RBC basics + erythropoiesis Flashcards by L W

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

erythrocytes

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complication of loss of biconcave RBC shape

sickle cell disease
hereditary spherocytosis
viscous → sludging in capillaries

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deficient pyruvate kinase (enzyme in glycolysis pathway)

no energy to RBC → RBC hemolyisis

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anisocytosis

RBC of varying sizes

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poikilocytosis

RBC of varying shapes

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polycythemia/erythrocytosis

too many RBCs

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reticulocytosis

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

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basophilic stippling

inhibition of enzyme that degrades RNA

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lead poisioning causes

basophilic stippling

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echinocyte (burr cell)

REGULAR, uniform spikes over surface

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uremia (renal failure) causes

echinocyte (burr cell)

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acanthocyte (spur cell)

IRREGULAR, spikes over surface

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

acanthocyte (spur cell)

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spherocyte

lose biconcave shape

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hereditary spherocytosis causes

spherocytes

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schistocytes

fragmented RBCs

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

schistocytes

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THAL
Thalassemia
Hemoglobin C disease
Asplenia
Liver disease

target cells

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pathologic RBCs seen in liver disease

target cells

acanthocytes (spur cells)

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sickle cells

crescent-shaped

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Howell-Jolly body

basophilic remnant of nucleus in RBC

no splenic macrophage to remove it

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

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target cells

howel-jolly body

complication of sickle cell disease

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infarction of spleen

Heinz bodies (looks like Howell Jolly bodies)

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

bite cells (degmacyte)

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

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)

``` Spleen Purges Nasty Inclusions from Damaged Cells Sulfonamides Primaquine Nitrofurantoin Isoniazid Fava beans Dapsone Chloroquine ```

heinz body vs howell-jolly body

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

myelofibrosis (BM infiltration)

teardrop cells

hereditary elliptocytosis

elliptocytes "pencil cell, cigar cell"

sideroblast

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

disorders of heme synthesis

anemia + | ringed sideroblasts in BM = sideroblastic anemia

ringed sideroblasts

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

causes of sideroblastic anemia

drugs chronic alcohol use myelodysplastic syndromes

transfusion with incompatible blood type

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

#1 cause of transfusion reactions

medical personnel

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)

erythroblastosis fetalis

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

erythroblastosis fetalis

prevent of erthryoblastosis fetalis in Rh- mom

``` 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 ```

look at ABO blood types

type AB blood

express A + B antigens on RBC surface | NO A or B antibodies → universal RECIPIENT of RBCs (only blood type that can receive AB)

type O blood

no antigens on RBC surface | A + B antibodies in blood→ universal DONOR (only can receive type O)

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

acute intermittent porphyria

treatment of acute intermittent porphyria

both inhibit ALA synthase (RLE): glucose heme

``` 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 ```

porphyria cutanea tarda: most common form of porphyria think of homeless man

porphobilinogen deaminase deficient in

acute intermittent porphyria

uroporphyrinogen decarboxylase deficient in

porphyria cutanea tarda

affects ALA-dehydratase + ferrochelatase

lead poisioning

child causes: | exposed to lead paint (

lead poisioning

adult causes: | factory with lead

lead poisioning

adult with neuro sx: headache memory loss demyelination

lead poisioning

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

lead poisioning

treatment of lead poisioning

child or adults: EDTA or succimer | child with severe toxicity: dimercaprol + succimer

causes of polycythemia

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)

4 EPO producing tumors

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

RBC basics + erythropoiesis Flashcards

(54 cards)