Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Hematology FPP > Anaemia > Flashcards

Anaemia Flashcards

1
Q

What is anaemia

A

Decrease in RBC to a level that’s insufficient for respiration

Or decrease in O2 carrying capacity of blood

Decrease in the Hb conc, to a level where O2 delivery becomes compromised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

When does O2 delivery become compromised in adult Male and female

A

When Hb conc is less than 13g/DL for male
12g/dL for women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

When does O2 delivery become compromised for children

A

When Hb is less than 12g/dL (4-16 yrs)
11g/dL (30days- 6yrs)

13..5g/dL (0-30days)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What volume of O2 does 1g of Hb bind

A

1.34ml of O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

If the Hb conc ie 15g/dL , what’s the volume of O2 that can be carried

A

1.34 (for 1g of Hb) X 15
= 20ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is oxygen tension

A

The amount of O2 present in 100ml of blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the normal O2 tension

A

20ml. (1.34 X 15)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens to O2 tension with reduction in Hb concentration

A

Reduces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What’s the partial pressure of O2 when the O2 tension is 20%

A

100mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What’s the normal Hb conc, O2 tension and partial pressure in 100ml of blood

A

Hb conc: 15g/dL
O2 tension : 20 volume %
Partial pressure of O2: 100mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the partial pressure of O2 in blood if the O2 tension falls from 20-15 volume%

A

It falls from 100mmHg to 40mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When the O2 tension in the artery is 20volume% whats the O2 tension in the veins

A

15volume%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What’s the areterovenous O2 difference

A

5volume%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

In every 100ml of blood, how much O2 is given to tissue and how much is retained

A

5volume% is given to tissue and 15volume% is retained

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

In every 100 ML of blood how much oxygen is given to the tissue and how much is it retained?

A

5ml is given to the tissue and 15ml is retained

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What happens when an individual HB concentration is as low as 10 g/dL

A

The arterial partial pressure would fallen lower than the Venous partial pressure of oxygen hence, the pression gradient that’s allows oxygen to be driven tissue is lost.

If the Hb conc is 10g/dL, that means the O2 tension is 13.4volume% (instead of the normal 20volume% from 15g/dL Hb)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What happens when the Hb conc, the O2 tension and the O2 PP all reduce

A

The body adapts and tries to find a way to get O2 to all the pets of the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the 5 adaptations to anaemia

A

•Modulation Hb/O2 affinity
•CVS adaptive mechanism
•Redistribution of blood flow
•Widen arterovenous O2 difference (by reducing venous O2 tension below 15volume%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What kind of carrier of O2 is Hb

A

A reversible carrier
Binds to O2 at high O2PP but readily parts at low O2PP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is high O2 affinity Hb

A

An abnormal Hb that has excessive affinity for O2

Complex with O2 at high or low PP ma don’t part , hence there could be Hb conc, but low O2 for tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is Low O2 affinity Hb

A

An abnormality where the Hb has excessively low affinity for O2 hence only binds under excessively high PP of O2

The little O2 they have is delivered to tissues but it’s not enough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What happens to the affinity of O2 for Hb in anemia

A

Reduced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What pathway does RBC use to make ATP under normal conditions

A

Glycolytic pathway (Embden-meyerhof)

G3P—1,3DPG—3PG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What happens to O2 when it complexed with Hb

A

Emits a proton (to be acidic, hence in the absence of enough O2, the cytoplasm is alkaline)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

In Anemia, what does the RBC produce

A

Hb instead of ATP

Converting 1,3DPG to 2,3 DPG by 1,3DPG mutase - then from 2,3 DPG TO 3 PG by 2,3 DPG phosphatase Rapport- Luebering shunt
Instead or 1,3DPG to 3PG directly(to produce ATP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What pathway tries to help to pass O2 to tissues in anemic conditions

A

Energy clutch pathway/ Rapport Luebering shunt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What feature of the RBC cytoplasm stimuthates conversion of 1,3DPG to 2,3DPG

A

The alkalinity in anemic situations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What’s the function of 2,3DPG

A

It’s is capable of complexing with Hb and allow O2 detach from Hb at low O2 PP (to the tissues)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What’s the most adaptive mechanism of anemia

A

The generation of 2,3DPG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What makes the cytoplasm alkaline in anemia

A

The presence of HHb instead of HbO2 in the cytoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the CVS adaptive mechanism of anemia

A

•Increased vascular dilatation
•Decreased peripheral resistance
•Myocardial dilatation (increased volume of the 4 chambers)
•Increased HR
•Increased CO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What’s the O2 tension of 5L of blood (physiological CO)

A

100ml—20 ml
5000ml—X

X= 1000ml O2 carrying capacity(available to tissues per minute) of 5L of blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Of the 1000ml of O2 available to the body per minute, what goes to the brain, myocardium, muscle and the whole body

A

The body only requires 250ml
•60ml - Brain
•50ml- myocardium
•60ml- muscle mass

And the rest distributed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Which parts of the body are O2 sensitive

A

Brain, Heart, Skeletal muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What happens to the O2 distribution if the Hb conc was 10g/dL instead of 15g/DL

A

The HR would have increased to ~ 100 instead of 72 and the SV would be ~ 100 instead of 70
The CO would be like 10L instead of 5L

So instead of having 1000ml of O2 available for distribution, there would be 1340ml available (replacing 13.4 for 20, and 10L for 5L in the calculation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Compare the CVS adaptation and the Modulation of Hb/O2 affinity

A

They are both equall vital but the CVS adaptation has energy implications and could easily fail if Hb clc falls extremely low

The failure of CVS adaptation is usually the cause of death in severe anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

When will the CVS adaptation fail

A

When the Hb conc goes lower than 7g/dL
However in children under 5, it may not fail till the Hb conc is as low as 5g/dal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is severe anemia

A

When the Hb conc is lower than 8g/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Features of failure of CVS adaptation

A

•Fast HR (greater than 100-120bpm)
•Biventricukar heart failure
• Redistribution of blood flow
• More capillaries are opened up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Features of biventricular heart failure (Right and Left)

A

Right ventricular Heart failure
•Raised Jugular pressure
•Hepatomegaly
•Ascitis
•Gravity Dependent pedal edema

Left ventricular heart failure
•Pulmonary edema (Basal crepitations on ascaultation due to fluid at the base of lung : Heamic murmur) ;chokes to death

41
Q

Explain redistribution of blood flow

A

Redistribution of blood to more O2 sensitive areas at the expense of O2 less send areas

42
Q

What part of the body is less O2 sensitive

A

Predominantly the skin
Also kidney (only needs 4ml per minute instead of 100 that’s given to it)

43
Q

Explain the opening of more capillaries

A

•This is to ensure tissues are better perfused
•There’s more plasma that RBC drying anemia , makes the blood more viscous hence need more push (reduced peripheral resistance helps)

44
Q

If the cause of the anemia is not due to bone marrow failure, why other mechanism can be used to adapt

A

Compensatory increase of erythropoesis as sim in sickle cell anemic patients

45
Q

What’s the classification of anemia

A

•Morphological classification
•Etiological classification

46
Q

What is the morphological classification of anemia

A

refers ot the physical appearance of red cell together with the red cell indices as the base of classification

47
Q

What are the three types of anemia based on morphological classification

A

•MACROCYTIC normochromic anemia
•Microcytic hypochromic anemia
•Normocytic normochromic anemia

48
Q

What is macrocytic normochromic anemia

A

Large RBCs with normal Hb on them

As a result of impairment of DNA synthesis but not impairment of RNA transcription

49
Q

What’s another name for macrocytic normochromic anemia

A

Megaloblastic anemia

50
Q

What is Microcytic hypochromic anemia

A

Small cell size with small Hb content

As a result of impairment of Hb synthesis, deficiency of iron, or failure of iron utilization

51
Q

Explain normocytic normochromic anemia

A

•Normal cell size and normal Hb content
•Associated with chronic disorders
•Also called **Anemia of chronic disorder **

52
Q

What are the types of anemia based on the etiologies classification

A

•Anemia of blood loss/Hemorrhagic anemia
•Anemia of decreased RBC/Hemolytic anemia
•Anemia of bone marrow survival failure

53
Q

Explain Hemorrhagic anemia

A

•Blood loss could be acute or chronic
Acute hemorrhagic anemia
-Acute obstetric hemorrhage
-Disseminated Intravascular coagulopathy
-Post partum hemorrhage
-Bleeding from animal poison

Chronic hemorrhagic anemia
-Hematomosis (bleeding from mouth)
-Hemoptosis (coughing blood)
-Epistasis (sneezing blood)
-Bleeding stool

54
Q

What’s the most common cause of hemorrhage all over the world

A

Road traffic accident

Others include, violent injuries, injuries from building collapse

55
Q

Explain acute obstetric hemorrhage

A

-Placenta Previa (cause of antepartum hemorrhage)
-Abruptio placenta
-Ectopic gestation
-Uterine rupture

56
Q

Causes of post partum hemorrhage

A

-Placenta retention
-Uterine atomy

57
Q

What causes Hematemesis

A

This is bleeding from mouth, includes vomiting blood
-Gastric ulceration
-Duodenal ulcers
-Gastric carcinoma
-Bleeding from esophageal varices

58
Q

Causes of hemoptosis

A

This is coughing blood
-Chronic chest infection
-Collagen Wagener’s granulomatosis
-Heart failure
-Pulmonary infarction
-Lung/Bronchial cancer

59
Q

Causes of epistasis

A

This is sneezing blood
-Weakened or loss of integrity of vessels
-Severe hypertension
-Systemic diseases (thrombocytopenia)
-impairment of platelet function

60
Q

Causes of Hematochezia

A

This is bleeding in stool
-upper GIT bleeding
-Lower GIT bleeding

61
Q

What’s the characteristic of upper GIT bleeding

A

Malena stooling - dark colored foul smelling
Same causes as hematemesis

62
Q

Causes of lower GIT bleeding

A

Bleeding hemorrhoids
Colonic diverticulosis
Anal tear
Colonic/ceacal carcinoma
Inapparrnt GIT blood loss

63
Q

What causes in apparent GIT blood loss

A

Blood sucking intestinal parasites (hookworm)

64
Q

Causes of Hematuria

A

Bleeding into the urethra
-pathology in bladder, kidney , urethra , ureter

Kidney pathology
•payelonephrotis
•Renal papillary necrosis (ss)
•Carcinoma

Ureter pathology
•Ureteric stones (leading to erosion)

Bladder pathology
•Infections (schistosoma hematobium)
•Carcinoma
•Stones (erosions)

Irethra pathology
•Obstruction/Fibrosis ( from gomococcal infection)

65
Q

Causes of Memoragia

A

This is vaginal bleeding
-Vaginitis
-Cervicitis
-Cervical cancer
-Fibroid
-Endometriosis
-Endometrial cancer
-Dysfunctional uterine bleeding

66
Q

Causes of Hemathrosis and Hematoma

A

Hemathrosis- Bleeding into joints
Hematoma- Bleedimg into soft tissue
-Coagulative protein disorder

67
Q

Causes of Purpura

A

This is bleeding into skin
-Platelet disorder
-VW disease
-Vascular collagen disorder (Ehler Dahlos syndrome )

68
Q

What % of RBC are removed and replved daily

A

~1%

69
Q

What is hemolytic anemia

A

When the life span of RBC is shorten to as low as 20 days ( seen in HbSS) or 50-60 days (seen in HbSC)

And the bone marrow’s ability to increase production RBC and Hb conc is impaired

70
Q

What are the 2 causes of hemolytic anemia

A

Intracapsular pathology
Extracapsular pathology

71
Q

What are the 2 types of intracapsular pathology

A

-Cell membrane pathology
-Cytoplasmic pathology

72
Q

What are the 2 types of RBC membrane pathology

A

Acquired and Inherited membrane pathology

73
Q

What causes acquired RBC membrane pathology

A

•As a result of paroxysmal nocturnal hemoglobinurea (PNH) due to deficiency of decay attack mechanism (perforated proteins lose the membrane)
• Also as a result of Zeid’s triad

74
Q

What does the Zeids triad consist of

A

Alcoholic Liver disease
Hyperlipidemia
Hemolytic anemia

75
Q

Who is an alcoholic

A

Takes at least 80g of alcohol daily

76
Q

How does the Zeids triad come about

A

Because of the liver disease, liver cannot oxidize the lipids to form energy, then the lipid go back into the blood causing hyperlipidemia , then it goes into the cell causing too much lipid in the cell then causing lyses

77
Q

What are the types of Inherited RBC membrane pathology

A

•Inherited spherocytocis
•Inherited acanthocytosis
•Inherited stomatocytosis
•Inherited ovalocytosis
•Inherited elliptocytosis
•Inheritedpyropoikilocytosis

78
Q

A as what are the 2 types of cytoplasmic pathology

A

Enzymopathies
Hemogliobinopathy

79
Q

What are the 2 types of enzymopathy

A

Deficiency of enzyme in glycolysis
Deficiency of enzymes in reducing pathway

80
Q

What enzymes are deficient in glycolytic enzymopathy

A

All the enzymes can be deficient but the commonest is hexokinase and pyruvate kinase

81
Q

What does deficiency of glycolytic enzymopathy lead to

A

Leads to reduction in ATP generation
Which causes Na/K ATPase failure, hence Na influx and Water influx , which leads to is osmotic cell lyses

82
Q

What is the reducing power of RBC

A

NADPH2

83
Q

Why does RBC need NADPH2

A

It is required by RBC to reduce oxidized membrane macromolecules including membrane proteins and membrane lipids

84
Q

When do we say a carbon atom is fully reduced

A

When the valency points is fully occupied by H atom

85
Q

What happens when a reduced carbon atom is oxidized

A

We want carbon atoms to be full reduced
When a oxidizing molecule is brought to a reduced carbon, it changes its single bonds to double bonds and makes it easy to break
With each oxidation, it’s easier to break, causing membrane lipid / protein damage

86
Q

What does the RBC use to reduce oxidized membrane macromolecules

A
87
Q

What is Glutathione

A

A tripeptide consisting of Glutamine, Cysteine, Methionine

88
Q

What 2 enzymes does the RBC use to synthesize the GSH and their role

A

•Gamma-glutamyl-cysteinyl-transferase- Joins Glutamime to cysteine
•Glutathione synthase - Add methionine to the glutamine, cysteine comples

89
Q

How does the GSH help reduce oxidizes macromolecules

A

It’s gives of its H atom to the oxidized molecule and becomes an unstable G-S
Then two G-S fuse to become a stave G-S-S-G , a stable oxidized glutathione

90
Q

What enzyme links tow unstabe G-S to stabilize it G-S-S-H

A

Glutathione peroxidase

91
Q

What enzyme helps to fuse the unstable G-S to stabilize it to G-S-S-G

A

Glutathione peroxidase

92
Q

Why does the oxidized glutathione (G-S-S-G) have to get reduced back to GSH

A

Because the RBC does not have tha capacity to keep synthesizing new GSH

93
Q

What converts the oxidized G-S-S-G back to a reduced GSH

A

RBC reducing power NADPH2 (and then becomes NADP)

94
Q

What enzyme does RBC use to reduce oxidized membrane macromolecule

A

Glutathione

95
Q

What enzyme converts the oxidized G-S-S-G back to a reduced GSH

A

Glutathione reductase

96
Q

How is the oxidized NAPD reduces back to NADPH2

A

Glucose-6-phosphate is converted to 6-phosphoglutamate using G-6-P dehydrogenase

97
Q

What’s the most important enzyme in producing reducing power

A

Glucose-6-phosphate dehydrogenase (converts G-6-P to 6-phosphoglutamate and produces NADPH2)

98
Q

What happens to people deficient in G-6-P dehydrogenase

A

They cannot reduce oxidized NADP which in turn cannot reduce oxidized glutathione which in turn cannot reduce oxidized membrane macromolecules

99
Q

List all the enzymes involved in the reducing pathway of RBC

A

•Gamma-Glutamyl-Cystyl-trasferase
•Glutathione synthase
•Glutathione peroxidase
•Glutathione reductase
•Glucose -6-phosphate dehydrogenase

Hematology FPP (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions