RBCs Flashcards

Question 1

Q

RBC Path-Terms

Answer

A

MCV (mean cell volume): Average volume of RBC expressed in fentoliters (um3)
NORM value = 80-96 fL
MCH (mean cell hemoglobin): Average content mass of Hb per RBC (Picograms)-^{Should be about the SAME SIZE as Macrophage}
NORM 27-31 picograms/cell
MCHC (Mean cell Hb content)=Average conc of Hb in given volume of packed RBCs-Hgb/Hct
NORM 32 to 36 grams/deciliter
RBC distrubution width (RDW): Coefficient of variation of RBC vol
NORM 11.5-14.5%

Question 2

Q

RBC Morphology

Answer

A

Normal RBC = same size as macrophage w/small hole in middle
Howell-Jolly Body = RBC w/nuclear material present ^{ALWAYS a SIGN OF SPLENIC DYSFUNCTION}
Microcytic/Hypochromic = anemia with a LOW MCH
Target Cell = Seen in hemoglobin C (crystal) or Beta & Alpha thalassemia ^{(Target appearance due to Bleb in center)}
Spherocyte: Loss of bi-concave appearance found in hereditary spherocytosis & autoimmune hemolytic anemia

Question 3

Q

RBC Morphology (2)

Answer

A

Schistocytes=fragmented RBC “helmet appearance found in Micoangiopathic hemolytic anemia ^{(MAHA)}
Nucleated RBC=Found in fetus/New born beyond that shows disorder w/blood producing mech
Reticulocyte=Stain blue and show mesh like network of RNA ^{(immature RBCs)}
- Polychromatopheila ^{(LARGE # of immature RBCs seen)}
- Supravital stain ^{(Blue staining of RNA ribosome)}
Basophilic stippling=Tiny blue dots found around RBC associated w/Lead poisoning

Question 4

Q

Hemolytic Anemia Outline

Answer

A

“Normocytic”
Results from INCREASE in rate of RBC destruction
Premature destruction of RBCs dut to:
Intrisic ^{(Heptaglobin increased to save Iron)}
Extrinsic ^{(Jaundice & Splenomegaly)}
Hemolytic anemias are classfied based on intrisic or extrinsic causes
Site of destruction: Based on presence or absence of FREE Hb & Hb products
Shortened RBC life span = bone marrow hyperplasia
“Compensated hemolytic disorders” = Anemia is absent BUT reticulocytosis & erythroid hyperplasia of marrow SEEN

Question 5

Q

Hemolytic Anemia (Intrinsic)

Answer

A

Normocytic
Acute process
Destruction of RBCs w/in circulation W/release of Free Hb ^{(incomp blood transfusion)}
**Haptoglobin decrease **^{(binds to Hb)}
Membrane defects:
Hereditary spherocytosis ^{(Cytoskeleton membrane tethering-Spectin, ankryin, Band 3.1)}
Hb Defects:
Sickle cell disease
Thalassemias
Enzyme defects:
G6PD def
Acquired:
Paroxysmal nocturnal hemoglob

Question 6

Q

Hemolytic anemia (Extrinsic)

Answer

A

Exaggeration of normal mech of removing aged RBCs
RBCs recognized as abnormal by Recticulo-endothelial system ^{(LYMPH & SPLEEN)}= Phagocytosed prematurely ^{(Hereditary Spherocytosis)}
Acquired-
Immune mech:
Hemolytic disease of newborn
Incomp blood transfusion
Drug induces
Non-immune:
Mechanical-Mico angiopathic hemolytic anemia (MAHA)
Cardiac prosthetic valve
Misc:Due to infections, burns, lead poisoning

Question 7

Q

Haptoglobin (RBC breakdown)

Answer

A

Increased Hb breakdown intravas & extravas:
Haptoglobin made in liver & binds to free Hb (Fe+3)
Hb small enough to pass thru the normal glomerulus (Iron wasted)
HB + haptoglobin large and cannot be excreted
Following release of Hb into circulation-Plasma Haptoglobin lvls fall & return to normal after 3-6 days
Presistant hemoysis = LOW haptoglobin lvls
Haptoglobin (Hb only) reduced in BOTH types Intrinsic & extrinsic

Question 8

Q

Hemopexin (RBC breakdown)

Answer

A

Plasma Hemopexin:
Binds to FREE HEME in 1:1 ratio
NO bind to Hb
If Hb from hemoysis exceeds haptoglobin lvls-Hb turned into Metheglobin
Methemoglobin turns into ferriheme & globin
Ferriheme BINDS to hemopexin-LOST through glomerular filtration
Associated w/Intravascular hemolysis=LOW hemopexin lvls

Question 9

Q

RBC breakdown

Answer

A

Iron released from Heme & combines with transferritin 1/3 saturated (iron-binding protein)
Carried to bone marrow or body iron stores (Ferritin/Hemosiderin-Storage form)

Increased Extravascular (reticulo):
Jaundice due to Hyperbilirubinemia
Bilirubin is unconj & does not appear in urine
Increased Intravascular = Low hemopexin lvls
Reticulocytes: (Normal 0.2 to 2%)
Bone marrow hyperplasia ^{(erythroid)}
Extra medullary hematopoiesis ^{(liver, spleen)}
Cholelithiasis^{ (pigment gall stones)}
Skeletal abnormalites

Question 10

Q

Hereditary Spherocytosis (HS)

Answer

A

Inherited disorder due to intrisic defects in RBC membrane
Vulnerable to splenic sequestration & distortion = ^{Phagocytosed by macrophages}
Mutation of ankyrin & Spectrin:
Increaed permeability to Na+=countered by active transport out of Na+
Result is increase in glycolytic rate = DEPLETES ATP
PH falls = Inhibiting glycoloysis membrane LOSS
Increase in MCHC

Question 11

Q

HS lab investigations

Answer

A

Hb: Decreased
Histo:
Spherocytes
absence of central pallor
anisocytosis - RBCs are of un = size
Howell-Jolly Bodies = Small dark nuclear remnants - Asplenic pts
Osmotic fragility test:
Normal RBCs able to increase in size w/increasing hypotonic conc of saline sol.
BUT spherocytes RUPTURE
Reticulocytes increased
Extravascular hemolysis = Increased serum bilirubin - Unconj-Gallstones

Question 12

Q

HS Clinical Features

Answer

A

Anemia
Splenomegaly
Jaundice
Gall Stones ^{(increase unconj bilirubin)}
Aplastic crisis=^{Associated w/Parvovirus 19:}
Virus kills RBCs progenitors
Worsens already anemic pts
Further REDUCED reticulocytes
Hemolytic crisis:
Increased splenic destruction of spherocytes
Darkening of unrine
Can be assoc w/infectious mononucleosis ^{(Epstein-barr & herpes virus)}
Treatment: Splenectomy ^{(done after 7 yrs immune system established)}

Question 13

Q

G6PD def properties

Answer

A

X-linked Recessive
Glucose-6 phosphate dehydrogenase reduces NADP to NADPH
NADPH helps in the conversion of ^{OXIDIZED} glutathione to ^{REDUCED} glutathione
This reduction helps w/Oxidant injury ^{(FREE RADICALS H2O2 build up in Def.)}
Def-Leads to reduced levels of G6PD:
Neutrophils & macrophages poor bactericidal properties
Back pain assoc hemogloburia hours after oxidative stress ^{(anti-malarials, Fava beans)}

Question 14

Q

G6PD def Pathogenesis

Answer

A

Hemolysis occurs due to oxidative stress from:
Drugs - anti malarials (Primaquine, Chloroquine, sulfonamides)
Infections - Viral hep, pneumonia, typhoid fever
Fava bean (mediterrian G6PD) - Favism in children or immunocomprimised people
G6PD def RBCs:
Exposed to oxidants = Oxidation of reactive sulfhydryl group on Hb Chain
Chain is denatured = membrane bound inclusion^{ (HEINZ BODY)}
Heinz body damages cell membrane=^{INTRAVASCULAR HEMOLYSIS}
Spleen macrophages eat heinz = Bite cells

Question 15

Q

G6PD def Lab diagnosis

Answer

A

Hb: Decreased can be mild or severe
Histo: Heinz bodies & Bite cells
Low G6PD lvls:
plasma Hb = increased ^{(hemoglobinemia)}
Haptogloben = reduced
Hemoglobinuria
Clinical features:
Acute hemolysis^{ (2 to 3 days following oxidant stress & can last 7 days)}
Associated stressors: Anti-malarial, infection, fava bean

Question 16

Q

HbS-Extravascular Hemolysis

Answer

A

Sickle Cell anemia (HbS)
Point mutation @ 6th pos of Beta globin chain = Sub of Valine for Glutamic acid
Homozygous state almost ALL Hb in RBCs are HbS (90-95%)
Heterozygous (carrier)-undergo sickling ONLY under severe hypoxic states
Pathogenesis:
Distorted/rigid RBCs block small BVs = Ischemia
Repeated sickle-unsickle cycles results in ^{RBCs MORE FRAGILE} - Then REMOVED by splenic macrophage
Sickling REDUCES flow rate & RBCs begin to adhere ^(STAGNATE)=Further reduces O2 tension MORE sickling
FInal result = Ischemia ^{(painful crisis)}

Question 17

Q

HbS Lab investigations

Answer

A

Hb = Decreased
RBC measurement = Increased MCHC ^{(mean corp hemoglobin conc)}
HIsto:
Micocytic & Hypochromic
10-15% are sickled RBCs
Sickling test-
observering for RBC sickling when treated w/2% Na+ Metabisulfite (Hetero & Homo)
Hb electrophoresis:Sep based on charge
Chorionic Villi biopsy-Fetal DNA analysis in 1st trimester

Question 18

Q

HbS Clinical Features

Answer

A

Severe anemia
Vaso-oculsive complications:
Hypoxic injury & infarction
Severe pain
“Hand-Foot” syndrome = Dactylitis ^{(redness/swelling in palms and soles)}
Micro-infarction of carpal & tarsal bones
Acute-chest syndrome-Fever, dry cough, chest pain & pulmonary infiltrates ^{(due to SLUGGISH pulmonary blood flow)}
Due pneumonia infection
CNS=seizures/strokes hypoxia
Aplastic crises-Transient bone marrow failure of erythropoiesis
Infection by parvovirus B19=Worsening anemia & reduced reticulocytes
Chronic hyperbilirubinemia (extavascular hemolysis) = Gallstones

Question 19

Q

HbS Sequestration crises

Answer

A

Sequestration Crises:
Massive sequestration of sickled cells in spleen
Rapid splenic enlargement, hypovolemia, ^{POSSIBLE SHOCK-}Seen in children
Susceptibility to early infections due to:
Congestion & poor blood flow in spleen ^{(Immune center)} in children
Infarction & autosplenectomy ^{(shrunken)} in adults
Infections:
Pneumococci ^{(sepsis)} & hemophilus influenzae
Osteomyelitis by salmonella parathyphi
Loss of renal function ^{(vasocculsive)}

Question 20

Q

Beta Thalassemias properties

Answer

A

Beta = Def synthesis (B+) or TOTAL ABSENCE (B0) -Chromosome 11
genetic point mutation
Lack of adequate HbA (a2b2)=^{Microcytic&hypochromic}
Excess free Alpha chains in comparison to reduced Beta chains
Insol. precipitated aggregates in RBCs=destroyed & ineffective erythropoiesis
INCREASED absorption of Iron
Secondary hemochromatosis
Inclusions of alpha chains damages cell membrane = vulnerable to phagocytosis ^{(extra-vascular hemolysis)}
Beta Carriers are protected from plasmodium malaria

Question 21

Q

Beta Thalassemia Major Lab/Features

Answer

A

Hb: Severe anemia
_HIsto: _
Anisopoikilocytosis (RBCs vary in size)
Target cells-Fargmented RBCs, reticulocytosis, nucleated RBCs
Biochem studies:
Bilirubin & Iron
Clinical features:
Pallor & Jaundice
Bone marrow transfusion ^{Lead to secondary hemochromatosis}(excess iron)
Bronze Diabetes - Overload of iron due to melanin to unexposed skin-_^{Use penacillamine to get rid of iron}_
Growth retardation
Skeletal system abnormalites ^{(Crewcut skull)}
Gall stones
Infections-Parovirus B19 (aplastic)

Question 22

Q

Beta Thalessemia Minor

Answer

A

Diff from Iron def anemia
Iron def anemia improved w/Iron therapy
B-thalassemia trait (minor) worse with Iron therapy
Important for Lab:
Serum Iron
Ferritin
Transferrin
Total iron binding capacity (TIBC):
Increased in Iron Def
NORMAL in B-thalassemia minor
Serum iron & ferritin:
Decreased in iron def
Normal or slightly increased in thalassemia minor

Question 23

Q

Alpha Thalassemia

Answer

A

Due to deletion of alpha synthesis
Affects: Hb-A, Hb-A2 & Hb-F
Severity depends on # of Alpha chains missing
4 alleles on Chormosome 16
Silent carrier = Deletion of single alpha chain
Alpha trait = deletion of 2 alpha chains
HbH = Deletions of 3 alpha chains (B4)
Barts = 4 gamma chains-VERY HIGH Affinity for O2=NO O2 delivered to periphery
Clinical picture similar to SEVERE Rh-Incompatibility

