Prednisone and other Flashcards
What is leukocytosis?
an increase in the number of white cells in the blood, especially during an infection.
What is neutrophilic leukocytosis?
is an abnormally high number of neutrophils (a type of white blood cell) in the blood. Neutrophils help the body fight infections and heal injuries. Neutrophils may increase in response to a number of conditions or disorders.
What is the specific cellular MOA for prednisone?
-Glucocorticoids diffuse across the membrane of the cell, bind with a specific receptor and then enter the nucleus and interact specifically with DNA
What is the MOA of prednisone in the body?
-Anti-inflammatory effects: inhibits production of almost ALL cytokines and pro inflammatory mediators –Inhibit innate immunity–suppresses phagocytic function of neutrophils and macrophages, causes neutrophilic leukocytosis –Decrease the number of circulating T cells -with chronic administration, decrease in IgG and IgA
What is the MOA of prednisone?
-anti-inflammatory –inhibit phagocytosis (neutrophils and macrophages) –cause neutrophilic leukocytosis –decrease # circulating T cells –with chronic admin, decrease IgA and IgG
Why would you use prednisolone ?
–used alone or in combo with other agents for a wide variety of medical conditions involving an undesirable immunologic response
What undesirable immunologic responses do you use prednisolone for?
-prophylaxis for prevention of rejection of transplanted organ -autoimmune disease -inflammatory disorders -allergic conditions -malignancies
What is the cushingoid appearance?
round moon face, buffalo hump, big belly also giving them cortisol so patient tends to gain weight
What is atherosclerosis?
is a disease in which plaque (plak) builds up inside your arteries.
What are the prednisolone adverse effects? (11 things)
- skin thinning and purport 2. cushingoid appearance 3. weight gain 4. HTN 5. HDL –> may lead to atherosclerosis 6. GI= gastritis, ulcers, may initially increase appetite (then later on will decrease b/c of gastritis) 7. osteoporosis 8. neuropsychiatric (initially euphoria/insomnia, can lead to depression, mania or psychosis) 9. Hyperglycemia –> leading to DM 10. Hypothalamic-pituitary-adrenal-insufficiency 11. Heightened risk of typical and opportunistic infections
What do you need to monitor with these patients? 3 all time, 2 long term
- Blood pressure 2. Lipids (b/c of HDL) 3. CMP (BG b/c of DM) Long term: 1. DEXA scan (bone density) 2. Ophthalmic exam (glaucoma, cataracts)
What are the specific questions you will need to address in the patient instructions? 4 questions
How to take it When to take it What to watch for When to go to the ED
When should patient take prednisone?
Take with food because of GI upset, take in morning and noon because of insomnia
What should the patient watch for when taking predisone short term?
HTN– monitor BP BG–if diabetic watch BG Psychosis –strange behavior or voices–>immediate help Follow up closely
What should you tell the patient to watch for if on long term prednisone?
HTN, BG, Psychosis, close follow up and: Osteoporosis Check lipids because of HDL Hypothalamic pitiitary renal insufficiency glaucoma and cataracts
When should the patient go to the ED?
Chest pain, SOB, HTN, pounding headache, psychosis
What is the concern with hypothalamic-pituitary-adrenal-insufficiency?
Giving puts corticosteroids surpasses the bodies action to make them. If pt gets sick, trauma, their adrenal glands will not produce cortisone or mount a response so you have to give them some or they will die
What is Cyclosporine?
immunosuppressant
What is tacrolimus?
immunosuppressant
What is sirolimus?
immunosuppressant
What is azathioprine (Imuran)?
immunosuppressant
What is cyclophosphamide(cyc)?
immunosuppressant
What is pneumocysistis? And pneumocystis jirovecii?
Pneumocysistis is a parasitic protozoan that can cause fatal pneumonia n peple affected with immunodeficiency diseases.
Pneumocystic jerovecii is a FUNGAL infection of the lungs
When are combined immunodeficiences termed “severe”?
