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Cardiopulm > PowerPoints > Flashcards

PowerPoints Flashcards

1
Q

3 basic steps of a reflex arc

A
  1. Sensory input to CNS
  2. Triggers Response
  3. Initiates motor outflow to “do” something
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2
Q

Touching a hot stove triggers what receptors?

A

Nociceptors (pain receptors)

They are brought to threshold and an AP travels down to the nerve to her spinal cord, depolarizes the pre-synpatic membrane of the axon from the nociceptors

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3
Q

What happens in the “Autonomic Reflex Arc”?

A

Afferent neuron → dorsal side of spinal cord then to brain (Big gap because for smooth muscle we always send it to the brain- lower levels (brainstem, hypothalamus) and not cortex) → then to ventral side and efferent signal (ANS)

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4
Q

Do we have afferent neurons in the viscera (organs)?

A

Yes

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5
Q

The ANS of the viscera is the equivalent of the motorneurons/efferent arm we used to produce the withdrawl reflex

A

True

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6
Q

What does the ANS control?

A

Smooth muscle, blood flow, glands

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7
Q

How many ANS neurons to effector cell?

A

2: pre-ganglionic and post-ganglionic

Speed is not our main goal- thus we have 2 neurons from brain to effector location

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8
Q

Do the sympathetic and parasympathetic leave the CNS in different places?

A

Yes

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9
Q

Where does the pre-ganglionic axon synapse?

A

On the post-ganglionic neuron which goes to target organ and synapses on it

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10
Q

“en passant” synapse for smooth muscle

A

Mailman tossing mail onto lawn..doesn’t matter because receptors on smooth muscle are much more widely distributed so it will still find a receptor

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11
Q

What are varicosities?

A

They are swellings on autonomic nerves, along the axon, that contain the NT

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12
Q

On the effector organ, at the synapse between the post-ganglionic axon and smooth muscle (or whatever we’re trying to affect) we don’t nAChR…we have instead….

A

mAChR

Activates a G protein

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13
Q

Inhibitory G protein means what?

A

Inhibiting cAMP…so it could lead to an increase in activity. cAMP does different things in different places

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14
Q

G-protein: M2

A

Cardiac: (inhibitory G-protein)

↓ cAMP→ ↑ gK+

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15
Q

G-protein: M3 (widely distributed in body)

A

Gq coupled

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16
Q

G-protein: M4

A

Neurons

↓ cAMP→ ↓ ACh release

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17
Q

Synapse between pre and post ganglionic synapses are the same for sympathetic/parasympathetic

A

True

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18
Q

All of the NE/epi receptors are serpentine (G-protein coupled receptor ) receptors that connect to both α and β receptors

A

True

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19
Q

α-adrenergic

A

Higher affinity for NE than epinephrine

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20
Q

β-adrenergic: 3 subtypes

A

All ↑ cAMP (G-stimulatory protein)

Higher affinity for epinephrine

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21
Q

Adrena medulla (equivalent of a sympathetic ganglion)

A

Makes chromaffin cells → makes epinephrine

Pre-ganglionic fiber going into adrena medulla → releases ACh (same as all pre) →acts on nAChR on chromaffin cells inside adrena medulla → release epinephrine into blood

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22
Q

What do α-adrenergic receptors do to radial muscle of iris?

A

Contract the muscle → dilation of pupil → allows more light in

*(α-adrenergic receptors almost always contract muscle)

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23
Q

What do β-adrenergic receptors do to the ciliary muscle of the lens?

A

Relax smooth muscle→flattens lens → focus on far objects

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24
Q

What do β1 and β2 adrenergic receptors do to the heart?

A

Both ↑ HR and ↑ strength of contraction

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25
Q

General rule of thumb for α and β receptors of vascular smooth muscle:

A

α receptors: contraction → vasoconstriction

β receptors: relaxation → vasodilation

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26
Q

Most arteries and veins have both α and β receptors

A

True

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27
Q

What systems have only α receptors on them?

