Brainscape's Knowledge GenomeTM

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


See full index

Z - M2 Heme/Onc > Heme/Onc - Week 3 Review - Part 2 > Flashcards

Heme/Onc - Week 3 Review - Part 2 Flashcards

1
Q

Primary Hemostasis - 3 Major Steps

A

1) Trasient Vasoconstrition (Neurogenic + Endothelial Release)
2) Platelet Adhesion (vWF binds sub-endothelial collagen + GP1b from Platelets)
3) Platelet Aggregation - Platelets bind vWF + Each other via GPIIB/IIIA - Release granules with TXA2 + ADP)

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

vWF Production - 2 Places

A

1) Alpha Granules of Platelets

2) Wiebl-Palade Bodes if Endothelial Cells (Also produce p-selectin for speed bumps in inflammation)

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

Disorders of Primary Hemostasis - 2 Major Classes + 6 Disorders

A

Disorders of Platelet Quantity

1) Acute Immune Thrombocytopenic Purpura
2) Chronic Immune Thrombocytopenic Purpura
3) Microangiopathic Hemolytic Anemia - Thrombocutopenic Purpura
4) Hemolytic Uremia Syndrome - Microangiopathic Hemolytic Anemia

Disorders of Platelet Quality

5) Bernard Soulier
6) Glanzmann Disroder

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

Major Features of Primary Hemostatsis (5)

A

1) Skin + Mucousal Bleeding
2) Petechia = Thrombocytopenia
3) Low Platelet Count
4) High Bleeding Time
5) Normal PT/PTT (No Coagulation Factors involved)

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

Immune Thrombocytoic Purpura (ITP) - 2 Forms + Pathopyhsiology

A

Acute - Children after Viral Infection
Chronic - Adults - SLE + CLL

Autoimmune IgG Antibody against Platelets Antigen (GPIIb/IIIa) - Antibody bound platelets consumed in macrophages

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

Immune Thrombocytoic Purpura (ITP) - Key Lab Findings (4) + Treatment (2)

A

Findings

1) Large Platelets
2) Increase MK Cells in Marrow
3) Thrombocytopenia
4) Long Bleeding Time with Normal PT/PTT

Treatment

1) Steroids
2) IVIgG

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

Fetal-Maternal ITP - Key Facts (2)

A

1) Material IgG attacks fetal platelets

2) HPA-1A = Most Common

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

Microangiopathic Hemolytic Anemia - Definition Causes (4) + Classic Findings (3)

A

Anemia caused by RBC desctruction when the crash into micro-thrombi - causes using up/damage to platelets

Causes

1) TTP
2) HUS
3) DIC
4) Mechanical Heart Valves

Classic FIndings

1) Skin/Mucosal Bleeding (vs. Joints in Secondary Hemostasis disoders)
2) Renal Symptoms (worse in HUS)
3) CNS Symptoms (worse in TTP)

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

Microangiopathic Hemolytic Anemia - Lab Findings (5)

A

1) Thromboyctopenia
2) Normal PT/PTT with elevated Bleeding Time
3) Schistocytes (Half cells with points from microthrombi damage)
4) Increased Mega-K Cells in Marrow
5) Elevated LDH

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

Thrombocytopenic Purpura (TTP) - Mechanism + Cause (3)

A

ADAMTS13 - Normally cleaves vWF allowing for degradation - No ADAMTS13 - No vWF degradation = over-production of micro thrombi

Causes

1) Congenital
2) Acquired - Antibodies to ADAMTS - Treat with plasmapheresis to remove the Ab

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

Thrombocytopenic Peurpura vs. DIC (2 Differences) vs. Hemolytic Uremic Syndrome (1 Key)

A

TTP vs. DIC
TTP has Normal D-Dimer (not breaking down clots causing fibrin split products)
TTP has either low ADAMST13 of Ab’s - DIC Does not

TTP vs. HUS
TTP = Worse CNS S/Sx
HUS = Worse Renal S/Sx

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

Hemolytic Uremic Syndrome (HUS) - Mechanism + Causes (2)

A

Mechanism - Microthrombi production due to endothelial damage

Acquired = E. Coli 157:H7 -Shiga Verotoxin damages endothelium
Congenital/Atypical = Complement Factor H Defect (CD46 Issues)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Qualitative Platelet Disorders (2) + Mechanism

A

1) Bernard Souiler - Genetic GP1b deficiency - issue with platelet adhesion (can’t bind vWF
2) Glanzamann - Genetic GPIIb/IIIa deficiency - issue with platelet aggregation (can’t bind each other + form fibrin cross links)

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

Bernard Souiler - 2 Key Findings

A

1) Large Platelets with Thrombocytopenia (Platelets Die)

2) Ristocetin Test - Abnormal

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

Major Tests for Heme/Onc (8)

A

1) Nitro Blue - Chronic Granulomatous Disease
2) D-Dimer - DIC
3) Schilling Test - B12
4) Metabisulfite Test - HbS - Trait/Disease
5) Osmotic Fragility - Heriditary Spherocytosis
6) Sucrose Test - PNH + CD55 Follow-Up
7) Ristocetin Test - Benard Soulier + vWF Disease
8) Mixing Test - Lack of a Factor vs. Ab against a Factor

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

PT vs. PTT - Pathway Measured + Medication Checked

A

PT
Extrinsic = Tissue Factor/ FVII
Checks Coumadin

PTT
Intrinsic = XII, XI, IX, VIII
Checks Heparin

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

Hemophila A - Inheritance Pattern + Defect + Findings (4)

A

X-Linked Recessive VIII Deficiency

1) Normal PT with Elevated PTT
2) Hemarthrosis (Joint Bleeding)
3) Deep/Surgical Bleeding
4) FVIII binds vWF for stabliization - loss of vWF can mimic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Hemophila B - Inheritance Pattern + Defect + Findings (3)

A

X-Linked Recessive IX Deficiency

1) Normal PT with Elevated PTT
2) Hemarthrosis (Joint Bleeding)
3) Deep/Surgical Bleeding

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

Disorders of Primary vs. Secondary Hemostasis - Findings - 2 Major Differences

A

Primary

1) Normal PT/PTT (No Coagulation Factors Impacted) + Increased Bleeding Time
2) Typically Superficial Bleeding (Mucousal/Skin/Gums)

Secondary

1) Typically changes in either PT or PTT (Coagulation involved)
2) Typically deep bleeding - Hemarthrosis (Joint) + Surgical

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

Coagulation Factor Inhibitor Disease

A

Acquired Ab against factor - VIII and XIII Most Common

Mixing Test - Acquired Ab won’t respond to plasma infusion vs. Inherited Will

21
Q

vWF Disease - Genetics + Mechanism + Findings (3)

A

Most Common Bleeding Disorder - Normally Autosomal Dominant

No vWf - No Adhesion - Also limited FVIII (Stabalizes)

Findings

1) Increased bleeding time with normal PT
2) PTT may or may not be elevated (FVIII)
3) Ristocetin Test

22
Q

Vitamin K Deficiency - Mechanism - Affected Factors (6) + Common Causes (2)

A

Gamma-Carboxyglutamate Restoration of Factors

Factors - II + VII + IX + X + C + S
Impact on VII Impacts PT Most

Causes

1) Newborns
2) Long Term Antibiotics

23
Q

Heparin Induced Thrombocytopenia - Mechanism + Causes (2) + Treatment + Key Point

A

Antibodies to Heparin Factor IV Complex

Causes - Heparin (High Risk) vs. Enoxoprin (Low Risk)

Treatment - Direct Factor X Inhibitors - E.g. Aragtroban + Lepirudin

Increases risk for Warfarin induced skin necrosis

24
Q

Disseminated Intravascular Coagulation (DIC) - Mechanism + Causes (6)

A

Mechanism - Pathological activation of coagulation cascade - Leads to microthrombi with endothelial damage + ischemia –> Uses of platelets (bleeding)

Causes

1) Pregancy (Extra tissue thromboplastin)
2) Rattlesnake Bite
3) Sepsis (Gram -)
4) AML-M3 (with auer rods + 15/17)
5) Adenocarcinoma (Mucin actiation)

CLASS ONLY
6) Crush Injury

25
Q

DIC Lab Findings (4) + Treatment

A

1) Thrombocytopenia (all platelets used up)
2) Elevated PT/PTT (factors used up)
3) Microangiopathic Anemia
4) Increased Fibrin split products + D-Dimer

Treatment - Underlying disease

26
Q

Meningcoccemia - Key Points (3)

A

1) Cram (-) Cocci Induced Endothelial Damage + DIC
2) Waterhouse-Friderichsen Syndrome
3) Specific to adrenal cortex

27
Q

Hermansky Pudlak Syndrome - Key Points (3)

A

1) Autosomal Recessive
2) Dense Granule Failure (Platelets)
3) Albinism + Platelet Disease

28
Q

Ehlers-Danlose Syndrome - Key Points (2)

A

1) Collagen Defect

2) Hyper-elastic skin = adhesion issues

29
Q

Sickle Cell Disease Case - Genetics + Physical Exam Findings (3) + Labs (7)

A

Autosomal Recessive

PE

1) Jaundice (Intravascular Hemolysis)
2) Anemia (Pale
3) Asplenia/Removed Gallbladder

30
Q

Sickle Cell Disease Case - Labs (7)

A

Labs

1) Normocytic Anemia
2) Increased MCHC
3) Sickle Cells
4) Target Cells
5) Elevated LDH (Intravascular)
6) Elevated Platelets (Marrow trying to response)
7) Reticulocyte Count (Corrected) - Shows bone marrow responding = Hemolysis

31
Q

GP6D Case - Genetics + Type of Anemia + Cause (5)

A

X-Linked Recessive

Normocytic Anemia with Intravascular Hemolysis

Causes - Oxidative Stress

1) Fava Beans
2) Malaria Mediaction (Primiquine)
3) DKA
4) Infection
5) Sulfamides

32
Q

GP6D Case - Lab Findings (6)

A

1) Bite Cells
2) Heinz Bodies
3) Elevated LDH
4) Corrected Reticulocyte Count > 3%
5) Low Heptaglobin (Lots of Free Hb being bound)
6) High Bilirubin (Intravascular)

33
Q

Rapid Fire Markers - CD20

A

Mature B-Cell

34
Q

Rapid Fire Markers - CD10

A

ALL

35
Q

Rapid Fire Markers - CD4/8

A

T-Cell

36
Q

Rapid Fire Markers - CD103

A

Hairy Cell Leukemia

37
Q

Rapid Fire Markers - CD34

A

HSC

38
Q

Rapid Fire Markers - CD15

A

Reed Sternberg

39
Q

Rapid Fire Markers - CD30

A

Reed Sternberg

40
Q

Rapid Fire Markers - CD55

A

Negative = No DAF = No GPI = PNH

41
Q

Rapid Fire Markers - CD46

A

Atypical HUS (Compliment I Issues)

42
Q

Rapid Fire Markers - CD5

A

CLL + Mantle + T-Cell Tumors

43
Q

Rapid Fire Markers - CD23

A

CLL (with CD5)

44
Q

Solitary Meyloma - Keys (2)

A

1) Plasmacytoma

2) Solidatry Lesion of Bone/Soft Tissue - Monoclonal Plasma Cells

45
Q

Lymphoplasmacytic Lymphoma - Keys (3)

A

1) Mixed Neoplastic B-Cell Plasma Tumor
2) Secretes IgM (vs. IgG in normal Multiple Myeloma)
3) Triggers Waldenstrom Macroglobulinemia (big cells are hyperciscous)

46
Q

Porphyria Cutanea Targa (PCT) - Key Findings (3)

A

1) Funky Hands

2) Cutaneous Porphyria with photosensitivity

47
Q

Congenital Erythropoietic Porphyria (CEP) - 2 Keys

A

1) Vampire Disease

2) Gunther’s Disease

48
Q

Acute Intermittent Porphyria (AIP) - Cause + Findings (5)

A

Neuroviscreal Porphyria - Lack of PBD (Porphobilinogen Deaminase)

5 P’s

1) Abdominal Pain
2) Polyneuropathy
3) Port-wine urine
4) Psych S/Sx
5) Precipitated by starvation, drugs and phenotyonin

49
Q

Rapid Fire Markers - CALLA - Positive (4) and Negative (4)

A

CD10

Positive
All B-Cell Disease - Especially ALL + Burkitt + B-Cell Lymphoma

Negative
AML
CLL
Mantle Cell
Marginal

Z - M2 Heme/Onc (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions