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Hem/Onc > Pathology > Flashcards

Pathology Flashcards

1
Q

What happens to the CBC in acute blood loss anemia?

A

There are proportional decreased in blood count, including WBC and platelets.

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2
Q

What happens to reticulocyte production in acute blood loss? Does it increase or decrease?

A

Increases

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3
Q

This is the condition where there are premature destruction of RBC’s, ↑ EPO levels, and accumulation of Hb degredation products.

A

Hemolytic anemia

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4
Q

Is there more unconjugated or conjugated forms of bilirubin in hemolytic anemia?

A

Unconjugated

since theres an overload of Hb that can’t all be conjugated imemdiately

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5
Q

What happens to the levels of erythroid precursors/normoblasts in the marrow in hemolytic anemia?

A

Normoblasts ↑

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6
Q

This is the hemolysis of RBC’s within vessels.

A

Intravascular hemolysis

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7
Q

What is the protein responsible for picking up free Hb?

A

Haptoglobin

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8
Q

When haptoglobin’s reserves are depletes, what will the rest of the free Hb eventually be oxidized to?

A

Methemoglobin

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9
Q

So in intravascular hemolysis, what happens to the following values?

Blood Hb
Urine Hb
Urine hemosiderin
Blood haptoglobin

A

Blood Hb ↑ (hemoglobinemia)
Urine Hb ↑ (hemoglobinuria)
Hemosidinuria
↓ serum haptoglobin

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10
Q

If there is hemolysis in places other than the vessels, what is that condition called?

A

Extravascular hemolysis

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11
Q

What is the main organ that causes extravascular hemolysis?

A

Spleen’s sinusoids

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12
Q

Why would the spleen be a little biatch and break down RBC’s? What might be wrong with the RBC’s?

A

the RBC’s can become less deformable –> get stuck in the spleen sinusoids –> get phagocytoses and broken down

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13
Q

What happens to the gross spleen in extravascular hemolysis diseases?

A

Splenomegaly

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14
Q

This is an inherited defect int eh RBC cytoskeleton (tethering proteins) which causes weird RBC shapes and extravascular hemolysis?

A

Hereditary spherocytosis

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15
Q

What are the 3 main proteins affected by hereditary spherocytosis?

A

Spectrin
Ankyrin
Band 3.1

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16
Q

If theres loss of cytoskeletal proteins in herediatry spherocytosis, what might happen to the the SHAPE of the RBC?

A

It causes it to be spheres (lol it’s in the name) instead of disc-shaped

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17
Q

If there are sphere-shaped (pac man ghost shaped) RBC’s in hereditary spherocytosis, what happens in the spleen?

A

They can’t get through the sinusoids –> consumed by splenic marophages –> anemia

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18
Q

What happens to the color of the RBC’s in herediatary spherocytosis?

A

They lose their central pallor (cuz they’re all big and fat)

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19
Q

What happens to the RDW levels and MCHC levels in hereditary spherocytosis?

A

RDW ↑

MCHC ↑

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20
Q

What are the clinical manifestations of herediatary spherocytosis?

A

Splenomegaly
Jaundice with unconjugatted bilirubin (like any other hemolysis)
Biliribin gallstones

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21
Q

What is the test u should do to test for hereditary spherocytosis?

A

Osmotic fragility test

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22
Q

What is the 1 treatment for hereditary spherocytosis?

A

Splenectomy

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23
Q

After the splenectomy in hereditary spherocytosis, what might still appear in RBC’s on blood smear?

A

Howell Jolly bodies

fragments of nuclear material

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24
Q

This is a XR disorder wher ethe HMP shunt or glutathione metabolism are problematic.

A

G6PD deficiency

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25
Q

What is the main product of the HMP shunt (mainly by the G6PD enzyme), which helps reduce glutathione?

A

NADPH

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26
Q

What can the reduced glutathione break down so there arent oxidative injuries and hemolysis?

A

H2O2 (and other free radicals)

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27
Q

What is the form of G6PD deficiency where there is a mildly reduced half-like of G6PD, leading to mild hemolysis with oxidative stress?

A

African variant

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28
Q

What is the form of G6PD deficiency where there is MARKEDLY reduced half-like of G6PD, leading to marked intravascular hemolysis with oxidative stress?

A

Mediterranean variant

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29
Q

Regardless of the variant, G6PD deficiency has a protective role against which infection?