A

Skin/mucosa (so you don’t bleed as much when bit by T-Rex)

Salivary glands (dry mouth)

Brain (α receptors only activate and thus get blood when BP is VERY high)

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28
Q

Making it easy to get oxygen in:

Bronchial smooth muscle and Bronchial glands receptors

A

Bronchial smooth muscle:
-β2: smooth muscle relaxation → bronchodilation

Bronchial glands (if I’m running and taking deep breaths we need to protect airway from dry air)

  • α1: ↓ secretion
  • β2: ↑ secretion
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29
Q

Fight or Flight: Motility

A

Motility→usually decrease motility (stop digestion)
-α1 and β

Sphincters
-α1 → contraction

Secretion
α2→ ↓ secretion

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30
Q

Fight or flight: Liver and Adipose Tissue

A

Liver
-α1 and β2→glycogenolysis (release of glucose)

Adipose Tissue
-α1, β1 and β3→ ↑lipolysis

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31
Q

Summary slide of “fight or flight”

A

Eyes (dilate in fear- get more light in, focus on distance)

  • Radial muscle: α adrenergic; dilate pupil
  • Ciliary muscle: β adrenergic; allow distance vision
Cardiovascular
-Heart: β2: increase strength and rate of contraction (more blood)
-Vasculature: 
α: constrict and send blood away
β: dilate and increase blood flow
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32
Q

3 steps of Hemostasis

A
  1. Formation of primary plug
  2. Formation of blood clot
  3. Fibrinolysis- removal of clot
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33
Q

Structure of Fibrinogen

A

Made up of 3 subunits: α, β, γ that exist as dimers with domains D and E

Thrombin cuts off A and B sites- left over portions of A fit into γ subunit of another fibrinogen. Cutting off A exposes sites in the E domain that match complementary sites in D domain. B chains interact to form a 3 dimensional wall…maybe how they stick together?

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34
Q

How is a hard clot formed?

A

D+E are H-bonds but still not hard

Covalent bond formed between NH2 of GLUTAMINE and NH3 of LYSINE via factor 13a (transglutaminase) which is activated by Thrombin (it also activates Fibrin)

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35
Q

How does clot localization occur?

A

Prothrombin has to be modified

Extra COO- attached to Glutamic acids. There is carboxylation of several glutamic acid residues- adds another charge to side R-group on amino acid- “-2” negative charge- called γ-carboxyglutamate

Glutamate —- (carboxylase) —→ γ-carboxyglutamate

This -2 charge helps localize prothrombin to damaged vessels. These vessels release Ca 2+ and so it binds Prothrombin, and then Ca 2+ binds platelets which have exploded, uncovering negatively charged phospholipids as they invert

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36
Q

Vit K recycling uses what enzyme and why is Vit K important?

A

Epoxide reductase (helps reduce Vit K so it can be used again)

**Warfarin inhibits this enzyme (anti-clotter)

Important because: Modification of Prothrombin (carboxylation) requires Vit K

37
Q

What 2 things are competitive inhibitors of epoxide reductase (which helps recycle Vit K)?

A

Warfarin (rat poison) and Dicoumerol

(Anti-clotting drugs)- inhibit the addition of carboxylic acid groups to prothrombin→ so things aren’t localized

38
Q

Intrinsic vs Extrinsic pathway

A

Extrinsic is the SPARK (creates some thrombin= kindling)→start up intrinsic

Intrinsic: workhorse

39
Q

What is exposed during platelet damage?

A

PF3 (Platelet factor 3) and phospholipids

On interior of platelets and exposed when platelets disrupted

40
Q

What does the Extrinsic pathway require to get started?

A

Tissue Factor 3

7+3a→7a+3a

(A very small amount of 7a is floating around waiting for damage which triggers Tissue Factor 3 (3a)

41
Q

What is given quickly after a stroke to dissolve a clot?

A

TPA (protein)

42
Q

What activates Hormone Sensitive Lipase (HSL)?

A

Activated by phosphorylation by PKA (Triggered by glucagon, epi, norepi)

Glucagon, epi, norepi → act. PKA via cAMP and GPCR cascade→ phosphorylates/activates HSL

(Glucagon, epi, norepi=promote lipolysis in adipocytes)

(Insulin inhibits lipolysis)

43
Q

What inactivates HSL?

A

Dephosphorylation by PP1 (protein phosphatase 1)

Insulin → act. PP1 → Inactivates HSL

44
Q

How can we target obesity via Perilipin?

