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Allergy and Immunology > Prednisone and other > Flashcards

Prednisone and other Flashcards

1
Q

What is leukocytosis?

A

an increase in the number of white cells in the blood, especially during an infection.

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2
Q

What is neutrophilic leukocytosis?

A

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.

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3
Q

What is the specific cellular MOA for prednisone?

A

-Glucocorticoids diffuse across the membrane of the cell, bind with a specific receptor and then enter the nucleus and interact specifically with DNA

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4
Q

What is the MOA of prednisone in the body?

A

-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

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5
Q

What is the MOA of prednisone?

A

-anti-inflammatory –inhibit phagocytosis (neutrophils and macrophages) –cause neutrophilic leukocytosis –decrease # circulating T cells –with chronic admin, decrease IgA and IgG

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6
Q

Why would you use prednisolone ?

A

–used alone or in combo with other agents for a wide variety of medical conditions involving an undesirable immunologic response

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7
Q

What undesirable immunologic responses do you use prednisolone for?

A

-prophylaxis for prevention of rejection of transplanted organ -autoimmune disease -inflammatory disorders -allergic conditions -malignancies

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8
Q

What is the cushingoid appearance?

A

round moon face, buffalo hump, big belly also giving them cortisol so patient tends to gain weight

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9
Q

What is atherosclerosis?

A

is a disease in which plaque (plak) builds up inside your arteries.

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10
Q

What are the prednisolone adverse effects? (11 things)

A
  1. 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
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11
Q

What do you need to monitor with these patients? 3 all time, 2 long term

A
  1. 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)
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12
Q

What are the specific questions you will need to address in the patient instructions? 4 questions

A

How to take it When to take it What to watch for When to go to the ED

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13
Q

When should patient take prednisone?

A

Take with food because of GI upset, take in morning and noon because of insomnia

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14
Q

What should the patient watch for when taking predisone short term?

A

HTN– monitor BP BG–if diabetic watch BG Psychosis –strange behavior or voices–>immediate help Follow up closely

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15
Q

What should you tell the patient to watch for if on long term prednisone?

A

HTN, BG, Psychosis, close follow up and: Osteoporosis Check lipids because of HDL Hypothalamic pitiitary renal insufficiency glaucoma and cataracts

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16
Q

When should the patient go to the ED?

A

Chest pain, SOB, HTN, pounding headache, psychosis

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17
Q

What is the concern with hypothalamic-pituitary-adrenal-insufficiency?

A

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

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18
Q

What is Cyclosporine?

A

immunosuppressant

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19
Q

What is tacrolimus?

A

immunosuppressant

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20
Q

What is sirolimus?

A

immunosuppressant

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21
Q

What is azathioprine (Imuran)?

A

immunosuppressant

22
Q

What is cyclophosphamide(cyc)?

A

immunosuppressant

23
Q

What is pneumocysistis? And pneumocystis jirovecii?

A

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

24
Q

When are combined immunodeficiences termed “severe”?

A

When they lead to early death from overwhelming infection, typically within the first year of life

25
Q

What is lymphadenopathy?

A

a palpable enlargement of the lymph node

26
Q

What is lymphocytosis?

A

Lymphocytosis is an increase in the number or proportion of lymphocytes in the blood

27
Q

What is thrombocytopenia?

A

deficiency of platelets in the blood. This causes bleeding into the tissues, bruising, and slow blood clotting after injury

28
Q

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?)

A

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

29
Q

What is the clinical presentation of XLA, Burtons, hypogammaglobulinemia?

A

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

30
Q

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?

A

–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

31
Q

Selective IgA immunoglobluin deficiency

When is it diagnosed?

What is the pathophys?

A

****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)

32
Q

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?

A
  • incidental finding (normal IgG and IgM)
  • increased incidence of sinopulmonary infections, GI, resp tract, and conjuctivae infections

–increased incidence of :

  • asthma
  • allergies
  • autoimmune diseases
33
Q

Selective IgA immunoglobulin deficiency

What is the treatment? What do you not want to do?

A

–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

34
Q

What is the pathology for CVID (common variable immunodeficiency)? When does it present? How long does it take to find?

A
  • 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)

35
Q

What is the clinical presentation for CVID (common variable immunodeficiency)?

A

-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

36
Q

You would consider CVID (common variable immunodeficiency) in patients that presented with:

A
  • 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
37
Q

What is bronchiectasis?

A

abnormal widening of bronchi or their branches, causing a risk of infection

38
Q

What is pernicious anemia?

A

Pernicious anemia is a decrease in red blood cells that occurs when the intestines cannot properly absorb vitamin B12

39
Q

What is atrophic gastritis?

A

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.

40
Q

What is the treatment for someone with CVID?

A

IVIG or SCIG/IGSC

–premedicate with antihistamines and steriods

Antibiotics

And *wait to give live vaccines (MMR, Varicells) until treated

41
Q

What are the important function of T-cells in helping to control and regulate?

A

control viral and fungal disease

monitor/control bad cell changes (dysplastic cellular changes)

provide TH cells for effective B cell response (humoral)

42
Q

What is the pathophys for DiGeorge syndrome (thymic aplasia)?

When is DiGeorge syndrome diagnosed?

A

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

43
Q

What is the clinical presentation of DiGeorge syndrome (thymic aplasia)?

A

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)

44
Q

What is the treatment for DiGeorge syndrom (thymic aplasia)?

A
  • 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

45
Q

What is the pathophys for Severe combined immunodeficiency (SCID)? When is the onset? What are the two types?

A

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

46
Q

Clinical presentation of SCID?

A
  • failure to thrive
  • pneumocystis
  • diaper rash and diarrhea
  • severe thrush and candidas
  • common and fatal viral infections to RSV, CMV,
47
Q

Treatment for SCID?

A

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

48
Q

What is wiskott-aldrich and ataxia-tenagiectasia?

A

Combined B and T cell immunodeficiencies

49
Q

What is the pathophys for (HAE) Hereditary angioedema?

A

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

50
Q

What is the clinical presentation of HAE? What are the increased risks of having this disease?

A

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

51
Q

What is the treatment for HAE?

A

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

Allergy and Immunology (9 decks)

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