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Cardiopulmonary I > Test 1 (Part 5) > Flashcards

Test 1 (Part 5) Flashcards

1
Q

Agonist vs Antagonist

A

AGONISTS:
- Activate the RECEPTOR to Signal as a Direct result of Binding to it

  • Some AGONISTS activate a Receptor to produce all of the Receptor’s BIOLOGIC FUNCTIONS
  • Some agonists selectively promote ONE Receptor FUNCTION more than another

ANTAGONISTS:
- Bind to receptors but DO NOT ACTIVATE generation of a Signal

  • Interfere with the ABILITY of an AGONISt to ACTIVATE the RECEPTOR
  • Some Agonists SUPPRESS the basal signaling of RECEPTORS that are constitutively ACTIVE
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2
Q

Agents that act on the ANS

A

1) CHOLINERGIC Agents: Drugs that mimic ACH
- AChR Agonists
- Acetylcholinesterase Inhibitors

2) CHOLINOCEPTOR- Blocking Drugs
- AChR Antagonists

3) SYMPATHETIC Agents: Drugs that mimic or enhance Alpha and Beta Receptor Stimulation
- Agonists, drugs that enhance Catecholamine release, drugs that BLOCK REUPTAKE

4) ADRENOCEPTOR- BLOCKING Drugs
- Alpha and Beta Receptor Antagonists

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3
Q

Autonomic Nervous System

A

Efferent portion of the Nervous System:

1) SOMATIC: Consciously controlled actions
- Movement, Respiration, Posture

2) ANS: Unconscious Actions
- Cardiac output, Blood flow to various Organs, Digestion

ANS Subdivisions:
1) SYMPATHETIC (Thoracolumbar, Fight or Flight)

2) PARASYMPATHETIC (Craniosacral, Rest and Digest)

*****Actions of these Subdivision GENERALLY OPPOSE EACH OTHER!!!!!

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4
Q

Parasympathetic vs Sympathetic

A

PARASYMPATHETIC:

  • Neurotransmitters: ACh
  • Receptors: nAChR, mAChR

SYMPATHETIC:

  • Neurotransmitters: NE> Epi (DA): ACh
  • Receptors: Alpha, Beta, (D), nAChR, mAChR
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5
Q

Neurotransmitters of the ANS

A

1) ACETYLCHOLINE (Cholinergic)
- The major neurotransmitter of the Parasympathetic Nervous System

  • All PREganglionic Autonomic Fibers
  • All POSTganglionic PARASYMPATHETIC Fibers
  • Few Postganglionic SYMPATHETIC Fibers (Sweat Glands)

2) NOREPINEPHRINE (Adrenergic)
- The major Neurotransmitter of the Sympathetic Nervous System
- The vast majority of POSTganglionic Sympathetic Fibers

3) EPINEPHRINE (Adrenergic)
- SYNTHESIS only occurs in the ADRENAL MEDULLA and in a FEW EPINEPHRINE-contaiing NEURONAL PATHWAYS in the Brainstem

4) DOPAMINE (Dopaminergic)
- NE and Epi Precursor
- Acts on the CNS and Renal Vascular Smooth Muscle

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6
Q

Review of Cholinergic Neurotransmission

A

1) Junctional Transmission
A) Synthesis of Acetylcholine (ACh)

B) Storage

C) Release

D) Destruction

2) ACh Signaling
3) End Organ Effects

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7
Q

nACh Receptor

A

(IONOTROPIC)
- MOSTLY PARASYMPATHETIC!!!!!!!

Tissue Location:

  • CNS
  • Autonomic Ganglia (Nn)
  • **ADRENAL MEDULLA: Only part that is SYMPATHETIC
    - Releases CATECHOLINES

Function:
- Excitatory

Agonist:
- Acetylcholine Nicotine

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8
Q

mACh Receptor

A

(METABOTROPIC)
- MOSTLY PARASYMPATHETIC!!!!!!!

