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Boards > Pathoma Ch. 4 - Blood > Flashcards

Pathoma Ch. 4 - Blood Flashcards

1
Q

4 steps of primary hemostasis (w/ molecular causes)

A
  1. Vasoconstriction (reflex neural stim., ENDOTHELIN)
  2. Platelet adhesion (Collagen + vWF + Gp1b)
  3. Degranulation (ADP, TxA2)
  4. Aggregation (2b/3a + fibrinogen)
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2
Q

Functions of ADP and TxA2 from platelet degranulation

A

ADP – promote exposure of 2b/3a receptor

TxA2 – promote aggregation

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3
Q

Petechiae = ____ (NOT ___)

A

Thrombocytopenia (NOT qualitative disorder)

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4
Q

Purpose of giving IVIg

A

Compete with the actual problematic antibodies for the splenic macrophages –> reduce splenic hemolysis

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5
Q

ITP - where do antibodies come from?

A

Plasma cells in the spleen

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6
Q

TTP - why is ADAMTS13 deficient?

A

Acquired autoimmune antibody to it

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7
Q

HUS - why the symptoms? (3)

A

Verotoxin (Shiga-like toxin) causes endothelial cell damage –> thrombus formation in the kidney small vessels

Thrombi –> consumes platelets –> petechiae

Thrombi –> mechanical destruction of RBCs –> hemolytic anemia + schistocytes

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8
Q

TTP - why the neuro symptoms?

A

Thrombi form in small vessels of brain

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9
Q

Treatment for HUS and TTP

A

Plasmapheresis (remove antibodies)

Corticosteroids (stop antibody synthesis)

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10
Q

Qualitative platelet disorder + enlarged platelets

A

Bernard-Soulier (“Big Suckers”)

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11
Q

How does uremia affect platelet function?

A

Disrupts adhesion AND aggregation

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12
Q

Function of the coagulation cascade

What happens after that?

A

Produce thrombin, which converts fibrinogen to fibrin in the platelet plug

Fibrin is cross-linked –> STABLE

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13
Q

How to tell if clotting factor is deficient or being destroyed by antibodies?

A

Deficient –> mixing study corrects it

Antibodies –> mixing study does NOT correct it

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14
Q

Epoxide reductase

A

Activator of Vitamin K in the liver

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15
Q

Function of Vitamin K

What does that mean?

A

Gamma-carboxylation of factors 2, 7, 9, 10, C and S

Allows for CALCIUM to bind

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16
Q

Hemorrhagic disease of the newborn

A

Vitamin K deficiency (no gut bacteria)

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17
Q

Effect of liver failure on coagulation is measured via ___

A

PT

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18
Q

Function of Protein C
Function of Protein S
Function of Antithrombin 3

A 
C = inhibit 5 and 8
S = activate C (w/ thrombomodulin)
AT3 = inhibit 10 and 2 (thrombin)
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19
Q

HIT…explain

What to watch for?

What NOT to give? Why?

A

Heparin binds to PF4 on platelets
The body creates antibodies against these complexes
The spleen destroys the complexes (thrombocytopenia)

Platelet bits into circulation –> activation of others –> THROMBOSIS

Warfarin (risk of warfarin skin necrosis)

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20
Q

Warfarin skin necrosis…explain

Tie in w/ HIT?

A

Warfarin –> decreased Protein C and factor 7 FIRST –> increased coaguability –> blood clots in skin vessels

HIT –> thrombosis risk –> Warfarin INCREASES thrombosis risk –> tissue necrosis

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21
Q

Rattlesnake bite –> starts bleeding

A

Venom –> activates clotting cascade –> DIC

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22
Q

Sepsis –> bleeding from everywhere

A

Endotoxin + TNF/IL-1 –> endothelial cells express tissue factor –> DIC

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23
Q

Obstetric complication –> bleeding from everywhere

A

Tissue thromboplastin in the amniotic fluid

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24
Q

D-dimer comes from where?

A

Splitting of CROSS-LINKED fibrin

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25
Q

Functions of plasmin

What inactivates it?

A
  1. Cleave fibrin
  2. Destroy serum fibrinogen
  3. Block platelet aggregation

Alpha-2 anti-plasmin (serum protease inhibitor)

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26
Q

Radical prostatectomy –> excess bleediing

A

Release of UROKINASE activates plasmin

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27
Q 
Bleeding everywhere
Increased PT/PTT
Increased bleeding time
Normal platelet count
Normal qualitative studies
No D-dimer

Treatment?

A

Plasmin overactivation (cirrhosis, prostatectomy)

Tx = Aminocaproic acid (blocks plasminogen activation)

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28
Q

Lines of Zahn

Other way to distinguish from post-mortem clot

A

Alternation of platelets/fibrin w/ RBCs

Attachment to vessel wall

29
Q

Anti-thrombotic functions of endothelial cells (5)

A
  1. Block exposure to collagen and tissue factor
  2. PGI2 and NO –> vasodilation and inhibited aggregation
  3. Heparin-like molecules –> enhanced AT3
  4. tPA
  5. Thrombomodulin
30
Q

Describe the interaction between folate, B12, and homocysteine

Why is this important? (the homocysteine part)

A
  • THF circulates as methyl-THF
  • Methyl transferred to B12 –> THF drives thymidylate synthase (dTMP production)
  • Methyl transferred to homocysteine –> converted to methionine

Elevated homocysteine = THROMBOSIS via endothelial cell damage

31
Q

Long, slender fingers, lens dislocation, mental retardation, vessel thrombosis

Explain

A

Homocysteinuria

CBS deficiency (or B6 deficiency)

32
Q

Prothrombin 20210A

A

Inherited point mutation in prothrombin –> increased gene expression –> increased coagulation

33
Q

OCP hypercoaguability

A

Estrogen –> increased coagulation factor production

34
Q

Laparascopic surgery –> respiratory distress

A

Gas embolus (air pumped into abdomen)

35
Q

Amniotic fluid embolus – finding?

A

Squamous cells and keratin debris in the embolus

36
Q

What is required for a PE to cause symptoms?

A

Infarction of large or medium artery + pre-existing cardiopulmonary compromise (usually)

37
Q

PE – pathology

A

Hemorrhagic, wedge-shaped infarct

38
Q

Microcytic anemias (4)

A 
Iron deficiency
Anemia of chronic disease (functional deficit of iron)
Sideroblastic anemia (deficit of protoporphyrin)
Thalassemia (deficit of globin)
39
Q

Absorption location of…

  • Iron
  • Folate
  • B12
A 
Iron = duodenum
Folate = jejunum
B12 = ileum
40
Q

Gastrectomy –> iron deficiency

A

Acid keeps iron in 2+ state (“goes 2 the blood”)

41
Q

Functions of hepcidin (2)

A
  • Sequester iron, limiting transfer to RBCs

- Suppress EPO

42
Q

Increased free erythrocyte protoporphyrin

A

Iron deficiency of some kind

43
Q

Alpha vs. Beta thalassemia – genetics

A 
Alpha = gene DELETION
Beta = gene MUTATION (promotor or splice site)
44
Q

Microcytic, hypochromic RBCs
Increased RBC count
Target cells
Increased HbA2 and HbF

What causes target cells? (in general) (2)

A

Beta-thalassemia minor

Decreased cytoplasm OR increased membrane

45
Q

Microcytic, hypochromic anemia as an infant
Crewcut x-ray
Chipmunk facies
HSM

Increased risk for what? (2)

A

Beta-thalassemia major

Infusion-induced hemochromatosis
Aplastic crisis (B19)
46
Q

Beta-thalassemia major – see what on blood smear

A

Target cells

Nucleated RBCs

47
Q

Beta-thalassemia major - Hb type(s)?

A

Increased HbA2 and HbF

48
Q

Macrocytic anemia w/o megaloblastic change (3)

A
  • Alcoholism
  • Liver disease
  • 5-FU (ex.)
49
Q

Folate vs. B12 deficiency - time frame

A

Folate - months

B12 - years

50
Q

Causes of folate deficiency (6)

A
  • Alcoholic (poor diet)
  • Elderly (poor diet)
  • Pregnancy (demand)
  • Cancer (demand)
  • Hemolytic anemia (demand)
  • Methotrexate (inhibition)
51
Q

Describe pathway of B12 absorption (5)

A
  • Amylase liberates it
  • Bound by R-binder
  • Proteases in duodenum detach it
  • B12 binds IF in small bowel
  • B12-IF complex absorbed in terminal ileum
52
Q

Causes of B12 deficiency (5)

A
  • Pernicious anemia
  • Pancreatic insufficiency (no protease to detach it)
  • Crohn’s disease (ileum damage)
  • D. latum (ileum damage)
  • Vegans (dietary)
53
Q

Larger RBCs with bluish cytoplasm

A

Reticulocytes (residual RNA)

54
Q

How to determine true reticulocyte count?

Why?

What do the results mean?

A

RC x Hct/45

Anemia –> FALSE increased reticulocyte value

3+% = good marrow response (destruction)
Under 3+ = poor marrow response (underproduction)

55
Q

Normocytic anemia + extravascular hemolysis (3)

A

Hereditary spherocytosis
Sickle cell anemia
Hemoglobin C

56
Q

Normocytic anemia + intravascular hemolysis (5)

A 
PNH
G6PD deficiency
Immune hemolytic anemia
Microangiopathic hemolytic anemia
Malaria
57
Q

Sickle cell - increased risk of sickling (3)

A

Acidosis
Dehydration
Hypoxemia

58
Q

Intravascular hemolysis in sickle cell

See what on blood smear?

A

Damaged membrane due to sickling –> DEHYDRATES –> hemolysis, decreased haptoglobin, etc.

TARGET CELLS (dehydration)

59
Q

Sickle cell + gross hematuria and proteinuria

A

Renal papillary necrosis

60
Q

Microscopic hematuria, some HbS found

A

Sickle cell trait (only sickles in renal medulla)

61
Q

Metabisulfite test

A

Any amount of HbS –> sickling

Positive in the disease OR the trait

62
Q

Hemoglobin C - cause

See what on blood smear?

A

Glu –> Lys mutation (causes MORE positive charge)

HbC crystals

63
Q

PNH - deficiencies

A

No GPI –> no DAF –> no inhibitor of C3 convertase

64
Q

PNH - 3 tests for diagnosis

A
  • Sucrose test
  • Acidified serum test
  • Flow cytometry for CD55 (DAF)
65
Q

Death in PNH

A

Thrombosis of hepatic, portal, or cerebral veins

66
Q

**2 complications of PNH

A
  • Iron deficiency anemia (chronic hemolysis)

- ***AML

67
Q

Causes of IgG immune hemolytic anemia (5)

A

SLE, CLL, Penicillin, Cephalosporins, Alpha-methyldopa

68
Q

Causes of IgM immune hemolytic anemia (2)

A

Mycoplasma, Infectious Mononucleosis

69
Q

IgG vs. IgM immune hemolytic anemia – hemolysis

A 
IgG = extravascular
IgM = intravascular

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