Cellular Physiology and Hemotology (Part 1 / Lecture 1)

Question 1

What constitutes plasma?

Answer 1

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)

Question 2

“Interstitial fluid”

Answer 2

= “Plasma” – “Proteins”

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

Question 3

Albumin

Answer 3

carrier protein

Question 4

Fibrinogen

Answer 4

clotting material

Question 5

Transferrin

Answer 5

transfers iron

Question 6

ferritin

Answer 6

stores iron,mostly in the liver

Question 7

Globulins

Answer 7

immnunoglobulins (IgG’s)

Question 8

Oncotic Pressure

Answer 8

**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.

Question 9

Liver/Kidney Disease & Malnutrition

Plasma (Clinical Significance)

Answer 9

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

Question 10

Hematopoiesis

Answer 10

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

Question 11

Why does it matter that all proteins have a charge?

Answer 11

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

Question 12

Megakaryocytes

Answer 12

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

Question 13

Thrombopoetin (TPO)

Answer 13

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

Question 14

Thrombocytopenia

Answer 14

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)

Question 15

Platelets (Thrombocytes)

Membrane Receptors for :

Answer 15

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)

Question 16

Intracellular Granules

of platelets

Answer 16

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!

Question 17

Intrinsic Activation

Answer 17

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

Question 18

Extrinstic Activation

Answer 18

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

Question 19

Hemostasis and coagulation

Answer 19

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)

Question 20

Fibrin

Answer 20

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

The morter in the brick wall

Question 21

Initial response to injury

Answer 21

Involves vasoconstriction and the formation of a hemostatic plug

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

Hemostatic Plug : formed by activated platelets

Question 22

Prostacyclin

Answer 22

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.

Question 23

What allows the conversion of fibrinogen to fibrin?

Answer 23

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

Question 24

Thromboxane A2

Answer 24

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

Question 25

vWF ( Von Willebrand Factor) Receptor's role

Answer 25

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

Question 26

Glycoprotein receptor

Answer 26

binds fibrinogen causing platelets to stick to each other. receptor makes it extra sticky

Question 27

Thrombin-platelet activating factor role

Answer 27

1) wake up sleepy platelets | 2) take freely floating fibrinogen turning it into fibrin

Question 28

Fibronolysis

Answer 28

tearing the clot apart

Question 29

Plasminogen to Plasmin

Answer 29

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

Question 30

tPA

Answer 30

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

Question 31

Where do the smallest clots get broken down?

Answer 31

The lung : bound and filtered.

Question 32

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

Answer 32

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

Question 33

Leukocyctes

Answer 33

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)

Question 34

Colony Stimulating Factors

Answer 34

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

Question 35

Neutrophils

Answer 35

Type of Leukocyte: -Phagocytose bacteria -produce H2O2 50-60% More(+) N = + WBC. Less(-) N = -WBC

Question 36

Lymphocyte

Answer 36

Type of Leukocyte: - Activate immune system - Produce antibodies (B cells) - Cell lysis (cytotoxic T and NK cells) ( promote cell death) 20-40%

Question 37

Eosinophils

Answer 37

Type of Leukocyte: Major basic protein --> cytotoxic to parasites. involved in allergies ( histamine, leukotrienes) - coat parasite and signal to kill them

Question 38

Basophils

Answer 38

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

Question 39

Monocyte

Answer 39

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

Question 40

Normal Body temperature range

Answer 40

35.8-37.9 C

Question 41

Rectal temperature

Answer 41

0.5C higher than oral. | most accurate

Question 42

Tympanic

Answer 42

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

Question 43

Axillary

Answer 43

(armpit) 1C lower than oral unrealiable

Question 44

What controls the body temp?

Answer 44

The hypothalamus

Question 45

Fever

Answer 45

Temp higher than 37.9C by an oral thermometer. changing the set point in the thalamus to allow for an increase in body temp

Question 46

Hyperpyrexia

Answer 46

extreme elevation due to disease / disorder : not infection

Question 47

Hyperthermia

Answer 47

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

Question 48

Blood flow to the skin

Answer 48

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

Question 49

Pyrogen

Answer 49

something that initiates fever. Usually toxins or bacterial antigens. Carried via the blood

Question 50

Circumventricular organ system ( CVOS)

Answer 50

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

Question 51

How does PGE2 activate the febrile response?

Answer 51

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).

Question 52

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

Answer 52

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

Question 53

Value to a fever?

Answer 53

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.