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Physiology (BAS 118) > Cellular Physiology and Hemotology (Part 1 / Lecture 1) > Flashcards

Cellular Physiology and Hemotology (Part 1 / Lecture 1) Flashcards

1
Q

What constitutes plasma?

A

Water - 92% (total blood volume)

Proteins - 7%
(so water stays in blood vessels and doesnt run out)

Nutrients & waste products - 1%
(Amino acids, ions, vitamins, glucose, O2, CO2, lipids, nitrogenous waste, trace elements – these are not always bound (to alumin) to something and can be found dissolved in the fluid of plasma)

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2
Q

“Interstitial fluid”

A

= “Plasma” – “Proteins”

*this ends up in your tissues. Holes are small enough to let in liquid, but not the proteins.

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3
Q

Albumin

A

carrier protein

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4
Q

Fibrinogen

A

clotting material

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5
Q

Transferrin

A

transfers iron

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6
Q

ferritin

A

stores iron,mostly in the liver

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7
Q

Globulins

A

immnunoglobulins (IgG’s)

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8
Q

Oncotic Pressure

A

**allow water to stay in the muscles, to maintain blood volume. Otherwise, we would all faint.

*water pulled out of interstitial fluid into capillaries due to the presence of plasma proteins.

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9
Q

Liver/Kidney Disease & Malnutrition

Plasma (Clinical Significance)

A

results in decrease in plasma proteins (albumin) –> (increase) edema (swelling) in lower limbs

*frothy urine, like eggwhites

  • Can’t make albumin as much/as quickly as you used to
  • Can’t keep water in the vessels
  • Kidney may lose ability to keep proteins in when it’s filtering
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10
Q

Hematopoiesis

A

Cellular development from pluripotent stem cell (which are found in bone marrow) to the various cellular elements found in whole blood

  • Megakaryocytes/thrombocytes
  • Red Blood Cells
  • Mast cells
  • Leukocytes
  • B/T/NK (natural killer) cells
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11
Q

Why does it matter that all proteins have a charge?

A

All proteins have a charge, therefore they bring water with them when they move.

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12
Q

Megakaryocytes

A

extend into capillaries and shed fragments of their extensions
(Fragments = thrombocytes aka platelets)

they stay in the bone marrow and poke out to add thrombocytes to the blood

Regulated by TPO

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13
Q

Thrombopoetin (TPO)

A

regulates megkaryocytes. made in the liver and a small amount in the kidney.

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14
Q

Thrombocytopenia

A

too few platelets in the blood cused by :

1) decreased production :(cancer, chemo, viral infection of marrow)
2) Increased Destruction (autoimmune, inflammation, reaction to medication)

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15
Q

Platelets (Thrombocytes)

Membrane Receptors for :

A

Von Willebrand factor
- helps platelets stick to collagen

Fibrinogen
Helps platelets stick together

ADP
(omnipresent, weak vasoconstrictor, and clotting factor)

Thromboxane A2
(help platelet activation)

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16
Q

Intracellular Granules

of platelets

A

1)Serotonin
Vasoconstrictor, pinch off area so blood clot can form more easily
2)ADP

3) Clotting factors
4) Platelet derived growth factor (PDGF) *
5) Platelet activating factor (PAF) *

function : coagulation or making more platelets

*Activate sleepy platelets and recruit more!

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17
Q

Intrinsic Activation

A

damage to the endothelium exposes collagen

  • blood vessel completely cut
    ex) cut yourself , and the collagen is exposed.

platelets go from disk to spiney after activation and quickly form a clot to stop you from bleeding out

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18
Q

Extrinstic Activation

A

tissue factor (thromboplastin) is released from damaged endothelial cells.

  • inside of cells makes up the tube (tissue factor) ; if that gets into the circulation, it activates the platelets.
  • stubbed toe
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19
Q

Hemostasis and coagulation

A

Endothelium and platelets interact/communicate during the process of repair

both extrinsic and intrinsic activation may happen at the same time

both boil down to the same pathway : making Thrombin (protein)

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20
Q

Fibrin

A

Provides structural stability for the clot, form a definitive clot.

The morter in the brick wall

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21
Q

Initial response to injury

A

Involves vasoconstriction and the formation of a hemostatic plug

Vasoconstriction : Mediated by seritonin, and TXA2 (Thromboxane A2)

Hemostatic Plug : formed by activated platelets

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22
Q

Prostacyclin

A

1) Helps keep platelet inactive.
2) Constantly released in healthy endothelium
3) Platlet sedative - ensures they stay inactive

Activation of ADP, TXA2, , and thrombin override prostacyclin.

23
Q

What allows the conversion of fibrinogen to fibrin?

A

Conversion of fibrinogen to fibrin occurs in the presence of thrombin
Common pathway of coagulation

24
Q

Thromboxane A2

A

Weaker vasoconstrictor, activates platelets : doesn’t do anything very well

25
Q

vWF ( Von Willebrand Factor) Receptor’s role

A

vWF receptor – binds vWF leading to platelets adhering to exposed collagen

2) anchor, granules release a substance that activates the platelet that it came from & others around it. Makes a SUPER STRONG association with collagen

26
Q

Glycoprotein receptor

A

binds fibrinogen causing platelets to stick to each other.

receptor makes it extra sticky

27
Q

Thrombin-platelet activating factor role

A

1) wake up sleepy platelets

2) take freely floating fibrinogen turning it into fibrin

28
Q

Fibronolysis

A

tearing the clot apart

29
Q

Plasminogen to Plasmin

A

Plasmin (active form)

  • Plasminogen activated by a number of enzymes, including tissue-type Plasminogen Activator (tPA)
  • Plasmin functions to breakdown fibrin and fibrinogen, therefore breaking down the structural integrity of a clot
30
Q

tPA

A

tissue-type Plasminogen Activator (tPA)
Enzyme

goes around and eats fibrin, serves to break down blood clots

Given in the ER for Myocardial infraction (MI)

Happy, newly healed endothelial cells release tPA

31
Q

Where do the smallest clots get broken down?

A

The lung : bound and filtered.

32
Q

NSAIDs : what are they, and how does this affect coagulation?

A

Non-steroidal Anti Inflammatory drugs.
ex) asprin etc.

COX (cyclooxygenasis makes TXA2).

It inhibits coagulation by not activating platelets, not having vasoconstriction, and makes it more difficult to make blood clots.

May prevent second heart attack , but causes ulcers : doesn’t prevent the first heart attack

33
Q

Leukocyctes

A

Produced in the bone marrow

Produced by pleury-potent blood cells.

  • live for 10 days
  • 75% of all hematopoiesis is the creating of WBC’s. 25% RBC

We are able to choose which WBCs to produce deoending on the environment ( infection, inflammation, tissue damage)

34
Q

Colony Stimulating Factors

A

Synthesized by Leukocytes, Endothelial cells, Fibroblasts of Bone Marrow
Regulate the production of various leukocytes

35
Q

Neutrophils

A

Type of Leukocyte:

-Phagocytose bacteria
-produce H2O2
50-60%

More(+) N = + WBC.
Less(-) N = -WBC

36
Q

Lymphocyte

A

Type of Leukocyte:

  • Activate immune system
  • Produce antibodies (B cells)
  • Cell lysis (cytotoxic T and NK cells) ( promote cell death)
    20-40%
37
Q

Eosinophils

A

Type of Leukocyte:

Major basic protein –> cytotoxic to parasites.

involved in allergies ( histamine, leukotrienes)

  • coat parasite and signal to kill them
38
Q

Basophils

A

Type of Leukocyte :

similar to mast cells, but not the same.
active in amplifying allergic reactions, work with histamine, IgE receptor (hypersenstivity)
can alter severity of reactions

39
Q

Monocyte

A

Type of Leukocyte :

Baby macrophages. become macrophages when entering tissues.
Phagocytose bacteria and debris ( like a cellular vacuum)

40
Q

Normal Body temperature range

A

35.8-37.9 C

41
Q

Rectal temperature

A

0.5C higher than oral.

most accurate

42
Q

Tympanic

A

0.8C higher than oral.
reliable if done correctly
(ear)

43
Q

Axillary

A

(armpit)
1C lower than oral
unrealiable

44
Q

What controls the body temp?

A

The hypothalamus

45
Q

Fever

A

Temp higher than 37.9C by an oral thermometer.

changing the set point in the thalamus to allow for an increase in body temp

46
Q

Hyperpyrexia

A

extreme elevation due to disease / disorder : not infection

47
Q

Hyperthermia

A

not fever, externally induced ( environment) or secondary to drugs ( anathetics)

48
Q

Blood flow to the skin

A

loss / conservation of heat largely involves changing the blood flow to the skin

  • radiate more heat = more blood flow to the skin

trap heat - subcutaneous fat as an insulator = less blood flow to the skin

49
Q

Pyrogen

A

something that initiates fever. Usually toxins or bacterial antigens.

Carried via the blood

50
Q

Circumventricular organ system ( CVOS)

A

cluster of cells that originate in the hypothalmus.
- project through the blood brain barrier ( BBB) like with a fishing rod, and looks for pyrogens.

Also monitors BP, GI activity, and appetite

If it interacts with a pyrogen, then the blood goes below the fat layer and we turn up the thermostat

51
Q

How does PGE2 activate the febrile response?

A

Pyrogens activate specific neuronal receptors( hypothalmus) within the CVOS and prostaglandins (PGE2 through COX enzymes) are created.

PGE2 activates the febrile response within the hypothalamus

  • Initiates change in set point
  • Activation of diverse processes to conserve heat (decreased blood flow to skin – less radiant heat).
52
Q

Why to NSAIDs like acetaminophen have the ability to reduce fever?

A

Tylenon blocks COX, so the hypothalmus cannot be activated to turn up the heat

53
Q

Value to a fever?

A

Debated.

Yes :

  • enhances immune response
  • impairs bacterial and viral replicaion
  • anorexia ( decreased blood glucose levels : starves bacteria)
  • liver makes acute phase proteins (that bind to cations, so that pyrogen cannot bind)

Harmful :
irreversible damage if fever nis higher than 40C
- Brain damage beyond 43C,
-loss of thermoregulation beyond 45C

  • burden of fever needs to be dependant on a patient. ie) immunocompromised patient probably should not endure the fever.

Physiology (BAS 118) (4 decks)

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