A

Perilipin coats lipid droplets→ limits access to HSL (We want to get rid of Perilipin b/c it’s protecting the fat)

By inhibiting Perilipin → break down more fat

Phosphorylation via PKA → we can reach HSL → lipolysis

45
Q

What is olestra and what does it do?

A

A synthetic fat

Absorbs Vit D,E,K,A → Vit deficiency

(Abdominal cramps, bloating, diarrhea)

46
Q

What are Lipoproteins used for?

A

Transport

47
Q

What are 3 functions of Apolipoproteins?

A

Stabilize lipoproteins
Transport lipids
Cofactor for enzymes that act on lipids

48
Q

What do statin drugs do?

A

Lower cholesterol

They mimic structure of HMG CoA…they inhibit HMG CoA reductase

You’re blocking cholesterol synthesis in your body…you also lose out on Heme A, Ibiquinon etc

49
Q

What cells release NO?

A

Endothelial cells ..causes relaxation

Mechanical change (stretching) can cause hormones to be released. Smooth muscle (when damaged) can activate itself

50
Q

Can we get smooth muscle contraction w/o an AP?

A

Yes- use hormones can trigger Ca 2+ release

51
Q

Smooth muscle contraction steps

A

(Smooth muscle is not dependent on troponin)

  1. Ca 2+ enters from SR or ECF
  2. Ca 2+ binds calmodulin (CaM)
  3. Ca 2+/CaM activates myosin light chain kinase (MLCK)
  4. MLCK phosphorylates light chains in myosin heads and ↑ myosin ATPase activity (need ATP)
  5. Active myosin crossbridges slide along actin and create muscle tension
52
Q

Smooth muscle contraction: the latch mechanism

A
  1. Dephosphorylation of light chain
  2. Cycle proceeding very slowly
  3. Any attached cross-bridges are still generating tension
  4. Way to ↑ tension and ↓ ATP usage
53
Q

Smooth muscle relaxation

A

The Phosphate can be taken off the myosin light chain at any point in the cycle- the cycle will continue VERY SLOWLY. A new cycle can’t be started

A new cycle can’t be started b/c once myosin light chain is dephosphorylated, it’s “stuck”…the other ATP can’t get in very easily because the latch position is crowding it out…needs to be phosphorylated to start a new cycle

54
Q

Smooth muscle has much more what than skeletal muscle?

A

Many more thin filaments and less thick filaments (doesn’t have sarcomeres)

55
Q

Length-Tension Relationships in Smooth muscle

A

The chart looks like little blips on the x-axis

Smooth muscle gets rid of passive tension VERY quickly b/c the thick/thin filaments aren’t arranged in a sarcomere

Passive Tension= Comes from stretching the membranes
-but in smooth muscle it rapidly dissipates (falls back to zero)

When I stretch smooth muscle these thick/thin elements can rearrange…the thick filament can find a new thin filament to interact with

As smooth muscle is stretched, the myosin heads, once free from the actin, will interact with a DIFFERENT thin filament

This does 2 things:

  1. Reduces passive tension by reducing strain on points of attachment
  2. Allows smooth muscle to continue to generate active tension over a wide range of length…always an actin available for the myosin head
56
Q

What happens when you eat a large Thanksgiving dinner?

A

As my stomach stretches, I got rid of passive tension b/c the thick filament that had been binding with one thin filament let go and found another thin filament to bind to (anchored to cell membrane but in different place) and we generate active tension with this new arrangement. Passive tension was dissipated and active tension was maintained…this is crucial to how smooth muscle functions

57
Q

What are the 4 steps of Hemostasis?

A
  1. Vascular spasm (clamp off blood flow)
  2. Form platelet plug
  3. Form blood clot
  4. Repair damage
58
Q

What stimulates the formation of platelets?

A

Thrombopoietin (TPO) in liver/kidney

-Amine terminal is like erythropoietin (EPO)…thrombopoietin (liver) can trigger cell growth of other cell lineages

59
Q

What receptor do platelets express for thrombopoietin?

A

MPL

Found on platelets, and all hematopoietic cells

60
Q

What happens with thrombopoietin when platelets #’s are high?

A

Lots of TPO (thrombopoietin) bound to MPL receptor on platelets → internalize TPO and destroy it → not much free to act on megakaryocytes

61
Q

What happens from a mutation in the TPO receptor?

A

Causes polycythemia vera- platelets are unable to destroy TPO so it’s action becomes continuous…and you get too much TPO…may increase platelet function

62
Q

On platelets are glycoproteins which do what?

A

Sticky

63
Q

Platelets have receptors for collagen

A

True

64
Q

Production of platelets is controlled by Thrombopoietin

A

True

65
Q

What are the causes of vascular spasms?

A

Myogenic affect- direct response to injury. Doesn’t require anything

Platelet factors: serotonin, TXA2- both make sure it stays contracted

66
Q

How is the platelet plug formed?

A

W/ damage, collagen exposed → platelets bind collagen (needs Von Willebrand protein- links collagen and platelet)

  1. Binding causes platelet swells
  2. Contraction
  3. Granules leave platelet
  4. Platelets stick to vessel wall and to each other (TXA2 and ADP→sticky)
67
Q

What are the 3 major steps in clot formation?

A
  1. Formation of prothrombin activator
  2. Activation of Thrombin
  3. Create fibrin from fibrinogen

(then clot retraction-stabilizes)

68
Q

What is Clot Retraction?

A

Get rid of excess fluid within clot

Solidify clot

Platelets required (bind fibring together)

Requires Ca 2+ for contraction

69
Q

What’s the role of platelet-derived growth factor in healing?

A

Secreted by platelets

Stimulates fibroblast to grow into area → differentiate into different cells

70
Q

How are clots removed?

A

Plasminogen (made by liver)

Activated by “Tissue plasminogen activator” (TPA)-released by damaged tissue

If I need the clot to stick around, then tPA inhibitor inhibits its destruction

71
Q

How do we get rid of the tPA inhibitor?

A

Endothelial cells secrete →thrombomodulin→thrombin binds and this becomes an anti-coagulant→inhibiting/undoing clot

Protein C inhibits “tPA inhibitor”→tPA can create plasmin which gets rid of fibrin

72
Q

What systems limit clotting?

A

Blood vessels (smooth lining prevents platelets from rupturing)

Glycocalyx- repels platelets

73
Q

How does Fibirin prevent clotting?

A

Binds thrombin and prevents it from working

74
Q

How does PGI2 prevent clotting?

A

Made at time of injury by endothelial cells

Vasodilation

Limits platelet aggregation

75
Q

How does Antithrombin 3 prevent clotting?

A

When thrombin binds to it, works as anticoagulant

Heparin ↑ antithrombin efficiency

76
Q

Activated protein C does what?

A

Activated protein C → inactivation of tPA inhibitor → inactivation of 8a and 5a →Inhibition of further fibrin creation

Protein C, when activated, inactivates factors 5 and 8

Mutation in factor 5 leads to blood clots.

77
Q

What is the major cause of phase 0 of a neural AP?

A

Increased Na+ conductance

78
Q

Which of the following maintains the neural resting potential?

A

K+ conductance

Potential is determined by the most permeable or highest conducting species

79
Q

Which of the following contributes to phase 1 of the neural AP?

A

Opening of K+ gates

80
Q

How do I calculate the Ejection Fraction?

A

Ejection Fraction= SV/EDV x 100

SV= EDV- ESV

81
Q

What would stimulating Beta 1 receptors on the SA node do?

A

↑ HR (increasing slope of depolarization in the process)

82
Q

In order for shortening to occur, Ca 2+ must bind to what?

A

Troponin…which then affects tropomyosin

83
Q

What is attached at the Z line?

A

Actin

84
Q

The A band is comprised of what?

A

Myosin

85
Q

During phase 2 the extracellular potential is ____ mV?

A

Between 0- -15

86
Q

NO

A

Made on demand by endothelial cells and can diffuse straight through the membrane b/c it’s very lipid soluble

87
Q

ACh binds to muscarinic receptors on the actual smooth muscle cell

A

True

88
Q

Intrinsic innervation (neural)

A 
Gut, trachea
Via neurons (sensory and motor)
89
Q

Extrinsic via ANS

A

Allows CNS to control viscera (internal organs)

Cardiopulm (3 decks)

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