blood vessels that branch off from the larger coronary arteries.

39
Q

How muscle is regulated at rest and exercise?

A

Rest: Sympathetic nervous system is the primary regulator of blood flow to the skeletal muscle

Exercise**: **local metabolic mechanisms are dominant (lactate, adenosine and K+)

40
Q

Capillary Recruitment

A

Shortens the distance for nutrients to travel

41
Q

Skeletal muscle pump

A

Emptying of muscle veins lowers intramuscular venous pressure

Helps drive arterial blood into skeletal muscle.

42
Q

Issues with blood flow to muscle during exercise?

A

Blockage during isometric contraction

Edema due to increased capillary filtration

43
Q

Arteriovenous anastomoses (AVAs)

Where are they located?

Innervated by?

Controlled by?

A

In acral/apical skin (hands, feet, nose, ears)

Sympathetic nervous system

Hypothalamus

44
Q

What three variables affect directly the mean arterial pressure

A

Heart Rate

Stroke Volume

Vessel Diameter

45
Q

Baroreceptors

Where are they located?

Function?

Pressure range?

A

High Pressure

The carotid sinus near bifrucation (50-200 mmHg)

The aortic arch (100-200 mmHg)

Low Pressure

Cardiopulmonary (right atrium)

Buffer acute changes in blood pressure

46
Q

What do low-pressure baroreceptors monitor & control?

A

They monitor venous volume STRECH

The help to control blood volume through reflex release of antidiuretic hormone

47
Q

What is it and the function of cardiovascular center

A

Collection of neurons in the medulla of the brain

Receives multiple inputs and sets the point for systemic arterial blood pressure, and initiate reflex to maintain BP.

48
Q

What if arterial baroreceptors are removed?

What if both arterial and cardiopulmonary receptors are removed?

How do baroreceptors work during chronic hypertension?

A

Fluctuations of BP, Not really change in mean blood pressure

Fluctuations and shift to high blood pressure

Not so well (only acute control). They set the new set point.

49
Q

What is the chemoreceptor function?

Why they are sensitive to specific molecules?

Effects on activation?

Where are they located? What do they monitor?

A

Monitor acute changes in pO2 (hypoxemia), pCO2 (hypercapnia), and pH (acidosis)

They have high rate of O2 consumption

Results in vasoconstriction, low pO2 < 60 mmHg causes hyperventilation

Carotid and aortic bodies – oxygen, carbon dioxide, and pH

Medula oblongata – carbon dioxide and pH

50
Q

Renin Angiotensin Aldosterone System

What is is triggered by?

Speed?

A

Renal perfusion pressure

Slow – hormonal for long-term blood pressure rgulation

51
Q

Mechanisms that regulate BP except

baroreceptors and RAAS

Comparison of different control mechanisms over time

A

CNS Ischemic response – pCO2 stimulates vasomotor centers

Cushing Response – pressure and constriction leading to increased pressure and flow

Vasopressin (ADH) – acitvated by low-pressure baroreceptors and causes vasocontrction (V1 receptors) and water absorption (V2)

Natriuretic peptides (ANP, BNP) – released from atrial because of strech cause vasorelaxation, sodium and water secretion, and inhibits renin.

52
Q

Preload and afterload definition

A

Preload = pressure that reults in filing of the heart

Afterload = pressure required to eject blood

53
Q

What are cardiac factors that determine cardiac output?

What are coupling that determine cardiac output?

A

Cardiac: HR and contractility

Coupling factors: Preload (central venous pressure) and afterload (peripheral resistance)

54
Q

Cardiovascular regulation diagram 1

A
55
Q

Cardiovascular regulation diagram 2

A
56
Q

Cardiovascular regulation diagram 3

A
57
Q

Cardiovascular regulation diagram 4

A
58
Q

How blood vessels solve the problem with standing?

How is the change in posture problem solved?

A

The valves in vein present pressure buildup

By mechanial responses (muscle pump, venous valves, and respiratory pump) and ANS (HR, contractility, and vasocontriction0

59
Q

How respiratory pump affects blood flow?

A

During inspiration, venous blood is sucked back into the thorax, increasing venous return and preload.

60
Q

Effect of prolonged standing

A
61
Q

How lack of of RAAS affects response after hemorage?

A
62
Q

Circulatory shock

A

Loss of more than 1 to 1.5 L which cannot be compensated by regulatory mechanisms

63
Q

How blood flow to muscle can increase 20 fold?

A

Metabolic vasodilation

Capillary recruitment

64
Q

What is the effect of NE and EPI on their receptors?

