Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Anatomy & Physiology I > Topic 4.1 - Blood > Flashcards

Topic 4.1 - Blood Flashcards

1
Q

Circulatory System

A
  • Main transport system in humans
  • Consists of the heart & the blood vessels through which the blood flows in the body
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

3 types of blood vessels

A
  • Arteries
  • Veins
  • Capillaries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Functions of Blood

A

Transport
- Delivering O2 & Nutrients
- Metabolic waste removal
- Hormones

Regulation
- Body temperature – Distribution, conservation, dissipation
- pH in body tissues using buffers (alkaline reserve of bicarbonate ions)
- Maintaining adequate fluid volume in circulatory system

Protection
- Preventing blood loss – Plasma proteins and platelets in blood initiate clot formation
- Preventing infection – Agents of immunity (antibodies, complement proteins, white blood cells) carried in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Composition of Blood

A
  • Only FLUID tissue in body
  • Formed elements suspended in plasma (eryth, leuko, platelets)
  • More dense, 5x more viscous than H₂O (due to solutes)
  • pH – 7.35 - 7.45 (slightly alkaline)
  • Temp – 38 C
  • Colour – Scarlet (O₂ rich), Dark red (O₂ poor)
  • 8 % Body Weight (5 - 6 L ♂; 4 - 5 L ♀)

When # RBCs ↑ normal range → Blood more viscous, slower flow
When # RBCs ↓ normal range → Blood thinner (less viscous), faster flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Buffy Coat

A
  • Present in erythrocyte-plasma junction
  • <1 % of whole blood
  • Leukocytes (white BC)
  • Platelets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Composition of Plasma

A
  • Straw-coloured, 55 % of whole blood
  • Less dense than erythrocytes
  • 90% water + MANY solutes :

Plasma proteins: Produced in liver (except gamma globulins), functional proteins which remain in blood
- Albumin (60% of all plasma proteins) – Major osmotic protein (holds water molecules), carrier of various molecules, important blood buffer, blood constantly adjusted to keep its composition / pH within normal range

Electrolytes: Na, CL, etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the hematocrit ?

A
  • Percentage of erythrocytes in a blood sample
  • About 45 %

MEN = 47 % +- 5 %♂
WOMEN = 42 % +- 5 % ♀

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Formed elements

A
  • *Erythrocytes – Bags of hemoglobin
  • Leukocytes – Complete cells (full complement of organelles)
  • Platelets – NO organelles, cytoplasmic granules containing signaling substances → blood clotting
  • Most formed elements short-lived / disposable
  • Most do not divide → Continuously replaced by red bone marrow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Structure & Function of Erythrocytes & RBCs

A
  • Diameter : Small, 7.5 μm, larger than some capillaries
  • Biconcave, “dented” disc shape
  • Anucleate, essentially has no organelles
  • Contain proteins to maintain PM and regulate cell shape
  • Cannot grow, divide or make new proteins

Spectrin – Lines internal surface of RBC, provides flexibility so that they can change shape (squeeze through tiny capillaries and “pop” back into shape)
- Spleen always monitoring, improper shape → destruction

Filled with hemoglobin (Hb) for gas transport
- Dedicated to the transport O2 from lungs to tissues
- Transport 20% of CO2 back to lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Special Characteristics of RBCs that Optimize Function

A

3 features make for efficient gas transport:

  • Small size concave shape offers huge SA:V ratio for gas exchange
  • Hemoglobin (Hb) makes up 97 % of cell volume (not counting H2O)
  • RBCs have no mitochondria (ATP production is anaerobic, create 2 ATPs, enough to power RBC)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Erythrocytes & Hemoglobin

A
  • 2.5 x 108 Hb molecules / RBC
  • Hemoglobin : Red heme pigment bound to the protein globin