A

Falciparum malaria

think like theyre always a little under stress and the malaria that enters the RBC just gets pimp slapped

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30
Q

The oxidative stress in G6PD deficiency causes the formation of what of RBC inclusions?

A

Heinz bodies

ketchup in G6PD deficiency

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31
Q

What type of things can cause oxidative stress and are not warrarented in G6PD deficiency?

A

infections
drugs (primaquine, sulfa drugs, and dapsone)
Fava beans

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32
Q

In G6PD deficiency, when the Heinz bodies are removed from the RBC’s by splenic macrophages, they take a bite outta the RBC, causing the change to which morphology?

A

Bite cells

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33
Q

What is the presentaton of G6PD deficiency hourse after exposure to oxidative stress?

A

Hemoglobinuria and back pain

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34
Q

So to screen for G6PD deficiency, what cells do you look for?

A

Heinz bodies and bite cells

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35
Q

This is a disease where a point mutation in the 6th codon substitutes a Bal for a Glutamate.

A

Sickle cell

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36
Q

When there are low levels of what do you see polymerization of HbS and thus the sickle shape?

A

Oxygen

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37
Q

What form of Hb inhibits HbS, sometimes make it hard to Dx in infance?

A

HbF

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38
Q

What is the inheritance of HbS?

A

AR

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39
Q

What infections is HbS act as a protective role?

A

P. falciparum

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40
Q

In sickle cell disease, which system removies RBCs with damaged membranes, leading to anemia, jaundice with unconjugated hyperbilirubinemia, an increased risk for bilirubin gallstones (extravascular hemolysis patterns)?

A

Reticuloendothelial system (RES)

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41
Q

In sickle cell, if there is intravascular hemolysis, there is dehydration of the RBC cytoplasm, leading to what RBC morphology?

A

Target cells

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42
Q

In sickle cell disease, what happens to haptoglobin levels as intravascualr hemolysis persists?

A

↓ haptoglobin levels

they’re all getting bound by the new free Hb

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43
Q

If there is ANY hemolysis, what happens to erythroid precursors?

A

They undergo hyperplasia to compensate

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44
Q

In sickle cell disease, there is an expansion of hematopoieses into the skull and facial bones, leading to what facial morphology?

A

“Crewcut” appearance and chipmunk face

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45
Q

In sickle cell, irreversible sickling can lead to this condition, where there is swollen hands and feet due to vaso-occlusive infarcts int he bones, commonly in infants.

A

Dactylitis

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46
Q

In sickle cell, irreversible sickling reads to a this conition, which is characterized by a shrunked, fibrotic spleen.

A

Autosplenectomy

lol literally u take out ur own spleen

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47
Q

If there is autosplenectomy in sickle cell, what 3 bugs are u at risk for getting?

A

Encapsulated organisms, such as…

Strep pneumoniae
H influenza (most common cause of death in children)
Ssalmonella paratyphi osteomyelitis

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48
Q

What bodies are seen on blood smear in sickle cell>

A

Howell-Jolly bodies

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49
Q

In sickle cell disease, this is the condition where there is vaso-occlusion in the pulmonary microcirculation, leading to chest pain, SOB, lung infiltrates, and often precipitated by PNA.

A

Acute chest syndrome

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50
Q

Acute chest syndrome is the most common cause of death in what sickle cell age pts?

A

Adults

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51
Q

And again, what is the most common cause of death in kids with sickle cell?

A

H. influenza from autosplenectomy

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52
Q

What is the renal manifestations of Sickle Cell disease?

A

Renal papillary necrosis (hematuria and proteinuria)

remember the “SOAP” acronym for papillary necrosis?

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53
Q

This is the form of sickle cell condition where there is the presenc of 1 mutated and 1 normal.

A

Sickle Cell TRAIT

just like being heterozygous

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54
Q

True or False: sickle cell trait is generally asymptomatic as there is never any sickling of the cells.

A

FALSE

There is sickling of the RBC’s with <In which50% except in the renal medulla

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55
Q

In which condition (disease or trait) do you see sickle and target cells on blood smear?

A

Sickle cell disease

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56
Q

What is the screen for sickle cells which causes cells with ANY amount of HbS to sickle, yielding a + result in both disease and trait?

A

Metabisulfite screen

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57
Q

Infection with which virus can complicate the already poor production and cause aplastic crisis (low reticulocyte count) in sickle cell disease?

