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CAM III > Heme part 2 > Flashcards

Heme part 2 Flashcards

1
Q

Thrombosis

A

Occurs when balance is disturbed between:
Procoagulant factors
Anticoagulant factors

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2
Q

Procoagulant factors that get disturbed in thrombosis

A

Coagulation factors
Platelets
Leukocytes

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3
Q

Anticoagulant factors that get disturbed in thrombosis

A

Protein C
Protein S
Antithrombin

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4
Q

Thrombosis RFs

A

Age
Smoking
Obesity
Estrogen use

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5
Q

Types of thrombophilia

A

Inherited thrombophilic conditions

Acquired thrombophilic conditions

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6
Q

Factor V Leiden

A

The MC inherited thrombophilia
Point mutation (G1691A) in the factor V gene
Leads to an amino acid substitution that renders factor V resistant to inactivation by activated protein C (APC)

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7
Q

Dx of factor V Leiden

A

APC resistance assay
-Assess the ability of protein C to inactivate factor Va
PCR testing of the gene

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8
Q

Prothrombin G20210A

A

Gene mutation is the second most common inherited risk factor for VTE
Pts have slightly higher levels of circulating prothrombin (factor II)

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9
Q

Dx of prothrombin G20210A

A

PCR testing of the prothrombin gene

Obtaining factor II activity levels is NOT helpful

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10
Q

Pathophysiology of antithrombin deficiency

A

Antithrombin is an enzyme that interrupts the coagulation process, mainly by inhibitin thrombin and activated factors IX and X

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11
Q

Antithrombin deficiency types

A

Type I: quantitative

Type II: qualitative

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12
Q

Antithrombin deficiencies are typically _______

A

Heterozygous

Homozygous deficiencies are typically not compatible with life

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13
Q

Acquired cases of antihrombin deficiency that must be ruled out

A 
Acute thrombosis
Heparin therapy
Liver dz
Nephrotic dz
Protein-loosing enteropathy
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14
Q

Labs for antithrombin deficiency

A

Genetic testing

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15
Q

Tx for antithrombin deficiency

A

Antithrombin concentrates may be used as adjunctive therapy with routine pharmacologic VTE prophylaxis or as a supplement when treateing VTE

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16
Q

Pathophysiology of Protein C deficiency

A

Protein C is a vit K-dependent natural anticoagulant

It is converted during the coagulation process to APC (which inactivates coagulation factors Va and VIIIa)

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17
Q

Types of protein C deficiency

A

Type I: quantitative

Type II: qualitative

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18
Q

Acquired conditions in protein C deficiency

A

Acute thrombosis
Warfarin therapy
Liver dz
Protein-losing enteropathy

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19
Q

Labs for protein C deficiency

A

Protein C activity assay

Genetic testing

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20
Q

What is protein C deficiency a risk factor for?

A

Primary VTE
Recurrent VTE
Arterial thromboembolism

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21
Q

When can protein C concentrate be given?

A

Indicated in infants with catastrophic thrombotic complications

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22
Q

Pathophys of Protein S deficiency

A

Natural vit K-dependent anticoagulant

Cofactor for APC

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23
Q

Labs for protein S deficiency

A

Protein S activity

Free protein S antigen

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24
Q

Acquired conditions in protein S deficiencies

A 
Acute thrombosis
Warfarin therapy
Liver dz
Inflammatory states
Estrogens
Protein-loosing enteropathy
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25
Q

What is protein S deficiency a RF for?

A

Primary VTE
Recurrent VTE
Arterial thromboembolism

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26
Q

Other inherited disorders

A

Dysfibrinogenemias- rare
Elevated homocysteine level
-Polymorphisms in the methylene tetrahydrofolate reductase (MTHFR) gene
Elevated plasma factor VIII levels

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27
Q

RFs for acquired thrombotic conditions

A 
Surgery
Trauma
Hospital or nursing home confinement/immobility
Malignancy
Central venous catheters
Pacemaker placement
Estrogen
Pregnancy
Obesity
Inflammatory disorders
Chemo
Glucocorticoid therapy
Smoking
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28
Q

Surgery, trauma, hospitalization and immobility in acquired thrombotic conditions

A 
Higher risk with:
Hip and knee arthroplasty
CA surgery
Pelvic surgery
Abdominal surgery
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29
Q

40% of VTEs are associated with _________

A

Hospitalization

Either during or within 3 mos after d/c

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30
Q

CA and VTE

A

20% of all VTEs occur in pts with CA
Active CA increases VTE risk 5-6 fold
-Hx of CA, or CA that has undergone curative therapy without residual dz
6% of pts with unprovoked VTE have an undiagnosed CA at the time of the VTE
10% of pts with unprovoked VTE will be diagnosed with a CA in the year following the VTE dx

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31
Q

Antiphospholipid antibody syndrome

A

Acquired autoantibodies against phospholipids and phospholipid-binding proteins such as cardiolipin and B2-glycoprotein
Autoimmune, malignancy, drugs
Increases the risk of venous and arterial thrombosis

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32
Q

Labs for antiphospholipid antibody syndrome

A 
Lupus anticoagulant
Anticardiolipin antibodies
-False pos syphilis test
Anti-B2-GPI antibodies
Presence of APLAs are found in nearly 505 of pts with SLE but only 1-5% of the general population
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33
Q

Tx of antiphospholipid antibody syndrome

A

Pts with APS and a hx of unprovoked VTE should received anticoag therapy for life
-Target INR range is 2-3
Catastophic APS is rare and results in multiorgan failure
-Tx includes: anticoagulation, high-dose glucocorticoids and other immunosuppressants, and plasma exchange

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34
Q

Meds in acquired thrombotic conditions

A 
Estrogen-progestin contraceptives
-Highest with progesting drospirenone
Contraceptive patches and rings
Hormone replacement therapy
Chemo
Tamoxifen
Anastrozole
Bevacizumba
Erythropoiesis-stimulating agents
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35
Q

Hemodynamically stable pts and transfusions

A

Transfusion threshold hgb level of < 7 g/dL is recommended based on data

36
Q

Transfusion strategies

A

Erythropoietin and darbepoetin are used to promote RBC production and reduce the need for transfusion
-Higher hemoglobins have increased risks
Preoperative autologous blood donation
-Reduces blood transfusion risks
Interoperative hemodilution or use of intraoperative cell salvage technology

37
Q

FFP

A

Replacement solution for plasma exchange
Prevention of coagulopathy form massive transfusion
Tx of bleeding associated with multiple acquired clotting factor deficiencies (DIC)
Major warfarin-associated hemorrhage

38
Q

Cryoprecipitate

A

Congenital or acquired fibrinogen deficiency
Dysfibrinogenemia
Factor XIII deficiency
Tx of hemophilia A and vWB dz when another more suitable product is not available

39
Q

Immune globulin

A

Acquired or congenital hypogammaglobulinemia

Autoimmune disorders

40
Q

Albumin

A

Replacement solution for plasma exchange

Spontaneous bacterial peritonitis

41
Q

Prothrombin complex concentrates

A

Major warfarin-associated hemorrhage

42
Q

Factor VIII

A

Hemophilia A

Tx and prevention of bleeding

43
Q

Von Willebrand protein-rich factor VIII

A

Von Willebrand dz

Tx and prevention of bleeding

44
Q

Factor IX

A

Hemophilia B

Tx and prevention of bleeding

45
Q

Fibrinogen

A

Congenital fibrinogen deficiency

Tx of bleeding

46
Q

Thrombin

A

Small vessel bleeding despite standard surgical techniques or when surgical intervention is not feasible (topical application)

47
Q

Protein C concentrate

A

Severe congenital protein C deficiency

Prevention and tx of venous thrombosis and purpura fulminans

48
Q

Antithrombin

A

Hereditary antithrombin deficiency

49
Q

Alpha 1 antitrypsin

A

Congenital alpha 1 antitrypsin deficiency

50
Q

C1-esterase inhibitor

A

Hereditary angioedema

Acute attacks

51
Q

Conventional approaches to medical oncology

A

Histologic dx and clinical staging

Surgery, radiation therapy, chemo

52
Q

New approaches to medical oncology

A

Molecular profiling

Targeted therapy, immunotherapy, use of immunoconjugates

53
Q

What must be done before oncology pts can be treated?

A

Staging
Individualized clinical assessment
Mutually determine goals of therapy

54
Q

T staging oncology- size or direct extent of the primary tumor

A

Tx: tumor cannot be assessed
Tis: carcinoma in situ
T0: no evidence of tumor
T1, T2, T3, T4: size and/or extension of the primary tumor

55
Q

N staging oncology: degree of spread to regional lymph nodes

A

Nx: LNs cannot be assessed
N0: no regional lymph nodes metastasis
N1: regional lymph node metastasis present; at some sites, tumor spread to closest or small number of regional LNs
N2: tumor spread to an extent between N1 and N3
N3: tumor spread to more distant or numerous lymph nodes

56
Q

M staging oncology- presence of distant metastasis

A

M0: no distant metastasis
M1: metastasis to distant organs (beyond regional lymph nodes)

57
Q

Performance status in oncology

A

Indicates a pt’s well-being and ability to perform daily activities
-Karnofsky score
-Zubrod score
Pts with an excellent performance status typically have a better overall prognosis and the ability to tolerate more aggressive therapies

58
Q

How is Karnofsky performance status scale scored?

A

100 is best, 0 is dead

59
Q

How is the Zubrod scale scored?

A

O is nl activity, 4 is bedridden

60
Q

MItotic rate

A

Measure of how fast CA cells are dividing and growing

Higher mitotic rates are linked with lower survival rates in oncology

61
Q

Overall survival

A

Refers to the time from initiation of therapy until death

Frequently quoted as the median survival time

62
Q

Progression-free survival (progression-free interval)

A

The time from initiation of therapy until the time therapy is not longer controlling the tumor growth

63
Q

Overall response rate

A

The percentage of pts involved in a clinical trial whose tumor undergoes a prespecifed degree of shrinkage in imaging studies

64
Q

Surgical resection

A

Primary tx for locoregional solid tumor malignancies

65
Q

Adjuvant therapy

A

Chemo and/or radiation given after definitive surgery with curative intent

66
Q

Neoadjuvant therapy

A

Chemo and/or radiation given before planned definitive surgery with curative intent

67
Q

Traditional CA chemo

A

Cytotoxic agents with minimal selectivity for tumor cells over nl cells

68
Q

Personalized targeted agents

A

Have more selective toxicity on tumor cells based on specific tumor biology
Tumor markers

69
Q

Ovarian CA

A

Leading cause of GYN cancer-related deaths

Median age is 63 yrs

70
Q

RF for ovarian CA

A

FHx (BRCA1/2 mutations)
PCOS
Endometriosis
Smoking

71
Q

Decreased RF for ovarian cancer

A

Previous pregnancy
Prior OC
Tubal ligation or hysterectomy

72
Q

Dx of ovarian CA

A

U/s
Bx
CA-125

73
Q

Tx of ovarian CA

A

Surgery

+/- adjuvant chemo

74
Q

Cervical CA

A

Mean age is 48 yrs
Invasive cervical CA incidence in the US by more than 80% since the 1940s owing to Pap smear screening
HPV subtypes 16 and 18

75
Q

S/sx of cervical CA

A

Postcoital bleeding

Vaginal bleeding between menstrual cycles or after menopause

76
Q

Colon Ca sx

A

Bright Red Blood Per Rectum
Melena
Chronic diarrhea or constipation
Cramping and bloating

77
Q

Dx of colon CA

A

Colonoscopy

CEA

78
Q

Tx of colon CA

A

Surgical resection
+/- adjuvant tx
5-fluorouracil

79
Q

Rectal CA: details and tx

A

Adenocarcinoma

Tx: surgery +/- neoadjuvant chemoradiotherapy

80
Q

Anal cancer

A

Epidermoid or squamous cell carcinoma

Typically associated with HPV

81
Q

Tx of anal cancer

A

Often curable with radiation therapy and concurrent chemo with mitomycin plus 5-FU

82
Q

Pancreatic CA

A

Surgical resection is the only potential curative intervention (CA 19-9)
Only 15-20% of cases are considered resectable at presentation
-Resectable tumors: IA, IB, IIA
-Borderline resectable- extends to nearby blood vessels but may be removed completely by surgery
-Unresectable

83
Q

Gastroesophageal CA

A

Virtual all gastric and gastroesophageal junction CAs are adenocarcinomas, as are approximately 95% of esophageal CAs
Pts with adenocarcinomas and squamous cell carcinoma receive the same tx

84
Q

Tx of gastroesophageal CA

A

Surgery

Chemoradiation

85
Q

Non-small cell lung CA

A

80-90%
Adenocarcinoma is MC subtype
+/- paraneoplastic syndromes (hypercalcemia)
Tx: surgery, radiation, chemo

86
Q

Small cell lung CA

A 
Neuroendocrine tumor- smokers
\+/- paraneoplastic syndromes (SIADH, hyponatremia)
Limited-stage: 1 hemithorax
Extensive-stage: beyond
Tx: mostly chemo

CAM III (12 decks)

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