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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
Beta 2 Adrenergic Receptor
G Protein and Effectors - Gs - INCREASE Adenyl Cyclase Agonist - Isoproterenol > EPINEPHRINE >> NOREPINEPHRINE - Terbutamine Tissue - Smooth muscle (Vascular, Bronchial, GI, GU) - Skeletal Muscle Responses - RELAXATION - Glycogenolysis; Uptake of K+
26
Beta 3 Adrenergic Receptor
G Protein and Effectors - Gs - INCREASE Adenyl Cyclase Agonist - Isoproterenol = Norepinephrine > Epinephrine Tissue - Adipose Tissue Responses - LIPOLYSIS
27
Sympathomimetic Agents: Drugs that mimic or Enhance Alpha and Beta Receptor Stimulation
1) Epinephrine: - Alpha 1 = Alpha 2 - Beta 1 = Beta 2 2) Norepinephrine: - Alpha 1 = Alpha 2 - Beta 1 >> Beta 2 3) Isoproterenol: - Beta 1 = Beta 2 >>>> Alpha
28
Rules of Thumb for Smooth Muscle and Autonomic Receptor
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
Direct Effects of Autonomic Stimulation
PARASYMPATHETIC ACTIVITY: | - Has NO EFFECT on the BLOOD VESSELS!!!!!!!!!!!!!!!!!
30
Response of Blood Vessels to Autonomic Nerve Impulses
- 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
mAChRs, EDRF (NO), and Vessel Relaxation
- 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
Adrenal Medulla
- 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
Baroreceptor Reflex as an Example of Compensatory Changes in the ANS
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
Coronary Heart Disease Causes
- 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
ST Segment Elevation | Acute Myocardial Infarction (AMI)
ECG - ST Segment ELEVATION - "Transmural" - Complete interruption of Blood Flow - CORONARY occlusion usually due to THROMBUS
36
PATHOBIOLOGU
- 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
Clinical Manifestations
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
AMI ECG
- Critical role in STRATIFICATION, TRIAGE, MANAGEMENT
39
STEMI
" 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
NSTEMI
- ST Segment DEPRESSION - T Wave INVERSION - Chest pain - Elevated CARDIAC ENZYMES
41
QT Duration Length of Ventricular Systole
- 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
Zones of Infarction
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
Anterior Wall Infarction
Artery: - Left Anterior Descending Artery (LAD) aka "Widow Maker" ( Anterior Interventricular Artery) Leads: - V1 to V7
44
Inferior Wall Infarction (RV Infarction)
Artery: - Right Coronary Artery (RCA)!!!!! Leads: - II, III, aVF - V3R - V6R ***Called DIAPHRAGMATIC INFARCT****
45
Lateral Wall Infarction
Artery: - Circumflex Artery Leads: - I, aVL - V5 to V6
46
Posterior Wall Infarction
Artery: - Posterior Descending Artery Leads: - V1 to V3
47
Picture of MI with Zone of Ischemia, Zone of Injury, and Zone of Infarction
- 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
NSTEMI MI
- ST Segment do not INSCRIBE a SIZEABLE Q WAVE!!!! | - T Wave INVERSION!!!!
49
Labs for MIs
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
Cardiac Biomarkers of Necrosis
- 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
Exercise
- 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
Exercise Graph
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
Hemorrhage
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
Hemorrhage
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
Changes in Posture
- 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
Responses to Standing
- 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
Standing Chart
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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