Brainscape's Knowledge GenomeTM

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


See full index

CPR > Anemia theme 2 > Flashcards

Anemia theme 2 Flashcards

1
Q

Whats osmotic fragility test?

A

its a test to putting RBCs in different concentrations of solution to see when the cells hemolysis. Normal RBCs rupture at .9% solution. If lyse say at 1% or .95% this is abnormal. Use this test to help diagnosis type of anemia. picks up anemias involving issues with the cytoskelton/membrane of the rbc

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

What is Hereditarty Spherocytosis? genetics? cause? what are its effects? CBC reading clues?

A

Its and autosomal dominate disorder effecting mostly N. European decent. Its a hemolytic anemia cause abnormal cytoskeletal proteins(spectrin, ankryin, band 3 and protein 4.2). This makes the RBC ridged c shape that breaks when cross things. The change in membrane causes Na+ to accumulate inside cell and K+ to escape. You will see spleenmegaly, gallstones due to inc bilirubin(bc destroy rbc). The CBC anemia with high MCHC, and high reticulocyte count

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

What definds anemia?

A

Low hemoglobin level

it also has low RBC # and low hematocrit %

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

Name the Macrocytic anemias?

A

the 2 main ones are:
B12 def
folate def
then there are a few others

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

Name the nomocytic anemias?

A

bone marrow def
hemolysis
blood loss

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

name the microcytic anemias?

A

Iron def
Thalassemia
Anemia of chronic inflammation

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

the difference between erythropoiesis and hematopoiesis?

A

ertythropoiesis is the making of RBCs

hematopoiesis is the making of all blood cells from one precusor steam cell

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

site of erythropoiesis in fetus?

A

start off from the yolk sac, then the liver (peak at 5months) & spleen (peak at 4 months). As bone marrow starts to take over the job and is sole contributor after birth

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

site of Erythropoiesis in adults and children?

A

Adults : vertebrae and pelvis (main ones) then sternum and ribs
Kids: Tibia and femur are major sites

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

What would happen if you have a mutation to GATA-1?

A

You would hender the ability make RBCs and platelets. GATA-1 is a very important gene regulator protein for RBC lineage. Other hematopoietic diseases have been linked to mutations in the GATA-1 gene

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

Describe the cell proliferation to a reticulocyte?

A

Its an amplification process with multiple rounds of division 11-12. It goes from Proerythroblast-> basophilic erythroblast-> polychromatophilic erythroblast-> orthochromic erythroblast-> reticulocyte (the last step is the only one that is truely linear)
along the way the cell becomes smaller, chromatin becomes condense through shutting off genes by GATA-1. Also more and more hemoglobin is added. Before the recticulocyte is release it expels its nucelus. There is still a little mitochondria and ribosome to add the remainder hemeglobin in a day or so in the blood stream.

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

Whats erythropoietin and why is it so important in RBC lineage?

A

Its a colony stimulating factor (CSF) that stim stem cells to make RBCs. erythropoietin is made in the kidney….. so if your patent has kidney failure Epo will go down and so will your RBCs

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

why is RBCs apoptosis, performed in the spleen or liver called erythroptosis?

A

RBCs lack a mitochondria so it lacks cytochrome C so it doesn’t have the primary signal for normal apoptosis

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

how would you calculate the number of RBCs destroyed each day?

A

1/# days it survives X #RBCs/L X # of L in body

this number will equal the number produce if the person is normal

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

How would you get the normal number of reticulocytes in your body?

A

calculate the % of RBCs destroyed in a day and X by 100 to give you the %

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

What effect does high altitude have on RBCs?

A

Inc their production
high altitude low levels of O2 leading to hypoxia-> stim the kidneys to make/release Epo-> stim stem cells in bm to make RBCs

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

Compare and contrast erythrocyte burst forming cell (BFU-E) & erythrocyte colony forming cell (CFC-E)

A 
They both make RBC
BFU-E comes before CFC-E in lineage (bc undergoes more cycles of cell division) 
BFU-E needs IL-3 to survive 
CFC-E need Epo to survive 
CFC-E divides it make 2 proerythroblasts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

why are reticulocytes bigger than RBCs?

