Therapeutics Iii Exam 3 - Post Tranplant Non-Infectious Diseases Questions

Front 1

What are the most common non-ID post transplant complications?

Back 1

-cardiovascular (HTN, diabetes, NODAT, hyperlipidemia)
-post-transplant malignancy
-osteoporosis

Front 2

What are the traditional risk factor for CVD?

Back 2

1. high blood cholestrol and lipproteins
2. high blood pressure
3. diabetes mellitus
4. tabacco use
6. physical inactivity
7. obsesity/overweight

Front 3

What are some common causes of transplant-associated hypertension?

Back 3

Hypertension is found in ~90% of kidney transplant recipients.
-poor graft function
-source of donor (deceased)
-native kidney disease
-CNIs, steroids

Front 4

HTN and Renal Allograft Outcome

Back 4

There is an increased risk of graft loss with each 10 mm Hg increase in SBP over 140/90.

Front 5

Blood pressure targets in kidney transplant recipients

Back 5

Diabetes mellitus: <130/80
Proteinuria: <125/75
No DM or proteinuria: <130/85

Front 6

What is the best drug to use to treat hypertension in kidney transplant recipients?

Back 6

nifedipine

Front 7

Why don't we use beta blocker to treat HTN in kidney transplant recipients?

Back 7

may contribute to hyperlipidemia

Front 8

Why don't we use most calcium channel blockers to treat HTN in kidney transplant patients?

Back 8

-increase blood levels of CNIs and may lead to over immunosuppression
-may worsen gingival hyperplasia

Front 9

Why don't we use ACE inhibitors or ARBs to treat HTN in kidney transplant patients?

Back 9

-may cause anemia, hypovolemia, and potassium retention
-may exacerbate vasoconstriction

Front 10

How do we characterize hyperlipidemia?

Back 10

-total cholesterol (>200 mg/dl)
-LDL (>130 mg/dl)
-triglycerides (>150 mg/dl)

Front 11

Target Serum Lipid Levels for kidney transplant recipients

Back 11

-total cholesterol: <200
-LDL: <100
-HDL >40
-triglycerides: <150

Front 12

What are some phamacological causes of hyperlipidemia?

Back 12

-calcineurin inhibitors
-mTOR inhibitors
-corticosteroids

Front 13

What would we typically use for hyperlipidemia in the transplant patient?

Back 13

Statins
-others include bile acid resins, nicotinic acid, and fibrates

Front 14

Max dose of lovastatin with cyclosporine use?

Back 14

20 mg

Front 15

Max dose of simvastatin with cyclosporine use?

Back 15

10 mg

Front 16

Max dose of fluvastatin with cyclosporine use?

Back 16

40 mg

Front 17

Max dose of rosuvastatin with cyclosporine use?

Back 17

5 mg

Front 18

Definition of NODAT

Back 18

No prior history of diabetes plus:
-casual plasma glucose >200 plus symptoms of polyuria, polydipsia, and unexplained weight loss
-fasting plasma glucose >126
-2-hour plasma glucose >200

Front 19

NODAT is associted with what other factors?

Back 19

-mortality
-morbidity
-renal graft failure
-higher risk of CVD
-higher rates of infection

Front 20

Traditional risk factors for NODAT?

Back 20

-age over 40
-black or hispanic
-BMI over 30
-family history of DM
-hepatitis C
(with 3 or more, give cyclsporine)

Front 21

Drugs that increase diabetogencicity?

Back 21

corticosteroids
calcineurin inhibitors

Front 22

Drugs used in patients at risk for NODAT?

Back 22

If a patient has more than 3 traditional risk factors we consider then high risk for NODAT. Maintenance therapy should be either CSA or MMF.

Front 23

Treatment of NODAT

Back 23

Stepwise approach
1. non-pharmacologic therapy
2. oral monotherapy (glipizide)
3. oral combo therapy (glipizide + thiazolidinedione)
4. insulin (long acting insulin glargine +/- regular insulin)

Front 24

What immunosuppressive regimen is considered the combo of least evil?

Back 24

TAC/MMF/Pred

Front 25

What is the typical pattern of post-transplant bone loss?

Back 25

-rapid bone loss for the first 3-6 months
-loss stabilizes after 6 months
-beyond 6 months patients begin gaining bone density
-at 2 years patients have higher bone density than their pretransplant levels

Front 26

Corticosteroid effects on bone density?

Back 26

-increases urinary calcium excretion
-reduces intestinal calcium absorption
-decreases skeletal growth factors
-increases bone resorption (osteoclasts)
-increases bone formation (osteoblasts)

Front 27

Cyclosporine effects on bone density?

Back 27

CSA causes high turn-over osteoporosis. Stimulates osteoclasts and osteoblasts but resorption rates exceed formation rates.

Front 28

Prevention and Treatment of Post-transplant Osteoporosis

Back 28

1. Calcium + D supplements (1000-1500mg calcium daily + 800IU of vitamin D)
2. Calcitriol 0.5mcg daily
3. Oral bisphosphonates

Front 29

Post-transplant malignancy - General facts

Back 29

Chronic use of immunosuppressants increase the long-term risk of malignancy
ATG is strongly associated with PTLD
It is usually cancer uncommon in the general population
-PTLD
-nonmelanoma skin cancers
-Kaposi's sarcoma
-renal carcinoma
-hepatobiliary tumors
-anogenital carcinomas

Front 30

Incidence of unusual malignancies post-transplant

Back 30

20 X increase in nonmelanoma skin cancers, Kaposi's sarcoma, and non-Hodgkin's lymphoma
15 X increase in renal cell cancer
5 X increase in melanoma, leukemia, hepatobiliary, cervical, and vulvovaginal cancer
3 X increase in testicular and bladder cancer

Front 31

Risk factor of post-transplant lymphoproliferative disease

Back 31

-overall level of immunosuppression
-EBV serostatus of the recipient (seronegative is bad)

Front 32

PTLD prevention

Back 32

-limit exposure to aggressive immunosuppressants
-taper immunosuppressants as soon as possible
-proper antiviral prophylaxis (EBV)

Front 33

PTLD treatment

Back 33

1. reduction of immunosuppression
2. chemotherapy
3. immune globulin
4. surgical resection
5. radiation therapy
6. interferon-alpha