A

Parvovirus B19

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58
Q

Generally, this is anemia due to decreased synthesis of the globin chains of Hb, which leads to microcytic anemia.

A

Thalassemia

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59
Q

Which infections are thalassemias good at resisting?

A

P. falciparum

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60
Q

How many alpha-globin genes do we have on chromosome 16?

A

4

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61
Q

What is the Sx of a-thalassemia with 1 gene deleted?

A

There arent any.

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62
Q

What is the Sx of a-thalassemia with 2 genes deleted?

A

mild anemia with increased RBC count

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63
Q

What is the form of a-thalassemia with 2 genes deleted where there an increased risk of severe thalassemia in the OFFSPRING?

A

cis deletion

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64
Q

Which demographics are at risk for cis deletions of the a-globin?

A

Asians

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65
Q

Which demographics are at risk for trans deletions of the a-globin?

A

African Americans

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66
Q

What is the Sx of a-thalassemia with 3 genes deleted?

A

Severe anemia

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67
Q

This is the form of Hb when 3 alpha-globin genes are deleted, forming a tetramers of B-chains, which can damage RBC;s.

A

HbH

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68
Q

What is the Sx of a-thalassemia with 4 genes deleted?

A

YOU DEAD

hydrops fetalis

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69
Q

This is the form of Hb where there are tetramers of gamma-globin chains

A

Hb Barts

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70
Q

Instead of deleting the whole gene, where on the DNA is there deletions to cause B-thalassemia?

A

usually in the PROMOTER region

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71
Q

This is the minor form of B-thalassemia, and is typically asymptomatic, an ↑ RBC count, and u see microcytic hypochromic RBC’s on blood smear.

A

ß-thalassemia minor (ß/ß+)

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72
Q

What special form of RBC’s do u see on blood smear for ß-thalassemia minor?

(think low cytoplasm)

A

target cells

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73
Q

For ß-thalassemia minor, what do u see on Hb electrophoresis?

A

↓ HbA with isolated HbA2

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74
Q

This is the form of ß-thalassemia which is more severe, there is high HbF, and alpha tetramers of aggregate and damage RBCs.

A

ß-thalassemia major (Bo/Bo)

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75
Q

Do you see extravascular or intravasuclar hemolysis in ß-thalassemia major?

A

Extravascular

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76
Q

ß-thalassemia leads to the same massive erythroid hyperplasia problems (weird skull, extra medullary hematopoiesis with hepatosplenomegaly, and risk of aplastic crisis with parvovirus B19) as what other extravascular hemolysis disease?

A

Sickle cell disease

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77
Q

What is the main treatment for ß-thalassemia?

A

Chronic transfusions

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78
Q

What is the main complication with chronic transfusions in the treatment of ß-thalassemia?

A

Secondary hemochromatosis

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79
Q

In addition to microcytic, hypochromic RBC’s and target cells, what type of RBC’s do u see in ß-thalassemia, as if they were make in the spleen or liver?

A

Nucleated RBCs

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80
Q

This is a defect in myeloid stem cells resulting an absent GPI, rendering cell susceptible to destruction by complement.

A

Paroxysmal Nocturnal Hemoglobinuria (PNH)

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81
Q

Is PNH inherited or acquired?

A

Acquired

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82
Q

What is the molecule on the surface of normal RBC’s which inhibits C3 convertase, which protects it from complement-mediated damage.

A

Decay Accelerating Factor (DAF)

AKA CD55

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83
Q

Which molecule secures DAF to the RBC membrane? It also secures CD59 to the membrane as well.

A

GPI

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84
Q

In PNH, there is a lack of GPI, leading to what problem?

A

Complement-mediated damage

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85
Q

What happens during the nightime, which causes the nocturnal hemoglobinuria?

A

Mild respiratory acidosis –> activation of complement –> lysis of RBCs and WBCs and platelets

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86
Q

In PNH, the intravascular hemolysis at night leads to what changes in the blood and urine?

A

hemoglobinemia
Hemoglobinura
Hemosidinuria (seen days after hemolysis)

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87
Q

What is the test that is used to screen for PNH?

A

Sucrose test

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88
Q

What is the confirmatory test for PNH?

A

Acidified urine test or flow cytometry to detect the lack of CD55 (DAF) on blood cells.

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89
Q

What is the main cause of death in PNH?

A

Thombosis of hepatic, protal, or cerebral veins

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90
Q

What are the 2 main complications to PNH?