A

NE: b1=a1 > a2=b2

EPI: b1=b2 > a1=a2

65
Q

List Sympathetic Agents

A
66
Q

Shock definition

Types?

A

A life-threatening condition that occurs when the body’s organs and tissues are not being adequately perfused

Types:

Hypovolemic

Vasodilatory (anaphylactic, septic, neurogenic)

Cardiogenic

67
Q

What recepotrs affect MAP?

What recepotrs affect systolic pressure?

What recepotrs affect diastolic pressure?

What recepotrs affect pulse pressure?

A

systolic pressure – SV (b1) TPR (a1,b2)

diastolic pressure – TPR (a1,b2)

pulse pressure – SV (b1)

68
Q

Dopamine effects on its effectors

A

D1 > b1=b2 > a2

69
Q

Clonidine effect on its receptors

A

Clonidine can activate presynpatic α2 receptors inhibiting sympathetic neurotransmitter release

Decrease sympathetic tone

70
Q

Tyramine problem with signalling

A

Tyramine is an indirect acting **sympathomimetic **

Found in many foods

It is taken up into postganglionic neuron by NET

If MAO inhibitor is present, it cannot be metabolized

Hypertensive crisis

71
Q

Parasympathetic Agents

A

+M bethanacol

+N nicotine

  • M atropine
  • NN trimetaphan
  • NM d-tubocurarine
72
Q

Incidence (absolute risk) =

Crude mortality rate =

Specific mortality rate =

Proportionate mortality =

Prevalence =

Incidence density =

Relative risk =

Attributable risk

Etiologic fraction =

Number needed to treat =

A

Incidence (absolute risk) = new cases / pop at risk

Crude mortality rate = deaths / population

Specific mortality rate = death / poulation (specific)

Proportionate mortality = death from disease / total deaths

Prevalence = cases / total people

Incidence density = new cases / patient days

Relative risk = Inc(exp)/Inc(con)

Attributable risk = Inc(con) - Inc(exp)

Etiologic fraction = (Inc(con) - Inc(exp))/Inc(con)

Number needed to treat = 1/(att risk)

73
Q

Summarize the role of the unconscious in motivation, according to psychodynamic theory

A

Human behavior must include the notion that human lives are goverend by internal forces of which they are unaware

74
Q

Describe the role of conflict in psychopathology, according to psychodynamic theory

A

Intrapsychic and interpersonal

Humans have incompatible goals and engagin in paradoxical actions.

75
Q

Describe the influence of the past on adult behavior, according to psychodynamic theory

A

The past, particulary the events of childhood, have a profound influence on behaviours of adults.

76
Q

Define defense mechanisms, paraphrase definitions of the defense mechanisms described in the chapter, and recognize examples of patient defense mechanisms in clinical vignettes

A

It is a way that ego wards off anxiety and control unacceptable instinctual urgest and unpleasnt affects or emotions.

77
Q

Define:

projection

acting out

denial

dissociation

primitive idealization (and devaluation)

reaction formation

intellectualization

altruism/ activism

suppression

sublimation

displacement

undoing

repression

regression

identification

A

Define:

(M) reaction formation (prevents the expression or the experience of unacceptable thoughts, feelings or actions by turning them inside out and turning them into their opposite)

(M) altruism/ activism (committing oneself to the needs of other rather than than self)

(M) suppression (consciously deciding not to attend to a particular feeling or circumstance)

(M) sublimation (Transforming socially objectionable or internally unacceptable aims into socially acceptable ones

**(N) intellectualization **(provide distance from intense affect)

(N) displacement (It involves the discharge of pent up emotions onto less dangerous objects- our spouse, dog, plant or doctor)

(N) undoing (involves trying to negate or undo an acceptable thought, wish or actual behavior)

(N) repression (exclusion from conciousnes)

**(I) dissociation **(against utter and complete helplessness of sexual abuse, rape and torture, it provides escape when there is no escape as in the face of a terminal dx. Diss disrupts individual’s sense of time, identity and perception in order to maintain a sense of psychological control when all appears lost)

(I) regression (going back to the previous stage of development)

(I) identification (one takes on traits or attributes of another for safety and a sense of security)

(I) fixation (inability to give up infantile patterns of behavior, inadequate personality)

**(I) denial **(pushes away difficult or intolerable external realities)

(I) acting out (acting on an unconscious wish or impulse in order to avoid being aware of the emotion that accompanies it)

**(I) projection **(unacceptable impulses, thoughts or feelings are disavowed and projected onto another person)

Block 2 (7 decks)

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