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DMD 5247 > Blood Pathology-Anemia- Bickmen > Flashcards

Blood Pathology-Anemia- Bickmen Flashcards

1
Q

Normal red blood cells, why are they paler in the center ?

A

Biconcave shape (on both sides)

becasue the cell has very little organelles

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2
Q

Complete Blood Count (CBC)

A

essential in determining the nature of a blood disorder

  1. RBC
  2. Hemoglobin (more –> reder)
  3. Heatocrit (ratio of RBC 50%)
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3
Q

MCV

A

mean corpuscular volume

(too small)microcytic–> normocytic–>macrocytic (too big)

cytic= size

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4
Q

MCHC

A

Mean corpuscular hemoglobin concentration

Hypochromic (lack of hemoglobin)

normochromic

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5
Q

anisocytosis

A

size variaiton

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6
Q

poikilocytosis

A

shape variation of RBC

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7
Q

Anemia

A

“without blood”

a reduction below normal in hemoglobin or RBC #

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8
Q

Symptoms of Anemia

A

Pale skin, mucous membranes
Jaundice (if hemolytic)
Breathlessness
Tachycardia
Dizziness
Fatigue

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9
Q

anemia causes

A
  1. Blood loss
  2. Excessive RBC destruction
  3. Insufficient RBC production
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10
Q

Excessive RBC destruction

A

Extracorpuscular reasons

Intracorpuscular reasons

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11
Q

Insufficient RBC production

A

too little material

too few erythroblasts

not enough room

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12
Q

Anemia

blood loss

A

cause: trauma resulting in acute blood loss
* after 2-3 days reticulocyte spike (normal 1%)

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13
Q

Reticulocytes

A

develop and amture in the red bone marrow and then circulate for about a day in the blood before developin into mature erythroctes

(kidneys release erthropotein to induce the relase of Red bone marrow)

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14
Q

Hemolytic Anemias

Signs of destruction

A

Increased bilirubin

Increased LDH (lactate dehydrogenase)

Reduced haptoglobin

Extracorpuscular

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15
Q

Hemolytic Anemias

Signs of Production

A

increased reticulocutes

nucleated red cells in blood

Intracorpuscular

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16
Q

Erythrocytes Destruction

A
  • Life span of RBC is about 120 days
  • RBC destroyed by resident macrophages in spleen and liver
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17
Q

RBC recyling

A
  • Globin (into AA)
  • Heme (Iron-containing part)
  • Remainder converted to bilirubin
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18
Q

Iron used in

A

variousn tissues

  • Liver
  • spleen
  • bone marrow
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19
Q

Unconjugated bilirubin

A
  • Is toxic
  • “Bilirubin+Albumin” (water insoluble)
  • Lipid soluble
  • Damage cell membranes
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20
Q

Bilirubin Eliminaiton

A
  • Unconjugated bilirubin is taken up by the liver
  • Conjugated via glucuronyl transferase
  • conjugated bilirubin is excreted with the bile to the small intestine
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21
Q

How is bilirubin eliminated from the body

A

as fecal material

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22
Q

what conjugates bilirubin

A

glucuronyl transferse

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23
Q

Some bilirubin in the intestine is converted to_____ by _________

A

urobilinogen by intestinal bacteria

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24
Q

Urobilinogen can be reabsorbed into the blood where

A

the liver can vurther metabolize it and excrete it as bile

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25
Q

small amounts of urobilinogen are excreted from the body to

A

to the kidneys in the urine

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26
Q

Jaundice

A

Excess biliruben accumulation in the body

  • Skin
  • nail beds
  • whites of the eye –>yellow
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27
Q

jaundice two causes

A

excess bilirubin produciton

decreased bilirubin excretion

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28
Q

Excess bilirubin production

Jaundice

A

due to RBC destruciton

surpasses livers ability to conjugate

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29
Q

Decreased bilirubin excretion

Jaundice

3

A
  1. Reduced hepatic uptake (hepatitis, cirrhosis)
  2. Decreased conjugation (hepatitis, cirrhosis, enzyme deficiency)
  3. Bile duct obstruction (tumor, stone)
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30
Q

Bilirubin very toxic to

A

brain cells

31
Q

Jaundice treatment

A
  • Treat cause of condition
  • Blood transfusion
  • Sun
32
Q

Light or clay colored feces and dark urine

A

Extrahepatic obstructive jaundice

obstruction of bile duct

(outlet for billirubin is urine)

33
Q

Normal to light colored feces and light colored urine

A

Intrahepatic obstructive jaundice

damaged hepatocytes

(hepatitis, cirosisi)

34
Q

Dark feces and urine

A

Hemolytic anemia

everything is working but you just have too much

35
Q

Besides color feces and urine what other techniques are used to diagnosis Jaundice

A

x-ray

ct scan

liver biopsy

(help determine stones, tumor, or cirrosis)

36
Q

A 63-year-old man has been an alcoholic for 30 years. His skin and eyes have a yellowish coloring. He is now most likely suffering from what:

A. Prehepatic jaundice
B. Intrahepatic obstructive jaundice
C. Extrahepatic obstructive jaundice
D. Hemolytic jaundice

A

B

(urine and feces are both light)

37
Q

Mircoangiopathic Hemolytic Anemia

A

Extracorpuscular (something is physically damaging the RBC)

  • Physical trauma to red cells
  • Schistocytes
38
Q

Schistocytes

A

RBC fragments

39
Q

Microangiopathic Hemolytic Anemia

Causes

A

Causes

  • Artificial heart valve
  • Malignancy
  • Obstetric complications
  • Sepsis
  • Trauma
40
Q

Autoimmune Hemolytic Anemia

A

Extracorpuscular - Abs attack RBC

warm

  • IgG
  • Spleen
  • Spherocytes

Cold

  • IgM, Complement
  • Intravascular hemolysis
  • Agglutination
41
Q

Autoimmune Hemplytic Anemia is based on

A

temp

IgG is more active at higher temps

IgM (C3b) more active at lower temps

(gives rise of where the anemia is happening)

42
Q

Sickle cell anemia

A

Intracorpuscular

  • Hemoglobinopathy
  • Single aa substitution in β chain (Val for Glut Acid)
  • -/+ vs. +/+
  • African ethnicity
43
Q

sickles causes

A
  • clog vessels and are fragile
  • Infarcted spleen with HbS
44
Q

Thalassemia

A

Intracorpiscular Hemolytic Anemia -point mutation

  • Can’t make enough α or β chain
  • Hypochromic, microcytic anemia
  • Increased RBC synthesis (EPO)
45
Q

Thalassemia

alpha:

beta:

A

α: SE Asian
β: Mediterranean

46
Q

Thalassemia, clinical manifestations

A

medullary expanision due to increased erythropoiesis

47
Q

Herditary Spherocytosis

A
  • Many spherocytes (round ball shape)
  • Caused by a spectrin defect
  • Splenectomy is curative
48
Q

Hereditary Spherocytosis RBCs

A

form polymers and get entrapped in spleen causing Splenomegaly

49
Q

Howell-Jolly Bodies

A

Evidence of markedly decreased splenic function

(intracorpuscular hemolytic anemia)

excessive RBC destruction

50
Q

G6PD Deficiency

A

intracorpuscular

  • decrease G6PD –> increase peroxide–> cell lysi
  • ROS exposure kills RBCs
  • Devlopment/removal of Heinz bodies
51
Q

G6PDH deficiency causes a loss in

A

glutathione

52
Q

what happens if there is a loss of glutathione?

A

build up radical peroxide which damages lipids and dna

53
Q

Heinz bodies

A

globin denatures, sticks to RBC membrane

forms bite cells

54
Q

what are the symptoms and triggers of Intracorpuscular

A
  • some asymptomatic other episodes
  • triggers: drugs or fava beans
55
Q

insufficient RBC produciton

too little material

anemia

A
  1. Iron deficiency
  2. Chronic disease
  3. Megaloblastic
56
Q

Insufficient RBC production

too few erythroblasts

anemia

A

aplastic anemia

57
Q

Insufficient RBC production

not enought room

anemia

A

Myelophthisic anemia

58
Q

Iron deficiency anemia

manifestations

A

Mircocytic, hypochromic anemia

  • atrophic glossitis
  • koilonychia
59
Q

Iron dieficiency anemia causes

A
  • Decreased iron intake
    • Poor diet
    • Poor absorption
  • Increased iron loss
    • GI bleeding
    • Menses
    • Hemorrhage
  • Increased iron requirement–>Pregnancy
60
Q

Anemia of chronic disease

causes

A

Normochromic, normocytic anemia

Cause:

Distrupted iron metabolism → moree hepcidin in liver

61
Q

Megalblastic Anemia

causes

A

Normochromic, macrocytic anemia

  • reduced B12/folate in the body (need to split the cell)
  • inadequate absorption through insufficient Intrinsic Factor
62
Q

Pernicious anemia

cause

treatment

A
  • decrease RBC synthesis due to low Vitamin B12 in body ( bc low intrinsic factor)
  • treatment B12 injections

type of Megablastic anemia

63
Q

Clinical manifestaions of Pernicious Anemia

A

low levels of B12 in the blood and low uptake of B12 from intestine

disease develops slowly due to large stores of B12 in liver

64
Q

B12 deficiency generally due to lack of intrinsic factor caused by:

A

​

  • Autoimmune disease of stomach
  • GI surgery (e.g., gastric bypass surgery)
  • Chronic gastritis
65
Q

Megaloblastic Anemia histological manifestations

A

large oval shaped RBC

Hypersegmented neutrophils

66
Q

Schilling Test

A

A clinical test to determine whether a patient has pernicious anemia

(via B12 absorption)

67
Q

Aplastic anemia

causes

A

Normochromic, normocytic anemia

  • Idiopathic
  • Drugs/chemicals
  • Viruses
  • Pregnancy
  • Fanconi anemia (DNA damage)
68
Q

Aplastic anemia

histological manifestations

A
  • pancytopenia (deficency of all blood cells)
  • Hypoplastic(empty) bone marrow
  • bleeding and compromised immune function
69
Q

Myelophthisic Anemia

causes

A

Normochromic, Normocytic amenia

  • infilatration of one marrow by tumors or fibrosis
  • possible pancytopenia
70
Q

Myelopthisic anemia histology

A

tear-dropped shaped RBX (dacryocytes)

71
Q

In sickle cell anemia, the globin portion of the molecule is abnormal due to the amino acid valine being substituted for which of the following amino acids?

A.Glutamine

B.Glutamic acid

C.Aspartic acid

D.Glycine

A

B

72
Q

From the following list select the THREE items associated with the normocytic classification of anemia.

A.Iron deficiency

B.Thalassemias

C.Aplastic anemia

D.Anemia of chronic disease

E.Liver disease

F.Vitamin B12 and folate deficiency

G.Acute and chronic blood loss

A

C,D,G

a,b(microcytic)

73
Q

The Schilling test may be used to detect:

A.Folate deficiency

B.Aplastic anemia

C.Pernicious anemia

D.Myelophthisic anemia

A

C

DMD 5247 (7 decks)

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