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DIT topics > RBC basics + erythropoiesis > Flashcards

RBC basics + erythropoiesis Flashcards

1
Q

no nucleus
biconcave (large SA for gas exchange) and flexible: both due to cytoskeleton protein SPECTRIN
rely on glucose for energy (no mito): 90% is aneorbic metabolism from glucose → lactate, 10% is HMP shunt metabolism
life span: 120 days

A

erythrocytes

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2
Q

complication of loss of biconcave RBC shape

A

sickle cell disease
hereditary spherocytosis
viscous → sludging in capillaries

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3
Q

deficient pyruvate kinase (enzyme in glycolysis pathway)

A

no energy to RBC → RBC hemolyisis

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4
Q

anisocytosis

A

RBC of varying sizes

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5
Q

poikilocytosis

A

RBC of varying shapes

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6
Q

polycythemia/erythrocytosis

A

too many RBCs

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7
Q

reticulocytosis

A

immature RBCs: when BM is producing more → leak out into blood

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8
Q

basophilic stippling

A

inhibition of enzyme that degrades RNA

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9
Q

lead poisioning causes

A

basophilic stippling

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10
Q

echinocyte (burr cell)

A

REGULAR, uniform spikes over surface

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11
Q

uremia (renal failure) causes

A

echinocyte (burr cell)

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12
Q

acanthocyte (spur cell)

A

IRREGULAR, spikes over surface

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13
Q

both these cause:
liver disease
abetalipoproteinemia (state of cholesterol dysregulation)

A

acanthocyte (spur cell)

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14
Q

spherocyte

A

lose biconcave shape

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15
Q

hereditary spherocytosis causes

A

spherocytes

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16
Q

schistocytes

A

fragmented RBCs

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17
Q

pathologic intravascular clotting (fibrin in blood vessels) → RBC sliced by fibrin (microangiopathic hemolytic anemia):
DIC
TTP/HUS

A

schistocytes

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18
Q 
THAL
Thalassemia
Hemoglobin C disease
Asplenia
Liver disease
A

target cells

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19
Q

pathologic RBCs seen in liver disease

A

target cells

acanthocytes (spur cells)

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20
Q

sickle cells

A

crescent-shaped

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21
Q

Howell-Jolly body

A

basophilic remnant of nucleus in RBC

no splenic macrophage to remove it

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22
Q

asplenia (due to trauma or ITP treatment, complication of sickle cell disease- infarcted spleen) causes

A

target cells

howel-jolly body

23
Q

complication of sickle cell disease

A

infarction of spleen

24
Q

Heinz bodies (looks like Howell Jolly bodies)

A

oxidation of hemoglobin → denatured hemoglobin precipitates in RBC →splenic macrophages bite it → bite cells

25
Q

bite cells (degmacyte)

A

splenic macrophages bite denatured hemoglobin (Heinz body) out of RBC

26
Q

G6PD deficiency: can’t go through HMP shunt → no NADPH produced → no reduction of glutathione → no detoxification of free radicals → Hb is oxidized → Heinz body + bite cells

sensitive to drugs that cause oxidative damage (cause Heinz bodies + bite cells)

A 
Spleen Purges Nasty Inclusions from Damaged Cells
Sulfonamides
Primaquine
Nitrofurantoin
Isoniazid
Fava beans
Dapsone
Chloroquine
27
Q

heinz body vs howell-jolly body

A 
howell-jolly body: remnant of nucleus (only 1 per cell)
heinz body (many per cell)
28
Q

myelofibrosis (BM infiltration)

A

teardrop cells

29
Q

hereditary elliptocytosis

A

elliptocytes “pencil cell, cigar cell”

30
Q

sideroblast

A

nucleated red cell precursor
granules of iron in mitochondria
found in BM (normal finding)

31
Q

disorders of heme synthesis

A

anemia +

ringed sideroblasts in BM = sideroblastic anemia

32
Q

ringed sideroblasts

A

sideroblast can’t use iron stored in mitochondria →excess iron granules form ring around nucleus
found in BM

33
Q

causes of sideroblastic anemia

A

drugs
chronic alcohol use
myelodysplastic syndromes

34
Q

transfusion with incompatible blood type

A

Ab-mediated type II HSR: circulating Ab binding to RBC antigens → hemolysis, fever, shock, kidney failure, death

35
Q

1 cause of transfusion reactions

A

medical personnel

36
Q

Rh-D (-) mom only have antibodies to Rh-D due to exposure to Rh-D + baby’s (during delivery/trauma of first pregnancy, no problems)
more abundant maternal Abs (anti-Rh-D = IgG cross placenta) to fetal Rh-D + baby (2+ pregnancy)

A

erythroblastosis fetalis

37
Q

anemia due to hemolysis of RBCs by maternal Abs → release Hb → bilirubin
jaundice → possible kernicterus
hydrops fetalis: generalized fetal edema
intrauterine death

A

erythroblastosis fetalis

38
Q

prevent of erthryoblastosis fetalis in Rh- mom

A 
anti-Rh-D immunoglobulin (bind to fetal RBC and hide from mom's Ab) at:
28 wks
any traumatic event (MVA)
any abortion/miscarriage
within 3 days of delivery
39
Q

look at ABO blood types

A

k

40
Q

type AB blood

A

express A + B antigens on RBC surface

NO A or B antibodies → universal RECIPIENT of RBCs (only blood type that can receive AB)

41
Q

type O blood

A

no antigens on RBC surface

A + B antibodies in blood→ universal DONOR (only can receive type O)

42
Q

abdominal pain: neuropathic: intermediate heme precursors are neurotoxic
“port wine” urine: excess heme precursors in blood, spill into urine
polyneuropathy
psych disturbances
precipitated by drugs: barbiturates, seizure drugs, rifampin, metoclopramide

A

acute intermittent porphyria

43
Q

treatment of acute intermittent porphyria

A

both inhibit ALA synthase (RLE):
glucose
heme

44
Q 
blistering of skin in sun (esp hands): photosensitivity
"tea-colored" urine
hypertrichosis: excessive hair growth
facial hyperpigmentation
↑LFTs: AST, ALT
associated with hep C + alcoholism
A

porphyria cutanea tarda: most common form of porphyria

think of homeless man

45
Q

porphobilinogen deaminase deficient in

A

acute intermittent porphyria

46
Q

uroporphyrinogen decarboxylase deficient in

A

porphyria cutanea tarda

47
Q

affects ALA-dehydratase + ferrochelatase

A

lead poisioning

48
Q

child causes:

exposed to lead paint (

A

lead poisioning

49
Q

adult causes:

factory with lead

A

lead poisioning

50
Q

adult with neuro sx:
headache
memory loss
demyelination

A

lead poisioning

51
Q

CNS toxicity:
encephalopathy
memory loss
delerium
mental deterioration: learning disabilities
headaches
foot/wrist drop
lead lines (dark blue/black) on gingiva: burton lines
lead lines on long bones along metaphyses (child)
colicky ab pain
renal failure
microcytic anemia with basophilic stippling: denatured rRNA in cell

A

lead poisioning

52
Q

treatment of lead poisioning

A

child or adults: EDTA or succimer

child with severe toxicity: dimercaprol + succimer

53
Q

causes of polycythemia

A

1) polycythemia vera: monoclonal proliferation of RBCs
2) chronic hypoxia (pulm disease/COPD, sleep apnea, cyanotic heart disease, high altitudes): kidneys recognize ↓ O2 saturation→ ↑ EPO→ ↑ RBC → ↑ O2 carrying capacity
3) ↑ ectopic epo:
EPO-producing tumor
4) trisomy 21 (60% at birth)

54
Q

4 EPO producing tumors

A 
Potentially Really High Hematocrit
Pheochromocytoma
Renal cell carcinoma
Hepatocellular carcinoma
Hemangioblastoma (vascular CNS tumor)

DIT topics (115 decks)

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