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MHD Block 5: Renal > anemia I&II > Flashcards

anemia I&II Flashcards

1
Q

What maintains the unique shape of RBCs?

A

biconcave shape is maintained by:

-membrane skeleton = ankryin + spectrin

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2
Q

Describe the maturation and normal life span of an RBC

A
  • pleuripotent stem cell > reticulocyte > RBC
  • 120 days life span
  • removed from circulation by spleen and components are separated and recycled:
  • heme: iron
  • poryphorin: bilirubin
  • globin: amino acids
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3
Q

Name the three main categories of anemia?

A
  • blood loss: loss of RBCs
  • hemolytic: increased destruction
  • decreased production
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4
Q

What is the MCV and what does it tell us about types of anemia?

A

MCV: mean cell volume

80-100: normal range
100: macrocytic

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5
Q

Name the two main categories of hemolytic anemia

A

intrinsic: within the RBC; genetic OR acquired
extrinsic: outside of RBC; usually in the spleen

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6
Q

What are the main causes of intrinsic hemolytic anemia?

A

genetic:
- membrane defects: spherocytosis
- enzyme defects: GP6 deficiency
- low [hemoglobin]: thalassemia

acquired: Paroxysmal Nocturnal Hemoglobinuria

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7
Q

What are the main causes of extrinsic hemolytic anemia?

A
  • antibody mediated
  • chemical trauma
  • infections
  • chemical injury
  • splenomegaly
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8
Q

What is haptoglobin?

A

-haptoglobin is what binds to free hemoglobin released from hemolyzed RBCs

so if there is a lot of hemolysis, then [haptoglobin] will be low.

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9
Q

Describe spherocytosis: DDEPCT

A

D: abnormally shaped RBCs—discoid > spherically shaped

D: MCH + MCHC: elevated; osm fragility test (spherocytes take decreased amount of time to lyse when placed in hypotonic solution)

E: hereditary—auto dom. or auto rec

P: defect in ankyrin protein leads to decreased amounts of spectrin [membrane skeleton proteins]
= less interaction of RBC bilayer and cytoskeleton
= decreased membrane stability

C:

  • splenomegaly
  • anemia
  • jaundice
  • aplastic anemia: overworking of the bone marrow + infection = sudden drop of hemoglobin

T: splenectomy: decreases destruction of RBCs

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10
Q

Describe G-6-PD deficiency: DEPCT

A

D: deficiency in enzyme required to regenerate NADP in order to neutralize oxidative substances via reduced glutathione

E: x-linked, polymorphic, triggered by infections/toxins

P: w/o G-6-PD — heinz bodies
production due to oxidative substances denaturing hemoglobin
>cause intravascular hemolysis and damage to endothelium
>extravascular hemolysis: heinz bodies go to spleen, macrophages in the spleen bite the heinz bodies and spherocytes; spherocytes get stuck in spleen too

C: histo—–heinz bodies [crystal violet stain]

T: treat underlying infection, no specific treatment

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11
Q

Describe sickle cell disease: DEPCT

A

histo — automatic or induced sickling of RBCs on smear, gel electrophoresis: HgbS and HgbA migrate differently on gel

D: sickle shaped RBCs due to defective hemoglobin (HgbS)

E: African americans

P: mutation in beta globin gene causes hgb to aggregate and polymerize > distortion of RBCs to sickle shape
>hemolytic anemia
>occlusion of small vessels

C: splenomegaly (then fibrosis & auto-splenectomy), ischemic disease and infarct, increased risk of infection, aplastic anemia

T: pain control, blood transfusion, BM transplant

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12
Q

Describe alpha thalassemia: DEPCT

A

D: decreased alpha strand of hgb synthesis

E: genetic; alpha strand is encoded by two genes = so four total possible mutation leads to variation in the disease severity

P: decreased amount of alpha strands
>leads to less hgb
>imbalance of alpha and beta strands may lead to toxicity

C: anemia

T: no treatment, nutrient supplement, transfusion (severe)

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13
Q

Describe beta thalassemia: DEPCT

A

histo—target cells

D: absence of beta hgb strand synthesis

E: only 1 gene involved

P: decreased beta = aggregation of excess alpha
>RBC damage and decreased plasticity
»excess phago + hemolysis

C:
>minor: anemia —- trait: only one defective allele
»major: expansion of bone marrow (crew cut appearance)
»>splenomegaly + hematopoeisis in liver and spleen

T: tranfusions

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14
Q

Describe paroxysmal nocturnal hemoglobinuria: DPC

A

D: abnormal membrane protein

P: mutation in GP1 anchor protein in RBC membrane leads to activation of complement pathway

C:
>intravascular hemolysis
>thrombosis
>aplastic anemia

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15
Q

Which diseases include BOTH Intravascular and extravascular hemolysis?

A
  • sickle cell
  • g6pd deficiency
  • spherocytosis
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16
Q

Which two types of anemia may be mistaken for each other?

A

Thalssemia minor and Fe deficiency. IMP to rule out the other via:

> iron study: is iron low?
>Beta strand gel electrophoresis: normal or abnormal beta?
»levels of alpha strands a2 = increased, normal alpha is decreased

17
Q

Describe anemia caused by mechanical trauma: DEPCT

A

caused by:
-prosthetic cardiac valves: RBCs destroyed when they run into heart valves

  • microangiopathic hemolytic anemia: TTP, HUS, DIC
  • *schistocytes caused by abnormal fibrin deposits (via coag cascade) that destroy RBCs
18
Q

Describe iron deficiency anemia: DEPCT

A

histo—widened central palor + outer thin ring of hgb
D: microlytic anemia

P: chronic blood loss leads to: 
>depletion of ferritin
>circulating Fe depletion
>increased iron binding capacity (last resort)
>dec hgb + hemolytic anemia
C: 
>fatigue
>spoon nose
>smooth tongue
>interstitial malabsorption

T: iron supplements
figure out cause of blood loss

19
Q

Describe megaloblastic anemia: DEPCT

A 
D: anemia found in large RBCs
E: caused by Vit b12 OR folate low in diet and impaired absorption
>ileal resection
>IF deficiency
>tapeworm

P: defective DNA synthesis and maturation leads to large
oval nucleated [immature] RBCs

C: affects parts of the body that are actively dividing
>GI: gastritis
>blood and BM: decreased blood cell components
>CNS effects: seizures, encephalopathy, etc. [decrease methylmalonate] *only in Vit b deficiency

T: vitamin B12 supplements

20
Q

Describe anemia of chronic disease: DEPCT

A

How to differentiate with Fe deficiency anemia: increase Fe stores in BM and no increase in binding capacity (Fe deficiency: increased IBC)

D: anemia caused by increased hepcidin levels

E: common in hospitalized pts: chronic infection, malignancy, chronic immune disorders

P: hepcidin blocks transfer of Fe from macrophages to erythroid precursors
>decreased hgb
>microcytic anemia

C: anemia

T: treat underlying disease

21
Q

Describe aplastic anemia: DPCT

A

histo: more fat cells than stem cells in the the bone marrow

D: suppression of stem cells in the bone marrow

P: radiation, exposure to toxic chemicals, viral infections

C: anemia+ granulocytopenia + thrombocytopenia = pancytopenia

T: T cell suppression, stem cell transplant

MHD Block 5: Renal (13 decks)

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