When they lead to early death from overwhelming infection, typically within the first year of life
What is lymphadenopathy?
a palpable enlargement of the lymph node
What is lymphocytosis?
Lymphocytosis is an increase in the number or proportion of lymphocytes in the blood
What is thrombocytopenia?
deficiency of platelets in the blood. This causes bleeding into the tissues, bruising, and slow blood clotting after injury
Hypogammaglobulinemia, XLA, Burtons
When is it diagnose, what gender is it found it, and what is the pathophysiology?
(x or y linked, does it affect B and or T cells?)
Diagnosed in infants
Mostly in males unless dad is affected and mom is a carrier and/or affected
pathophys:
mutant tyrosine kinase
virtual absence of B cells
ALL immunoglobulins are decreased
T-cell is still fine
What is the clinical presentation of XLA, Burtons, hypogammaglobulinemia?
IN INFANTS:
–reccurant, PYROGENIC, bacterial infections such as otitis media, sinusitis, and pneumonia from: Streptococcus pneumoniae, Haemophilus influenzae
–may have absence of tonsils and lymph nodes
–may have failure to thrive
–serious skin infections, abcesses, pneumonia
What is the treatment for XLA, burtons, hypogammaglobulinemia? What does this treatment help with? What should you check with these patients during treatment and how should you counsil?
–replacement of immunoglobulin by:
IVIG (IV IgG) or Sub Q IgG (SCIG, IGSC)
Treatment helps with decreasing the number and intensity of infections
Check levels of IgG to see how treatment is going
Council on blood transfusions
Selective IgA immunoglobluin deficiency
When is it diagnosed?
What is the pathophys?
****dont diagnose before 4yo b/c there can naturally be a decrease of Ab w/ ANY immune dysfunction
-MOST common in adults
Pathophys:
B cells cant differentiate into mature plasma cells that secrete IgA (NORMAL amounts of other Ab)
Selective IgA immunoglobulin deficiency
What is the clinical presentation, meaning what other diseases and secondary infections will you see or are increased with this deficiency?
- incidental finding (normal IgG and IgM)
- increased incidence of sinopulmonary infections, GI, resp tract, and conjuctivae infections
–increased incidence of :
- asthma
- allergies
- autoimmune diseases
Selective IgA immunoglobulin deficiency
What is the treatment? What do you not want to do?
–no specific treatment
–PROMPT abx for infections
–RECOMMEND vaccines
-do not give pts blood or treat patients with gamma globulins because:
if they have a decrease in the IgA, it means they are making the IgA then their body is destroying it
If you give these pts immunoglobulins (which have trace IgA in them) anaphylxis may occur as will higher destruction of their own IgA ab
What is the pathology for CVID (common variable immunodeficiency)? When does it present? How long does it take to find?
- impared B cell differentiation
- decrease in IgG, A, and or M
- POOR response to vaccines
- not a SINGLE disease, but multiple hypogammaglobunemia symdromes from many genetic disorders
–B cells nomers that are immature, recognize Ag, respond with proliferation but have impared abiltiy to become memory and plasma cells
–presents in 20’s-40’s
–5-7 years from onset to diagnosis(mutl specialists)
What is the clinical presentation for CVID (common variable immunodeficiency)?
-reccurent sinopulmonary infections : TB, sinustitis, pneumonia, bronchitis
Evidence of immune downregulation leading to–>
inflammatory and autoimmune disorders as well as malignant disease such as :
*chronic lung disease
*GI & liver problems
*splenomegly
*malignancy
*lymphoid issues
You would consider CVID (common variable immunodeficiency) in patients that presented with:
- chronic pulm infections (some with bronchiectasis)
- chronic GI: giardia, intestinal malabsorption, atrophic gastritis with pernicous anemia
S&S suggestive of lymphoid malignancy including:
- weight loss
- anemia
- thrombocytopenia
- splenomegly
- generalized lymphadenopathy
- lymphocytosis
What is bronchiectasis?
abnormal widening of bronchi or their branches, causing a risk of infection
What is pernicious anemia?
Pernicious anemia is a decrease in red blood cells that occurs when the intestines cannot properly absorb vitamin B12
What is atrophic gastritis?
is a process of chronic inflammation of the stomach mucosa, leading to loss of gastric glandular cells and their eventual replacement by intestinal and fibrous tissues.
What is the treatment for someone with CVID?
IVIG or SCIG/IGSC
–premedicate with antihistamines and steriods
Antibiotics
And *wait to give live vaccines (MMR, Varicells) until treated
What are the important function of T-cells in helping to control and regulate?
control viral and fungal disease
monitor/control bad cell changes (dysplastic cellular changes)
provide TH cells for effective B cell response (humoral)
What is the pathophys for DiGeorge syndrome (thymic aplasia)?
When is DiGeorge syndrome diagnosed?
pharyngeal pouch not developed fully–thymus, thyroid, parathyroid, heart, aorta, face all affected
-causes congenital hypothyroidism and hypoparathyroidism
B cells normal!
T-cells reduced, decerase in T cell function
Diagnosed:
at birth
What is the clinical presentation of DiGeorge syndrome (thymic aplasia)?
many malformations: cardiac, hypocalcemia w/ poss tetany
facial abnormailites: low set ears, slanting eyes, short philtrum, hypertelorism, micrognathia, high arched palate with bifid uvula
other abn.: esophageal dysmotility, GI and GU anomalies, autoimmune diseases
SEVERE viral, bacterial, and fungal inffections
pneumonia (pneumocystis) and thrush (candida albicans)
What is the treatment for DiGeorge syndrom (thymic aplasia)?
- treat heart problems (tetrology of fallot)
- control Ca deficiency
—ONLY give irradiated blood b/c non-irradiated can result in fatal host disease
-ONCE stable, pts more suseptilbe to chronic rhinitis, pneumoina, candida, diarrhea
–MAY consider thymic implant from stillborn if reccurent infections, severe T-cell deficiency, and failure to thrive
What is the pathophys for Severe combined immunodeficiency (SCID)? When is the onset? What are the two types?
X-linked (most common) autosomal
Presents at infancy
pathophys is: absence of thymus tissue, tonsils, and lymph nodes
lymph nodes devoid of lymphocytes,
Ig levels are low
B & T cells are completely absent OR B & T cells present but dont function properly
Clinical presentation of SCID?
- failure to thrive
- pneumocystis
- diaper rash and diarrhea
- severe thrush and candidas
- common and fatal viral infections to RSV, CMV,
Treatment for SCID?
IVIG
enzyme replacement therapy
Bone marrow transplant (1-3 mo = high success rate)
cord blood transplant
**patient doesnt require immunosuppresants because there is no immune system to supress
AVOID ALL VACCINES
What is wiskott-aldrich and ataxia-tenagiectasia?
Combined B and T cell immunodeficiencies
What is the pathophys for (HAE) Hereditary angioedema?
No C1 esterase inhibitor
C1 cleaves C4 which activates C3a and C5a which inhance inflammation, and lead to capillary permeability and edema in many organs
What is the clinical presentation of HAE? What are the increased risks of having this disease?
either spontaneous or by trauma:
angioedema=face, lips, throat, abdomen, trunk, visera, extremeties and upper airway
Have increased risk of autoimmune disease like: SLE, sjogrens syndrome, crohns, or sceroderma
What is the treatment for HAE?
1 assess airway and intubate if stritor or resp distress
Acute: severe laryngeal, GI or cutaneous attacks–>
Human plasma derived C1 inhibitor concentrate (C1INHRP)
Recombinant C1 inhibitor
Icatibant–> bradykinin B2 receptor antagonist
Ecallantide –> kallikeren inhibitor (only in USA)
Chronic/prophylactic:
FFP
androgens that include a C1 inhibitor: androgens, methyltestosterone
