Slide set 6 Flashcards

1
Q

What is arteriosclerosis

A

Thickening of walls of arteries and loss of elasticity

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2
Q

What is athersclerosis

A

A progressive disease characterized by the formation of lesions on the walls of medium and large arteries called atherosclerotic plaques

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3
Q

What is coronary artery disease

A

Accumulation of atherosclerotic plaques in coronary arteries; reduced blood flow to myocardium

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4
Q

Damaging effects of hypertension that are untreated

A

Blood vessels (thickening of tunica media - the middle part ( muscle) of the vessel

Heart (left ventricle enlarges, weakens)
Brain (stroke)
Kidney (thickening of arterioles; more renin secretion)

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5
Q

Lifestyle changes against hypertension

A
Weight loss
Limit alcohol intake
Exercise
Reduce sodium intake
Do not smoke
Manage stress
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6
Q

Drug treatment to Hypertension

A

Diuretics(reduce the amount of liquid int he circulation),

vasodilators, (nitroglycerine, also sublingual one-very quick action)

ACE inhibitors (block Ang II formation-widen, or dilate, your blood vessels. That increases the amount of blood your heart pumps and lowers blood pressure. They also raise blood flow, which helps to lower your heart’s workload),

beta blockers (beta adrenergic receptor blocker- blocking adrenaline , help open up veins and arteries to improve flow)

Statins

Ca -channel blockers (reduce the force of contraction-heart work less hard)

Aspirin- anticoagulant, less viscous, heart easier to pump

Angioplasty (A procedure in which a small balloon at the tip of the catheter is inserted near the blocked or narrowed area of the coronary artery with a stent that will provide support inside the coronary artery)

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7
Q

Unstable vs stable angina

A

If the pain happens during certain activities and goes away with rest, it’s called stable angina. However, if the chest pain becomes more severe or frequent, lasts longer, or occurs while resting it’s called unstable angina.

Unstable-heart attack can happen any time

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8
Q

Blood consists of ___

A

Fluid(plasma) -55%and formed elements (cell)-45%

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9
Q

Percentage of plasma and formed elements change with

A

Disease
Drug use
Altitude

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10
Q

What proteins male up plasma and what is their percentage

A

6% of proteins in plasma of which
Albumins-58%
Globulins-38%
Fibrinogen-4%

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11
Q

How much water in plasma

A

92%

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12
Q

What are solutes in plasma?

A
In total they are 2 % of plasma
Ions
Nutrients
Waste products
Gases
Regulatory substances
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13
Q

What has the highest proportion of formed elements in the blood

A

erythrocytes

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14
Q

Name leukocytes and their percentage

A
Neutrophils-60-70%
Lymphocytes- 20-25%
Monocytes- 3%-6%
Eosinophis- 2%-4%
Basophils 0.5%-1%
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15
Q

The place where plasma proteins are synthesized

A

Liver

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16
Q

Function of albumins

A

Carriers for various substances

Contributors to colloid osmotic pressure of plasma

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17
Q

Globulins: function

A

Clotting factors, enzymes, antibodies, carriers for various substances

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18
Q

Systemic arterioles carry ___ blood

A

Oxygenated

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19
Q

Fibrinogen function

A

Forms fibrin threads essential to blood clotting

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20
Q

Transferrin function

A

Iron transfer

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21
Q

Osmotic pressure vs hydrostatic pressure

A

Whereas hydrostatic pressure (capillary hydrostatic pressure) forces fluid out of the capillary, osmotic pressure draws fluid back in. Osmotic pressure is created by the proteins in the blood.

The plasma proteins suspended in blood cannot move across the semipermeable capillary cell membrane, and so they remain in the plasma. As a result, blood has a higher colloidal concentration and lower water concentration than tissue fluid. It therefore attracts water.

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22
Q

The pressure created by the concentration of colloidal proteins in the blood is called ___

A

the blood colloidal osmotic pressure (BCOP). It is determined by albumin concentration

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23
Q

Why is liver disease associated with edema

A

albumin is produced by the liver-> liver is ill->poor plasma protein production->no right BCOP

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24
Q

division in WBCs

A

Granulocytes (neutrophills,basophills,eosinophills)

Agranulocytes (monocytes, leucocytes)

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25
Q

The size of RBCs

A

7.5 micrometers

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26
Q

What is the structure of spectrin and what is it and function

A

Spectrin is a cytoskeleton protein that binds to the cytosolic side of the membrane protein

Spectrin is partly responsible for their elastic strength under deformation

Each spectrin molecule sonsists of 2 interwined polypetide chains (alpha and beta)

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27
Q

In RBCs have how much hemoglobin molecules

A

200 to 300 million

28
Q

Structure of one hemoglobin

A

2 aplha and 2 beta globins each with a heme group. Each heme has 1 iron

29
Q

Who binds to Oxygen and CO2 in hemoglobin

A

Oxygen-heme group

CO2-globulin

30
Q

CO2 transfer in the body (3 ways)

A

70% bicarbonate buffer system through H2CO3-> HCO3 and H, and Cl will be taken inside the cell to have an exchange will HCO3
4% dissolved directly in blood
23% by carbaminohemoglobin

31
Q

RBC differentiation

A

Take 4 days

All blood cells are derived from hematopoietic stem cells (hemocytoblast)

Differentiation begins with the appearance of proerythroblasts

Mitotic divisions then produce basophilic erythroblasts

Then polychromatic erythroblasts-these produce hemoglobin

These cells lose their nuclei and become reticulocytes

after that additional 24-36 hours they become mature

32
Q

RBC differentiation happens in

A

Bone marrow

33
Q

From stem cell you can get

A

Both WBCs and RBCs -depends on the stimuli

34
Q

Platelets originate from

A

Breaking off Megakaryocyte

35
Q

What is aplastic anemia

A

A reduction in the production of RBCs

36
Q

Leukopenia is

A

A reduction of WBCs

37
Q

A reduction in the production of thrombocytopenia is

A

reduction in the production of platelets, leaving the person at high risk of hemorrhage

38
Q

Bone marrow cell production can be suppressed by

A

Drugs or radiation therapy

39
Q

What is eryhtropoietin

A

Cytokine- glycoprotein

It is produced in response to low oxygen levels in the kidneys

40
Q

Function of erythropoietin

A

Stimulates the bone marrow to accelerate its production of RBC, then stopped secreted ( negative feedback)

41
Q

Why would athletes train at high altitudes

A

Less oxygen-> more stimulation of RBCs production

42
Q

how destruction of RBCs happens

A

Macrophage cells in the liver and spleen will recognize warn out RBCs and perform phagocytosis on the them

This process results in the breakdown of Hemoglobin with the release of amino acids, iron, and pigmented bilirubin

43
Q

What happens to all substituents of RBC after its destruction

A

Iron is returned to the bone marroe

Bilirubin is transported to the liver where it is excreted into the intestine as part of bile or urine

AAs are used for energy or the synthesis of new proteins

44
Q

How iron is transferred after the absorption in the intestine to the bone marrow

A

Transferrin

Or to the liver and transformed to ferritin for storage

45
Q

PCV or hematocrit is

A

Packed cell volume is the percent of RBC-> centrifugation separation

46
Q

Normal hematocrit is

A

45% RBC for men and 42 for women , WBC and platelets (buffy coat) 1%

47
Q

Change in PCV reasons

A

Anemia- reduced PCV

Polycythemia- increased PCV

48
Q

Polycynthemia is

A

Bad, because increased blood viscosity

More RBCs

49
Q

Function of neutrophils

A

Highly mobile and very active phagocytic cells

Capable of diapedesis( migrate out of BV and enter tissues; cytoplasmic granules contain lysosomes for destruction of bacterial cells

50
Q

Function of eosinophils

A

Numerous in lining of respiratory and digestive tracts
Weak phagocytes
Provide protection against infections caused by parasitic worms and allergic reactions. Release anti-inflammatory substances in allergic reactions

51
Q

Basophils function

A

Motile and capable of diapedesis; cytoplasmic granules contain histamine (inflammatory chemical) and heparin (anticoagulant)

52
Q

Function of lymphocytes

A

Have T and B cells, Produced in thymus

T cells directly attack infected or cancerous cell, when B cells produce antibodies against specific antigens

53
Q

Function of Monocytes

A

Mobile and highly phagocytic, ingests bacteria and cancerous cells

54
Q

Lymphocytes have little ___

A

cytoplasm, most is nucleus

55
Q

3 important properties if platelets

A

Agglutination, adhesiveness, and aggregation

56
Q

Hemostasis is

A

Refers to stoppage of blood flow; however if injury is extensive, the blood-clotting mechanism is activated to assist

57
Q

What is done in order platelets do not stick to each other in the normal state

A

endothelium of BV release prostacyclin and NO that prevents adhesion

58
Q

What happens when the collagen is damaged

A

Plateles start to clamp, because there is no NO and prostacyclin and as a positive feedback it attracts more platelets ->temporal clot

then the coagulation cascade is activated-> activation of thrombin->conversion of fibrinogen to fibrin-> binds to platelets

59
Q

The first thing that happens when we have damage to the blood vessel

A

Vasoconstriction to reduce the amount of blood loss

60
Q

3 steps in blood clotting mechanism

A
  1. Release of clotting factors by both injured tissue and sticky platelets
  2. Formation of thrombin
  3. Formation of fibrin and trapping of blood cells to form a clot
61
Q

ABO blood groups are named according to

A

Antigens present on RBCs

62
Q

Types of ABO groups

A
Type A(antigen A, antobodies for B)
Type B(antigen for B, antobodies for A)
Type AB (antigen for A and B, no antibodies, universal recipient)
Type O (no antigen, universal donor, has antibodies against A and B)

Have from birth

63
Q

+ and - in blood groups meaning

A

Rh factor

64
Q

What does + and - Rh factor mean

A

-, meaning that you do not have Rh naturally present on the surface of RBCs,

65
Q

What will happen if you get not the right blood

A

Agglutination (clumping)

66
Q

Anti Rh antibodies can appear under what circumstances

A

If Rh negative comes in contact with Rh positive

67
Q

What will be given to a woman who has Rh- and her baby is Rh+

A

RhoGAM stops from making antibodies to Rh