4 Heme groups :
- A Fe ion in the center of an organic ring called porphyrin
- 1 O2 mol reversibly binds to Fe ion in heme group (1O2 / Fe)
- Each heme can transport 4 mol of O2 (4 binding sites)
- No comp. between O2 & CO2, different binding sites
- Oxygenated Hb different shape & colour than deoxygenated Hb

Globin – 4 polypeptide chains (2α & 2β)
- CO2 binds to globin (carbaminohemoglobin)

Hb is contained in erythrocytes rather than being a plasma protein :
- Keeps it from fragmenting / being lost
- Keeps it from contributing directly to osmotic pressure & blood viscosity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Hematopoiesis

A
  • Production of living blood cells → formed elements
    – Occurs in the red bone marrow in a network of reticular connective tissue containing :
  • Immature blood cells
  • Macrophages
  • Fat cells
  • Reticular cells (secreting the CT fibers)

Hemocytoblast (hematopoietic stem cell)
- _Origin stem cell for all formed elements_ → Cells become committed to a particular pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Erythropoiesis

A
  • Production of RBCs (erythrocytes)
  • Takes about 15 days
  • All occurs in bone marrow
  • Spleen gets rid of RBCs

Phase 1 : Ribosome synthesis
Phase 2 : Hemoglobin accumulation from ribosomes
Phase 3 : Once full complement of hemoglobin has been made, nucleus is ejected (resulting in biconcave disc shape)
- Reticulocyte – Cell that will be released into blood stream, within days transforms into erythrocyte
- Immature (has residual protein synthesizing machinery)
- Mature loses machinery in 2-3 days, becomes RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Reticulocyte Count

A
  • Makes up 1-2 % of erythrocytes
  • Provides info on the bone marrow’s ability to produce new red blood cells (RBCs)
  • Helps distinguish between various causes of anemia
  • Helps monitor bone marrow response and the return of normal marrow function following :
    – Chemotherapy
    – Bone marrow transplant
    – Post-treatment follow-up for iron deficiency anemia, vitamin B12 or folate deficiency anemia, or renal failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Regulation of Erythropoiesis

A
  • Homeostatic balance between production & destruction
  • Too few – Anemia, reduced O2 carrying capacity in blood, can lead to hypoxia (low oxygenation in organs)
  • Too many – Polycythemia, resulting in ↑ blood viscosity
  • To maintain balance, new RBCs produced at rlly fast rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Hormonal Controls – _Erythropoietin (EPO)_

A
  • Glycoprotein produced in kidneys

Always some EPO in blood, more release by the kidney if hypoxia due to:
- High altitude or pneumonia
- Increased demand
- Hemorrhage / excess RBC destruction
- Insufficient Hb / RBC

  • Production depressed if too many erythrocytes OR excessive O2 (control of EPO dependent on RBCs ability to transport blood)
  • Enhances maturation rate of committed RBC precursors (1-2 days to see results)
  • Route of stimulation : Hypoxia sensed by kidneys → Increased release of EPO → Activation of bone marrow → More reticulocytes → More mature RBCs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What disease is linked to anemia ?

A

Kidney disease is linked to anemia
- Losing RBC as they are constantly are pulled out of bloodstream
- There is no ability to produce EPO in kidneys so cannot replace RBCs
- Treated with recombinant EPO injections

Renal failure patients face a lack of EPO (RBCs can be 50% of normal amount)
- Treated with recombinant EPO injections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Athletes & EPO Abuse

A

Theory – Injecting EPO increases RBCs, enhancing O2 carrying capacity → Better endurance
- EPO causes ↑ hematocrit from 45% to 65%
- BUT ↑ viscosity + dehydration during race can cause clotting, stroke, heart failure (heart needs to work twice as harder)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the effect of testosterone on EPO ?

A
  • Enhances output of EPO production
  • Increases responsiveness of bone marrow to EPO (effectiveness)

Why women have slightly lower hematic rate (also menstruation → huge amount of RBCs lost)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Erythropoiesis Dietary Requirements

A
  • Iron & B-vitamins

Iron – Available from diet
- 65% of iron found in hemoglobin, with the rest in liver, spleen, and bone marrow
- Free iron ions are toxic so iron is bound with proteins:
Stored in cells as ferritin and hemosiderin, Transported in blood loosely bound to protein transferrin
- Body does good job at recycling iron, but not 100% efficient – Lost in feces, urine, menstrual cycle

Vitamin B12 and folic acid necessary for DNA synthesis for rapidly dividing cells such as developing RBCs
- Help in nuclear maturation
- Absence → Gigantic immature blood cells that lose ability to become RBC

21
Q

Life Cycle of Red Blood Cells

A
  • Useful lifespan: 100-120 days

1. Low oxygen levels in blood stimulate kidneys → produce EPO
2. EPO levels rise in blood
3. EPO & necessary raw materials in blood promote erythropoiesis in red bone marrow (production of RBCs)
4. New erythrocytes enter bloodstream
5. Mature RBCs become rigid, fragile with time (no organelles to support or synthesize proteins for repair)
6. Hb begins to degenerate
7. Aged / damaged RBCs engulfed by macrophages in spleen, liver & bone marrow
- Spleen = RBC graveyard, pull RBCs out of circulation & break down hemoglobin into components, most of which are recycled

22
Q

RBC Breakdown

A

Heme, iron, & globin are separated
- Iron binds to ferritin or hemosiderin + is stored for reuse
- Heme is degraded to yellow pigment bilirubin → Secreted by liver in bile into intestines → Degraded to pigment urobilinogen → Transformed into brown pigment stercobilin in feces
- Globin is metabolized into functional amino acids & released into circulation

23
Q

Erythrocyte Disorders

A

Anemia & Polycythemia

24
Q

Anemia

A
  • Blood has abnormally low O2-carrying capacity that is too low to support normal metabolism
  • Symptoms : fatigue, pallor (pale colour in mucous membrane), dyspnea (shortness of breath), & chills (metabolic functions toned down due to ATP, byproduct heat so not enough)

3 groups based on cause :
- Blood loss
- Not enough RBCs produced
- Too many RBCs being destroyed

25
Q

1. Blood Loss Anemia

A
  • Hemorrhagic anemia
  • Characterized by rapid blood loss (severe wound)
  • Treated by blood replacement
26
Q

2. Insufficient # of RBCs produced

A
  • Iron-deficiency Anemia : Caused by hemorrhagic anemia, low iron intake, impaired absorption
  • Pernicious Anemia : Autoimmune disease that destroys stomach mucosa that produces intrinsic factor needed to absorb B12
  • Renal anemia : Caused by lack of EPO
  • Aplastic anemia : Destruction / inhibition of red bone marrow
27
Q

3. RBCs Destruction

A
  • Incompatible transfusion
  • Hemolysis :
    Thalassemia - 1 globin chain absent / faulty
    Sickle-cell anemia - Hemoglobin S (mutation)
28
Q

Polycythemia

A
  • Abnormal excess of RBCs; increases blood viscosity, causing sluggish blood flow
  • Polycythemia vera – Bone marrow cancer leading to excess RBCs, hematocrit may go as high as 80%, treated with therapeutic phlebotomy
  • Secondary polycythemia – Caused by low O2 levels (e.g. High altitude) or increased EPO production
  • Blood doping – Artificially induced polycythemia
29
Q

Platelets

A
  • Cytoplasmic fragments of megakaryocytes contain purple-staining granules that contain clotting factors & enzymes essential in hemostasis
  • Function in temporary platelet plug formation
  • Platelet formation regulated by the hormone thrombopoietin (liver & kidney)
  • Anucleate
  • Lifespan : Around 10 days
  • Not as structurally bound as RBCs
  • 150,000-400,000 platelets/μl blood
  • Megakaryoblast → Committed to becoming platelet
  • Final Step → Very large cell (Megakaryocyte) taking off projections in capillaries, become sinusoids in bone & platelets
30
Q