A

Iron deficiency anemia

Acute myeloid leukemia (AML)

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91
Q

This is the antibody-mediated (IgG or IgM) destruction of RBCs.

A

Immune hemolytic anemia (IHA)

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92
Q

Which IHA involved EXTRAvascular hemolysis (IgM or IgG)?

A

IgG-mediated

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93
Q

In IHA, when does the IgG’s bind to the RBC, which is then consumed by splenic macropahges, leading to spherocytes?

A

In warm temperature (warm agglutinin, like in the central body)

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94
Q

What is the autoimmune disorder associated with IgG IHA?

A

SLE

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95
Q

PCN and cephalosporins can cause IgG IHA because of what mechanism?

A

Drug attaches to RBC membrane –> Ab attaches to drug –> extravascular hemolysis

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96
Q

The drugs (like a-methyldopa) that can cause IgG IHA can leave a resdual effect, where you might start producing what molecules, leading to extravascular hemolysis?

A

Autoantibodies

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97
Q

What is the treatment for IgG IHA?

A

Cessation of the offending drug, steroids, IVIG, and if necessary, splenectomy

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98
Q

What is the IHA conditon that involved intravascular hemolysis?

A

IgM-mediated

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99
Q

Under what condition does IgM bind RBCs and fix complement?

A

Relatively cold temperatures

cold agglutinin, like in the extremities

100
Q

What 2 infections is associated with IgM IHA?

A

Mycoplasma pneumoniae and infectious mononucleosis

101
Q

This is the test that is used to Dx IHA.

A

Coombs test

102
Q

This is the form of Coombs test where Anti-IgG is added to pts RBCs, and see if agglutination occurs (they do if RBC’s are already coated with Ab).

A

Direct coombs test

103
Q

What is the procedure for the INdirect coombs test?

A

It sees in Ab’s are in the SERUM…

anti-IgG and test RBCs are mixed with the pts serum, and agglutination occurs if the serum antibodies are present.

104
Q

This is the condition where there is microangiopathic hemolytic anemia from O157:H7 bacteria.

A

HUS

105
Q

What is the O157:H7 toxin that damages endothelial cells, leading to platelet microthombi?

A

Verotoxin (pathoma version)

Shiga or Shiga-like toxin (Moscatello version)

106
Q

In normal B12 metabolism, what is bound to B12 as it enters the mouth and protects it until it reaches the duodenum?

A

R-binder

107
Q

Once the B12 reaches the duodenum, it gets complexed to Intrinsic Factor, which come from what GI cells?

A

Gastric parietal cells

108
Q

Where in the bowel is the B12-IF complex absorbed?

A

Terminal ileum

109
Q

After how long do u need to develop B12 deficiency? Why?

A

YEARS

the liver stores a lot of it, so u see this in strict vegans and stuff

110
Q

This is the most common anemia to cause B12 deficiency, where there is autoimmune destruction of parietal cells, leading to the absence of IF.

A

Pernicious anemia

111
Q

What can cause damage to the terminal ileum, leading to B12 deficiency from a lack of uptake from the GI?

A

Chron disease

Diphyllobothrium latum tapeworm

112
Q

Both B12 and folate deficiencies lead to what morphological change in RBCs?

A

Macrocytic RBCs

113
Q

What happens to the neutrophils in B12 deficiency?

A

Theyre hypersegmented

114
Q

What happens to the tongue in B12 deficiency>

A

Glossitis

115
Q

What happens in the spinal cord in B12 deficiency?

A

Subacute combined degeneration

(B12 is required for the conversion of methylmalonic acid –> succinyl CoA for FA metabolism, so it impairs spinal cord meylinization)

116
Q

For blood labs, what happens to vitamin B12, serum homocysteine, and methylmalonic acid levels in B12 deficiency?

A

B12 ↓
↑ serum homocysteine (↑ risk for thrombosis)
↑ methylmalonic acid (unlike folate deficiency)

117
Q

Folate and B12 are necesary for the synthesis of what in the cell?

A

DNA

118
Q

In order to be transferred from methyl THF to folate, what molecule must pick up the methyl group?

A

B12

119
Q

The Methyl-B12 molecule then transfers the methyl to which other molecule to produce methionine?

A

Homocyteine

120
Q

Where in the gut is folate absorbed?

A

Jejunum

121
Q

How long must it take to develop a folate deficiency?