Question 24

Q

Hydrops fetalis & Alpha Thalassemia

Answer

A

Hydrops fetalis: deletion of all 4 alpha chains ^{(Barts)}
Fetal distress occurs @ 3rd trimester = Intrauterine DEATH
CIS deletion spontaneous abortion Asians
Fetus characteristics:
Pallor
Generlized edema
MASSIVE hepatosplenomegaly
Mother has frequent toxemia (TOXINS in blood) of pregers

Question 25

Q

Paroxysmal nocturnal hemoglobinuria

Answer

A

Rare & chronic ^{(STEM CELL DISORDER AFFECTS ALL CELL LINES)}
Intravascular hemolysis-Intermittent hemoglobinuria ^{(@ night resp acidosis=Comp activation)}
Defect in Red cell membrane (DAF)
Pathogenesis:
Mutation in phophatidylinositol glycan-A gene X-linked ^{(PIGA)}
PIGA-enzyme important for production of cell surface proteins
Ex. Decay accelerating factor-CD55/DAF deficient due to gene mutation
This deficiency=abnormal sensitivity of erythrocytes to complement mediated hemolysis ^{(Includes neutrophils&Platelets)}
Comp activation = Fall in PH, infections, Surgery, Strenuous exercise

Question 26

Q

PNH Features

Answer

A

Aquired later in life
Low lvls of MAC inhibitor CD-59
Low lvls of C8 (comp system)
Passage of red/brown urine in morning ^{(night resp acidosis-comp activation=LOW PH)}
Chronic hemolysis-Hemosideriuria ^{(Excess binding of Hapto-Hb is excreted)}
Affects platelets-Thrombosis (liver, dermal cerebral) main cause of DEATH
Lab findings:
Hb = low @ time of diagnosis
Reticulocyte = Increase
WBC = Reduced
Platelets = Reduced
Bone marrow = hyperplastic ^{(increased erythropoesis)}
Screening test = Sucrose hemolysis ^{(LOW-IONIC SOL observe for LYSIS)}

Question 27

Q

Immunohemolytic Anemias (warm-IgG)

Answer

A

IgG auto-immune ^{(assoc w/SLE & CLC)}
Extravascular hemolysis by splenic macrophages->Eat away membrane=Spherocytes
Primary (idiopathic-Spontaneous)
_Secondary: _
B-cell lymphoid neoplasms ^{(CHRONIC LYMPOCYTIC LEUKEMIA)}
Autoimmune ^{(SLE)}
Drugs ^{(a-methyldopa, penicillin, quinidine)}
Clinical presentations-
Severe anemia
Increased MCV^{ (MORE RETICULOCYTES)}
Hyperbilirubemia ^{(extavascular hemolysis) }Conjugated or unconj
Diagnose w/Direct coomb’s test
B-cell neo: bone marrow (IgG)

Question 28

Q

Immunohemolytic Anemias (cold-IgM)

Answer

A

IgM Ab in Cold can coagulate = Reynaud’s syndrome ^{(WHITE & PAINFUL)}
Intravascular Fixes comp
Associated w/extremeties
Acute Causes:
Mycoplasma infection (WALKING PNEUMONIA=Productive cough)
Infectious mononucleosis (EpsteinBarr & 1 type of herpes Virus)
Histo: Shows Clumping-AutoAb against erythrocyte membrane
Chronic:
Idiopathic
B-cell lymphoid neoplasms:
Lymph (IgM)

Question 29

Q

Hemolytic Anemia-mech trauma

Answer

A

Microangiopathic hemolytic anemia
Cardiac valvle prostesis
Narrowing or partial obstruction of vasculture
Blood smear shows fragmented RBCS ^{(Schistocytes)}
TTP & HUS present similar BUT:
TTP-Defect in Adams 13 (stabilizes w/VwF&FACTOR 8)
Purpura
Mental confusion
**_HUS-_Caused by 0157:H7 E.coli **
Acute kidney failure
Affects children
DIC also shows similar symptoms BUT BT, PT, PTT are INCREASED

Question 30

Q

Malarial Parasites (intravascular w/SOME extravascular)

Answer

A

Transmitted from salvia ^{(SPOROZONITES) }of infected female
Infects live liver parenchymal remain dormant ^{(hypozonites)}
Parenchymal cells rupture w/meronts released into blood ^{(INFECT RBCs)}
P. Falciparum = MOST COMMON & deadly
RBCs burst everyday aquire **CHARGED **proteins ^{(PECAM-CD31 & ICAM-1)}
RBCs aggregrate/lyse-in postcap venules ^{(MICROTRHOMBI->COMA->CONVULSION & DEATH)}
Plasmodium vivax & ovale: burst loose every other day
Symptoms = Fever/chills, drenching sweats ^{(TERTIAN MALARIA)}
Plasmodium malariae: Burst @ 72 hours
Symptoms = Fever/chills ^{(Quartan malaria)}

Question 31

Q

Iron Absorption

Answer

A

Daily diet (10-20Mg) & absorb 1-2 mg/Lose 1-2 mg from desqua of GI epithelia
Absorbed by Duodenum in Ferric form (Fe+2) converted by Dcytb enzyme
DMT1 tansports ferric iron in
Ferroportion transport iron out
Once in circulation Hepcidin (^{sequesters Iron so bacteria cannot use it to divide)}
Also put into storage form Ferritin
Hemosidrin: degraded/aggregated_ _of ferritin ID by Prussian blue
Small scattered blue granules in cytoplasm of macrophages ^{(ALSO GOLDEN-BROWN)}
40% of normoblasts small blue granules=^{Sideroblasts OR if nucleus expelled Siderocytes}

Question 32

Q

Transferrin & Ferritin

Answer

A

Transferrin-Has 2 binding sites for ferric iron (Fe+2) BUT common only 1/3 binding sites occupied
Unbound Iron is TOXIC ^{(catalyst of free radical formation)}
Normal conc is 60-150 = ^{(LARGE PORTIN is BOUND IRON-Transferrin)}
TIBC=_{unbound transferrin + bound transferrin}= _{MAX cap} from iron binding ^{(300-360)}
% of transferrin saturated w/Ferric is best indicator of stored iron
Transferrin transports iron to:
Hemoglobin/Erythropoeisis
Ferritin ^{(storage form of Fe+3 in liver/Heart)}
Other proceses (5-15%)
Exceptions of Ferritin increase:
chronic inflammation
In heptocellular disease
in neoplasias (abnormal cell growth)

Question 33

Q

Iron Def. anemia general

Answer

A

4 reasons:
Diet LACK
Impaired absorption
Increased requirements ^{(menstruation/Pregers)}
Chronic Blood loss:
Peptic ulcer
Hemorrhoids
carcinoma stomach/colon (60 yr male)
Menorragha (50 yr female)
Aspirin
HOOK worm
Esophageal varices
Lab Diagnosis:
Hb - reduced
Hematocrit - reduced
RBCs - MCV, MCH, MCHC all Decreased
Ferritin - Down and TIBC - Up

Question 34

Q

Iron def anemia Lab findings

Answer

A

Microcytic & hypochromic ^{(central pallor)}
Ansiocytosis ^{(RBCs various sizes)}
Poikilocytosis (^{RBCs variation in shape)}
Increase in platelet count-Thrombocytosis 3x increase from normal 150-350 ^{(unknown)}
Bone marrow:
Hyperplastic
Microctic maturation
LOSS of stainable iron in macrophage ^{(prussian blue)}
Biochem tests:
FEP increased (free protoporphirin-no iron to bind)
Iron & ferritin ^{DECREASED}
TIBC ^{(total iron binding capacity)}-measure of amount of transferritin in blood=^{INCREASED}

Question 35

Q

Iron def anemia-Clinical features

Answer

A

Early stage = Normocytic anemia
Fatigue & Tachycardia
PICA
Pallor & glossitis ^{(smooth red tongue)}
Angular chlilitis ^{(inflammtion on side mouth)}
Kolionychia ^{(spoon shaped concavity of nails)}
Plummer-Vinson Syndrome ^{(Triad findings)}:
Microcytic hypochromic anemia
Atrophic glossitis
esophageal webbing (Protruding part of esophagus membrane)-**Dysphsia problems w/shallowing **

Question 36

Q

Anemia of Chronic Disease

Answer

A

Liver will secrete Hepcidin (sequesters Iron) - due to chronic infections (IL-6)
Examples:
Chronic microbal infections (Osteomyelitis, Bacterial endocarditis, Lung Abscess)
Chronic immune disorders (Rheumatoid arthritis)
Neoplasms (Hodgkin Lymphoma)
Lab Findings:
Normocytic-Normochromic
circulating Iron reduced
Ferritin is INCREASED ^{(Bronze Diabetes)}
TIBC REDUCED
Bone marrow = Iron increased

Question 37

Q

Sideroblastic Anemia

Answer

A

Defect in protoporphyrin production
Genetic defect rate limiting step ALAS
All have abnormal erythropoesis in bone marrow ^{(mitochondria)}
Abnormal intramitochondrial accumulation of iron ^{(pre-cursor RBCs)}
Sideroblast = Erythroblasts w/Iron granules in their cytoplasm ^{(ring)}
Defect in heme synthesis w/in mitochondria
Lab: RBCs are dimorphic ^{(micro & macro)}, sideroblats, siderocytes ^{(non-heme iron)}
Bone marrow: Hyperplasic ^{(ring sideroblasts w/Prussian blue)}
Secondary: seen in pyridoxine antagonists used in Tb (isoniazid)-Vit B6 def-needed in ALAS
Lead ^{(denature ALAD/Ferrochelatalase)}

Question 38

Q

Megaloblastic Anemia

Answer

A

2 causes:
Folate def
B12 def ^{(pernicious anemia)}
- ^{Intrisic factor def in stomach}
- ^{Absorbed in terminal Illeum}
Both are co-enzymes required in synthesis of Thymidine ^{(DNA)}
Def = defective nuclear muturation ^{(DELAY/BLOCK in CELL DIVISION)}
Increase in homocysteine ^{(CH3-transfer)}
Cytoplasmic maturation unaffected ^{(Nuclear/Cytoplasmic asynchrony seen)}
Cellular RNA & protein synthesis OK
Granulocytic precursors LARGE & abnormally immature chromatin
Multiloped Neutrophils

Question 39

Q

Folate Def

Answer

A

Increased requirements ^{(pregers)}
Decreased intake:
Fruits & Vegetables
Alcoholism
Phenytoin ^{(anticonvulsant)}
Oral contraceptives ^{(interfere w/absorption)}
Imparied utilization-Folic acid antagonists (Methothrexate-Anti-cancer)
Clinical features are similar to Vit B12 except No neuro
Body stores are minimal
Lab values:
increased Homocysteine
Normal methyl malenoic
Absorbed in Jejunum

Question 40

Q

Pernecious Anemia

Answer

A

Auto-immune destruction of Parietal cells
Older age group-50 to 80
Common cause Vit B12 def.
Hypersegmented Neutrophils seen in ^{EARLY STAGE} before anemia
Pathogenesis:
Chronic atrophic gastritis ^{(autoimmune of parietal cells)-}atrophy of fundic glands
Achlorhydria ^{(reduced gastric acid-related with intrisic factor def)}
MCV = 110 fL^{ (normal 82-92)}
Large platelets ^{(pancytopenia=Issues with cell lineage)}
Bone marrow = Nuclear features, lace-like chromatin, Large nuclei
Urine = increased Methylmalonic acid

Question 41

Q

Pernicious Anemia (Types)

Answer

A

Type 1 Ab - Blocks binding of VitB12 to IF
Type 2 Ab - Blocks binding of VitB12-IF complex to ileal receptors
Type 3 Ab - Produced against alpha & beta subunits of gastric proton pump
Clinical (Anemia + Neuro)-
^{Syphilus presents same neuro symptoms}
Lemon tint (skin)- anemia
Glazed & beefy red tongue-Atrophy of papillae^{ (Burning pain on swallowing)}
Sysmetric numbness
Tingling
Loss of gait & position
Demyla of Post/Lat columns^{(spastic ataxia)}
Supplemeting B12-FAILS to resolve Neuro
Schilling test = Radioactive B12 ingested
Histamine test = stim parietal cells

Question 42

Q

Aplastic anemia

Answer

A

_Pancytopenia: _genetically altered stem cells due to drug exposure/infection
Activates TH1 T-cell = ^{IL-1, TNF, IFN-G}=Kill hemapoietic progenitors
Anemia, leukopenia, thrombocytopenia
Results from aplasia of BM=Reduction of hemopoietic tissue & Increase in fatty marrow
BM test=Fat & glycogen ^{(HYPOCELLULAR)}
NO splenomegaly
Reticulocytosis ABSENT
Bone Marrow transplantation effective

Question 43

Q

Aplastic like symptoms

Answer

A

Myelodysplasia= fibrosis & malignant caused by Radiation or household chems
- Leukemia & Hairy cell*
Tear drop RBCs due to no where in marrow to mature - leukoerythroblastosis
Marrow myelofibrosis - Bone marrow issue=Tear drop RBCs
Clinical features-
Pallor
Weakness
Easy bruising
Infections