Hemostasis

A
  • Fast series of reactions for stoppage of bleeding
  • Requires clotting factors + substances released by platelets & injured tissues

3 Steps involved :
1. Vascular spams
2. Platelet plug formation
3. Coagulation

31
Q

1. Vascular Spasms

A
  • Vasoconstriction of smooth muscles in walls of vessels in response to damage
  • Only sympathetic innervation (enhances / reduces activity at the vessel)

Triggered by :
- Damage to vascular smooth muscle
- Chemicals from endothelial cells & platelets
- Pain receptor reflexes

Purpose – Stops bleeding after break in blood vessel to prevent blood loss (hypovolemic shock)
- Reduces blood flow to site of injury
- Localized in area of damage

32
Q

2. Platelet Plug Formation

A
  • Usu. platelets do not stick to each other or to endothelial linings
  • Under normal conditions – NO (Nitric Oxide) & PGI2 (prostacyclin or PGI2) produced by endothelial cells inhibit platelet aggregation (keep blood flow continuous)

When vessel damage occurs:
- Exposed collagen causes platelet adhesion
- von Willebrand factor (large plasma protein) helps adhesion by forming a bridge between the collagen and platelets

Platelets activated → Swell, become spiky & stickier; degranulate (release chemical messengers that attract more platelets – positive feedback mechanism)
- Adenosine diphosphate (ADP) – Enhances aggregation & degranulation
- Serotonin & thromboxane A2 – Enhance vascular spasm & aggregation

33
Q

3. Coagulation

A
  • Blood is transformed from liquid to gel
  • Reinforces platelet plug with fibrin threads
  • Blood clots effective in sealing larger vessel breaks
  • Series of reactions use clotting factor (procoagulants), mostly plasma proteins (numbered I to XIII in order of discovery)
  • Vitamin K needed to synthesize 4 factors, produced internally in microbiome, gut + diet
  • When no damage, anticoagulants dominate in intact vessel
  • Rate limiting step in process → Everything quickly occurs after here - Cascading effect

3 phases :
1. Prothrombin Activator formed
2.Prothrombin to Thrombin
3. Fibrinogen molecules ⇒ Fibrin mesh

34
Q

Coagulation Phase 1 - 2 Pathways to Prothrombin Activator

A
  • Each pathway cascades toward and ends with the activation of Factor X

Intrinsic pathway : Clotting of blood outside the body (in a tube or slightly damaged vessel)
- Triggered by neg charged surfaces (e.g. collagen, activated platelets, even glass of a test tube)

Extrinsic pathway : Clotting of blood in response to damage → Release of tissue factor (TF), aka factor III
- Bypasses several steps of intrinsic pathway, so faster pathway
- Factor X then complexes with Ca2+, PF3 (platelet factor 3), and factor V to form prothrombin activator
- Once achieved, clot forms in 10-15 sec via Phase 2 & 3 common pathways

35
Q

Coagulation Phase 2 - Pathway to Thrombin

A
  • Prothrombin activator catalyzes transformation of prothrombin to active enzyme thrombin
36
Q

Coagulation Phase 3 - Common Pathway to the Fibrin Mesh

A
  • Thrombin converts soluble fibrinogen to fibrin strands - form structural basis of clot
  • Fibrin causes plasma to become a gel-like trap catching formed elements
  • Thrombin (along with Ca2+) activates factor XIII (fibrin stabilizing factor), which cross-links fibrin & strengthens and stabilizes clot
37
Q

Procoagulants

A
  • Blood clotting factors

Factor I - Fibrinogen :
- Plasma protein
- Source – Liver
- Common pathway; Converted to fibrin (insoluble weblike substance of clot)

Factor II - Prothrombin :
- Plasma protein
- Source – Liver (synthesis requires Vit K)
- Common pathway; Converted to thrombin (converts fibrinogen to fibrin)

Factor III - Tissue factor (TF)
- Plasma membrane glycoprotein
- Source – Tissue cells
- Activates extrinsic pathway

Factor IV - Calcium ions (Ca²+)
- Inorganic ion
- Source – Plasma
- Needed for essentially all stages of coagulation process ; Always present

Factor XIII - Fibrin Stabilizing Factor (FSF)
- Plasma protein
- Source – Liver, bone marrow
- Crosslinks fibrin, forming a strong, stable clot

38
Q

Clot Retraction & Fibrinolysis

A
  • Clot must be stabilized and removed when damage has been repaired

Clot retraction :
- Actin and myosin in platelets contract within 30–60 minutes
- Contraction pulls on fibrin strands, squeezing serum from clot (serum is plasma minus the clotting proteins)
- Draws ruptured blood vessel edges together

Vessel is healing even as clot retraction occurs :
- Platelet-derived growth factor (PDGF) released by platelets, stimulates division of smooth muscle cells & fibroblasts to rebuild blood vessel wall
- Vascular endothelial growth factor (VEGF) stimulates endothelial cells to multiply and restore endothelial lining

Fibrinolysis :
- The process of clot removal when it is no longer needed
- Begins within 2 days & continues until clot is dissolved
- Key enzyme is plasmin [precursor = plasminogen a plasma protein that gets incorporated into the clot]
- Plasminogen is activated by tPA (tissue plasminogen activator) released by endothelial cells

39
Q

Factors Limiting Clot Growth OR Formation

A

2 mechanisms limit clot size :
- Swift removal and dilution of clotting factors
- Inhibition of activated clotting factors

Clot formation requires MORE procoagulation factors > anticoagulation factors
1.Normally flowing blood washes away procoagulants
2. As thrombin forms, adsorbed onto fibrin threads (limits clot size)
3. Antithrombin III (plasma protein) inactivates any escaping thrombin
4. Antithrombin III & protein C (plasma protein) inactivate many intrinsic pathway procoagulants
5. Heparin (basophils & mast cells) – enhances activity of antithrombin III
6. Smooth endothelial lining of undamaged blood vessels prevents undesirable clotting; also heparin & endothelial-derived NO & prostacyclin)

40
Q

Disorders of Hemostasis

A
  • Thromboembolic Disorders
  • Bleeding Disorders
41
Q

Thromboembolic Disorders

A
  • Undesirable intravascular clotting
  • Thrombus – Clot that develops and persists in unbroken blood vessel
  • May block circulation, leading to tissue death
  • Embolus – Thrombus freely floating in bloodstream
  • Embolism – Embolus obstructing a vessel (e.g. Pulmonary or cerebral emboli)
  • Risk factors : Atherosclerosis, inflammation, slowly flowing blood or blood stasis from immobility
  • Treatment : Drugs such as tPA, streptokinase to dissolve clots via plasmin
  • Aspirin is an antiprostaglandin, inhibits
42
Q

Bleeding Disorders

A
  • Interference with normal clotting (thrombocytopenia, liver disorders, hemophilia)

Thrombocytopenia – Deficient number of circulating platelets
- Due to suppression or destruction of red bone marrow (e.g. malignancy, radiation, drugs)
- Platelet count < 50 000 / μl is diagnostic
- Treatment : Transfusion of concentrated platelets provides only temporary relief bc they die in 10 days

Impaired Liver Function – Inability to synthesize procoagulants (clotting factors)
- Causes : Vitamin K deficiency, hepatitis, or cirrhosis
- Liver disease can also prevent liver from producing bile, which is released in GI tract to help absorption of fatty meals & Vitamin K (fat-soluble)

Hemophilia – Includes several similar hereditary bleeding disorders
- Hemophilia A: most common type (77% of all cases), factor VIII deficiency
- Hemophilia B: Factor IX deficiency
- Hemophilia C: Factor XI deficiency, milder
- Symptoms : Prolonged bleeding, especially into joint cavities
- Treatment : injections of genetically engineered factors has eliminated need for plasma transfusion and risk of contracting hepatitis or HIV

43
Q

Blood Transfusion

A

Cardiovascular system minimizes effects of blood loss by:
Reducing volume of affected blood vessels
Stepping up production of RBCs

Body can compensate for only so much blood loss
15–30% causes pallor and weakness; >30% results in potentially fatal severe shock
Volume must be replaced immediately with
Normal saline OR multiple-electrolyte solution (Ringer’s solution) that mimics plasma electrolyte composition
Replacement of volume restores adequate circulation BUT does not replace oxygen-carrying capacities of RBCs
Whole Blood Transfusion : Substantial blood loss or thrombocytopenia
Packed red cells (PRBC) for anemia

Donor blood mixed with heparin (Ca2+ chelator, anticoagulant)
Human blood groups of donated blood must be determined because transfusion reactions can be fatal
Blood typing determines groups

44
Q

Human Blood Groups

A
  • RBC membranes bear different many antigens (referred to as agglutinogens, promote agglutination)
  • Mismatched transfused blood is perceived as foreign and may be agglutinated and destroyed → Potentially fatal reaction
  • Humans have at least 30 naturally occurring RBC antigens
  • Presence or absence of each antigen is used to classify blood cells into different groups
  • Some blood groups (MNS, Duffy, Kell, and Lewis) are only weak agglutinogens, not usually typed unless patient will need several transfusions
  • Antigens of ABO and Rh blood groups cause most vigorous transfusion reactions (trigger immune system); therefore, they are major groups typed
45
Q

ABO Blood Groups

A
  • Based on presence or absence of two agglutinogens (A and B) on surface of RBCs
  • Type A has only A agglutinogen, agglutinates with anti-A
  • Type B has only B agglutinogen, agglutinates with anti-B
  • Type AB has both A & B agglutinogens, agglutinates with both sera (universal recipient)
  • Type O has neither A nor B agglutinogens, does not agglutinate with either (universal donor)
46
Q

Agglutins

A
  • Blood may contain preformed anti-A or anti-B antibodies (agglutinins)
  • Act against transfused RBCs with ABO antigens not present on recipient’s RBCs
47
Q

Rh Blood Groups

A
  • 52 named agglutinogens (Rh factors)
  • C, D, E most common
  • Rh + indicates presence of D antigen → 85 % Americans are Rh+
  • Anti-Rh antibodies not spontaneously formed in Rh- individuals, form if Rh- individual receives Rh+ blood, or Rh- mom is carrying Rh+ fetus
  • Second exposure to Rh+ blood will result in typical transfusion rxn
  • Rh- mothers carrying Rh+ babies are treated with RhoGAM (anti-Rh serum) to prevent erythroblastosis fetalis → Hemolytic disease of the newborn
48
Q

Transfusion Reactions

A
  • Occur if mismatched blood is infused
  • Problem is recipient’s agglutinins (antibodies), not donors
    → Agglutinate & clog small vessels
    → RBCs rupture and release Hb into bloodstream

Overall result :
1. Blocked flow to tissues
2. Reduced O2-carrying ability of blood
3. Hb precipitates/clogs kidney tubules ⇒ possible kidney failure

Symptoms : Fever, chills, nausea, vomiting, general toxicity - critical to prevent kidney failure by administering alkaline fluids to dilute & dissolve Hb; also diuretics

  • Autologous transfusion (e.g. 1 unit/4 days up to 3 days before surgery)
49
Q

Blood Typing

A
  • Donor blood is mixed with antibodies against common agglutinogens
  • If agglutinogen is present, clumping of RBCs will occur
  • Blood is typed for ABO and for Rh factor in same manner

Cross matching : Typing between specific donor and specific recipient
- Mix recipient’s serum with donor RBCs
- Mix recipient’s RBCs with donor serum

Anatomy & Physiology I (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions