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Mam Physiology > Slide set 6 > Flashcards

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
The size of RBCs
7.5 micrometers
26
What is the structure of spectrin and what is it and function
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)
27
In RBCs have how much hemoglobin molecules
200 to 300 million
28
Structure of one hemoglobin
2 aplha and 2 beta globins each with a heme group. Each heme has 1 iron
29
Who binds to Oxygen and CO2 in hemoglobin
Oxygen-heme group | CO2-globulin
30
CO2 transfer in the body (3 ways)
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
RBC differentiation
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
RBC differentiation happens in
Bone marrow
33
From stem cell you can get
Both WBCs and RBCs -depends on the stimuli
34
Platelets originate from
Breaking off Megakaryocyte
35
What is aplastic anemia
A reduction in the production of RBCs
36
Leukopenia is
A reduction of WBCs
37
A reduction in the production of thrombocytopenia is
reduction in the production of platelets, leaving the person at high risk of hemorrhage
38
Bone marrow cell production can be suppressed by
Drugs or radiation therapy
39
What is eryhtropoietin
Cytokine- glycoprotein It is produced in response to low oxygen levels in the kidneys
40
Function of erythropoietin
Stimulates the bone marrow to accelerate its production of RBC, then stopped secreted ( negative feedback)
41
Why would athletes train at high altitudes
Less oxygen-> more stimulation of RBCs production
42
how destruction of RBCs happens
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
What happens to all substituents of RBC after its destruction
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
How iron is transferred after the absorption in the intestine to the bone marrow
Transferrin Or to the liver and transformed to ferritin for storage
45
PCV or hematocrit is
Packed cell volume is the percent of RBC-> centrifugation separation
46
Normal hematocrit is
45% RBC for men and 42 for women , WBC and platelets (buffy coat) 1%
47
Change in PCV reasons
Anemia- reduced PCV | Polycythemia- increased PCV
48
Polycynthemia is
Bad, because increased blood viscosity More RBCs
49
Function of neutrophils
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
Function of eosinophils
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
Basophils function
Motile and capable of diapedesis; cytoplasmic granules contain histamine (inflammatory chemical) and heparin (anticoagulant)
52
Function of lymphocytes
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
Function of Monocytes
Mobile and highly phagocytic, ingests bacteria and cancerous cells
54
Lymphocytes have little ___
cytoplasm, most is nucleus
55
3 important properties if platelets
Agglutination, adhesiveness, and aggregation
56
Hemostasis is
Refers to stoppage of blood flow; however if injury is extensive, the blood-clotting mechanism is activated to assist
57
What is done in order platelets do not stick to each other in the normal state
endothelium of BV release prostacyclin and NO that prevents adhesion
58
What happens when the collagen is damaged
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
The first thing that happens when we have damage to the blood vessel
Vasoconstriction to reduce the amount of blood loss
60
3 steps in blood clotting mechanism
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
ABO blood groups are named according to
Antigens present on RBCs
62
Types of ABO groups
``` 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
+ and - in blood groups meaning
Rh factor
64
What does + and - Rh factor mean
-, meaning that you do not have Rh naturally present on the surface of RBCs,
65
What will happen if you get not the right blood
Agglutination (clumping)
66
Anti Rh antibodies can appear under what circumstances
If Rh negative comes in contact with Rh positive
67
What will be given to a woman who has Rh- and her baby is Rh+
RhoGAM stops from making antibodies to Rh

Mam Physiology (16 decks)

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