Tissue Location:

  • CNS
  • Autonomic Ganglia
  • Effector Organs (Cardiac and Smooth Muscle, Gland Cells, Nerve Terminals)
  • ***SWEAT GLANDS: Only part that is SYMPATHETIC!!!!!!!!
    - Sweat Secretion

Function:
- Excitatory and Inhibitory

Agonist:
- Acetylcholine Muscarine

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9
Q

Cholinergic Receptors

A 
M1
M2
M3
M4
M5

Nm
Nn

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10
Q

M1 Cholinergic Receptor

A

Location:
- CNS, Ganglia

Structural Features:
- GPCR, Gq/11

Mechanism:

  • Activation of Phospholipase C (PLC)
  • IP3, DAG Cascade
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11
Q

M2 Cholinergic Receptor

A

Location:
- HEART, Nerves, Smooth Muscle

Structural Features:
-GPCR, Gi/0

Mechanism:

  • INHIBITION of ADENYL CYCLASE (AC)
  • Decrease in cAMP Production
  • ACTIVATION os K+ Channels

***DECREASES the rate of FIRING and FORCE of Contraction

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12
Q

M3 Cholinergic Receptors

A

Location:
- Glands, SMOOTH MUSCLE, Endothelium

Structural Features:
- GPCR, Gq/11

Mechanism:

  • Activation of PLC
  • IP3
  • DAG Cascade

***Smooth Muscle contraction to stop release of bowels

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13
Q

M4 Cholinergic Receptor

A

Location:
- CNS

Structural Features:
- GPCR, Gi/0

Mechanism:

  • Inhibition of AC
  • Decrease in cAMP production
  • Activation of K+ Channels
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14
Q

M5 Cholinergic Receptors

A

Location:
- CNS

Structural Features:
- GPCR, Gq/11

Mechanism:

  • Activation of PLC
  • IP3
  • DAG Cascade
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15
Q

Nm Cholinergic Receptor

A

Location:

  • SKELETAL MUSCLE
  • Neuromuscular Junction

Structural Features:

  • Pentamer
  • Alpha 2, Beta d, and Gamma/ Epsilon

Mechanism:
- N+, K+ depolarizing ION CHANNEL

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16
Q

Nn

A

Location:

  • POSTGANGLIONINC CELL BODY
  • Dendrites
  • CNS

Structural Features:

  • Alpha and Beta Only
  • (Alpha 4)2 (Beta 4)3
  • (Alpha 7)5

Mechanism:
- N+, K+ Depolarizing Ion Channel

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17
Q

Catecholamine Synthesis

A

1) Occurs in the NERVE CYTOPLASM:
A) Tyrosine —-> DOPA

B) DOPA —-> Dopamine

2) Occurs in the Vesicle:
A) Dopamine —> Norepinephrine

B) Norepinephrine —> Epinephrine

3) Occurs MAINLY in the Adrenal Medulla:
A) Norepinephrine —> Epinephrine

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18
Q

Synthesis, Storage, Release, and Reuptake

A

1) Na+ Dependent TYROSINE Transporter:
- Transports Tyrosine into the Nerve Terminal

2) VASICULAR Monoamine Transporter (VMAT-2)
- Transport NE, Epi, DA, and Serotonin into Vesicles (promiscuous)

  • RELEASE upon ACTION POTENTIAL and Ca2+ INFLUX

3) NE Transporter (NET)
- Imports NE into the Nerve Terminal

  • DAT Imports DA into the Nerve Terminal
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19
Q

Termination of Catecholamine Signaling

A

1) Reuptake into Nerve Terminals:
- Major Mechanism that terminates the ACTIONS of Catecholamines

  • NET (Norepinephrine Transporter) and DAT (Dopamine Transporter)
  • After REUPTAKE, Catecholamines are STORED in Vesicles by the VMAT-2

2) Metabolism of Catecholamines (2 Main Enzymes)
A) MONOAMINE OXIDASE (MAO)

B) CATECHOL-O- METHYLTRANSFERASE (COMT)

***In contrast to Cholinergic signaling, termination of Catecholamine action by Degradative enzymes (Ex: AChE) is nonexistent in Adrenergic Signaling

*****VMA is a marker for a specific type of tumor an Individual can get

***COMT and MAO help create the VMA!!!

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20
Q

Adrenergic Signaling

A

1) Catecholamines activate TWO SUBSETS of Adrenergic Receptors:
- Alpha and Beta

2) Alpha Receptors:
- GPCR
- Pre and Postjunctional
- Two major subtypes (Alpha1, Alpha2)

3) Beta Receptors:
- GPCR
- Pre and Postjunctoinal
- Three Major Subtypes (Beta1, Beta2, Beta3)

4) DA Receptors:
- GPCR
- 5 Types (D1- D5)

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21
Q

Adrenergic Receptors

A

Alpha 1

Alpha 2

Beta 1

Beta 2

Beta 3

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22
Q

Alpha 1 Adrenergic Receptor

A

G Protein and Effectors

  • Gq
  • Increase Phospholipase C
  • IP3 and DAG, Intracellular Ca2+

Agonist

  • Epinephrine > Norepinephrine&raquo_space; Isoproterenol
  • Phenylephrine

Tissue

  • Vascular, GU Smooth Muscle
  • Liver
  • Intestinal Smooth Muscle
  • HEART

Responses

  • CONTRACTION
  • Glycogenolysis; Gluconeogenesis
  • Hyperpolarization and relaxation
  • Increased Contractile Force; Arrhythmias
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23
Q

Alpha 2 Adrenergic Receptor

A

G Protein and Effectors

  • Gi, Go
  • DECREASE in Adenyl Cyclase
  • DECREASE in cAMP

Agonist

  • Epinephrine > Norepinephrine&raquo_space; Isoproterenol
  • CLONIDINE

Tissue

  • Pancreatic Islets (Beta Cells)
  • Platelets
  • Nerve terminals
  • Vascular Smooth Muscle

Responses

  • DECREASED INSULIN Secretion
  • Aggregation
  • Decreased RELEASE of Norepinephrine
  • CONTRACTION
24
Q

Beta 1 Adrenergic Receptor

A

G Protein and Effectors

  • Gs
  • INCREASE in Adenyl Cyclase, cAMP,
  • L Type Ca2+ Channel Opening

Agonist

  • Isoprotenol > EPINEPHRINE&raquo_space; NOREPINEPHRINE!!!!!!!!
  • DOBUTAMINE

Tissue

  • Juxtaglomerular Cells
  • HEART

Responses

  • Increased RENIN Secretion
  • Increased FORCE and RATE of Contraction and AV Nodal Conduction Velocity
25
Q

Beta 2 Adrenergic Receptor

A

G Protein and Effectors

  • Gs
  • INCREASE Adenyl Cyclase

Agonist

  • Isoproterenol > EPINEPHRINE&raquo_space; NOREPINEPHRINE
  • Terbutamine

Tissue

  • Smooth muscle (Vascular, Bronchial, GI, GU)
  • Skeletal Muscle

Responses

  • RELAXATION
  • Glycogenolysis; Uptake of K+
26
Q

Beta 3 Adrenergic Receptor

A

G Protein and Effectors

  • Gs
  • INCREASE Adenyl Cyclase

Agonist
- Isoproterenol = Norepinephrine > Epinephrine

Tissue
- Adipose Tissue

Responses
- LIPOLYSIS

27
Q

Sympathomimetic Agents: Drugs that mimic or Enhance Alpha and Beta Receptor Stimulation

A

1) Epinephrine:
- Alpha 1 = Alpha 2
- Beta 1 = Beta 2

2) Norepinephrine:
- Alpha 1 = Alpha 2
- Beta 1&raquo_space; Beta 2

3) Isoproterenol:
- Beta 1 = Beta 2&raquo_space;» Alpha

28
Q

Rules of Thumb for Smooth Muscle and Autonomic Receptor

A

1) Alpha-1 Receptors:
- Stimulate CONTRACTION of all SMOOTH MUSCLE

  • Vascular Smooth Muscle - VASOCONSTRICTION

2) Beta-2 Receptors:
- Relax Smooth Muscle- VASODILATION

3) Muscarinic Receptors:
- CONTRACT Smooth Muscle (Different Intracellular Signal than Alpha 1 Receptors)

29
Q

Direct Effects of Autonomic Stimulation

A

PARASYMPATHETIC ACTIVITY:

- Has NO EFFECT on the BLOOD VESSELS!!!!!!!!!!!!!!!!!

30
Q

Response of Blood Vessels to Autonomic Nerve Impulses

A
  • Blood Vessels are INNERVATED by ADRENERGIC RECEPTORS, which cause Vessel Constriction when ACTIVATED (SYMPATHETIC)
  • Smooth Muscle of Blood Vessels is NOT INNERVATED by PARASYMPATHETIC Neurons
  • neither mAChRs nor nAChRs are found on SMOOTH MUSCLE of Blood Vessels
  • Blood Vessels RELAX in response to PARASYMPATHETIC RELEASE of ACh as long as the Epithelium is INTACT!!!!
31
Q

mAChRs, EDRF (NO), and Vessel Relaxation

A
  • Activation of mAChRs on EPITHELIAL CELLS causes production and release of Endothelium- derived Relaxing Factor (EDRF) also known as NITRIC OXIDE (NO)
  • Stimulation of NO release can occur from ACh, VASOACTIVE PRODUCTS, and Physical Stimuli
32
Q

Adrenal Medulla

A
  • SYMPATHETIC Innervation
  • EPINEPHRINE and NOREPINEPHRINE is triggered by the RELEASE of ACh from the PREGANGLIONIC FIBERS
  • ACh binds to NnAChRs and produce a localized Depolarization
  • RELEASE in approximately:
    80%: Epinephrine
    20%: Norepinephrine
33
Q

Baroreceptor Reflex as an Example of Compensatory Changes in the ANS

A

1) Baroreceptor:
- BP Increases with PHENYLEPHRINE

  • BP Decreases with HISTAMINE

2) Parasympathetic Nervous System:
- BP Increases with PHENYLEPHRINE

  • BP Decreases with HISTAMINE

3) Sympathetic Nervous System:
- BP Decreases with PHENYLEPHRINE

  • BP Increases with HISTAMINE
34
Q

Coronary Heart Disease Causes

A
  • Now out of Six Adults in the US (380,000 deaths/ year)
  • One coronary event every 30 seconds
  • STEMI accounts for 30% of all MI’s
35
Q

ST Segment Elevation

Acute Myocardial Infarction (AMI)

A

ECG
- ST Segment ELEVATION

  • “Transmural”
  • Complete interruption of Blood Flow
  • CORONARY occlusion usually due to THROMBUS
36
Q

PATHOBIOLOGU

A
  • Erosion, Fissuring Orrupture of Plaque; THROMBUS (Platelet, Fibrin Rich Thrombus is generated)
  • If Coronary FLOW is occluded- STEMI
  • If Partial Occlusion- UA or NSTEMI
  • MOST MI CAUSED BY ATHEROSCLEROSIS; other causes include Vasospasm, Vasculitis, Dissection, Genetics
37
Q

Clinical Manifestations

A

History
- Chest discomfort (more severe with Angina)

  • HEAVY, Pressure, Crushing, etc
  • Retrosternal, left, across chest; Neck, Jaw, Left arm, Epigastrium
  • Nausea, Vomiting, Diaphoresis, Dyspnea
  • Not reliability relieved by NOTRO or REST
  • 20% AMI are painless (Silent); diabetics elderly women
38
Q

AMI ECG

A
  • Critical role in STRATIFICATION, TRIAGE, MANAGEMENT
39
Q

STEMI

A

” ST Elevation Myocardial Infarction”
- Elevation of 2mm in Two CONTINUOUS LEADS!!!!

  • ST elevation of 2mm of > at J POINT in V2-V3 in Men or 1.5 mm or > in Woman in absence of LVH or 1mm or > in 2 or more Contiguous Chest or limb leads
  • New LBBB (obscures ST elevation Analysis)
  • May need SERIAL TRACINGS (to see if there are any changes in the ECG)!!!!!!!!!
40
Q

NSTEMI

A
  • ST Segment DEPRESSION
  • T Wave INVERSION
  • Chest pain
  • Elevated CARDIAC ENZYMES
41
Q

QT Duration Length of Ventricular Systole

A
  • Myocardial Ischemia
  • Myocardial Injury
  • Myocardial Infarction
  • T WAVE: ISCHEMIC pattern is associated with INVERTED T WAVES and TALL, PEAKED T WAVES!!!!!!!
  • ST ELEVATION: Pattern of Injury
  • Q WAVE or QS COMPLEX: Pattern of NECROSIS or INFARCTION
42
Q

Zones of Infarction

A

1) Ischemia:
- Deficiency Blood Supply
- IMPAIRED REPOLARIZATION

*** T WAVE Changes!!!!

2) Injury:
- Deficient Blood Supply
- INABILITY to FULLY POLARIZE

***ST SEGMENT Shifts

3) Infarction:
- Dead Tissue
- LACKS DEPOLARIZATION

**Q Waves!!!!!!!!!!

43
Q

Anterior Wall Infarction

A

Artery:
- Left Anterior Descending Artery (LAD) aka “Widow Maker”
( Anterior Interventricular Artery)

Leads:
- V1 to V7

44
Q

Inferior Wall Infarction (RV Infarction)

A

Artery:
- Right Coronary Artery (RCA)!!!!!

Leads:

  • II, III, aVF
  • V3R - V6R

Called DIAPHRAGMATIC INFARCT*

45
Q

Lateral Wall Infarction

A

Artery:
- Circumflex Artery

Leads:

  • I, aVL
  • V5 to V6
46
Q

Posterior Wall Infarction

A

Artery:
- Posterior Descending Artery

Leads:
- V1 to V3

47
Q

Picture of MI with Zone of Ischemia, Zone of Injury, and Zone of Infarction

A
  • Ischemia causes INVERSION of T WAVE due to ALTERED DEPOLARIZATION
  • Muscle injury causes ELEVATION of ST Segment
  • Death (INFARCTION) of muscle causes Q or QS Waves due to absence of DEPOLARIZATION current from DEAD TISSUE and opposing currents from other parts of the Heart
  • During RECOVERY (Subacute and Chronic stages) ST Segment often is first to return to Normal, then T Wave, due to disappearance of ZONES of Injury and Ischemia
48
Q

NSTEMI MI

A
  • ST Segment do not INSCRIBE a SIZEABLE Q WAVE!!!!

- T Wave INVERSION!!!!

49
Q

Labs for MIs

A

1) INCREASE in WBC (12,000 - 15,000)
- Hours through 2 to 4 days

2) INCREASE in C Reactive Protein (CRP)
3) Brain Naturetic Peptide (BNP): Increased in Ventricular Wall Stress and Fluid Overload

50
Q

Cardiac Biomarkers of Necrosis

A
  • TROPONIN I (cTnI) or T (cTnT)
  • 1 to 4 hours DETECTABLE after onset AMI
  • 10 to 24 hours PEAK
  • Persist 5 to 14 days
  • RENAL Failure can cause FLASE POSITIVE cTnT!!!!!!!!
51
Q

Exercise

A
  • Body ANTICIPATES exercise and INCREASES SYMPATHETIC Outflow and DECREASES PARASYMPATHETIC
  • CO Increases and NON Active Tissues INCREASE RESISTANCE
  • Local Reflexes of CONTRACTING MUSCLE causes VASODILATION.
  • Tissue Mass can be GREAT ENOUGH that is could cause a LARGE REDUCTION of TPR and BP if ANTICIPATORY REFLEX has NOT ALREADY BEEN INVOKED!!!
52
Q

Exercise Graph

A

1) Exercise

2A) CENTRAL COMMAND:

  • Increases Sympathetic OUTFLOW
  • Decreases Parasympathetic OUTFLOW

Leads to:

  • Incr HR
  • Incr Contractility
  • Incr Cardiac Output
  • Constriction of Arterioles
  • Constrictoin of Veins
  • Decr in Unstressed Volume

2B) LOCAL RESPONSE:
- Increases VASODILATION Metabolites

Leads to:

  • Dilation of Skeletal Muscle ARTERIOLES
  • Decr in TPR

**AL OF THESE CAUSE an INCREASE IN BLOOD FLOW TO SKELETAL MUSCLE!!!!!

53
Q

Hemorrhage

A

DECREASED BLOOD VOLUME can be caused by:

  • Hemorrhage
  • Dehydration
  • Loss of Body Fluids

DECREASED Venous Return, Preload, Stroke Volume, CO, and BP

  • BAROCEPTOR REFLEXES are STIMULATED
  • HORMONAL REFLEXES are INITIATED
54
Q

Hemorrhage

A

1) Hemorrhage (DECREASES Arterial Pressure)

2A) BARORECEPTOR REFLEX:
- INCREASES Sympathetic OUTFLOW

Leads to:

  • Incr HR
  • Incr Contractility
  • Incr Cardiac Output
  • Constriction of Arterioles
  • Incr TPR
  • Constriction of Veins
  • Decr Unstressed Volume

2B) RENIN- ANGIOTENSIN II- Aldosterone
- INCREASE in AGIONTENSIN II

Leads to:
- Incr TPR

  • Incr Aldosterone —–>
  • Incr Na+ Reabsorption ——>
  • Incr Blood Volume

2C) CAPILLARIES:
- DECREASE Pressure in Capillaries

Leads to:

  • Incr in Fluid Absorption —->
  • Incr Blood Volume
55
Q

Changes in Posture

A
  • Normally upright movement INITIATES Muscle Pumps which pushes blood UPWARD towards the HEART past VALVES in the LIMBS
  • If NO MOVEMENT then VENOUS RETURN accumulate in LOWER LIMBS, INCREASING Venous and Capillary Hydrostatic Pressure
  • Venous pooling can result in EDEMA and/ or HYPOTENSION
  • REFLEXES will attempt to BRING BP BACK to NORMAL!!!
56
Q

Responses to Standing

A
  • DECREASED VENOUS RETURN
  • DECREASED CO and therefore DECREASED BP
  • Baroreceptor Reflex
  • Hormonal Reflex will also be initiated but probably TOO SLOW to have a significant IMPACT
  • ORTHOSTATIC HYPOTENSION!!!!
    • Fall in Systolic BP of at least 20 mm Hg or Diastolic BP of at least 10 mm Hg when a person stands!!!!
57
Q

Standing Chart

A

1) Standing
- Pooling of Blood in VEINS!!!

2) BARORECEPTOR REFLEX
- INCREASES Sympathetic OUTFLOW

Leads to A:

  • INCR HR
  • INCR Contractility
  • INCR Cardiac Output

Leads to B:

  • Constriction of Arterioles
  • INCR TPR

Leads to C:

  • Constriction of Veins
  • DECR Unstressed Volume

*****RESULTS IN an INCREASE IN ARTERIAL PRESSURE TOWARDS NORMAL!!!!!

Cardiopulmonary I (12 decks)

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