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Semester 3 > A&P300 (chapter 19) > Flashcards

A&P300 (chapter 19) Flashcards

1
Q

cardiovascular system consist of

A

Heart

blood vessels (arteries, capillaries, veins)

blood

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2
Q

major function of cv system

A

oxygen/CO2

waste/nutrient exchange

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3
Q

hematology

A

study of blood

study of disorders associated w/ blood

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4
Q

major function of blood

A

transportation (O2, CO2, waste, nutrients

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5
Q

2 fluids of body that responsible for transport

A

blood

ISF

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6
Q

blood vs ISF

A

.

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7
Q

blood is

A

liquid CT

liquid ECF –> called blood plasma

cellular portion –> WBC, RBC, platelets,

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8
Q

blood plasma contains

A

water (92%)

Plasma proteins

dissolved solutes (ions, etc.)

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9
Q

blood plasma vs ISF

A

similar to ISF

ISF has less proteins

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10
Q

serum vs plasma

A

blood serum is plasma without clotting factors /proteins

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11
Q

body composition

A

40-45% solid
55-60% fluid

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12
Q

body fluid composition

A

2/3 ICF

1/3 ECF

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13
Q

ECF composition

A

20% plasma

80% ISF

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14
Q

3 functions of blood

A

1) transport

2) regulate

3) protect (WBC)

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15
Q

what does blood transport?

A

dissolved gasses, nutrients, hormones, metabolic wastes

E.g.
O2 (lungs to tissue)
CO2 (tissue to lungs)

nutrients (GI tract or liver/adipose to other tissue)

hormones (glands to tissue)

wastes (to kidneys)

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16
Q

what does blood regulate?

A

regulation of pH, temperature, ion composition of ISF

E.g.
absorb/neutralize acid

diffusion b/w blood-ISF balances ions

maintain body temperature (36-37)
–> high body temp = blood to superficial
–> low body temp = blood to deep

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17
Q

how does blood protect?

A

restrict fluid/blood loss @ injury (blood clotting)

clot = temporary patch
–> enzyme-directed when vessel wall is broken

blood defends against toxins/pathogens
–> Via WBC/Ab (immunity)

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18
Q

some physical characteristics of blood

A

more viscous than water

temp 38 (ONE DEGREE HIGHER THAN BODY TEMP)

pH –> 7.35-7.45

colour –> bright to dark red
–> oxygenated = bright

about 5 litres of blood in average person

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19
Q

blood composition

A

fluid CT

blood with all components = WHOLE BLOOD

2 major components:
plasma
Formed elements (cells/cell fragments)

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20
Q

“whole blood”

A

blood with all components

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21
Q

formed elements

A

cellular portion of blood CT

cells and cell fragments (E.g. platelets)

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22
Q

blood composition percent

A

about 55% plasma

about 45% formed elements

can range
46-63 plasma,
37-54 formed elements

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23
Q

plasma consists of

A

plasma proteins

other solutes

water

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24
Q

formed elements consist of

A

platelets

WBC

RBC

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25
Q

more about plasma

A

similar composition to ISF (less proteins)

constant exchange of water/ions/solutes across capillary walls

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26
Q

some differences b/w ISF and plasma

A

presence of respiratory gases (O2, CO2) in blood

dissolved proteins in blood (plasma proteins cannot cross capillary walls

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27
Q

plasma proteins in blood vs ISF

A

each 100mL has 7.6g protein
–> 5x more than ISF

cannot leave bloodstream
–> due to large, globular shape

liver synthesizes 90% of plasma proteins

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28
Q

which organ synthesizes more than 90 percent of plasma proteins?

A

LIVER

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29
Q

main proteins in plasma?

A

Albumins

Globulins

Fibrinogen

other enzymes/hormones

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30
Q

what percentage of plasma water

A

92 percent water

7 percent plasma proteins

1 percent other solutes (electrolytes, organic nutrients/wastes)

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31
Q

plasma protein composition

A

mostly ALBUMINS (60% albumins)

some GLOBULINS (35% globulins)

least FIBRINOGEN (4%)

1% (?) enzymes/hormones

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32
Q

which plasma protein most?

A

mostly albumins

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33
Q

which plasma protein least?

A

least = fibrinogen

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34
Q

what are Albumins for?

A

for osmotic pressure

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35
Q

what are globulins for?

A

E.g.
antibodies (immunoglobulins) vs foreign proteins/pathogens

E.g.
transport globulins
–> bind ions, hormones, lipids, other compounds

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36
Q

what is fibrinogen for?

A

blood clotting –> they form FIBRIN

fibrin = large insoluble protein strands

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37
Q

fibrin

A

large insoluble protein strands

for clotting

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38
Q

other solutes (1%) of plasma

A

electrolytes

organic nutrients

organic wastes

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39
Q

electrolytes of plasma

A

major ions

E.g.
Na+, K+, Ca2+, Mg2+, Cl-, HCO3-, HPO4-, SO4^2-

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40
Q

organic nutrients of plasma

A

lipids

carbohydrates (CH2O)

amino acids

–> used for cell ATP production, growth/maintenance

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41
Q

organic wastes of plasma

A

taken to site of excretion/breakdown

E.g.
urea, uric acid, creatinine, bilirubin, NH4+ (ammonium)

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42
Q

blood composition – formed elements (“about 45%”)

A

RBC

WBC

platelets

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43
Q

what percentage of formed elements are RBC

A

99.9%

vast majority

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44
Q

what percentage of formed elements are WBC/platelets

A

<0.1% WBC

<0.1% platelets

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45
Q

platelets, AKA

A

thrombocytes

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46
Q

what are platelets?

A

small membrane-bound cell fragments, involved in clotting

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47
Q

which cells do platelets come from?

A

megakaryocytes

@ bone marrow

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48
Q

about WBC

A

body defense, 5 classes, each class different function

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49
Q

what are 5 classes of leukocytes (WBC)

A

Neutrophils

Lymphocytes

Monocytes

Eosinophils

Basophils

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50
Q

what are RBC mainly known for?

A

transport O2

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51
Q

Hematrocrit

A

“ratio of the volume of red blood cells to the total volume of blood.”

other definition:
“Percentage of whole blood from formed elements (mainly RBCs)”

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52
Q

why hematocrit generally concerned w/ RBC

(I.e. why WBC/platelet left out in other definition?)

A

99.9% of formed elements = RBC

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53
Q

hematocrit etymology

A

of blood

judge

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54
Q

average hematocrit

A

45%

(range 37-54%)

males slightly higher than females

male average 47%
female average 42%

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55
Q

why male hematocrit higher?

A

androgens stimulate RBC production

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56
Q

what does low hematocrit indicate?

A

anemia

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57
Q

high hematocrit

A

Polycythemia (also called Erythrocytosis?)

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58
Q

polycythemia

A

poly
cyte
hemia

many cell blood

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59
Q

erythrocytosis, luekocytosis

A

.

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60
Q

formation of blood cells

A

hematopoiesis (aka hemopoiesis)

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61
Q

hematopoiesis

A

process of formed elements developing

hemato
poiesis
= blood making

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62
Q

how long to RBCs live?

A

about 120 days

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63
Q

why RBC not live long?

A

no nucleus

no DNA, no regulatory/repair proteins, no repair wear/tear

no ER

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64
Q

what is rate of RBC replacement

A

3 million per second

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65
Q

about RBM

A

found b/w trabeculae of spongy bone

site of hematopoiesis –> production of RBC, WBC, platelet

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66
Q

where does hematopoiesis begin in embryo/fetus?

A

begins in yolk sac during Embryonic development

switches to liver, spleen, thymus

continues @ RBM during last 3 months pregnancy

continues @ RBM after that

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67
Q

blood cells –> which germ layer

A

all blood cells are from mesenchymal cells

from mesoderm

also from mesoderm:
blood, RBM, kidneys/ureters, muscle, cartilage/bone,

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68
Q

6 steps in formation of blood cells ****

A

1) pluripotent stem cells

2) specialized stem cells (myeloid/lymphoid)

3) progenitor cells (CFU – colony forming units)

4) precursor cells (blast cells)

5) “optional step” (for RBC/platelets)

6) fully developed formed elements

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69
Q

1) pluripotent stem cells

A

from Mesenchyme (mesenchymal cells)

(mesenchyme originates from mesoderm)

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70
Q

pluripotent stem cells give rise to 2 types of stem cells

A

a) lymphoid cells

b) myeloid cells

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71
Q

lymphoid cells

A

B cells, T cells, NK cells

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72
Q

myeloid cells

A

everything else:
RBC, platelet, Mast cell, Eosinophil, Basophil, neutrophil, monocyte/macrophage

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73
Q

2) the specialized stem cells (myeloid/lymphoid)

A

again lymphoid –> B cell, T cell, NK cell

myeloid –>
RBC
platelet
Mast cell
Neutrophil
Eosinophil
Basophil
monocyte/macrophage

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74
Q

what can myeloid/lymphoid cells do

A

can reproduce/differentiate

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75
Q

3) progenitor cells (CFU – colony forming units)

A

most myeloid stem cells become progenitor cells before becoming precursor cells (BLAST cells)

some myeloid stem cells develop directly into precursor (blast) cells

Lymphoid stem cells always directly develop into precursor (blast) cells, without intermediate progenitor cell (CFU)

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76
Q

which specialized stem cell does not differentiate into progenitor (CFU) cell, and directly develops into precursor (Blast) cell?

A

lymphoid stem cells

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77
Q

can progenitor (CFU) cells reproduce?

A

no

committed to differentiate into specific elements within blood

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78
Q

list progenitor (CFU) cells

A

CFU-E:
colony forming unit ERYTHROID

CFU-Meg (or CFU-MK):
colony forming unit Megakaryocyte

CFU-GM:
colony forming unit Granulocyte - Macrophage

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79
Q

CFU-E

A

CFU-E becomes erythrocyte (RBC)

CFU-E
–> Proerythroblast
–> (nucleus ejected) Reticulocyte
–> RBC (erythrocyte)

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80
Q

CFU-Meg (CFU-MK)

A

CFU-Meg becomes platelets

CFU-Meg
–> Megakaryocyte
–> platelets

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81
Q

CFU-GM

A

CFU-GM becomes
–> granulocytes (neutrophils, eosinophils, basophils)

–> and monocytes (macrophage)

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82
Q

granulocytes

A

neutrophils, eosinophils, basophils

“granular WBCs” (cytoplasm)

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83
Q

4) precursor cells

A

blast cells

immature cells

blasts then differentiate into actual blood cells

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84
Q

blasts cells E.g.

A

proerythroblast
megakaryoblast

myeloblast (to neutrophil)
eosinophilic myeloblast
basophilic myeloblast

monoblast

**
From lymphoid stem cells:
T lymphoblast
B lymphoblast
NK lymphoblast

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85
Q

granular vs agranular leukocytes

A

GRANULAR:
neutrophils
eosinophils
basophils

AGRANULAR:
3 lymphocytes
monocytes

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86
Q

5) “optional step” (for RBC & platelets)

A

one extra differentiation for RBCs and Platelets:

b/w blast cell and fully developed mature cell there is:
–> Reticulocyte (nucleus ejected) before RBC
–> Megakaryocyte before Platelet

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87
Q

6) developed formed element

A

blast cells become developed formed elements:

RBC (erythrocyte)
platelet (thrombocyte)
neutrophil
eosinophil
basophil
monocyte
T lymphocyte
B lymphocyte
NK cell

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88
Q

Hematopoietic growth factors

A

hormones that regulate steps within differentiation process

impact differentiation/proliferation

Esp:
differentiation of particular progenitor (CFU) cells

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89
Q

Hematopoetic growth factors E.g.

A

EPO – Erythropoietin

TPO – Thrombopoietin

Cytokines

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90
Q

EPO (erythropoietin)

A

stimulates production of RBC

released from KIDNEYS

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91
Q

where is EPO released?

A

KIDNEYS

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92
Q

TPO (thrombopoetin)

A

stimulates production of thrombocytes (platelets)

released from LIVER

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93
Q

where is TPO released?

A

LIVER

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94
Q

cytokines

A

stimulates WBC production

glycoproteins –> act as local hormones
–> colony-stimulating factors (CSFs)
–> Interleukins (from RBM)

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95
Q

Hematology Tests

A

..

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96
Q

why blood tests?

A

determine blood type

evaluate type/# of RBC, WBC, platelets

abnormal values indicate pathological conditions

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97
Q

how are blood samples generally obtained?

A

venipuncture

(withdrawal of blood from vein)

most commonly @ median cubital vein

other method is via finger/heel stick

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98
Q

CBC

A

complete blood count

1 cubic mL of blood (1uL):
RBC count
WBC count
erythrocyte indices (hemoglobin)
hematocrit
other

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99
Q

WBC differential count

A

part of CBC (?)

identified # of each WBC type

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100
Q

RBC tests

A

several types

Assess #, size/shape, maturity of RBCs

can detect problems that don’t have signs/symptoms (?)
–> E.g. internal bleeding (??)

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101
Q

RBC what percentage of cells in body

A

almost 85 %

20-30 trillion RBC

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102
Q

what percentage of volume of blood is RBC

A

about 45% (45 = formed elements; RBC = 99.99 of “)

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103
Q

major protein in RBC

A

hemoglobin

transport O2
some CO2 (?)

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104
Q

single drop of blood # of RBCs

A

slides say 260 million
–> overestimate most likely

single drop may have about 5 million RBCs

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105
Q

RBC death rate vs production rate

A

death rate = production rate

about 3 million die per second

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106
Q

how long RBC last?

A

about 120 days

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107
Q

why 120 days?

A

no nucleus, no ER, no regulatory/repair proteins etc

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108
Q

erythrocytes (RBC)

A

biconcave discs

(surface area)

–> also to facilitate movement in capillaries

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109
Q

when is nucleus ejected from precursor to RBC?

A

proerythrocyte –> reticulocyte (no nucleus) –> Erythrocyte

nucleus ejected @ reticulocyte

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110
Q

RBC structure/function (surface area)

A

filled w/ hemoglobin (protein that carries O2)

large surface area allows more oxygen exchange

total RBC surface area = 2000x total surface area of body

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111
Q

what are rouleaux

A

stacks that are formed by overlapping RBCs

facilitate transport in small vessels (I.e. capillaries)

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112
Q

RBC other physical properties (flexible/bendable)

A

RBCs can move through capillaries w/ smaller diameter than RBC

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113
Q

RBC anatomy (hemoglobin)

A

RBC cytosol = contains hemoglobin

” synthesized before loss of nucleus (lost @ reticulocyte)

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114
Q

what percentage of weight of RBC is hemoglobin?

A

about 1/3 (33%)

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115
Q

RBC plasma membrane

A

strong/flexible

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116
Q

RBC glycolipids

A

glycolipids acting as antigens for blood types

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117
Q

how many hemoglobin molecules per RBC

A

about 280 million

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118
Q

hemoglobin structure

A

globin protein
–> 4 polypeptide chains
(2 alpha chains, 2 beta chains)

+

heme
–> 4 ring-like structures
–> non-protein “
–> bind to each pp chain

centre of each heme
–> an IRON ion

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119
Q

oxyhemoglobin (HbO2)

A

each heme + iron ion
–> interacts w/ O2 molecule

–> forms OXYHEMOGLOBIN (HbO2)

–> makes “oxygenated blood”
(bright red)

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120
Q

Deoxyhemoglobin

A

reversible oxygen binding

–> hemoglobin not bound to oxygen = blood becomes dark red

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121
Q

what does RBC w/ 280million Hb molecules do?

A

carry oxygen from lungs to tissue –> carry CO2 from tissue to lungs

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122
Q

how many O2 molecules per RBC?

A

4 Heme rings per Hb –> so 4 O2 molecules per Hb

4*280 million (Hb)
= 1.1 billion O2 molecule per RBC

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123
Q

nitric oxide and Hemoglobin

Where does NO bind on Hb

A

nitric oxide binds on Heme ring of Hb

NO carried by Hb dilates microvasculature
–> increaes blood flow & oxygen delivery

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124
Q

how does Hemoglobin regulate blood pressure & blood flow?

A

NO binding to Heme ring on Hemoglobin regulates blood pressure & blood flow

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125
Q

what percentage of oxygen in blood is bound to Hemoglobin?

A

98-99% (VAST MAJORITY)

–> bound to Hb
–> remained is dissolved in PLASMA

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126
Q

carbon monoxide

A

toxic

byproduct of vehicle, furnace, heater fumes, even cigarette smoke

binds to heme group
–> @ 200x affinity vs O2
–> decreases O2 carrying capacity of Hb/RBC

can be fatal unless treated w/ pure O2
(E.g. oxygen chamber)

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127
Q

ERYTHROPOIESIS

A

.

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128
Q

where does erythropoiesis start?

A

starts in RBM

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129
Q

what are the steps in RBC production?

A

pluripotent stem cell
–> Myeloid stem cell
–> CFU-E progenitor cell
–> Proerythroblast precursor cell
–> Reticulocyte
–> Erythrocyte

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130
Q

proerythroblast – divide?

A

“divides several times”

–> previous notes said progenitor & blast cells do not divide, only differentiate

–> are there some exceptions?

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131
Q

about reticulocyte

A

reticulocyte gains BICONCAVE shape

unlike RBC, has some
–> mitochondria
–> ribosomes
–> ER

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132
Q

where do reticulocytes go?

A

pass from RBM to blood stream

–> develop into mature RBC within 1-2 days

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133
Q

a few extra steps b/w Proerythroblast & reticulocyte

A

proerythroblast becomes
–> Erythroblast
–> Normoblast

Normoblast ejects nucleus and becomes Reticulocyte

134
Q

at which stage does Hemoglobin production begin?

A

Erythroblasts begin creating Hb

135
Q

what percentage of Hemoglobin of mature RBC does Reticulocyte have?

A

80% of the 280million Hb molecules are already prepared in Reticulocyte

136
Q

hypoxia

A

cellular oxygen deficiency

E.g.
high altitude (less O2 in air)

anemia (not enough Hb or RBC = not enough O2)

circulatory problems (problem w/ O2 delivery?)

137
Q

Erythropoietin (EPO)

A

hormone produced by KIDNEYS

increases/facilitates Erythropoiesis

138
Q

Liver

A

Thrombopoietin (TPO)

> 90% of Plasma proteins

139
Q

Kidney

A

Erythropoietin (EPO)

140
Q

negative feedback loop of Erythropoietin from kidneys

A

decreased O2 delivery to tissues (including kidney)

–> kidney cells detect low O2

–> increase EPO production/secretion

–> Proerythroblast activity increases

–> more reticulocytes

–> more RBC

–> more Hb –> more O2 to tissues

–> return to homeostasis when kidney receives increased O2

141
Q

what happens to dead RBC?

A

removed from circulation

destroyed/recycled via FIXED macrophages
–> @ Spleen/Liver

breakdown products E.g. (Hb):
–> Globin (4 pp chains)
–> Heme ring (red/brown pigment w/ iron)

142
Q

RBC BREAKDOWN STEPS

A

..

143
Q

which macrophages break down RBC?

A

fixed macrophages

@ Spleen
@ Liver
or @ RBM

144
Q

what happens after macrophages break down RBC?

Which two parts of important molecules inside are split apart?

A

Globin & Heme portion of Hb molecules split apart

–> recall Globin protein = 4 Polypeptide chains

–> Hemes = Ring-shaped pigment structure

145
Q

what happens to Globin

A

4 polypeptide chains are broken into amino acids

–> recycled in other protein synthesis

146
Q

what happens to Heme structures?

I.e. what happens to Iron ion?

A

Iron is removed from heme portion

147
Q

what does Iron do?

A

Iron binds to Plasma protein TRANSFERRIN
(Iron transporter protein)

–> transports iron in blood

148
Q

where does Iron go?

A

Iron goes to
–> muscle fibres
–> liver cells
–> macrophages (liver/spleen)

then
–> detaches from Transferrin (@BV)
–> attaches to FERRITIN

Ferritin
–> Iron storage protein (@ cells)

149
Q

transferrin vs ferritin location

A

transferrin = plasma protein inside BV

ferritin = protein inside cells

150
Q

where does Iron go when released from storage (Ferritin)

or when absorbed via GI tract?

A

attaches to Transferrin (plasma protein) to be transported

–> to RBM (for Hb)

when not needed?
–> back to storage

–> @liver, spleen, marrow, duodenum, skeletal muscle and other anatomic areas.

151
Q

what happens to excess iron?

how can iron be excreted?

A

liver can excrete iron to some extent (?)
–> some sources state “

some sources also state some Iron can be excreted via sweat
+ shedding intestinal cells

also via blood loss

152
Q

what happens to Iron-Transferrin complex that goes to RBM

(after leaving storage)

A

RBC precursor cells use Iron

(proerythroblast? erythroblast? normoblast? reticulocyte?)

–> take Iron via Receptor mediated endocytosis

–> used for Hemoglobin synthesis
(reattached to Heme pigment portion)

153
Q

back to RBC breakdown –> what happens to non-iron portion of Heme?

A

converted to Biliverdin (green pigment)

Biliverdin converted to Bilirubin (yellow-orange pigment)

154
Q

what happens to bilirubin?

where is it taken?

what happens there?

A

enters blood –> transported to Liver

@ liver
–> bilirubin released to bile (component of bile?)

155
Q

where does bile+bilirubin go?

what happens there?

A

bile passes from liver (or gallbladder?)
–> to small intestine
–> then large intestine

Bacteria @ large intestine
–> converts bilirubin to UROBILINOGEN

156
Q

what happens to some urobilinogen

A

some urobilinogen goes to kidneys
–> via blood

converted to UROBILIN (yellow)
–> excreted in urine

157
Q

what happens to most urobilinogen

A

excreted via feces

–> in form of STERCOBILIN (brown)

“sterco” = excrement

158
Q

Iron overload

A

too many free iron ions can be damaging

Transferrin (plasma protein)
and
Ferritin (storage protein @ cells)
–> are protective
–> prevent too much free iron ions

159
Q

what happens if iron overload

A

amount of free iron increases

can cause damage
–> of heart
–> of liver
–> pancreas
–> gonads

can increase number of iron dependent MICROBES

160
Q

iron elimination

A

notes say:
“We have NO method of elimination excess iron”

–> other sources say liver can excrete to some extent
–> also say sweat can excrete to some extent
–> also via shedding of intestinal cells

otherwise iron is lost when blood is lost

161
Q

WHITE BLOOD CELLS

A

leukocytes

contribute to body defense

no hemoglobin

but nucleus/organelles present (unlike RBC)

162
Q

5 types of WBCs

A

neutrophils (majority)
eosinophils (2-3%)
basophils (<1%)

Monocytes (become macrophages)

Lymphocytes (T, B, NK cells

163
Q

granular vs agranular WBCs

A

neutrophil, eosinophil, basophil
= granular

monocyte, lymphocytes
= agranular

164
Q

what are similarities & shared characteristics of diferent WBCs

A

1) spend only short time in circulation

2) most located @ loose/dense CT (where infection occurs)

3) can migrate out of bloodstream

165
Q

where does infection often occur?

A

loose/dense CT

166
Q

what do all WBCs do to migrate out of bloodstream?

A

adhere to vessel walls @ infection site

squeeze out b/w adjacent endothelial cells

167
Q

what is it called when WBCs squeeze out of BV via adjacent endothelial cells?

A

“Emigration”

or
“Diapedesis”

dia = through
pedesis = leaping

168
Q

other shared characteristics b/w all WBCs

A

4) are attracted to chemical stimuli
–> this characteristic is called “POSITIVE CHEMOTAXIS” (or just chemotaxis)

chemotaxis guides WBCs to pathogens, damaged tissue, or other active WBCs

169
Q

what is (positive) chemotaxis?

A

here refers movement of WBCs up concentration gradient

–> going toward pathogens, damaged tissues, or other active WBCs

170
Q

what is similarity b/w Neutrophils, Eosinophils, and monocytes?

A

capable of phagocytosis

–> engulf pathogens/debris

171
Q

monocyte/macrophage

A

“Macrophages are monocytes that have moved out of the bloodstream”

172
Q

WBC count

A

about 7000 WBC per uL of blood

–> # can increase during infection, inflammation, injury, allergy, etc

173
Q

recall “differential count”

A

number of each type of WBC in sample

reported as percentage (per 100 WBCs)

174
Q

two classificaitons of WBC (granular vs agranular)

A

granular (granulocytes)
–> cytoplasmic granules
(secretory vesicles + lysosomes)
–> absorb “Histological Stains”

agranular (agranulocytes)
–> “smaller secretory vesicles/lysosomes”
–> “don’t absorb stains”

175
Q

histological staining

A

“Histological stains are chemical dyes used to treat histological specimens to make tissues more readily visible by light microscopy and demonstrate underlying characteristics of the tissue.”

“Staining is a technique used to enhance contrast in samples, generally at the microscopic level. Stains and dyes are frequently used in histology, in cytology, and in the medical fields of histopathology, hematology, and cytopathology that focus on the study and diagnoses of diseases at the microscopic level.”

176
Q

about granulocytes – including percentage (differential count)

A

“absorb histological stains (so are visible under the microscope)”

numbers (as % of WBCs):
Neutrophils (about 50-70%)
Eosinophils (about 2-4%
Basophils (<1%)

177
Q

about Neutrophils

A

“pale” colour – neutral stain

most numerous WBC

1st to arrive

engage in phagocytosis of bacteria

uses enzymes for destruction:
a) oxidants
b) LYSOZYMES
c) “defensins”

178
Q

about Eosinophils

A

“red/orange” colour – acidic stain

relationship to HISTAMINE (?)
–> note says “antihistamine” (???)

destroys parasites

destroys Ag-Ab complexes

179
Q

about Basophils

A

“blue/purple” colour – basic stain

releases
–> serotonin
–> heparin
–> histamine

important during allergic reactions

180
Q

defensins?

A

“Defensins are small … proteins … They are host defense peptides … either direct antimicrobial activity, immune signaling activities, or both.”

181
Q

about agranulocytes – including percentage (differential count)

A

“few, if any, cytoplasmic granules that absorb histological stain”
= not visible under the microscope

numbers (as % of WBCs):
Lymphocytes (20-40%)
Monocytes (2-8%)

182
Q

most vs least numerous WBC?

A

–> lymphocytes = second most numerous WBC
–> neutrophil = most numerus
–> monocytes = usually 3rd most numerus
–> eosinophil = 4th
–> basophil = 5th

183
Q

about Monocytes

A

kidney bean shaped (?) –> b/c of nucleus (???) “indented nucleus”

called monocytes @ blood
called macrophages @ tissue

main role:
phagocytosis of cells/debris

can be:
Fixed or Wandering

184
Q

about Lymphocytes –> includes 3 subtypes

A

T cells –> attack cancer cells, foreign/viral invasions

B cells –> become plasma cells, secrete Ab (w/ help from T cells)

NK cells –> attack cancer cells & infectious microbes

185
Q

lymphocytes, innate vs adaptive immune system

A

B/T cells are adaptive

NK cells are innate

186
Q

how long can WBCs live?

A

in healthy body –> several months/years

however
–> most only live a few days due to being destroyed during immune activity

E.g.
During infection phagocytic WBCs may live only a few hours

187
Q

WBC functions –> when pathogens enter body

A

WBCs combat pathogens

–> via phagocytosis
–> via immune response

188
Q

which leukocytes never return to bloodstream?

A

Granular Leukocytes (neutrophils, eosinophils, basophils)

& macrophages

189
Q

which leukocytes constantly recirculate?

A

Lymphocytes

constantly recirculate
I.e.
blood –> ISF –> Lymph –> blood

190
Q

what percentage of lymphocytes are circulating at a given time?

A

about 2% circulate

rest are in lymphatic fluid or organs (esp lymphoid organs)
E.g.
thymus, lymph nodes, spleen, and appendix

191
Q

some terms related to WBC functions

A

a) Emigration (Diapedesis)

b) Phagocytosis

c) Chemotaxis

192
Q

a) Emigration (Diapedesis)

A

how WBCs leave bloodstream

roll along endothelium
–> attach and squeeze out between endothelial cells

AKA Diapedesis
OR
“LEUKOCYTE EXTRAVASATION”

extra = out
vas = related to vessel

193
Q

ADHESION MOLECULES during diapedesis (emigration/ leukocyte extravasation)

A

adhesion molecules include
–> Selectins, Integrins

these help WBCs stick to endothelium

194
Q

b) Phagocytosis

A

eating/engulfing cell/microbe

195
Q

c) Chemotaxis

A

“the process by which chemicals released by toxins or damaged/inflamed tissue attract phagocytes”

WBC movement up concentration gradient to site of infection/inflammation/injury etc.

196
Q

other common terms related to WBCs

A

Leukocytosis

Leukopenia

Leukemia

Leukocytolysis

197
Q

leukocytosis

A

“increase in the number of WBCs”

“Normal, protective response to stresses such as invading microbes, strenuous exercise, anethesia and surgery”

can also be pathological

198
Q

Leukopenia

A

“An abnormally low level of WBC”

“May be caused by radiation, shock or chemotherapeutic agents”

199
Q

Leukemia

A

Cancer of WBCs

“WBCs differentiate and divide uncontrollably, producing non-functional WBCs”

200
Q

Leukocytolysis

A

WBC death

“Due to trauma, disease or chemicals”

201
Q

Platelets

A

Aka thrombocyte

“Cell fragments, have no nucleus”

“Short life span of 5 to 9 days”

“Aged and dead platelets are
–> removed by:
fixed macrophages in the spleen and liver”

202
Q

platelet function

A

“Platelets function primarily in the formation of plugs and release of other chemicals to assist in blood clot formation”

203
Q

thrombopoiesis

A

myeloid stem cells
–> progenitor CFU-Meg cells
–> Megakaryoblast
–> Megakaryocyte
–> Platelet

204
Q

how do megakaryocytes become platelets?

A

“megakaryocytes splinter into 2000-3000 cell fragments called a platelet”

205
Q

Thrombopoietin (TPO)

A

From liver

stimulates platelet production

206
Q

hemostasis

A

stop blood loss from damaged BV

quick, localized to damaged area

207
Q

three phases of hemostasis

A

1) vascular phase

2) platelet phase

3) coagulation phase

208
Q

hemorrhage define

A

loss of large amount of blood

209
Q

thrombosis define

A

clotting @ undamaged vessel

“local coagulation or clotting of the blood in a part of the circulatory system.”

210
Q

1) vascular phase of hemostasis

A

lasts about 30 minutes

endothelial response + vascular spasm
–> smooth muscle contracts

reduces blood loss @ damage vessel until next step

211
Q

what causes the spasm/contraction during 1) vascular phase of hemostasis?

A

a) Endothelial chemical release via damaged BV

b) platelet chemical release

c) nociceptor reflexes

212
Q

One of the substances that endothelial cells release

A

Endothelins

which cause:
a) smooth muscle contractions (vascular spasms)

b) division of cells (endothelial, smooth muscle)

c) division of fibroblasts

Note endothelial plasma membranes become “sticky”

213
Q

2) platelet phase of hemostasis

A

note that platelets always present

however when tissue damaged:
–> causes platelet adhesion
–> platelets stick to area of damaged BV

214
Q

why do platelets stick to area of damaged BV?

A

platelets bind to exposed collagen fibres of CT beyond damaged endothelial cells

215
Q

what happens after platelets adhere @ site of damage?

A

platelets are activated

interact with one another

release contents of vesicles

others platelets are attracted via contents (CHEMOTAXIS)

216
Q

which substances are released by platelets

A

ADP, thromboxane A2, setotonin

217
Q

what does each substance do?

A

ADP/thromboxane A2 attract other platelets

serotonin/ thromboxane A2 stimulate vasoconstriction

thromboxane A2 = both

218
Q

what happens after platelets release contents of vesicles?

A

more platelets attracted

area becomes sticky

arriving platelets adhere to existing platelets

PLATELET PLUG forms
–> later tightened by fibrin threads during clotting

219
Q

3) Coagulation phase of hemostasis

A

involves clotting cascade

via substances called “CLOTTING FACTORS”

ultimately involves formation of FIBRIN via FIBRINOGEN

& blood cells + platelets are trapped in “Fibrin Network” (Blood Clot)

it is an example of positive feedback system

220
Q

quick note about blood outside body

A

outside body blood thickens to:
–> Serum = blood plasma w/o clotting factors

–> Clot = gel-like, network of Fibrin (Insoluble protein fibres) + trapped formed elements

221
Q

what are Clotting factors (Procoagulants)

A

Ca2+

& 11 different proteins

many are “proenzymes” (I.e. inactive)

activated enzymes lead to “chain reaction” –> “Clotting Cascade”

222
Q

proenzymes define

A

“any of a group of proteins that are converted to active enzymes by partial breakdown”

223
Q

two different pathways that lead to same common pathway for blood clotting (coagulation step of hemostasis)

A

1) extrinsic pathway

2) intrinsic pathway

224
Q

1) extrinsic pathway to clotting

A

quicker than intrinsic pathway

extrinsic b/c involves factor from outside blood

225
Q

steps of extrinsic pathway to (Common pathway) blood clotting

A

1) broken tissue releases TF (tissue factor)
–> AKA thromboplastin, or factor iii

2) TF + Ca2+ = FACTOR X activated

detailed steps:
Factor iii + [Ca2+] + Factor vii –> Tissue factor complex
—> FACTOR X activated

226
Q

1) intrinsic pathway to clotting

A

takes few minutes to begin (slower than extrinsic pathway

called “intrinsic” b/c all factors are found directly inside blood

227
Q

steps of intrinsic pathway to blood clotting (Common Pathway)

A

1) factor xii activated via damaged platelets/endothelium

PF-3 (platelet factor)
+
Ca2+
+
Factor viii + ix
—>
Factor X activator complex

—> Activated Factor X (Common pathway)

228
Q

can both extrinsic and intrinsic pathways be active at once

A

yes

both tissue trauma and blood vessel trauma

229
Q

for simplified purposes (extrinsic/intrinsic pathways steps)

A

extrinsic
–> Factor iii + Ca2+ = Factor X activated

intrinsic
–> Factor xii + Ca2+ = Factor X activated

extrinsic factor ii
–> via tissue damage

intrinsic factor xii
–> via BV damage

230
Q

common pathway (of coagulation phase of hemostasis)

A

factor X activates “Prothrombinase”

231
Q

what does prothrombinase do

A

converts Prothrombin to thrombin

via Ca2+

232
Q

what is prothrombin

A

proenzyme

formed by liver

233
Q

what is thrombin

A

enzyme

234
Q

what does thrombin do

A

converts Fibrinogen to Fibrin (enzyme)

235
Q

what about Factor xiii

A

factor xiii + thrombin
–> Activates factor xiii

–> which strengthens Fibrin threads

236
Q

vitamin K

A

not directly responsible for clotting

contributes to production of some clotting factors

237
Q

fibrinolysis

A

dissolving of small/unneeded clots after repair

via “Fibrinolytic system”
–> Lysis of fibrin

238
Q

which enzyme/protein is responsible for fibrinolysis

A

plasminogen
–> inactive plasma protein
–> component

plasminogen converts to Plasmin
–> active plasma enzyme

plasmin breaks down fibrinogen in blood clots

239
Q

anticoagulants (hemostatic control mechanisms)

A

anticoagulant (substances that prevent unnecessary coagulation)
E.g.
Warfarin
Anti-thrombin
Heparin
APC (Activated Protein C)

240
Q

Warfarin

A

“aka Coumadin ® blocks Vit K, therefore production of clotting factors”

241
Q

Anti-thrombin

A

blocks thrombin formation

which blocks fibrinogen –> fibrin conversion

242
Q

Heparin

A

produced by Mast Cells & Basophils

–> helps activate anti-thrombin

243
Q

note mast cell vs basophil

A

structurally/functionally similar

244
Q

APC (Activated protein C)

A

blocks clotting factors

enhances plasminogen activation

245
Q

thrombolytic agents

A

note “thrombolysis”

thrombolytic agents:
–> synthetic/artificial chemicals
–> injected to dissolve clots

E.g.
Tissue plasminogen activator –> activates plasmin

Streptokinase –> produced by streptococcus bacteria –> helps dissolve clots

Aspirin
–> inhibits vasoconstriction (opens vessels)
–> prevents platelet aggregation (blocks thromboxane A2)

246
Q

intravascular clotting (thrombus)

A

thrombus
–> a clot in an unbroken or undamaged blood vessel

–> “usually self dissolves, happens in cases of minute traumas”

247
Q

intravascular clotting (embolus)

A

embolus:
“broken off piece of thrombus that travels the bloods stream”

“can have serious consequences if it lodges itself in small arteries”

“leads to arterial blockage”

“Can be blood clot, air bubble, fat or debris”

248
Q

embolism

A

“obstruction of an artery, typically by a clot of blood or an air bubble.”

249
Q

blood types

A

..

250
Q

what is blood type

A

determined by presence/absence of specific surface antigens on RBCs

antigen? “substance eliciting immune response”

251
Q

antigens on cells

A

“surface antigens embedded in plasma membranes”

“recognized as normal, or self, by immune system”

252
Q

what are antigens on surface of RBC composed of?

A

composed of:
–> glycoproteins
–> glycolipids

called “Agglutinogens”
–> “substance that acts as an antigen to stimulate production of specific agglutinin”

253
Q

agglutinogens, agglutin, agglutination

A

called “Agglutinogens”
–> “substance that acts as an antigen to stimulate production of specific agglutinin”

“AGGLUTININ is a substance (such as an antibody) producing agglutination.”

“Agglutination is a reaction in which particles suspended in a liquid collect into clumps usually as a response to a specific antibody”

254
Q

E.g. of antigens (agglutinogens) on RBCs

A

A antigen
B antigen

255
Q

agglutinin

A

“Agglutinins are substances that make particles (such as bacteria or cells) stick together to form a clump or a mass.”

“Antibodies can be agglutinins”

256
Q

E.g. of Agglutinins

A

anti-A antibody
anti-B antibody

257
Q

blood types E.g.

A

determined genetically

via which surface antigens are on RBC membrane

> 50 blood cell antigens

three most important:
A
B
Rh (or D)

258
Q

blood type A

A

surface antigen A

anti-B antibodies (in plasma)

259
Q

blood type B

A

surface antigen B

anti-A antibodies (in plasma)

260
Q

blood type AB (universal recipient)

A

surface antigens A & B

neither antibody in plasma

261
Q

blood type O (universal donor)

A

neither surface antigen

both antibodies in plasma

262
Q

ABO blood group

A

consists of four types:
A
B
AB
O

263
Q

reiterate blood types with different terms

A

type A
A agglutinogens (Ag)
B agglutinins (Ab)

type B
B agglutinogens (Ag)
A agglutinins (Ab)

type AB
A + B agglutinogens
no agglutinins

type O
no agglutinogens
A + B agglutinins

264
Q

Rh blood group

A

Named because the antigen was discovered in the blood of the Rhesus monkey

Rh+
RBCs have Rh antigen

Rh-
RBCs lack Rh antigen

265
Q

Rh blood type & anti-Rh antibodies

A

“Normally blood plasma does not contain anti-RH antibodies”

“If an Rh- person receives Rh+ blood the immune system will start to make anti-Rh antibodies”

Will cause agglutination/hemolysis in event of SECOND exposure to blood

E.g. blood of fetus Rh+, mother Rh-

266
Q

genetics of blood type

A

genetically determined

foreign exposure not needed to produce Ab (agglutinins)
–> Ab naturally present in plasma

Exception:
“Anti-Rh antibodies are not automatically present”
–>
“Rh-negative person will not have any anti-Rh antibodies until exposed to Rh-positive RBCs (sensitized); then develops anti-Rh antibodies”

267
Q

Blood transfusion

A

“transfer of whole blood or blood components into the bloodstream or directly into the red bone marrow”

for:
“Anemia, increase blood volume, improve immunity”

268
Q

incompatible blood transfusion

A

“Antibodies in the recipients plasma bind to the antigens on the donated RBCs and cause agglutination, or clumping of the RBCs”

–> Ab attack RBCs (?)

269
Q

hemolytic disease of newborn (Rh factor)

A

common problem with Rh incompatibility

“Normally there is no direct contact of fetal and maternal blood”

“Small amount can leak from the fetus through the placenta or @ delivery”

“If mother is Rh- and baby is Rh+, mother may create anti-Rh antibodies”

270
Q

hemolytic disease of newborn (Rh factor) 2

A

First pregnancy – mother creates antibodies

“Second pregnancy – the anti-Rh antibodies can cross the placenta and cause agglutination and hemolysis”

271
Q

treatment to prevent hemolysis of Rh+ fetus by (Rh-) mother’s Rh-antibodies

A

“Treatment – injection of … anti-Rh gamma globulin”

“bind to and inactivate the fetal Rh antigens before the mother’s immune system can respond”

272
Q

erythroblastosis

A

“abnormal presence of erythroblasts in the circulating blood”

273
Q

“erythroblastosis fetalis”

A

“erythroblastosis fetalis, type of anemia in which the red blood cells (erythrocytes) of a fetus are destroyed in a maternal immune reaction resulting from a blood group incompatibility between the fetus and its mother.”

274
Q

blood type test

A

“Drops of person’s blood are mixed with solutions containing antibodies to surface antigens A, B, and Rh”

“Clumping (agglutination) occurs where sample contains the corresponding antigen”

“Typing is necessary to avoid transfusion reactions (cross-reactions occurring from transfusing mismatched blood)”

“Donor and recipient blood types must be compatible (will not cross-react)”

275
Q

transfusion reaction

A

cross-reactions occurring from transfusing mismatched blood

276
Q

blood pathologies

A

..

277
Q

anemia

A

“problem of not having enough healthy RBC or hemoglobin to carry oxygen’

“oxygen-carrying capacity of blood is reduced”

symptoms:
Fatigue
Intolerant of cold
Skin appears pale
Dyspnea with mild exertion

278
Q

dyspnea

A

difficult or labored breathing.

279
Q

iron-deficiency anemia

A

a) Inadequate absorption of iron

b) Excessive loss of iron (menstruation)

c) Increased iron requirement

d) Insufficient intake of iron

280
Q

hypermenorrhea, polymenorrhea, oligomenorrhea

A

Heavy menstrual bleeding (hypermenorrhea)

more frequently than 21 days is considered abnormal (polymenorrhea)

less frequently than every 37 days is considered abnormal (oligomenorrhea).

281
Q

menstruation, meno, month

A

word “menstruation” is etymologically related to “moon”

meno = month
rrhea = flow

monthly flow

282
Q

megaloblastic anemia

A

Inadequate Vit B12 or folic acid (Vit B9) levels

Red bone marrow produces large, abnormal RBCs

Ineffective at carrying oxygen

283
Q

megaloblast

A

“large erythroblast that appears in the blood especially in pernicious anemia”

megaloblastic

284
Q

pernicious anemia define

A

“Pernicious anemia is a relatively rare autoimmune disorder that causes diminishment in dietary vitamin B12 (cobalamin) absorption, resulting in B12 deficiency and subsequent megaloblastic anemia.”

285
Q

megalo

A

prefix meaning “large, great, grand, abnormally large.”

286
Q

pernicious anemia

A

A type of megaloblastic anemia

“Vit B12 deficiency resulting from an inability of the stomach to produce intrinsic factor which is needed for absorption of vit B12”

autoimmune disorder:
“immune system attacks the actual intrinsic factor protein or the cells in the lining of your stomach that make it”

287
Q

hemorrhagic anemia

A

Excessive loss of RBCs

“bleeding from large wounds, ulcers or heavy menstruation”

288
Q

heavy menstrual bleeding

A

aka
hypermenorrhea, menorrhagia

289
Q

acute blood loss

A

“Recovery enhanced by increase in EPO levels” (kidneys)

“marrow response is marked by reticulocytosis “

290
Q

reticulocytosis

A

“increase in reticulocytes, immature red blood cells”

“commonly seen in anemia”

“bone marrow is highly active in an attempt to replace red blood cell loss such as in haemolytic anaemia or haemorrhage”

291
Q

chronic blood loss

A

Iron stores eventually depleted, hemoglobin ends up low

292
Q

hemolytic anemia

A

premature RBC plasma membrane rupture

“inherited defects, parasites, toxins or antibodies”

“possibly see jaundice with hemolytic anemia”
–> Note Heme-ring pigment structure
–> Bilirubin

293
Q

jaundice (hemolytic anemia)

A

“when too much bilirubin builds up in the body. Jaundice can occur if: Too many red blood cells are dying or breaking down and going to the liver.”

Can also occur with liver dysfunction

294
Q

hemolytic anemias E.g.

A

Thalassemia

Sickle cell disease

Infections: malaria, HIV

Medications

295
Q

thalassemia

A

deficient synthesis of hemoglobin (one globin chain)

Autosomal recessive blood disorder

“RBCs are small, pale and short-lived”

“reduced rate of synthesis or no synthesis of one globin chain”

296
Q

autosomal recessive define

A

“Autosomal recessive is a pattern of inheritance characteristic of some genetic disorders.”

“‘Autosomal’ means that the gene in question is located on one of the numbered, or non-sex, chromosomes.”

“‘Recessive’ means that two copies of the mutated gene (one from each parent) are required to cause the disorder”

297
Q

thalassemia most common in which ethnicities

A

populations from countries bordering the Mediterranean Sea

“South Asian, Italian, Greek, Middle Eastern, and African descent.”

298
Q

thalassemia (continued)

A

“reduced rate of synthesis or no synthesis of one globin chain”

“β-Thalassemias or α-Thalassemias”
(depending on which chain is affected?)

299
Q

thalassemia prognosis

A

Can be fatal early in life depending on severity

Some forms are mild and present as mild anemia

300
Q

thalassemia treatment

A

“If severe, may require regular blood transfusions”

301
Q

sickle cell disease

A

an abnormal hemoglobin
–> Hb-S

when O2 released
–> “forms long, stiff, rodlike structures that bend the RBC into a sickle shape”

“sickled cells rupture easily”

302
Q

sickle cell anemia vs sickle cell trait

A

Sickle Cell Anemia
–> Two copies of gene (one from each parent)
–> Rapid breakdown of RBCs

Sickle Cell Trait
–> One copy of gene
–> usually no symptoms

303
Q

more about sickle cell disease

A

inherited

found in populations that live in “malaria belt”
–> “Mediterranean Europe, sub-Saharan Africa, tropical Asia”

304
Q

sickle cell disease and malaria

A

“Sickle cell trait gives protection against malarial infection”

“cells that obtain malaria parasite sickle and are removed from circulation”

HOWEVER:
“Sickle cell anemia is worse during malarial infection (not advantageous)”

305
Q

sickle cell disease symptoms

A

Degree of anemia

Mild jaundice

Joint or bone pain

Breathlessness

Rapid heart rate

Abdominal pain

fatigue

306
Q

sickle cell disease treatment

A

Pain medication

Fluid therapy for hydration

Oxygen

Antibiotics

Blood transfusions

307
Q

aplastic anemia

A

destruction of red bone marrow

toxins, gamma radiation, viral hepatitis, medications

308
Q

aplastic anemia signs/symptoms

A

“Slowly progressive anemia”

“causes insidious development of weakness, pallor, and dyspnea”

thrombocytopenia
–> petechiae
–> ecchymoses

Granulocytopenia
–> frequent minor infections
–> sudden onset of chills, fever

309
Q

thrombocytopenia

A

deficiency of platelets in the blood

“bleeding into the tissues, bruising”

“slow blood clotting after injury”

310
Q

petechiae

A

“a small red or purple spot caused by bleeding into the skin.”

“tiny spots of bleeding under the skin or in the mucous membranes. The pinpoint-sized purple, red or brown dots are not a rash”

311
Q

ecchymosis

A

“a discoloration of the skin resulting from bleeding underneath, typically caused by bruising.”

312
Q

aplastic

A

“characterized by the failure of an organ or tissue to develop or to function normally.”

aplastos = unshaped

313
Q

“aplastic” anemia

A

“Stem cells in the bone marrow produce blood cells”

“In aplastic anemia, stem cells are damaged.”

As a result, the bone marrow is either empty (aplastic) or contains few blood cells (hypoplastic).

314
Q

granulocytes

A

neutrophil
eosinophils
basophil

315
Q

splenmegaly & aplastic anemia

A

absent in aplastic anemia

“you’re just not making any blood cells. The spleen has nothing to recognize as abnormal, which means your spleen isn’t going to enlarge.”

316
Q

leukemia

A

“group of red bone marrow cancers in which abnormal WBCs multiply uncontrollably”

“Interferes with normal processes and causes”
–>Reduced oxygen-carrying capacity
–> Increase susceptibility to infection
–> Abnormal blood clotting

“Spread to lymph nodes, liver and spleen”

317
Q

leukemia symptoms

A

Anemia
Weight loss
Fever
Night sweats
Excessive bleeding
Recurrent infections

318
Q

leukemia risk factors

A

Genetics (ie. Down syndrome)

Family Hx

Smoking

Radiation, chemotherapy (previous cancer treatment)

319
Q

leukemia treatment

A

Chemotherapy
Radiation
Stem cell transplant
Antibodies
Blood transfusions

320
Q

hemophilia

A

“inherited deficiency of clotting in which bleeding may occur spontaneously or after only minor trauma”

“Usually affects males”

“Different types of hemophilia are due to deficiencies of different blood clotting factors”

321
Q

hemophilia treatment

A

Transfusions, clotting factors

322
Q

hemochromatosis

A

Primary
Inherited

Secondary
Caused by anemia, alcoholism or other disorders

323
Q

hemochromatosis etymology

A

chromato- (“color”) +‎ -osis (“condition, disease”)

324
Q

about hemochromatosis

A

causes body to absorb and store too much iron

“Extra iron builds up in the body’s organs and without treatment can cause them to fail”

325
Q

normal iron absorption vs iron absorption with hemochromatosis

A

“Normally we absorb 10% of the iron in our food”

“Someone with hemochromatosis absorbs up to 30%”

326
Q

hemochromatosis symptoms

A

Arthritis

Liver disease

Damage to pancreas
Heart abnormalities

Thyroid deficiency

Abnormal pigmentation of skin – gray/bronze

327
Q

hemochromatosis treatment

A

take blood

Monitor ferritin levels

328
Q

jaundice

A

“abnormal yellowish discoloration of the sclerae of the eyes, skin and mucous membranes due to excessive bilirubin in the blood”

329
Q

3 categories of jaundice

A

Prehepatic –>
Due to excessive production of bilirubin

Hepatic –>
Abnormal bilirubin processing by the liver

Extrahepatic –>
Due to blockage of bile drainage by gallstones or cancer of bowel or pancreas

330
Q

excess breakdown of RBC

A

prehepatic jaundice (?)

excess breakdown = “excessive production of bilirubin” (??)

Semester 3 (32 decks)

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