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CCTC STUDY MATERIALS AND QUESTIONS > Review > Flashcards

Review Flashcards

1
Q

CNI

A

TACROLIMUS

CYCLOSPORINE

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2
Q

ANTIPROLIFERATIVE AGENTS/ANTIMETABOLITES

A

AZATHIOPRINE
MYCOPHENOLATE MOFETIL
MYCOPHENOLATE SODIUM

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3
Q

MTOR INHIBITORS

A

SIROLIMUS

EVEROLIMUS

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4
Q

ANTIBODIES

A 
ATGAM
THYMOGLOBULIN
BASILIXIMAB
RITUXIMAB
ATEMTUXUMAB
IVIG
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5
Q

PROTEASOME INHIBITOR

A

BORTEZOMIB

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6
Q

POLYCLONAL ANTIBODIES MOA

A

T-CELL DEPLETION
CYTOTOXIC ACTIVITIES
MODULATION OF T CELL ACTIVATION

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7
Q

POLYCLONAL ANTIBODIES ADVERSE REACTIONS

A 
CYTOKINE RELEASE SYNDROME
LEUKOPENIA/THROMBOCYTOPENIA
SERUM SICKNESS
ANAPHYLAXIS
INFECTION
MALIGNANCIES-PTLD
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8
Q

POLYCLONAL ADVANTAGES

A

STRONGER, CAN BE USED TO TREAT REJECTION

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9
Q

POLYCLONAL DISADVANTAGES

A

ACUTE SIDE EFFETS
HIGHER INFECTION RATES
HIGHER MALIGNANCY RATES

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10
Q

MONOCLONAL ADVANTAGES

A

NO ACUTE SIDE EFFECTS

NOT ASSOCIATED WITH HIGH INFECTION OR MALIGNANCY RATES

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11
Q

MONOCLONAL DISADVANTAGES

A

WEAKER, CANNOT BE USED TO TREAT REJECTION

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12
Q

TACROLIMUS DOSING

A

0.1-0.15 MG/KG/DAY PO DIVIDED BID

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13
Q

CYCLOSPORINE MOA

A

INHIBITS FIRST PHASE OF T CELL ACTIVATION

REDUCES LEVEL OF CIRCULATING T CELLS

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14
Q

CYCLOSPORINE DOSING

A

5-10 MG/KG/DAY DIVIDED BID

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15
Q

CNI NEPHROTOXICITY

A

TAC=CYCLO

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16
Q

CNI HYPETENSION

A

CYCLO>TAC

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17
Q

CNI DM

A

TAC>CYCLO

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18
Q

CNI NEUROTOXICITY

A

TAC>CYCLO

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19
Q

CNI COSMETIC EFFECTS

A

CYCLO>TAC

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20
Q

CNI GI EFFECTS

A

TAC>CYCLO

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21
Q

CNI HYPERKALEMIA

A

TAC>CYCLO

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22
Q

CNI HLD

A

CYCLO>TAC

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23
Q

CNI LOW MAG

A

CYCLO=TAC

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24
Q

THINGS THAT INCREASE CNI LEVELS

A
  • ZOLES
  • MYCINS
  • GRAPEFRUIT/POMEGRANATE JUICE
  • DILT, VERAPAMIL, AMIO
  • FLUOXETINE
  • PROTEASE INHIBITORS
  • REGLAN
  • SIMEPRAVIR
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25
Q

THINGS THAT DECREASE CNI LEVEL

A
  • MG/AL ANTACIDS
  • KAYEXOLATE/OCTREOTIDE
  • CHOLESTRYAMINE
  • ANTI-EPILEPTICS
  • RIFAMPIN
  • NAFCILLINE
  • ISONIAZID
  • CARBAMEZEPINE
  • HERBS (ST. JOHNS WART)
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26
Q

MTOR MOA

A

INHIBITS T CELL ACTIVATION AND PROLIFERATION

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27
Q

SIROLIMUS DOSING

A

6-12 MG LOADING DOSE

2-5 MG MAINTENANCE DOSE

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28
Q

SIROLIMUS/EVEROLIMUS SIDE EFFECTS

A
  • NEUTROPENIA, THROMBOCYTOPENIA, LEUKOPENIA
  • INCREASE ANEMIA
  • HLD, HYPERTRIGLYCERIDEMIA
  • DELAYED WOUND HEALING
  • N/V/D
  • MOUTH ULCERS
  • INTERSTITIAL PNEUMONITIS
  • THROMBOTIC MYCROANGIOGRAPHY
  • PROTEINUREA
  • LYMPHOCELE/LYMPHODEMA
  • BONE PAIN
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29
Q

SIROLIMUS BLACK BOX WARNING

A
  • HEPATIC ARTERY STENOSIS

- BRONCHIAL ANASTOMOTIC DEHISCENCE

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30
Q

EVEROLIMUS DOSING

A

0.75 MG PO BID

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31
Q

AZATHIOPRINE DOSING

A

1-3 MG/KG/DAY

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32
Q

AZATHIOPRINE MOA

A

INHIBIT PURINE SYNTHESIS

INHIBIT T CELL PROLIFERATION

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33
Q

AZATHIOPRINE DRUG INTERACTIONS

A

ALLOPURINON-> PANCYTOPENIA-> DEATH

MYCOPHENOLATE MOFETIL-> BONE MARROW SUPPRESSION. SEPERATE MEDS BY 24 HOURS

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34
Q

MYCOPHENOLATE MOFETIL MOA

A

INHIBIT PURINE SYNTHESIS

INHIBIT T AND B CELL PROLIFERATION

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35
Q

MYCOPHENOLATE SIDE EFFECTS

A
  • N/V/D
  • ANEMIA, THROMBOCYTOPENIA
  • INFECTION
  • GASTRITIS, GI BLEED
  • CMV TISSUE INVASIVE DISEASE
  • MALIGNANCY
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36
Q

MYCOPHENOLATE MOFETIL DURG INTERACTIONS

A
  • ANTIVIRALS/SIROLIMUS-> INCREASED BONE MARROW SUPPORESSION
  • CYCLOSPONINE-> DECREASED LEVELS OF MPA
  • AZATHIOPRINE-> BONE MARROW SUPPRESSION. SEPERATE BY 24 HOURS
  • CHOLESTYRAMINE-> LOWERS DRUG LEVEL
  • AL/MG-> DECREASE ABSORPTION. SEPERATE BYT 2-4 HOURS
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37
Q

CORTICOSTEROIDS MOA

A

BLOCKS LYMPHOCYTE PROLIFERATIONS

ANTIINFLAMMATORY

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38
Q

METHYLPREDNISONE DOSING FOR REJECTION

A

250-1000 MG IV X 3 DAYS

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39
Q

CORTICOSTEROID SIDE EFFECTS

A
  • EUPHORIA/DEPRESSION/MOOD DISORDERS
  • HTN
  • HBP
  • HBS
  • INFECTION
  • MYOPATHY
  • IMPAIRED WOUND HEALING
  • HIRSUTISM
  • ACNE
  • WEIGHT GAIN/INCREASED APPETITE
  • CUSHINGOID FACE
  • OSTEOPOROSIS
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40
Q

PLASMAPHERESIS

A

MECHANICAL REMOVAL OF AB. DOES NOT DO ANYTHING TO THE B CELLS

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41
Q

IVIG DOSE

A

1-2 GM/KG

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42
Q

IVIG SIDE EFFECTS

A
  • BACK PAIN
  • HA
  • FEVER/CHILLS
  • BRONCHOSPASM
  • HYPOTENSION
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43
Q

RITUXIMAB MOA

A

MONOCLONAL AB TARGETED AGAINST CD20 ANTIGEN ON B LYMPHOCYTES

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44
Q

RITUXIMAB DOSING

A

PREVENTION OF REJECTION- 375 MG/M2
TREATMENT OF REJECTION- 375 MG/M2
TREATMENT OF PTLD- 375 MG/M2/DOSE EVERY WEEK X 4 DOSES

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45
Q

RITUXIMAB SIDE EFFECTS

A
  • HYPOTENSION
  • FEVERS/CHILLS
  • BRONCHOSPAMS
  • ARRYTHMIAS
46
Q

CMV causes what in the liver?

A

Vanishing bile duct

47
Q

CMV causes what in the heart?

A

Coronary artery vasculopathy

48
Q

CMV causes what in the lung?

A

Bronchiolitis obliterans

49
Q

CMV causes what in the kideny?

A

Glomerulopathy

50
Q

Staph is a

51
Q

c-diff is a

52
Q

Salmonella is a

53
Q

Psuedonomas is a

54
Q

Listeria is a

55
Q

Candida is a

56
Q

Aspergillus is a

57
Q

PCP is a

58
Q

Histoplasma is a

59
Q

Coccidio is a

60
Q

Blastomycosis is a

61
Q

Influenza is a

62
Q

Herpes is a

63
Q

EBV is a

64
Q

Varicella is a

65
Q

CMV is a

66
Q

Toxoplama is a

67
Q

Cryptosporidium is a

68
Q

What causes increased risk of CMV reactivation?

69
Q

CMV causes

A

inflammation of organs
decreased WBC
Decreased Plts
Increased LFTs

70
Q

EBV can cause

A

mononucleosis -> PTLD

71
Q

What are the symptoms of PTLD?

A
  • mono like
  • fever
  • abd pain
  • jaundice
  • gi bleed
  • change in CNS
  • renal dysfunction
  • hepatic dysfunction
  • splenomegaly
72
Q

What is the main treatment for PTLD?

A

Stop or lower immunosuppresion

73
Q

Treatment for varicella

A

varicella zoster immunoglobulin within 72 hours or IV acyclovir

74
Q

Treatment for C-diff

A

Flagyl or oral vanco

75
Q

How do you treat nocardia?

