Exam 1 Review Flashcards

1
Q

Active Transport

A

Energy mediated transport of molecules and ions across a cell membrane

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2
Q

Cell Membrane

A

Bilipid membrane that encloses the cell

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3
Q

Centrioles

A

cylindrical organelle near the nucleus occuring in pairs and involved in development of spindle fibers during cell division

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4
Q

Connective Tissue

A

Fibrous tissue: bone, ligaments, tendons, cartilage, adipose(fat) tissues

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5
Q

ligament

A

connects 2 bones or cartilages or holds together a joint

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6
Q

Diffusion

A

movement from area of high to low concentration

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7
Q

Ectoderm

A

Embryonic tissue that gives rise to epithelial, nervous, tissue

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8
Q

Endoderm

A

Gives rise to digestive and respiratory tubes

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9
Q

Endoplasmic Reticulum

A

protein production

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10
Q

endothelium

A

single layer of cells lining organs: blood vessels, heart, lymphatic vessels

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11
Q

epithelium

A

thin tissue on bodys outer surface

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12
Q

exocytosis

A

contents of a cell vacuole are released

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13
Q

facilitated diffusion

A

passive diffusion by use of ion channels and carrier proteins

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14
Q

organs

A

group of tissues with coordinated function

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15
Q

tissues

A

cells with common qualities

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16
Q

glycolysis

A

breakdown of glucose to release energy

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17
Q

golgi apparatus

A

modifies and packages proteins

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18
Q

krebs cycle

A

citric acid cycle- aerobic release of stored energy through oxidation of acetyl-CoA derived from carbohydrates, fats, and proteins

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19
Q

Lysosomes

A

Digestive enzymes

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20
Q

Proteosomes

A

Proteases that break down proteins tagged by ubiqutin

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21
Q

Mesoderm

A

Gives rise to skeletal muscles, smooth muscle, blood vessels, bone, cartilage, joints, connective tissue, endocrine glands, kidney cortex, heart muscle, urogenital organ, uterus, fallopian tube, testicles, and blood cells from the spinal cord and lymphatic tissue

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22
Q

nucleolus

A

structure within the nucleus; site of ribosome biogenesis

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23
Q

oxidative metabolism

A

aerobic metabolism

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24
Q

parenchyma

A

the functional tissue of an organ, as distinguished from the connective and supporting tissue

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25
Q

stroma

A

the supportive tissue of an epithelial organ, consisting of connective tissue and blood vessels

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26
Q

polyribosomes

A

polysomes: a group of ribosomes bound to an mRNA molecule

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27
Q

glycogen

A

polysaccharide store of carbohydrates

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28
Q

microtubules, microfilaments and intermediate filaments size

A

microtubules > intermediate filaments > microfilaments

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29
Q

peroxisomes

A

helps convert molecular oxygen to h2o2

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30
Q

phagosomes

A

a vacuole containing a phagocytosed particle

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31
Q

percentage of cell that is water

A

85

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32
Q

globular protein molecules

A

receptors, adhesion molecules, ion channels

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33
Q

extracellular matrix on which the epithelium sits

A

basal lamina

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34
Q

function of basal lamina

A

anchors cells to the extracellular matrix

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35
Q

contents of extracellular matrix

A

proteins, carbohydrates, electrolytes

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36
Q

junctional complexes

A

gap junctions (allow exchange between cells), desmosomes and occluding junctions

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37
Q

how cancer cells spread easily (metastacize)

A

they lack junctional complexes, so they detac more easily and spread throughout the body

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38
Q

ph of cytoplasm

A

slightly basic, retains acidic dyes (acidophilia)

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39
Q

lifespan of mitochondri

A

1-10 days

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40
Q

membrane of mitochondria

A

double membrane with inner leaf called cristae

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41
Q

enzymes along the cristae

A

oxidases, reductases, dehydrogenases

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42
Q

function of smooth ER

A

contains enzymes such as P450, metabolic degredation of drugs, hormones, and steroid metabolism

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43
Q

ER stress reaction

A

proteins begin to misfold, so their production is stopped and they begin to be degraded

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44
Q

products of golgi

A

glycoproteins and lipoproteins, secretions

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45
Q

secondary lysosomes

A

lysosomes fused with damaged organelles

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46
Q

autophagy

A

the process by which lysosomes degrade damaged organelles

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47
Q

lipofuscin

A

lipid-rich brown pigment present in residual bodies digested by liposomes

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48
Q

abnormalities in synthesis of enzymes normally present within lysosomes

A

lysosomal storage diseases

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49
Q

secondary system to degrade intracellular components

A

ubiquitin proteasome system

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50
Q

composition and function of microtubules

A

tubulin, contraction and scaffold

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51
Q

examples of microfilament proteins and function

A

actin and myosin; transport, cell division, motility

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52
Q

examples of intermediate filament proteins and function

A

keratins, desmin, gfap, neurofilaments; structure and transport

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53
Q

condensed chromatin

A

heterochromatin: supercoiled

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54
Q

divided chromatin

A

euchromatin

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55
Q

pyknosis

A

shrinkage and wrinking of the nucleus

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56
Q

fragmentation of the nuycleus

A

karyorrhexis

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57
Q

fading of nucleus

A

(karyoloysis)

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58
Q

cachexia

A

weakness and wasting of the body due to illness

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59
Q

degree of differentiation- well differentiated

A

the neoplastic cell simulates its parent or progenitor cell

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60
Q

degree of differentiation - poorly differentiated

A

the neoplastic cell is bizarre or deformed

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61
Q

clinical grade

A

low grade cancer cells spread more slowly than high grade

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62
Q

hematogenous spread

A

cells of a primary tumor penetrate into blood vessels

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63
Q

lymphatic spread

A

common in carcinomas but not in sarcomas

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64
Q

carcinomas

A

most common type of cancer, develop in epithelial or endothelial cells, which cover the internal organs and outer surfaces of the body (skin, mucous membranes

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65
Q

sarcomas

A

develop from mesenchymal cells: bones, blood vessels, cartilage, nerves, muscles, fat, joints, tendons, ligaments

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66
Q

adenocarcinoma

A

effects organs that produce fluids or mucous such as breasts or prostate; adenocarcinoma of the breast

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67
Q

basal cell carcinoma

A

affects the cells that form foundation of outer layer of skin

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68
Q

transitional cell carcinoma

A

affects transitional cells in the urinary tract, such as bladder, kidneys, and ureter

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69
Q

palliation

A

easing the severity of pain or disease without removing the cause

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70
Q

paraneoplastic effects

A

WBC attacks nervous system,: difficulty walking, swallowing, coordination, slurred speech, memory problems

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71
Q

tumor markers

A

substances found in higher than normal levels in the blood

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72
Q

benign neoplasms

A

lack the capacity to metastacize, but may kill patient if in a critical place, termed behavioral or positional malignancy

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73
Q

incorrectly called fibroids

A

leiomyomas (smooth muscle) of the uterus

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74
Q

suffix for benign neoplasms

A

tissue type + -oma: except melanoma, glioma, hepatoma (malignant), hematoma (swelling of blood) Example: fibroadenoma of the breast

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75
Q

incidence

A

number of new cases over a given time

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76
Q

prevalence

A

number of cases within a given population

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77
Q

etiology

A

cause of a disease or condition

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78
Q

dysplasia

A

loss of uniformity of cells or architecture

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79
Q

pleomorphism

A

variability of cell shape and size

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80
Q

anaplasia

A

loss of normal differentiation

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81
Q

aneuploidy

A

when the number of chromosomes is not a multiple of the haploid state

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82
Q

metastasis

A

spread of a malignancy to a distant site

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83
Q

Neoplasia:neoplasm

A

a new formation: abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of the normal tissues and persists in the same excessive manner after the stimulus is removed (autonomous)

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84
Q

lipoma

A

benign tumor of fat cells

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85
Q

naming neoplasias are based on

A

the embryologic origin of the tissue

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86
Q

endodermal benign tumor

A

adenoma of … breast, liver

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87
Q

Future classification of tumors

A

may be by the molecular pathway

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88
Q

do benign tumors ever metastasize

A

NO

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89
Q

histology of benign tumors

A

relatively normal

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90
Q

Stage 0

A

In situ cancer

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91
Q

Stage 1

A

Cancer confined to primary site

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92
Q

Stage 2

A

Cancer invasion locally

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93
Q

Stage 3

A

Cancer invades local nodes or vessels

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94
Q

Stage 4

A

Metastasis

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95
Q

Cancer staging performed by

A

Surgeon and Pathologist

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96
Q

TNM Staging

A

Tumor: primary site Node: extent of nodal involvement Metastasis: extent of metastatic spread (not used for hematopoietic and CNS cancers)

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97
Q

prefix c

A

clinical staging

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98
Q

prefix y

A

pathological staging

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99
Q

prefix r

A

recurrence or retreatmet

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100
Q

Cancer grade is done by

A

pathologist; a supplement to staging

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101
Q

G1

A

well differentiated

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102
Q

G2

A

moderately well differentiated

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103
Q

G3

A

poorly differentiated

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104
Q

G4

A

anaplastic (G3 and G4 are often combined)

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105
Q

a cancer that has not invaded the basal lamina

A

carcinoma in situ

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106
Q

what are the 3 steps of tumor invasion

A

attachment, dissolution, locomotion

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107
Q

what attaches the tumor cell to the basement membrane

A

lamanin

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108
Q

what breaks down the surface of basement membrane

A

Type IV collagenase

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109
Q

what is locomotion

A

when the tumor starts to diapedese through the basement membrane

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110
Q

carcinomas tend to spread

A

via lymphatic tissues

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111
Q

sarcomas tend to spread

A

via blood vessels

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112
Q

cancers may be spread

A

by either pathway

113
Q

iatrogenic manipulations

A

physician induced manipulations (needle biopsy can spread the metastasis)

114
Q

catastrophic hemmorage

A

when a major artery or vein is invaded and ruptures

115
Q

cachexia

A

loss of weight, wasting

116
Q

anaplasia

A

loss of function or features of a tissue

117
Q

Cachexia defined as

A

loss of 5% of pre-illness weight in 6 months

118
Q

What accounts for 80% of breast cancers

A

Invasive ductal adenocarcinoma

119
Q

How do the breasts connect to the lymphatics

A

360 degrees, axillary nodes, etc. The drainage is characteristic of where the tumor arises, many tumors are from the upper outer quadrant and drain to the axilla

120
Q

Critical point in treatment of breast cancer

A

Number of nodes: No nodes 85-95% survival >9 nodes = high mortality 0-1 node = lumpectomy or simple mastectomy

121
Q

Most important predictor in TNM

A

M1: metastasis

122
Q

What is a targeted therapy based on Estrogen receptor positive cells

A

oophorectomy and tamoxifen (reduces estrogen)

123
Q

In ER- patients what is the treatment

A

chemotherapy (methotrexate, adriamycin), biologics

124
Q

Her2 + tumors

A

receive herceptin + chemo

125
Q

what is triple negative and what is the treatment

A

ER, HER, Prolactin; combination of surgery, chemo, radiation

126
Q

What are determinants of treatment success

A

Type of tumor, grade and stage, metastasis, Influence the psychological state of the patient in counseling on these medications Tumor doubling time, patients health and attitude, quality of treatment facility, appropriateness of treatment protocol, complications

127
Q

Every type of cancer goes through this process

A

TNM and molecular characterization

128
Q

Positional malignancy

A

benign tumors growing in the wrong area`

129
Q

teratoma

A

benign tumor in utero where all 3 germ layers are present

130
Q

Total blood volume adult male

A

5L

131
Q

What is the composition in blood by number of cells in descending order

A

Erythrocytes, Platelets (thrombocytes), Leukocytes (Neutrophils, Eosinophils, Basophils), Lymphocytes, Monocytes and Macrophages

132
Q

What are the other components of blood

A

Albumin, Globulins, Fibrinogen, Salts (phosphates and bicarbonates), Metabolites (glucose, fats, aas, Water

133
Q

What is albumin and what are low levels indicative of

A

Albumin is a protein made by your liver. Albumin helps keep fluid in your bloodstream so it doesn’t leak into other tissues. It is also carries various substances throughout your body, including hormones, vitamins, and enzymes. Low albumin levels can indicate a problem with your liver or kidneys.

134
Q

What are globulins

A

The globulins are a family of globular proteins that have higher molecular weights than albumins and are insoluble in pure water but dissolve in dilute salt solutions. Some globulins are produced in the liver, while others are made by the immune system.

135
Q

What is fibrinogen

A

Fibrinogen (factor I) is a glycoprotein complex, made in the liver, that circulates in the blood of all vertebrates. During tissue and vascular injury, it is converted enzymatically by thrombin to fibrin and then to a fibrin-based blood clot. Fibrin clots function primarily to occlude blood vessels to stop bleeding.

136
Q

What are zymogens?

A

They act in the blood clotting cascade. They are pro-enzymes that are activated by cleavage. Reduced Vitamin K (GLA) is needed for phospholipid and calcium binding and hence the activation

137
Q

How many oxygens are carried and delivered by hemoglobin

A

Carry 4 oxygens and deliver 1

138
Q

What is hemocrit

A

The volume % of RBC in blood

139
Q

What is the difference between Hb and hemocrit

A

Hemoglobin is a protein in red blood cells and hematocrit is a measurement of the amount of red blood cells as related to total blood cell count.

140
Q

How many hemoglobins in RBC

A

approx 270m

141
Q

Reticulocyte

A

An immature RBC

142
Q

Corpuscular hemoglobin

A

The mean corpuscular hemoglobin , or “mean cell hemoglobin” (MCH), is the average mass of hemoglobin (Hb) per red blood cell (RBC) in a sample of blood. MCH is diminished in hypochromic anemias

143
Q

RBC distribution width

A

The difference from largest to smalles RBC

144
Q

Role of spleen in RBC

A

Removes old RBC, holds a reserve of blood, recycles iron

145
Q

Functions of the blood

A

•Respiratory gas exchange •Regulatory activity •Metabolic regulation •Hormone transport eg insulin, thyroid, glucuocorticoids,sex hormones, and many more •Maintenance of pH in tissues •Regulation of body temperature •Nutritive function •Excretion of metabolic endproducts •Immunological function

146
Q

Anemia

A

decrease in erythrocytes; reduction below normal limits of the total circulating red cell mass

147
Q

Leukopenia

A

decrease in leukocytes

148
Q

Neutropenia

A

decrease in neutrophils

149
Q

Granulocytopenia

A

agranulocytosis, decrease or lack of granulocytes

150
Q

Lymphocytopenia

A

Decrease in lymphocytes

151
Q

Thrombocytopenia

A

Decrease in platelets

152
Q

Pancytopenia

A

Decrease in red cells, white cells, and platelets

153
Q

Developmental hematopoiesis aspects

A

Early embryo all red cells derive from the yolk sac then migrate to the liver for the rest of development, and in the last few weeks it shifts to the bone marrow

154
Q

Utilized bone marrow in adults

A

1/3

155
Q

Ferritin

A

Ferritin is a universal intracellular protein that stores iron and releases it in a controlled fashion.

156
Q

Transferrin

A

Transferrin are glycoproteins found in vertebrates which bind to and consequently mediate the transport of Iron through blood plasma. It is produced in the liver and contains binding sites for two Fe³⁺ atoms.

157
Q

Ferritin v transferrin

A

Ferritin is stored in the body’s cells until it’s time to make more red blood cells. The body will signal the cells to release ferritin. The ferritin then binds to another substance called transferrin. Transferrin is a protein that combines with ferritin to transport it to where new red blood cells are made.

158
Q

Stem cells vs progenitor cells

A

The most important difference between stem cells and progenitor cells is that stem cells can replicate indefinitely, whereas progenitor cells can divide only a limited number of times. Progenitor cells have a tendency to differentiate into a specific type of cell

159
Q

All blood cells are derived in the ___ from ___

A

blood marrow; pluripotent hematopoietic stem cell

160
Q

Multilineage hematopoietic growth factors

A

Stem cell factor, IL1,3,6,11; GM-CSF; useful in pancytopenia

161
Q

Lineage specific growth factors

A

Erythropoietin, thrombopoietin, C-CSF/M-CSF, IL5,15,7

162
Q

Three main causes of anemia

A

Hemorrhage, inc hemolysis, dec hematopoiesis

163
Q

Signs and symptoms of anemia

A

Fatigue, pallor, malaise, poor concentration, dyspnea upon exertion, increased cardiac output (palpitations, sweat, heart failure), pica (appetite for non-nutritive substances)

164
Q

Diagnosis of anemia

A

CBC (complete blood counts): RBC level, shape and size, Hb level Reticulocyte count Assessment of ESR (erythrocyte sedimentation rate), ferritin, serum iron, B12, renal func Bone marrow examination

165
Q

Higher than normal reticulocytes may mean

A

hemolytic anemia

166
Q

Lower than normal reticulocytes may maean

A

iron deficiency anemia, aplastic anemia (bone marrow doesn’t make enough blood cells), pernicious anemia (B vitamins)

167
Q

MCV

A

mean corpuscular volume (average size and volume of RBC) (% hemocrit*10/RBC count)

168
Q

Anemia Size Based

A

Microcytic, Normocytic (w/ high or low retic count), Macrocytic

169
Q

Acute blood loss anemia results in

A

Shock, hemodilution on fluid replacement, erythrepoietin induction, normocytic with higher than normal reticulocyte count

170
Q

Chronic blood loss is only an anemic issue

A

If production outstrips production

171
Q

Mechanism and effect of hemolytic anemias

A

RBCs removed by mononuclear phagocytes in the spleen; shortened RBC life span

172
Q

Accumulation of catabolites in hemolytic anemias

A

bilirubin and Fe

173
Q

Anemia causes a marked increase in

A

red marrow (hematopoiesis) , accumulation of bilirubin and fe

174
Q

3 types of intravascular hemolysis

A

Trama, toxic, complement (autoimmune)

175
Q

hemoglobinemia

A

excess of hemoglobin in the blood plasma

176
Q

hemoglobinuria

A

presene of Hb in the urine

177
Q

Jaundice

A

skin turns yellow due to high level of bilirubin, common in anemia

178
Q

extracellular hemolysis occurs when

A

RBCs are wrong, foreign, or have loss of deformability

179
Q

hemosiderinuria

A

hemosiderin in the urine ) iron storage complex when breakdown of heme occurs

180
Q

herditary spherocytosis

A

deficient production of membrane proteins (membranes assume spherical shape and become trapped and destroyed in spleen)

181
Q

G-6-PDH deficiency

A

Failure to use G^P to convert NADP to NADPH, which normally regenerates glutathione (GSH) through the hexose monophosphate shunt, which damages the RBC membrane, which is sensitive to oxidant damage

182
Q

hemoglobinopathies

A

genetic disorders affecting the structure or production of Hb

183
Q

HbA

A

adult hemoglobin, hemoglobin A1 or α2β2

184
Q

HbF

A

Fetal hemoglobin, or foetal haemoglobin (also hemoglobin F, HbF, or α2γ2

185
Q

HbS

A

Sickle cell disease is caused by a variant of the beta-globin gene (causing valine for glutamic acid substitution) called sickle hemoglobin (Hb S) that manifests in homozygotes, manifested as pain and regional anoxia

186
Q

Pulmonary hypertension, a sign of sickle cell

A

Pulmonary hypertension is a type of high blood pressure that affects the arteries in your lungs and the right side of your heart

187
Q

Sickle mutation caues polymerization in which state

A

T state

188
Q

T state Hb

A

deoxyhemoglobin

189
Q

R state Hb

A

oxygenated hemogobin

190
Q

Sickle cell anemia causes damage to other parts of the body such as

A

child development, irregular bone growth and pain, kidney, genetalia, cardiopulmonary damage, retinal vessel damage, leg ulcerations, increased maternity risk

191
Q

Onset of sickle cell anemia can be retarded by

A

hydration, avoid cold, exertion, blood transfusions, infections

192
Q

Thalassemia

A

a group of genetic diseases resulting from impaired synthesis of either globulin chain

193
Q

Thalassemia defects by ethnic group

A

Alpha in asians, beta in meditteranean

194
Q

Major thalassemia

A

Cooley’s anemia; severe cases; homozygotes

195
Q

minor or intermedia thalassemia

A

minor, heterozygotes

196
Q

Effects of thalassemia

A

overgrowth of bone marrow, thin bones and distinctive facial appearance

197
Q

Treatment for thalassemia

A

Transfusion to prolong life into 20s or 30s

198
Q

Resulting from extravascular hemolysis in thalassemia

A

spleen accumulates iron and hypertrophies, treatment is iron chelation and splenectomy; risk of severe infection

199
Q

Genetics of thalassemia

A

there are 2 α and a single β gene, α deletions are common but β deletions are rare; classified as promoter region, chain terminator, or splicing

200
Q

An imbalance in α and β globulins resulting from thalassemia results in

A

erythroblasts dying in bone marrow, few abnormal cells leave containing unbound aggregates of “normal” globulins, which are hypochromic and destroyed, leading to increased ironabsorption in spleen and iron overload

201
Q

what monitors blood volume and quality

A

kidneys; release EPO (erythropoietin) that stimulates the bone marrow

202
Q

erythropoietic cells come from this bone marrow tissue

A

myeloid

203
Q

megakaryocytes make

A

platelets

204
Q

lifespan of erythrocyte

A

3-4 months

205
Q

how long it takes to replenish RBCs

A

2-3 weeks

206
Q

Causes of immunolytic anemias

A

sometimes autoimmune, sometimes drug induced

207
Q

cause of immunohemolytic anemias

A

antibodies or complement attaching to RBC and inducing hemolysis

208
Q

What is the test for immunohemolytic anemia

A

coombs antiglobulin test: RBC mixed within heterologous antisera for IgG and complement to detect agglutination

209
Q

warm antibody; mediated by

A

IgG mediated, Warm antibody hemolytic anemia is the most common form of autoimmune hemolytic anemia. It is defined by the presence of autoantibodies that attach to and destroy red blood cells at temperatures equal to or greater than normal body temperature. seen with lupus (SLE) and lymphoma; also assoc penicillin and antimethyldopa

210
Q

Cold agglutinin; mediated by

A

IgM, associated with infection and lymphoma

211
Q

cold hemolysin

A

acute intravascular hemolysis following cold exposure, or infection

212
Q

Erythroblastosis fetalis immunological factor and cause

A

Rh; mother is Rh negative and infant Rh positive; red cells from infant migrate to mother who develops antibodies which then migrate to the child which cause agglutination, hemolysis

213
Q

treatment and prevention of erythroblastic fetalis

A

infant is tranfused with fresh blood after birth; RhoGAM given at pregnancy and prior to birth to inhibit Rh antibody production

214
Q

What are examples of trauma leading to trauma induced anemia

A

cardiac valve prosthesis, narrowing or obstruction of microvasculature caused by disseminated intravascular coagulation, malignant hypertension, SLE

215
Q

Burr, helmet, and triangle cells are characteristic of

A

RBC fragments in trauma induced anemia

216
Q

Effect of CO odorless gas on RBC

A

Binds to hb 200-300x more than O2; locks Hb in R state

217
Q

Carboxyhemoglobin COHb results in this color

A

Cherry red

218
Q

Exposure to low level CO

A

headaches

219
Q

40% HbCO effect

A

impaired vision, tachycardia, hyperpnea

220
Q

60% HbCO effect

A

coma and death

221
Q

Treatment for CO poisoning

A

100% O2, control blood pH

222
Q

CO reacts with

A

all heme proteins, CYP450, cytochrome oxidase

223
Q

MetHb is hemoglobin in which

A

the iron is oxidized from Fe2+ to Fe3+ and thus cannot bind and transport O2

224
Q

How MetHb is formed

A

Nitrites or hydroxylamines react with Hb to form MetHb

225
Q

Sign of methemobloginememia

A

anoxia, ash blue complexion

226
Q

when metHb loses the heme group the globin is

A

denatured to form Heinz bodies

227
Q

Sign of megaloblastic anemia

A

many RBCs are macrocytic and hyperchromic, large neutrophils, marrow is hypercellular

228
Q

Hypercellularity in megaloblastic anemia is a response to

A

increased growth factors (EPO)

229
Q

Proerythroid cells in megaloblastic anemia

A

apoptose

230
Q

Cobalymin is a key factor in

A

methylation

231
Q

Cobalymin is critical for

A

neurological development

232
Q

Vitamin b12 is stored

A

in the liver

233
Q

vitamin b12 can only be absorbed from the gut after

A

complexing with glycoprotein intrinsic factor

234
Q

first step in methylation

A

cobalymin interacts with tetrahydrofolate to produce methylcobalymin

235
Q

diet and absorption of iron

A

10-15 mg/day in diet; 5-10% absorbed

236
Q

absorption of iron increased by

A

low levels, menstruation, pregnancy; regulated by absorption

237
Q

Storage sites of iron

A

intestinal epithelial cells, macrophages, spleen, hepatocytes

238
Q

iron is used in

A

erythroid precursors in bone marrow

239
Q

iron is transported in the blood by

A

transferrin

240
Q

storage and usage of iron is balanced by

A

ferritin/transferrin synthesis

241
Q

what is the most common cause of anemia

A

iron deficiency

242
Q

Lack of iron leads to insufficient and this type of anemia

A

Hb; microcytic hypochromic anemia

243
Q

Free iron is

A

toxic

244
Q

Ferritin and apoferritin

A

iron storage protein

245
Q

Transferrin receptor, divalent metal ion transproter, ferroportin 1

A

transports iron across membrane, part of iron hanling network

246
Q

Pancytopenia can be either

A

acquired or inherited

247
Q

What are the 3 phases of coagulation

A

Vascular phase, platelet phase, coagulation phase

248
Q

Hemostasis

A

cessation of bleeding from a cut or severed vessel

249
Q

Thrombosis is initiated when

A

endothelium is damaged or removed

250
Q

Thrombosis

A

local coagulation or clotting of the blood

251
Q

platelets accumulate and aggregate at the site of blood vesel injury to form the

A

primary hemostatic plug

252
Q

Platelets cause activation of

A

coagulation factors which eventually induce fibrin formation which reinforces the clot

253
Q

Fibrinolysis (thrombolysis)

A

dissolution and removal of the clot when damage is repaired

254
Q

What happens in the vascular phase of coagulation

A

Vessel constriction (Hemostasis only) and recruitment of platelets and coagulation factors (Thromboplastin/tissue factor - extrinsic; Collagen/Kallikrein - intrinsic)

255
Q

What happens in the platelet phase

A

Ca2+ induced alteration in platelet shape and ultimately activation of thrombin leading to fibrinogenolysis

256
Q

What happens in the coagulation phase

A

Fibrinogen is cleaved and then polymerizes by thrombin to form clot containing platelets, cells and debris

257
Q

What is the general process of clot formation

A

Cascade of protease function leads to zymogen activation>prothrombin>thrombin>converts fibrinogen to fibrin

258
Q

Zymogen

A

pro-enzymes activated by cleavage, (GLA domain mostly glutamate which is gammacarboxylated) by vitamin k in order to activate

259
Q

The clot formation cascade comes through either

A

Intrinsic or extrinsic pathways leading to factor Xa causing Ca2+ induced conversion of prothrombin to thrombin, which turn fibrinogen to fibrin

260
Q

What is a coagulation factor of the intrinsic pathway

A

Collagen/Kallikrein

261
Q

What is a coagulation factor of the extrinsic pathway

A

Thromboplastin (Tissue Factor TF)

262
Q

Collagen, thrombin, etc binds to receptors on platelets which

A

activates other platelets and causes them to bind fibrinogen, calcium makes the platelet sticky

263
Q

Activation of platelets is highly metabolic which generates

A

ADP which is another platelet activator

264
Q

Platelets are also involved in the conversion of

A

prothrombin to thrombin

265
Q

Fibrogen structure consists of

A

α β + λ chains

266
Q

Fibrinopeptide A and B

A

keep fibrinogen together; when it is cleaved, the fibrin monomers will cross link together, and transglutaminase secures the link, which is irreversible

267
Q

Clots are dissolved with

A

plasmin, which recognizes the coiled coil domain and dissolves them

268
Q

Plasminogen

A

is converted to plasmin by t-PA (PAI 1-2 inhibitors)

269
Q

reduced vitamin K is a factor for

A

λ glutamyl carboxylase, which creates functional zymogens

270
Q

Warfarins are inhibitors of

A

Vitamin K reductase

271
Q

What happens in fragility of the vessel wall

A

activators leak into the vasculature such as tissue factor

272
Q

What causes fragility of the vessel wal

A

infections>meningococcemia, drug reactionsleading to immmune complex deposition, impaired vascualar collagens - scurvy, amyloid infiltration

273
Q

thrombocytopenia

A

not enough platelets, no primary plug

274
Q

causes of thrombocytopenia

A

HIV, aplastic anemia, b12 def, leukemias, sequestration (splenomegaly)

275
Q

what causes decreased platelet survival

A

immune destruction, sle, pregnancy

276
Q

disseminated intravascular coagulation

A

a stimulus/trauma causes extensive release of tissue factor, which leads to too many clots/thrombosis: reduces ability to form clots as needed

277
Q

Bernard-Soulier syndrome

A

autosomal genetic disorder relted to loss of vWF response

278
Q

Drug mediated platelet functionality

A

Aspirin or other COX inhibitors

279
Q
A