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SUM'20 - Anatomy & Physiology > Hematology - Amanda > Flashcards

Hematology - Amanda Flashcards

1
Q

components of whole blood (and their %) are:

A
  • Plasma 55%
  • Erythrocytes 45%
  • <1% “buffy coat”: leukocytes and PLTs
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2
Q

What are we actually looking at for HCT?

A

erythrocytes

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3
Q

Of the plasma, what are the elements of it? (%)

A
  • Water 91%
  • Proteins 7%
  • other solutes 2%
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4
Q

Examples of plasma proteins (3)

A
  • Albumins (58%)
  • globulins (38%)
  • Fibrinogen (4%)
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5
Q

Globulins role:

A

is in defense

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6
Q

Fibrinogen role:

A

clotting protein

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7
Q

What elements make up the HCT?

A

Erythrocytes (~5million!!)
PLTs
Leukocytes

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8
Q

Name the different Leukoctyes: (5)

A
  1. Neutrophils
  2. Lymphocytes
  3. Monocytes
  4. Eosinophils
  5. Basophils
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9
Q

Most common leukocyte is

A

neutrophil (60-70%)

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10
Q

[blood] serum = (equation)

A

plasma - clotting factors

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11
Q

normal HCT for men

A

40-45%

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12
Q

normal HCT for females

A

35-40%

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13
Q

rates of RBC production in the bone do what with age?

A

decline in many bones

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14
Q

In early age, what bones are producing RBC’s?

A

all bones do

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15
Q

feature of immature cells:

A

they’re BIG

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16
Q

immature cells are found in

A

the bone marrow

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17
Q

mature cells are found in

A

the blood stream

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18
Q

immature cells are called

A

blast cells

-proerythroblast, lyphoblast, myeloblast, monoblast, megakaryoblast

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19
Q

a baby RBC is:

A

reticulocyte

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20
Q

Mature RBC’s are

A

erythrocytes

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21
Q

pluripotent hematopoietic stem cell (PHSC) is

A

what multiple forms of different blood cells are formed from in the bone marrow

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22
Q

3 functions of RBCs

A
  1. transport hgb
  2. transport O and CO2
  3. Acid-base buffer - pH control
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23
Q

Normal MCV =

A

90-95 mm^3

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24
Q

Erythrocytes/RBCs are missing what?

A

nucleus

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25
Q

w/o a nucleus, what can’t a RBC do?

A

replicate / divide

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26
Q

life span of RBC

A

120 days

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27
Q

Daily production and destruction rate of RBC:

A

1% produced/destroyed each day

**2 million/sec

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28
Q

what enzyme is important for CO2 transport in the plasma

A

carbonic anhydrase

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29
Q

Production of RBC intrauterine is in

A

liver
spleen
lymph node

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30
Q

production of RBC <5yo in

A

all bones

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31
Q

production of RBC > 20 years

A

vertebra, sternum, ribs, and hipbone

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32
Q

erythropoietin is released from:

it does what?

A

kidneys (90%) and liver (10%)

-regulates RBC production/ stimulates in bone marrow

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33
Q

what stimulates release of erythropoietin?

A

hypoxemia

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34
Q

what vitamins are required for rbc maturation?

A

B12 and folic acid

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35
Q

macrophages destroy old rbc’s by ____.

A

phagocytosis

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36
Q

HB is excreted as ___.

Iron is released to ___.

A
  • bilirubin

- transferrin

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37
Q

low levels of b12 and folic acid will show what in labs

A

more immature rbc’s

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38
Q

Hypoxia stimulates rbc production… name two other examples/causes of stimulation

A
  • high alt

- copd

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39
Q

negative feedback control in RBC production does what

A

inhibits the stimulation release of erythropoietin

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40
Q

when rbc production is stimulated, production increases within how many hours?

when will we see an increase in the count?

A
  • 24hrs

- 5 days

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41
Q

disease processes associated with reduced erythropoeitin response (anemia):

A
  • infections
  • AIDS
  • Hypothyroidism
  • Renal Disease
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42
Q

body stores Iron in:

A
  • Hb (65%)
  • liver
  • spleen
  • bone marrow
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43
Q

intracellular iron is stored in protein -iron complexes such as

A

Ferritin and hemosiderin

**stores are also low in anemia

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44
Q

circulating iron is loosely bound to the transport protein

A

Transferrin

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45
Q

the “graveyard” of RBCs is the

A

spleen

*Old RBC’s get rigid/less flexible and get TRAPPED in the spleen

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46
Q

macrophages engulf dying erythrocytes and

A

separate Heme and globin. Iron is salvaged for reuse

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47
Q

heme is degraded to

A

bilirubin

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48
Q

the liver secretes bilirubin into the intestines as bile and metabolize it into

A

urobilinogen

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49
Q

degraded pigment leaves the body in the feces is called

A

stercobilin

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50
Q

Globin is metabolized into

A

amino acids –> released into circulation

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51
Q

Hb released into the blood stream is captured by

A

haptoglobin and phagocytized by macrophages

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52
Q

Fe++

A

iron

“2 for us”

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53
Q

Fe+++

A

ferrous form

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54
Q

Heme (biliverdin) is

A

free bilirubin

  • insoluble in water
  • toxic to CNS
  • transported by albumin
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55
Q

Free bilirubin is removed from the blood by

A

the liver

-conjugated w/glucuronate and excreted in bile (not urine)

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56
Q

in the intestine, bacteria convert conjugated bilirubin to

A

urobilinogen (soluble)

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57
Q

some urobilinogen is REABSORBED into the blood and excreted as

A
  • urobilin in the urine

- stercobilin in feces

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58
Q

daily iron need

A

7mg/1000cal

~10% is absorbed

59
Q

iron absorption is INHIBITED by

A
  • oxalates (spinach, rubarb)
  • phosphates (vegetables)
  • tannate (tea)
  • carbonates
  • clay
60
Q

major site of iron absorption

A

duodenum and proximal jejunum

*HCl promotes absorption

61
Q

average daily loss for man and woman

A

men: 1mg/day
women: additional 14mg/period lost

62
Q

what process puts a higher demand on iron requirments?

A

pregnancy

63
Q

Transferrin has how many iron binding sites

A

2

64
Q

transferrin is responsible for

A

the pink color of plasma

65
Q

TIBC =

A

total iron binding capacity = 300 ug/ml

** this is less with disease

66
Q

ferritin accounts for how much total “strorage iron”

A

30%

67
Q

what is Hemosiderin? cause

A

Very high iron level
-can lead to multi-organ failure

  • typically r/o excessive blood transfusion
68
Q

hemoglobin consists of glboin (2 alpha, 2 beta polypeptide chains) and four heme groups. when all four heme groups are filled with iron, this =

A

100% saturated

69
Q

heme moiety-iron containing

A

porphyrin

70
Q

Fe++ binds to

A

O2

71
Q

Adult HbA =

A

Alpha2 and beta 2

72
Q

HbF has an increased affinity for O2. HbA facilitates the O2 movement from mother to fetus and:

A

a LEFT shift

more O2 loading

73
Q

methemoglobin is

A

iron in the ferric form Fe+++

-presentation seen as gray-blue discoloration in pts fingernails

74
Q

methemoglobin does not bind to O2 as readily, but has an increased afffinity for

A

CN-
cyanide

*resulting in defective O2 transpot = low o2 sat

75
Q

Causes of MetHgb:

A
  • Nitrates
  • Benzocaine
  • Prilocaine metabolites
76
Q

tx for methgb:

A

iv methylene blue

*converts ferric to ferrous form

77
Q

Causes for cyanide poisoning

A
  • Nitroprusside (CN ions released)
  • bitter almond oil
  • KCN (potassium cn)
  • wild cherry syrup
78
Q

s/s of CN poisoning

A

Tachy, hypotension, coma, acidosis, Increased venous O2,

–leads to rapid death

79
Q

Tx CN poisioning

A
  1. Sodium Nitrite and Amyl Nitrites to oxidize Hb to metHb (inducing metHb)
  2. the metHb binds to cyanide allowing cytochrome oxidase enzyme to go free and function (do its job)
  3. Use Thiosulfate to bind to cyanide - forming thiocynate which is excreted by kidneys
80
Q

Porphyrias are conditions of

A

(congenital) defective heme synthesis that leads to :
1. accumulation and
2. increase excretion of heme precursors (porphyrins)

81
Q

What environment element, if exposed, can cause similar condition (porphyria)

A

Lead

82
Q

Contraindications with porphyrias

A
  • Benzo’s
  • barbiturates

*should avoid these in any pt w/porphyrias

83
Q

Presenting Symptoms:
microcytic anemia, MR, HA, memory loss, demylination in adults

Condition and Affected enzyme:

A
  • Lead Poisoning

- Ferrochelatase

84
Q

Presenting Symptoms:
Painful abd, pink urine, Polyneuropathy, Psychological disturbance, Precipitated by durgs

Condition and Affected enzyme:

A
  • Acute Intermittent Porphyria

- Uroporphyrinogen-I-synthase

85
Q

Presenting Symptoms:
Blister, photosensitivity. most common porphyria

Condition and Affected enzyme:

A
  • Porphyria Cutanea tarda

- Uroporphyinogen decarboxylase

86
Q

most common porphyria

A

Porphyria Cutanea tarda

87
Q

porphyria’s essentially mean…

A

defective heme

88
Q

5 types of anemias

A
  1. Microcytic hypochromic anemia
  2. Macrocytic Anemia
  3. Hemolytic Anemia
  4. Hemoglobinopathies
  5. Aplastic Anemia
89
Q

presenting Hct and Hgb < what in male vs female

A

Male: < 12.5 g/dl and 40%
Women: <11.5 g/dl and 36%

90
Q

compensatory mechanisms to increase O2 delivery:

A

Increases in:

  • CO
  • 2,3 DPG
  • p50
  • Plasma Vol

Decrease in: blood viscosity (to improve bf)

91
Q

anemia shift O2-hb cure to

A

the RIGHT

92
Q

Definitive Diagnostic for anemia:

A

Blood Smear

-also get h/h, reti index, and RBC indices

93
Q

In a normal blood smear, the seen WBC’s have how many lobes

A

3

<6 is not abn

94
Q

Describe smear image of Microcytic Hypochromic cells

A

-small, pale cells, central white, almost colorless

95
Q

Microcytic Hypochromic anemia is known as

A

iron def. anemia

96
Q

Describe smear image of Macrocytic cells

A

Big cells , central white is almost diminished
- WBC is even bigger and have 6 lobes
(6+ is abn)

97
Q

Describe smear image of Sickle Cell anemia cells

A

you’ll see sickled cells

98
Q

MCV in MICROCYTIC HYPOCHROMIC Anemia

A

<80 fl

99
Q

tx for MICROCYTIC HYPOCHROMIC Anemia

A

if iron deficient:
- iron and rbc’s

chronic anemia: (RA, lupus, ca)
- tx underlying cause

100
Q

classic features of MICROCYTIC HYPOCHROMIC Anemia - iron deficient

A
  • iron deficient anemia
  • MCV < 80fl
  • HIGH TIBC (Increased Ferritin, Increased Serum Iron
101
Q

classic features of MICROCYTIC HYPOCHROMIC Anemia - chronic

A

Low TIBC (Increased Ferritin, Increased Serum Iron

102
Q

Iron deficiency anemia

Causes

A
  • Almost always due to blood loss e.g. menstrual loss, GI loss
  • Dietary deficiency
  • Breast feeding ( decreased iron) ,
  • pregnancy ( increased requirement)
  • Defective absorption of iron
  • decreased Heme synthesis
103
Q

“small pale cells”

A

Hypochromic microcytic

104
Q

male pts with iron def anemia, what do we assume?

A
  • bleeding
  • always colon cancer until r/o.

“he has it until we prove he doesn’t”

105
Q

Impaired utilization of iron and diminished response to erythropoietin

A

Anemia of chronic disease

106
Q

Low TIBC, Increased Ferritin, decreased serum iron

A

chronic anemia

107
Q

clinical features of iron deficiency anemia

A 
Pallor Hb < 7g/dl)
Fatigue, generalize weakness
Dyspnea on exertion
Orthostatic lightheadedness
Hypotension if acute
108
Q

Defective DNA synthesis due to folate or Vit B12 deficiency= (type of anemia)

A

megaloblastic anemia

109
Q

Macrocytic anemia (aka)

A

megaloblastic anemia

110
Q

reasons for megaloblastic anemia

A
  • B12 deficiency
  • Lack of Intrinsic factor
  • folate deficiency
111
Q

how and where is b12 absorbed

A
  • b12 binds to IF
  • absorbs in the terminal ileum
  • stored in liver for 3-4 yrs
112
Q

in terminal ileitis like crohn’s disease, what kind of anemia do you likely have?

A

megloblastic anemia/ b12 deficiency

113
Q

most common cause of B12 deficiency

A

pernicious anemia

- lack of IF

114
Q

s/s of this are similar to b12 deficiency w/o the NEUROLOGICAL SYMPTOMS

A

folate deficiency anemia (macrocytic anemia)

115
Q

MCV of Macrocytic anemia

A

> 100 fL

116
Q

Clinical findings of B12 deficiency

A
  • Neurological– paresthesia ,ataxia due to demyelination

- Cerebral and psychiatric manifestation; UMN lesions signs, dementia, incontinence, impotence

117
Q

Clinical findings

Megaloblastic anemia

A

-RBCs– large , oval, fragile

Hypersegmented polys : 6+ lobes “hallmark”

118
Q

“hallmark” finding in megaloblastic anemia

A

6+ lobes of the wbc; hypersegmented polys

** recognize in picture**exam

119
Q

what is the purpose of a Schilling test

A

– if corrects with IF –> pernicious anemia

  • if corrects with antibiotics –> bacterial overgrowth
120
Q

tx of megaloblastic anemia

A
  • Combination of folic acid and Vit B12 for life
  • Folic acid alone should NEVER be given in macrocytic anemia because it will fix the anemia but exaggerate neurological signs and symptoms.
121
Q

how to perform a schilling test

A
  • Intramuscular “flushing dose” of Vit B12 (unlabelled) is given to saturate binding sites
  • Oral radiolabelled VitB12 is given
  • % of radiolabelled VitB12 is measure in 24-hr urine
  • Low urinary excretion (<5%)oflabeled Vit B12supports absorption defect of Vit B12 (+ve Test)
  • Repeat the test with intrinsic factor (IF)
  • High urinary excretion of labeled Vit B12 shows that absence of IF is the cause. [Because Vit B12 needs IF for its absorption]
122
Q

Hemolytic anemia is the result of:

A

RBC membrane defects

  • Hereditary spherocytosis
  • Hereditary elliptocytosis
  • Acanthocytosis (change in shape “spiny” RBCs)
  • Stomatocytosis (deformed RBCs)
123
Q

Spectrin’s role

A

protein that keeps RBCs in shape

124
Q

Spectrin defect

A

hereditary spherocytosis form of hemolytic anemia

125
Q

RBC enzymatic deficiency

A

Glucose-6-phosphate dehydrogenase (G6PD) deficiency

126
Q

Most common enzyme deficiency disorder:

who and how get it?

A

G6PD deficiency

  • 1% of African American,
  • X-linked.
  • Reduce glutathione level
127
Q

in patients with a G6PD deficiency, what medications should be avoided?

A

***Avoid nitroprusside and prilocaine –> cyanide toxicity

Also avoid sulfa, aspirin, penicillin, streptomycin, quinidine, methylene blue –> hemolytic crisis

128
Q

Mismatched blood transfusion
Autoimmune hemolytic anemia

result in what form of anemia

A

hemolytic anemia

129
Q

Direct Coomb’s test is used to distinguish between

A

immune vs. nonimmune mediated RBC hemolysis

130
Q

hereditary spherocytosis looks like on blood smear:

A

small spherical RBCs with lack of central pallor)

– dark purple RBC

131
Q

Hemoglobinopathies include

A

sickle cell anemia

132
Q

sickle cell anemia is a result of:

A

Valine substitutes with glutamine in the 6th position of the beta-hemoglobin chain (HbS)

Distorted RBCs shape like sickle; short life span

133
Q

sickling of the RBC’s greatest complication

A

ischemia!

thrombosis, cvas and infections

134
Q

“autosplenectomy”

A

necrosis of spleen

135
Q

what vaccination’s must pts with sickle cell be sure to get?

**exam

A
  • PNA
  • salmonella

exam

136
Q

Prevention of sickle cell crisis:

A
  • Hydration
  • O2
  • Low PO2 triggers sickling (30-40 mmHg)
  • Maintain high cardiac output
  • Avoid stasis
137
Q

Preop considerations for sickle cell:

A 
Infection control
Hydration
Crit 30-40%
HbA ~ 50%
Partial exchange transfusion
**Avoid hypo or hyperthermia, hypoxemia or hypovolemia
138
Q

Treatment for sickle cell

A

Hydroxyurea (increased HbF) , BMT

HbF interferes formation of HbS

139
Q

Pancytopenia characterized by

A

severe anemia,
neutropenia,
thrombocytopenia

caused by failure or destruction of myeloid (bone marrow) stem cells – “DRY TAP”

140
Q

primary and secondary aplastic anemia

A

Primary
- Idiopathic

Secondary

  • Drugs- chemotherapy (MCC), antibiotics, antidepressants. ethanol
  • Chemical- benzene
  • Radiation, X-ray
  • Malignancy
141
Q

treatment of aplastic anemia

A

Withdrawal of offending agent, BMT

142
Q

thalassemia types

A

Alpha-thelassemia
– Underproduction of -globulin chain

Beta-thelassemia

    • beta-minor vs. Beta-major thalassemia
  • -Common in Mediterranean population (thalassa=sea)
    • Underproduction of beta-globulin chain
  • -Compensatory rise in HbF
  • -Result severe anemia, hepatosplenomegaly
143
Q

treatment of thalassemia

A
  • Packed RBC transfusions

- Folic acid

SUM'20 - Anatomy & Physiology (11 decks)

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