A

With sulfonamides and ceftriaxone

76
Q

What are the symptoms of Nocardia in different organs?

A

Brain-HA, lethargy, confusion, seizures
Lungs- PNA, fever, cough, CP
Skin-cellulitis

77
Q

Where is nocardia found?

A

In soil or water

78
Q

Where is legionella found?

79
Q

What is the treatment for Legionella?

A

Quinolones, marcrolides, cipro, zithromycin, rifampin

80
Q

What is the treatment for Hep B?

A

HBV immunoglobulin, enteravir, tenofovir

81
Q

What are the two types of polyomarvirus?

82
Q

What does BK affect?

A

-tubules and ureters

Biopsy shows tubules with epithelial cells containing the virus

83
Q

What does JC cause?

A

Progressive multifocal leukoencephalopathy.

The virus infects and lyses oligodendrocytes which leads to multifocal demyelination in the brain.

84
Q

Where is coccidomycosis found?

85
Q

Where is strongyloides found?

A

In tropical soil

86
Q

Where is toxoplasmosis found?

A

In cat feces

87
Q

Common post of complication for heart, heartlung

A

PNA d/t inactive phrenic nerve, long intubation times

88
Q

Common post of complication for heart?

A

CMV leading to CMV pneumonitis and gastritis

89
Q

Common post of complication for lung?

A

Colonization at the anastomosis site cause dehiscence, mediastinitis, bronchial stenosis.

90
Q

Common post of complication for kidney?

A

UTI, lymphocele, secondary infection or urine leak

91
Q

Common post of complication for Pancreas?

92
Q

Common post of complication for Liver?

A

Nosocomial gram- candida. Also, CMV, EBV, pneuomocystitis, aspergillus about 1-6 months post transplant.

93
Q

Common post of complication for intestine?

A

EBV-> PTLD

CMV most common

94
Q

3 was the immune system protects us

A
  • Defense
  • Surveillance
  • Homeostasis
95
Q

What are cytokines?

A
  • hormones
  • 1st to respond
  • T lymphocytes
  • cell mediated
  • responsible for allergic rxns
96
Q

When do you get an updated pra in a senistized pt, recent blood tx, VAD pt, ped/retransplant and non sensitized pt?

A
  • PRA >10% done monthly
  • blood tx- 1-2 weeks after
  • VAD pts- weekly
  • peds/retransplant- 3 months
  • no sensitization-6 months.
97
Q

How is a CDC crossmatch done?

A

Recipient serum is mixed with donor lymphocytes and complement. If there is lysis present then it is positive.

98
Q

How is a Flow cytometry cross match done?

A

Recipients serum is mixed with lymphocytes and fluorescein

99
Q

Major sign of Hyperacute rejection?

A

Thrombosis

100
Q

Major sign of acute ab mediated rejection?

A

Vasculitis

101
Q

Histological findings for acute ab mediated rejection?

A 
Capillary fragments
Hemorrhage
Infiltrates of neutrophils
Macrophages intravascularly 
Edema
Destruction of capillaries.
102
Q

Treatment for ab mediated rejection? Asymptomatic, mild, severe

A

Asymptomatic: hold steroid taper, change immuno meds
Mild: increase steroids, ATG, IVIG, change immuno meds
Severe: increase steroids, plasmapheresis, ATG, IVIG, change immuno meds.

103
Q

Histological changes seen in acute cellular rejection?

A 
Hemorrhage
Edema
Interstitial inflammation
Parenchymal damage
Endothelialitus
104
Q

Main symptoms of chronic rejections?

A

Vascular fibrosis

Kidney-nephropathy
Arteriosclerosis
Vanishing bile duct
Interstitial fibrosis
T-cell mediated
Bronchiolitis obliterans.
105
Q

Signs/symptoms of left sided heart failure

A

SOB, cough, wheezes, blood tinged sputum, tachycardia, cyanosis

106
Q

Signs/symptoms of right sided heart failure

A

Fatige, JVD, anorexia, edema, ascites, enlarged liver and spleen.

107
Q

Biopsy scale findings for antibody mediated rejection

A 
0= no acute cellular rejection 
1R= mild. Interstitial and or perivascular infiltrates with 1 focus of monocyte damage. 
2R= Moderate. 2 or more foci
3R= Severe. Diffuse infiltrates
108
Q

AB mediated rejection treatment based on phase

A

0 or 1R= no treatment, may adjust meds
2R= IV or oral steroids
3R= IV steroids. Thymo. Plasmapheresis. Mechanical support

109
Q

S/S of chronic rejection in heart transplant

A
  • CP
  • Fatigue
  • Dyspnea
110
Q

Diagnosis and treatment of chronic rejection in heart

A

Stress test/left heart cath

PTCA or retransplant

CCTC STUDY MATERIALS AND QUESTIONS (4 decks)

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