A

Months

122
Q

In what type of pts do you see a folate deficiency from poor diet?

A

Alcoholics and the elderly

123
Q

In what type of pts do you see a folate deficiency from increased demand?

A

Pregnancy, cancer, ane hemolytic anemia

basically any time you are using a lot of folate to make new DNA

124
Q

In what type of pts do you see a folate deficiency from folate antagonists?

A

Pts taking metrhotrexate, which inhbiits DHF reductase)

125
Q

What happens to the tongue in folate deficiency, like in B12 deficiency?

A

Glossitis

126
Q

What is the RBC morphology in folate deficiency, like in B12 deficiency?

A

Macrocytic RBCs

127
Q

What is the neutrophil morphology in folate deficiency, like in B12 deficiency?

A

Hypersegmented neutrophils (> 5 lobes)

128
Q

What are the serum levels of folate, homocysteine, and methylmalonic acid in folate deficiency?

A

Folate ↓
↑ homocyteine
NORMAL methylmalonic acid (in B12 deficiency it’s ↑)

129
Q

This is the type of anemia from ↓ iron levels, and is the most common type of anemia.

A

Iron deficiency anemia

130
Q

What is the RBC morphology in Iron deficiency anemia?

A

hypochromic microcytic

131
Q

Where in the gut is iron absorbed?

A

Duodenum

132
Q

What is the transporter on enterocytes that absorbed Fe into the cell?

A

DMT1

133
Q

What is the molecule that transports iron across the cell membrane into the blood?

A

Ferroportin

134
Q

What is the molecule that transports Fe in the blood and delivers it to liver and bone marrow macrophages for storage?

A

Transferrin

135
Q

What is the stored intracellular iron bound to, which prevents Fe from forming free radicals via the Fenton rxn?

A

Ferritin

136
Q

This is the measure of transferrin molecules in the blood,

A

TIBC

total iron-binding capacity

137
Q

True or False: the serum ferritin accurately reflexts iron stores in macrophages and the liver.

A

True

138
Q

Why do infants get Iron deficiency anemia?

A

Breast feeding (human milk is low in iron)

139
Q

Why do kids get Iron deficiency anemia?

A

poor diet

140
Q

What is the main cause in male and female adults in Iron deficiency anemia?

A

Males- peptic ulcer disease

Females- Menorrhagia or pregnancy

141
Q

What is the main cause of Iron deficiency anemia in the elderly in the Western world?

A

Colon polyps/carcinoma

142
Q

What is the main cause of Iron deficiency anemia in the elderly in the developing world?

A

Ancylostoma duodenale and Nieator ameicanus

143
Q

What happens to the ferritin and TIBC levels when storage iron is depleted in Iron deficiency anemia?

A

↓ ferritin

↑ TIBC (liver makes more transferrin to seek out more Fe)

144
Q

What is the intial stage of Iron deficiency anemia, characterized by bone marrow making fewer, but normal sized RBCs?

A

Normocytic anemia

145
Q

Normocytic anemia progresses to what RBC morphology in Iron deficiency anemia?

A

Microcytic hypochromic anemia

146
Q

This is the condition of Iron deficiency anemia where there is spoon-shaped nails.

A

Koilonychias

147
Q

This is the condition of Iron deficiency anemia where u eat random crap like dirt and hair.

A

Pica

148
Q

Why is the Free erythrocyte protoporphyrin (FEP) levels ↑ in Iron deficiency anemia?

A

Cuz when heme breaks down to Fe and protoporphyrin, since Fe is ↓ and protoporphyrin in normal, it gets free in the RBC

149
Q

What is the treatment for Iron deficiency anemia?

A

Supplemental iron (ferrous sulfate) and the underlying cause

150
Q

This is a manifestation of Iron deficiency anemia where there is esophageal webs and atrorophic glossitis, and presents as anemia, dysphagia, and a beefy-red tongue.

A

Plummer-Vinson syndrome

151
Q

What is the molecule that inhibits Ferriportin, which normally allows Ferrous ions out of the cell?

A

Hepcidin

152
Q

This is the anemia assocaited with chronic inflammation (endocarditis or autoimmune conditions, and is the most common type of anemia in HOSPITALIZED pts.

A

Anemia of chronic disease

153
Q

What is the important molecule produced in Anemia of chronic disease, which sequesters iron storage sites?

A

Hepcidin

154
Q

What are the 2 ways hepcidin sequesters iron storage?

A
  1. limiting Fe transfer from macrophages to erythroid precursors
  2. supressing EPO production
155
Q

What happesn to the ferritin, TIBC, serum iron, and FEP in Anemia of chronic disease?

A

↑ ferritin
↓ TIBC
↓ serum iron
↑ FEP

156
Q

In Anemia of chronic disease, what agent is used in the treatment, especially in those with cancer?

A

Exogenous EPO

157
Q

In Anemia of chronic disease, what is the role of hiding away all the Fe? What is it trying to prevent from accessing the iron?

A

Hiding away all the iron prevents the bacteria from accessing iron, which is necessary for their survival

(but it turn it leads to anemia cuz it takes the Fe from your own cells to use)

158
Q

This is the condition where there is reduced #’s of RBCs, WBCs, and platelets.

A

Pancytopenia

159
Q

This is the type of anemia where chemicals, viral infections, radiation, or drugs cause marrow suppression, leading to pancytopenia.

A

Aplastic anemia

“a-“ = without, “-plastic” = formation –> “without formation” anemia

160
Q

IF you take a bone marrow biopsy in aplastic anemia, what would the marrow look like?

A

Empty and fatty

161
Q

What is the treatment for aplastic anemia?

A

cessation of caustive drugs and supportive care with marrow-stimualting factors (EPO, GM-CSE, and G-CSE)

162
Q

What is the last resort treatment for aplastic anemia?

A

Bone marrow transplant

163
Q

This is the condition of a primary marrow disorder wehre erythroid progenitors are suppressed.

A

Pure red cell aplasia.

164
Q

What viral infection can cause pure red cell aplasia?

A

Parvovirus B19

165
Q

In what type of pts does an aplastic crisis occur with Parvovirus B19 infection?

A

Moderate-severe hemolytic anemias

166
Q

In addition to parvoviral infections, what causes pure red cell aplasia?

A

Thymoma + large granular lymphocytic leukemia
Drugs
Autoimmune disorders

167
Q

This is the condition where a pathological process (like metastatic cancer) replaces bone marrow, causing impairment of hematopoiesis, resulting in pancytopenia.

A

Myelophthisic process

168
Q

This is an abnormally high red cell count, usually with a corresponding increase in Hb levels.

A

Polycythemia

169
Q

This is the form of polycythemia from dehydration, vomiting, diarrhea, or excessive diuretic use.

A

Reactive polycythemia

170
Q

What is the main cause of the primary form of polycythemia (low EPO)?

A

Polycythemia vera

171
Q

What is the cause of secondary polycythemia from compensatory mechanisms?

A

Lung disease
High altitude living
Cyanotic heart disease

172
Q

What is the cause of secondary polycythemia from paraneoplastic mechanisms?

A

EPO-secreting tumor

173
Q

What might the change in Hb itself to cause secondary polycythemia?

A

Hb mutants with high O2 affinity

174
Q

What are the 2 things that can cause secondary polycythemia where there is stabilization of HIF-1a?

A

Chauvash polycythemia

Prolyl hydroxylase mutations

175
Q

Petechiae and purpuric hemorrhages can form in which infections?

A

Meningiococcemia

Other forms of septicemia
Infective endocarditis
Several rickettsioses

176
Q

What is the condition where there is deposition of drug-induced immune complexes in the vessel wall, leading to cutaneous petechiae and purpura?

A

Hypersensitivity (leukocytoclastic) vasculitis

177
Q

What 2 disorders can cause microvascular bleeding due to defects in collagen?

A

Scurvy and Ehlers-Danlos

178
Q

This is a condition form systemic hypersensitivity of unknown cause, and is characterized by purpuric rask, colicky abd pain, polyarthralgia, and acute glomerulonephritis.

A

Henoch-schonlein purpura

179
Q

This is an AD disease where dilated tortuous blood vessels with thin walls can bleed easily, and is common under mucous membranes of the nose, tongue, motuh, eyes, and GI tract.

A

Hereditary hemorrhagic telangiectasia

Weber-Osler-rendu

180
Q

Why can perivascular amyloidosis cause mucocutaneous purpura?

A

Amyloids weaken blood vessel walls and causes bleeding

181
Q

Under what platelet level do u determine thrombocytopenia?

A

< 100,000 platelets/uL

182
Q

What 2 general classes can thrombocytopenias be classifies?

A

Qualitative (↓ quality) and quanitative (↓ #)

183
Q

What are the 2 main classical Sx of thrombocytopenia?

A
  1. Mucosal bleeding

2. Skin bleeds (petichiae, purpura, ecchymosis, easy bruising)

184
Q

This is the form of thrombocytopenia where allantibodies are produced in response when platelets are transfused or cress the placenta from fetus into pregnant mother.

A

Neonatal thrombocytopenia

185
Q

This is the form of thromboytopenia where massive transfusion can cause a dilutional thrombocytopenia.

A

Transfusion thrombocytopenia

186
Q

This is the QUANTITATIVE thrombocytopenia where there is autoimmune production of IgG against the platelets Ag’s (GpIIb/IIIa).

A

Idiopathic Thrombocytopenic Purpura (ITP)

187
Q

True or False: ITP is the most common cause of thrombocytopenia in children and adults.

A

True!

188
Q

Which cells in the spleen make the autoantibodies for ITP?

A

Plasma cells

189
Q

Which cells then consumes the antibody bound platelets in ITP?

A

Splenic macrophages

Ab’s are made in the spleen and consumed in the spleen

190
Q

In which ages do u see the acute form of ITP weeks after viral infection or immunzation, and is typically self-limited?

A

Kids

191
Q

Who is at risk for the chronic form of ITP?

A

Women of child bearing age

192
Q

Though chronic ITP can be idiopathic, what is the main secondary condition that can cause it?

A

SLE

193
Q

Since the antiplatelet IgG can cross the placenta in chronic ITP, what might occur in the newborn?

A

Short-lived thrombocytopenia

194
Q

What happens to the serum platelet levels, PT/PTT, and megakeryocytes on bone marrow biopsy for ITP?

A

↓ platelets (usually < 50k/ul)
NORMAL PT/PTT (doesnt touch coag cascade)
↑ megakaryocytes (compensatory hyperplasia)

195
Q

Kids respond well with what treatment for ITP?

A

Corticosteroids

196
Q

What is the treatment for ITP that involves giving splenic macrophages something else to eat other than the platelets?

A

IVIG

197
Q

Why is a splenectomy killin 2 birds for the treatment of ITP?

A

You eliminate the source of Ab and the site of platelet destruction

198
Q

TTP and HUS are of what class of quantitative thrombocytopenias under what anemia?

A

Microangiopathic hemolytic anemia

199
Q

What happens in microangiopathic hemolytic anemia in the small vessels to cause hemolytic anemia?

A

Formation of platelet microthrombi –> partial lumen occlusion –> sharing of RBCs –> schistocyte formation –> hemolytic anemia

200
Q

What is the mrophology of the RBC’s in microangiopathic hemolytic anemias?

A

Shistocytes

pac man ghosts

201
Q

This is the form of microangiopathic hemolytic anemia where there is microthrombi formation from ADAMTS13 enzyme loss.

A

TTP

202
Q

What is the normal role of ADAMTS13 enzyme?

A

breaks down vWF multimers

203
Q

In adult females, what is the cause of the loss of ADAMTS13 seen in TTP?

A

auto-Ab

204
Q

What is the pentad of Sx in TTP?

A 
Fever
Thrombocytopenia
Microangipathic hemolytic anemia
****NEURO defects****
Renal failure
205
Q

HUS has basically the same Sx as TTP except what is enchanced?

A

RENAL FAILURE

hemolytic UREMIC syndrome

206
Q

Bernard-soulier, Glanzmann thromasthenia, ASA, and uremia are all what types of thrombocytopenia?

A

Qualitative disorders

↓ quality of the platelets

207
Q

What is the deficiency in Bernard-Soulier syndrome, causing problems with platelet adhesion?

A

GpIb deficiency

208
Q

What shows up on blood smears for Bernard Soulier syndrome?

A

Mild thrombocytopenia with enlarged platelets (Big Suckers)

209
Q

This is the a qualitative thropmbocytopena where there is a deficiency in GpIIb/IIIa, causing problems with platelet aggregation.

A

Glanzmann thrombasthenia

210
Q

What product of COX is lost if u give ASA, leading to impairment of platelet aggregation?

A

TXA2

211
Q

What problems may cause uremia, which disrupts platelet fxn and leads to both platelet adhesion AND aggregation problems?

A

Liver or renal problems

212
Q

How many variants are there for vW disease?

A

> 20

213
Q

What is the most common type of vW disease, where there is mild-mod vWF deficiency?

A

type 1 (AD inherited)

214
Q

Which type of vW disease shows ectremely low levels of vWF and severe manifestations, and is from frameshift mutations or deletions?

A

type 3 vW disease

215
Q

Which test is abnormal in vWF diease (specific for this disease)?

A

Ristocetin test

216
Q

What is the treatment of choice for vW disease?

A

Desmopressin

217
Q

Which type of vW disease shows qualitative defect in vWF (poor assembly), and has mild-mod bleeding?

A

type 2A

218
Q

Which factor is mutated in hemophilia A?

A

Factor VIII

219
Q

Which coag pathway is affected by hemophilia A?

A

Intrinsic pathway

220
Q

What is the inheritence of hemophilia A?

A

XR

221
Q

Where is the bleeding in hemophilia A?

A

Deep tissue, joint , and postsurgical bleeding

222
Q

So where is the bleeding in primary hemostasis disorders vs secondary?

A

Primary- in the mucosa and skin

Secondary- in deep tissues

223
Q

What happens to the PTT, PT, platelet count,annd bleeding time in hemophilia A?

A

↑ PTT

everything else normal

224
Q

What is the treatment for Hemophilia A?

A

recombinant FVIII

225
Q

Which coag factor is mutated in hemophilia B?

A

IX

226
Q

This is a pathologic activation of the coag cascarde, where there is widespread microthrombi causing ischemia and infarction.

A

DIC

227
Q

Which 5 things can cause DIC?

A 
Obstetric complication (amnitotic tissue has thromboplastin)
Sepsis
Adenocarcinoma (mucus)
APL
Rattlenake --[][][][][][][][][]D~

(that’s a snake not a ween)

228
Q

What happens to the platelet count, PT/PTT, and fibrinogen levels in DIC?

A

↓ platelets
↑ PT/PTT
↓ fibrinogen (cuz u use it all)

229
Q

What is the specific thing u can screen for in DIC whichi is the product of lysing cross linked fibrin, which tells u the entire coag cascade is activated so much u activate teh splitting of the cross-linked fibrin?

A

Fibrin split products (D-dimers)

230
Q

What is teh treatment for DIC?

A

to the cause, and transfuse and cryoprecipitate if needed

231
Q

What type of anemia is a manifestation of DIC?

A

Microangiopathic hemolytic anemia (like in TTP and HUS)

232
Q

This is a reduction in the # of neutrophils int eh blood.

A

Neutropenia

233
Q

This is a clinically significant reduction in neutrophils in the blood, and has a serious consequence of makign pt susceptible to bacterial and findal infections.

A

Agranulocytosis

234
Q

What is the most common cause of agranulocytosis?

A

Drug toxicity

(aminopyrine, chloramphenicol, sulfonamides, chlorpromazine, thiouracil, and phenylbutazone

235
Q

This the form of leukocytosis which is caused by acute bacterial infections and sterile inflammation.

A

Neutrophilic leukocytosis

236
Q

This the form of leukocytosis which is caused by allergic disorders.

A

Eosinophilic leukocytosis

237
Q

This the form of leukocytosis which is caused by myeloproliferative disease and is rare

A

Basophilic leukocytosis

238
Q

This the form of leukocytosis which is caused by chronic infections, bacterial endocarditis, rickettsiosis, malaria, and collagen vascular diseases and IBD.

A

Monocytosis

239
Q

This the form of leukocytosis which accompanies monocytosis in many disorders assocaited with chronic immunological stimulation, viral infections, and Bordetella pertussis infection.

A

Lymphocytosis

240
Q

This is a conditon where there is acute lympahdenitis in the cervical region likely due to microbial drainage from infections of teeth/tonsils.

A

Acute non-specific lymphadenitis

241
Q

What is the main cause of congestive splenomegaly?

A

Liver cirrhosis

242
Q

Where might there be thrombosis or pylephlebitis to cause congestive splenectomy?

A

Portal v.

243
Q

What can cause splenic rupture?

A

BLUNT TRAUMA

244
Q

What are the 4 predisposing factors for splenic rupture?

A

Mono
Malaria
typhoid fever
Lymphoid neoplasms

245
Q

Why are enlarged spleen UNlikely to rupture?

A

because of the toughening effect of extensive reactive fibrosis

Hem/Onc (5 decks)

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