A

reticulocytes have ribosome, mitochondria, and mRNA to synthesis the last 20% of hemoglobin
you can see the RNA in a new methylene blue stain

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

Whats the process if you lose RBCs?

A

Lose rbc-> inc Epo-> stim early release of reticulocyctes in kind of an immature form and accelarted cell cycle

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

What are the three things Epo does?

A

accelerate the cell cycle process for erythropoiesis
inhibts apoptosis of RBC precursor cells
stim the premature release of reticulocytes from the bone marrow

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

What are the 4 vitamins and nutrients needed for adequate RBC cell division?

A 
folic acid - converted to THF (n10 formy THF) makes purines G/A, (N5,N10 methylene) make thymidine 
vit B12 (cobalamin) converts N5-methyTHF back into THF 
def in these 2 leads to macrocytic anemia.. b12 def also see pernicious anemia 
also need iron, a.a def in these two leads to microcytic anemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is MCV? and what are some ranges

A 
MCV= mean corpuscular volume
the average vol of a circulating erythrocyte
norm range 80-100 normocytic 
below microcytic 
above macrocytic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

whats MCH

A

mean corpuscular hemoglobin
quantity of hemoglobin in ave eicrulating erythrocyte
not very useful because the rbc is usually fully tapped out

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

whats MCHC

A

concentration of hemoglobin in average erythorcyte in ciruclation
typically 31-37%
below is hypochomic
wont see hyperchromic because rbc will lysis it will be to big to handle

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

What is RDW and what info does it provide

A

is the distribution of size of RBCs (MCV)

changes sugges a mixed population of cells and indicate something is wrong

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

Whats RDW-CV and RDW-SD? and why do we either

A

RDW-CV curve width from +- 1 standard dev from the MCV then dividing by MCV . a normal value is 11.6-14.6% it minimize the effects of small pop of abnormal cells
RDW-SD measure curve width at the point where 20% of cells have that volume. normal range is 39-46fL. it is more sensitive to the smal pop of abnormal cells. Reticulocytes have a greater effect on it

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

What can effect the size of RDW?

A

ansicocytosis(odd size) or poikilocytosis (odd size)
Folate, B12, and iron deficinecyes elevate RBW if they cause anemia
Thalassemia also elevates RDW but not as much

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

Why is it important to have a corrected reticulocyte count and how would you interrupt the numbers?

A

You need the correct number so you can see if the bm is responding properly. In most anemias the reticulocyte level should be high, if its normal or low then there is a problem in the bm. Unless the anemia is because of iron def. You wont notice iron def anemia until later on when you have used up your extra store reticulocytes stores. There will be a inc in Epo just not a drastic inc in reticulocytes also

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

Whats the importance of the Hexose monophosphate pathway?

A

it synthesize NADPH+ in RBCs. the NADPH helps reduce oxidative products such oxidized glutathione. it gives its H+ so glutathione reductase and reduces glutathione disulfide back to glutathione as if not present the by oxidative by products will cause damage to the rbc

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

whats the most common def enzyme in glycolysis?

A

Pyruvate Kinase…. big players in anemias

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

How does 2,3 BPG relieve some of the symptoms of anemia?

A

It binds to Hb causing the rbc to have a lower affinity to the oxygen, so you can dumb more oxygen off in the tissue. It causes a right shift in the oxygen saturation curve

32
Q

What is the most common enzyme deficiency?

A

G6P dehydrogenase… has multiple class 1-5. 1 being the most sever (diffuclty surviving, hemolysis, jaundice in newborns). 5 being the least problems (asymptomatic with maybe light hemolytic events)

33
Q

Explain the folate bioavailability pathway for rbc?

A

folate-G-G-G-G-G the G tail is cleaved by gamma-glutamyl hydrolase-> folate-G enters rbc-> folypolyglutamate synthases(in cytosole) and converts it back into folate-G-G-G-G-G

34
Q

Whats sideroblastic anemia? how is it caused?

A

iron deposit in orgnells of the rbc bc hemoglobin carry of iron but not making the hem ring so iron deposist in various area around the cell. This is cause by a mutation in X-chromosome on the ALAS2 gene

35
Q

Whats Porphobilinogen synthase do? what is it susceptible too?

A

Its a zinc-dependant enzyme that is in a step to make hemoglobin. it is susceptible (inhibited) to heavy metal like lead. If have lead poisoning porphobilinogen will be inhibited and ALA will accumulate which leads to psychosis

36
Q

What are the two enzyme we have to be worried about having a deficency in for the formation of the heme synthesis? and what are the problems seen from the def?

A

uroporphyrinogen 3 synthase - accumulation of uroporphyrinogen 1 and coporphyrinogin 1 -> red urine, red/brown teeth, photosensitivity (light exposure get itchy and nothing will alleveate the itch)

ferrocheletase- less severelevate serum levels of porphyrin. get photosensitivity, red urine both not as drastic though because we degrade some of the porphyrin

37
Q

Explain the steps of Heme degradation?

A

heme oxidase opens up heme ring and becomes biliverdin
biliverdin reductase reduces this to bilirubin
albumin and glucuronidate transport bilirubin to the liver
it either secreted into bile, gut flora, or metabolized to urobiliogen
urobeiligen is further metabolized in the large intestine or kidney

38
Q

What is Jaundice? What is the cause of neonatal jaundice?

A

accumulation of bilirubin in blood, skin, sclearae, looking yellowish
delayed expression of bilirubin UDP-glucuronyl transferase (see a lot in premature babies)

39
Q

Name the causes of bone marrow damage?

A

autoimmune(idiopathic), toxins, infection, radiation, bone marrow infiltration

40
Q

whats aplastic anemia? what would you see in your lab results

A

T-cell mediate, where the cells go after the precursor cells in the marow. So you aren’t make blood cells-> low HGB, WBC, PLT
When you look at the bone marrow biopsy it will be acellular, you will see a lot more fat deposits

41
Q

What are Neutropenia, Thrombocytopenia(ITP) and AIHA?

A

autoimmune b-cell (humoral) autoantibodies anemia, the marrow is fine

42
Q

how to you distinguish between hypoplasia and aplasia?

A

you look at the bm cellularity %
if it great than 10% but less than normal for age =Hypoplasia
if it is less than 10% =aplasia

43
Q

The criteria for sever aplastic anemia

A

Neutropils

44
Q

Whats the initial treatment for idiopathic autoimmune anemia? What do you do if this doesn’t work

A

immunosuppressive agents and bone marrow growth factors (Neupogen)
if no improvement over a few months you move on to bm transplant

45
Q

What are some common causes of chemical bone marrow aplasia

A

Insecticides (DDT,lindane), Benzen, Chemotherapy(busulfan treat leukima wipes out bm first) toluene wood preservative, herbs

46
Q

What are common viruses that cause anemia?

A

Hep B, EBV, CMV, Pravo (effect just rbc), influenza

47
Q

What is myelophthisic anemia? the two types?

A

Its anemia due to marrow infiltration, basically things occupy the area preventing the production of norm blood cells
tumors are a big cause also is myelofibrosis whcich is the abnormal proliferation of fibrous tissue or even new bone formation in the bm

48
Q

what is anemia, leukopenia, lymphopenia, thrombocytopenia?

A

anemia- low Hgb/HCT
leukopenia- low levels of WBCs
lympopenia- low levels of lympocyctes
thrombocytopenia- low levels of platelets

49
Q

What is sideroblasitc anemia? what causes it? possible treatment?

A

You get ringed sideroblasts in the bm.
iron deposit in mitochondria that wthe incircle the nucleus forming the ring structure
ALA synthase reductase causes this, it is an X-link disorder
May respond to pyridoxine treatment

50
Q

Acute Intermittent Porphyria (AIP) cause?

A

deficiency in PGB deaminase leading to accumulation of prohobilinogen(PBG) in the cytoplasm
Its an autosomal dominant disorder, that effect woman more than men

51
Q

What triggers AIP attacks?

A

you usually experinece attacks between the ages of 18-40
things that trigger attacks are: drugs that inc the demand of heatic heme especially cytochrome P450, low carb diets, progesterone, cigarette smoking(induces cytochrome P450), metabolic stresses

52
Q

The symptoms of AIP and the main sequence of events of them

A
  1. abdominal pain 2. psychiatric symptoms 3. peripheral neuropathies-mainly motor
  2. can last for days
    2.CNS signs like seizure and blindness also
  3. Motor loss similar to Guillain-Barre syndrome- start from the most distal lower extremeties and moving there way up
    Pain diffuse pattern
    Depression is also very common
53
Q

How to you check for AIP?

A

check plasm, urine, stool porphyrin excretion ( they weren’t metabolized correctly

54
Q

What is Porphyria Cutanea Tarda (PCT)? causes?

A

It is the most common porphyria
Hepatic disorder, when uroporphyringogen decarboxylase activity is less than 20% of normal. This will lead to accumulation of porphyrins especially uroporphyrins
Can get from inheritance or acquired via, hep c, drug or alcohol use, or poisons such as halogenated hydrocarbons

55
Q

What is one of the major characteristics that you can use to test for PCT?

A

high levels of iron in the blood (iron overload)
disturbance of iron metabolism-> reactive oxygen species dec hepcidin expression-> lack regulation of iron levels-> accumulation of iron

56
Q

Whats PCT treatment

A

avoid sunlight, antimarials to form complex with porphyrins to excrete, repeate bhlebotomy goal to get get HCT

57
Q

What are the three categories of herediatry hemolytic anemias?

A 
RBC membrane defects (HS defects in either ankryin, spectrin, Band3, protein 4.2)(HE defect in SPATAN-1)
Metabolic defects (G6PD, Pyruvate Kinase)
Hemobloin Defects (sickle cell)
58
Q

Explain the linkage of the cytoplasma and cell membrane, and mutations that can lead to hereditary spherocytosis?

A

spectrin is connected to the cytoskelton (via connect with short actin filaments)-> connects with ankryin-> which binds to band 3-> which is in the cell membrane-> protein 4.2 helps assists the binding of ankryin to band 3

59
Q

How do you tell if a cell membrane mutation is in band 3 or the other proteins?

A

you look at the microvesicels it gives off. If they contain band 3 then the mutation isn’t in that protein. If the microvesicels don’t have band 3 then the mutation is in band 3

60
Q

The cause of spectrin mutation in HS?

A

mutation is either in alpha or beta chain. alpha gene is SPTA1 which if mutated is an autosomal recessive (early onset). beta gene is SPTB if mutated its an autosomal dominate

61
Q

Compare and Contrast hereditary elliptocytosis and hereditrary spherocytosis?

A

HE & HS can have mutated SPTA1 and SPTB but different effect HS you lose membrane over time, HE you don’t lose it but you mess up the assoication
HE effects African and mediterranean ppl more
HS effects more N. european decent

62
Q

Why does G6PD target RBC? and why is it such a big problem?

A

G6PD is used in the first step of the hexose monophosphate shunt which makes NADPH which is needed for to reduce glutahione so it can take care of the oxidative elements from glycolysis in the RBC to prevent damage. No reduced glutathione-> inc hydrogen peroxide -> extensive hemolysis. The reason it effects rbc so much over other cells is because other cells have mitchondria to take care of this problem, rbcs have nothing else

63
Q

what are the possible genetic mutation that lead to G6PD def and compare their effects on the def

A

G6PD A- : effects the stability of the enzyme, also effects just old rbc…. are aspmptomatic untill introduced to an oxidatvie stressor -> hemolytic anemia
G6PD B- : efects the stability and catalytic acitivity, also effects young and old rbc….. this defect is worse and is found in Medtirean pop… see extensive hemolysis

64
Q

Whats the effect of Pyruvate Kinase deficency on RBCs? How do patents compensate?

A

reduces atp production
also affects the membrane pumps that maintain membrane flexibilty and cell shape. The spleen then destroys the altered RBCs causing hemolytic anemia
They compensate by inc levels of 2-3 BPG to inc oxygen unloading and reduce their phenotypical symptoms
It is autosomal recessive

65
Q

What cause sickle cell disease? trait? detection of mutation

A

its a mutation on the b-globin gene switching a A(nt) to T causing a switch from gly to val. giving you a ridged c shape. It is auto recessive.
sickle cell trait is a person that is heterozygous but under low oxygen conditions can display symptoms of sickle cell anemia
Detect by doing a PCR followed by using a Mst2 restriction enzyme. If no mutation the sequence will be cut. If there is a mutation it won’t cut the affected allele

66
Q

Describe the diagnostic sequence for pernicious anemia?

A
  1. see if megaloblastic anemia-> inc MCV and hypersegmented neutrophils… check the bone marrow too
  2. if reticulocytes are normal or low if elevated then pernicious anemia
  3. Mechanism… shouldhave serum anti-intrinsic factor antibodies
67
Q

What is Pernicious anemia? what are its main causes

A

It is the lack of vit B12 absorption in gut due to lack of intrinsic factors (IF).
caused by:
1. anti-IF antibodies (IgG)
2. Parietal cell loss via anti H+/K+ -ATPase and anti-parietal cell H+/K+ - antibodies ATPase …. this causes damage to the gut lining making it accessible to the IgG antibodies to bind to IF before it binds to vit B12

68
Q

What is atrophic Gastritis? & what does it do for pernicious anemia?

A

causes damage to the stomach lining, by H. pylori infection & autoimmune attack. This allows access of the IgG to bind to the IF

69
Q

How does Helicobacter pylori add in the formation of pernicious anemia?

A

H. pylori attach to mucosal cells in the stomach-> degrades the cells cause release of urea-> cleaved by urease to make ammonia-> neturalizes the stomach acid so bact. can survive
the damage mucsoa cells cause inflammation that trigger an immune rspn to H. plyori-> this bring IgG into stomach-> they cross link alpha/beta sub-unit of H+/K+ ATPase pump because of the molecular mincry to H.pylori

70
Q

What is the pathophysiology of RDS? what are some risk factors?

A

deficiency of surfactant->low lung compliance-> progressive atelectasis
hypoxemia, intrpulmonary shunting, cyanosis
risk factors:
premature birth-> immature development of type 2 pneumocytes(which prd surfactant)
C section->reduced cortisol-> reduced surfactant
Maternal diabetes->high insulin->reduced surfactant

71
Q

What are the clinical presentations of a child with RDS?

A

dyspnea, respiratory distress, grunting, retractions, tachypnea, retractions, distress, hypoxemia, atelectasis-> R to L shunting (perf w/o vent)
C Xray “ground glass appearance
atelectasis is inversely proportional to age and weight = the older you are the bigger you are and less likely to have RDS issues bc bigger lungs less of a inward pull on them

72
Q

How does oxygen treatment for RDS lead to retinopathy of prematurity?

A

first ROP is a blindness. Oxygen is a drug. if you give to much oxygen to the kid it will mess with vasculature of the eyes leading to ROP

73
Q

What is Transient Tachypnea of the Newborn (TTN) and how do you treat?

A

its when the baby doesn’t fully reabsorb the fluid -> leads to tachypnea shortly after birth.
Usually their breathing hard so put on O2 had they will be fine in a few days… it spontanously fixes itself just fine in a few days

74
Q

What is meconium aspiration? and what do you do to treat it

A

This is when the fetus defecats in the uterus. when the baby is born it cries and breaths in the feces-> coarse crackles. also meconium plugs of small airways ->air trapping-> pneumothroax -> treat with needle aspartate if this doesn’t work you insert a small chest tube
possible prevention is tracheal suctioning (studies are so so right now)

75
Q

what causes Pneumonia in babies and treatment?

A

It is usually viral in babies. when of school age it becomes more Strep. Pneumonia the cause
risk factors instability, maternal infection, PROM
exam : distress, tep instabiltity, rash, hyopglycemia
treatment: empiric antibiotic - ampiciliin + cefotaxime… stay away from gentamicin bc can cause hearing loss

76
Q

Risk factors for SUIDS

A

sleep on stomach, sleep on soft surfaces, sleep on or under soft bedding
esposed to cigarette smoke in womb or environment, baby sleeps with adults

CPR (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions