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Immuno Flashcards

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1
Q

How Chronic granulomatous disease occurs?

A

Due to defect in NADPH oxidase no production of ROS result no respiratory burst in neutrophils

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2
Q

How to dx CGD?

A

Gene testing

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3
Q

How to manage Chronic granulomatous disease?

A

Pt should receive antimicrobial prophylaxis with TMP-SMX and itraconazole—lifelong

Pts with severe phenotype may benefit from IFN-ɣ injections

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4
Q

How Chédiak-Higashi syndrome occurs?

A

Defective microtubule due to mutate LYST gene result no phagosome-lysosome unfusion

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5
Q

Triad of Chédiak-Higashi syndrome

A

Progressive neurodegeneration with Lymphohistiocytosis
Albinism (partial) with recurrent pyogenic
Infections with peripheral Neuropathy

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6
Q

Dx findings of Chédiak-Higashi syndrome

A

Giant granules in granulocytes and platelets

Pancytopenia

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7
Q

Triad of Leukocyte adhesion deficiency

A

Late separation of umbilical cord
absent pus
Recurrent infections due to defective neutrophils

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8
Q

How Wiskott-Aldrich syndrome occur?

A

Mutated WAS gene result unorganized actin cytoskeleton result defective antigen presentation

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9
Q

Immunoglobulins status in Wiskott-Aldrich syndrome

A

Decrease to normal IgG, IgM

Increase IgE, IgA

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10
Q

How Hyper-IgM syndrome occurs?

A

due to defective CD40L on Th cells result no class switching defect

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11
Q

Immunoglobulins status in Hyper-IgM syndrome

A

Normal or increased IgM

Decreased IgG, IgA, IgE

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12
Q

How Ataxia-telangiectasia occurs ?

A

Unable to detect damage DNA as ATM gene is mutated

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13
Q

Important point of Ataxia-telangiectasia

A

Increase sensitivity to radiation (limit x-ray exposure)

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14
Q

Immune status in Ataxia telangiectasia

A

Increase AFP
Decrease all Immunoglobulins except IgM and IgD
Lymphopenia and cerebellar atrophy

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15
Q

How Severe combined immunodeficiency occurs?

A

defective IL-2R gamma chain (most common, X-linked recessive)
adenosine deaminase deficiency (autosomal recessive)
RAG mutation VDJ recombination defect

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16
Q

How to dx SCID?

A 
Decrease T-cell receptor excision circles
Germinal centers (lymph node biopsy), and T cells (flow cytometry)
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17
Q

Name the screening test for SCID

A

Absence of T cell receptor excision circles (circular DNA excreted by developing T cells in thymus)

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18
Q

How to dx X-linked (Bruton) agammaglobulinemia?

A

Decrease B cells as well as all immunoglobulin

Absent/scanty lymph nodes and tonsils (1° follicles and germinal centers absent)

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19
Q

Triad of Common Variable Immunodeficiency

A

Occurs due to B-cell not converted into plasma cells

Present during puberty and young adulthood (20-40yrs)

Recurrent Sxs of Respiratory tract and GIT esp diarrhoea

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20
Q

How Autosomal dominant hyper-IgE syndrome (Job syndrome) occurs?

A

Deficiency of Th17 cells due to STAT3 mutation result impaired recruitment of neutrophils to sites of infection

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21
Q

Triad of hyper-IgE syndrome (Job syndrome)

A

Cold (noninflamed) with staphylococcal Abscesses

retained Baby teeth with Coarse facies

Dermatologic problems (eczema) with bone Fractures from minor trauma

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22
Q

Name the organisms causing infection if Terminal complement deficiencies (C5–C9) occur

A

Increased susceptibility to recurrent Neisseria bacteremia

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23
Q

What are the Postsplenectomy findings?

A

Howell-Jolly bodies (nuclear remnants)

Target cells Thrombocytosis (loss of sequestration and removal)

Lymphocytosis (loss of sequestration)

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24
Q

Name the organisms cover by subunit vaccine

A 
HBV (antigen = HBsAg)
HPV (types 6, 11, 16, and 18)
acellular pertussis (aP)
Neisseria meningitidis (various strains), Streptococcus pneumoniae
Haemophilus influenzae type b.
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25
Name the organisms cover by Killed or inactivated vaccine
Hepatitis A Typhoid (Vi polysaccharide, intramuscular), Rabies Influenza Polio (SalK)
26
How Hyperacute rejection presents?
Widespread thrombosis of graft vessels----> ischemia and fibrinoid necrosis
27
How hyperacute rejection occurs?
Pre-existing recipient antibodies react to donor antigen (type II hypersensitivity reaction) activate complement
28
How acute rejections occurs?
If humoral antibodies developed after transplantation | If Cellular---> CD8+ T cells and/or CD4+ T cells activated against donor MHCs (type IV hypersensitivity reaction)
29
how acute rejections presents ?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate Prevent/reverse with immunosuppressants
30
How chronic rejection occurs?
CD4+ T cells respond to recipient APCs presenting donor peptides, including allogeneic MHC Both cellular and humoral components (type II and IV hypersensitivity reactions)
31
Important point
For patients who are immunocompromised, irradiate blood products prior to transfusion to prevent GVHD
32
MOA of MYCOPHENOLATE
reversible inhibitor of inosine monophosphate dehydrogenase (IMPDH), which is the ratelimiting enzyme in de novo purine synthesis
33
What is the main side effect of MYCOPHENOLATE?
bone marrow suppression.
34
MOA of AZATHIOPRINE
purine analog that is enzymatically converted to 6-mercaptopurine. It acts primarily by inhibiting purine synthesis.
35
What is the side effect of AZATHIOPRINE?
The major toxicity of azathioprine is dose-related diarrhea, leukopenia, and hepatotoxicity.
36
MOA of TACROLIMUS and CYCLOSPORINE
inhibiting the transcription of interleukin-2 and several other cytokines, mainly the T-helper lymphocytes.
37
Side effects of tacrolimus
nephrotoxicity and hyperkalemia | does not cause hirsutism or gum hypertrophy
38
Side effects of CYCLOSPORINE
Nephrotoxicity and neurotoxicity Gingival hypertrophy and hirsutism. Hypertension ( CCB as a TOC) Glucose intolerance
39
Important point
C1q levels are normal in hereditary angioedema and depressed in acquired forms,which Usually present much later in life. C4 levels are depressed in all forms of angioedema.
40
How to dx Hereditary angioedema?
complement testing Exaggerated cleavage of C4 by C1 complex causes depressed C4 levels Low levels of C1 inhibitor protein Or C1 inhibitor function confirmed the dx.
41
Important point
``` C1 inhibitor concentrate; a bradykinin antagonist (e.g icatibant) Kallikrein inhibitor (ecallantide) ```
42
How MuCcune albright syndrome occurs?
Defect in the G-protein cAMP-kinase function in the affected tissue, thereby resulting in autonomous activity of that tissue
43
Triad of MuCcune albright syndrome
precocious puberty pigmentation i.e. café au lait spots (large and irregular borders) and multiple bone defects (polyostotic fibrous dysplasia)
44
How Kallman syndrome occur?
Failure of migration of fetal GnRH and olfactory neurons result low FSH and LH Also loss of smell
45
Dysmorphic features of Prader Willi syndrome
Narrow forehead Almond shaped eyes Downturned mouth
46
Name the Complications occur due to Prader Willi syndrome
Sleep apnea DM type 2 Gastric distension/rupture Death by choking
47
How to dx Prader Willi syndrome?
Genetic testing is required to confirm diagnosis and begins with karyotype and methylation studies Followed by fluorescence in-situ hybridization, and then microsatellite probes
48
At what age DUCHENE and becker muscular dystrophy occur?
DUCHENE:::. 2-3 years of age Becker::: 5-15 years of age
49
Triad of Myotonic muscular dystrophy
Occur in 12-30 years of age Facial weakness with dysphagia Handgrip Myotonia
50
What are the complications of Myotonic muscular dystrophy?
Arrthymia Cataract Balding Testicular atrophy/infertility
51
How to dx DUCHENE muscular dystrophy?
Dx is confirmed by genetic testing (gold standard) biopsy shows muscle replacement by fat and fibrosis and absent dystrophin on immunochemistry staining
52
Important point
Myopathic pattern on electromyography (myotonic pattern in myotonic muscular dystrophy)
53
Triad of CONGENITAL CONTRACTURAL ARACHNODACTLY
Due to mutation in fibrillin gene 2 Tall stature with arachnodactyly multiple contractures involving large joints
54
Important point (very very important)
Unlike most cases of intussusception in children, which are ileo-colic, intussusceptions in HSP are more likely to be small-bowel or ileoileal Ileo-colic intussusceptions can be treated with air or contrast enema, but ileo-ileal intussusceptions that do not reduce spontaneously often require surgical management
55
Screening test of dyslipidemia
universal screening for dyslipidemia is recommended at age 9-11 and at age 17-21, as lipid levels are relatively stable just prior to and after puberty.
56
What are the causes of ACUTE URINARY RETENTION IN ELDERLY MEN?
BPH or prostatic CA neurogenic bladder or detrusor muscle inactivity
57
Important point
Spinal cord compression in lumbar region bowel/bladder incontinence (rather than retention)
58
Triad of Acute bacterial PROSTATITIS
Tender prostate with systemic symptoms Pyuria with positive urine culture SxS of lower urine tract like retention of urine, dysuria and pelvic pain
59
Triad of Chronic PROSTATITIS
Tender prostate without systemic symptoms LUTS with pyuria Due to Recurrent UTI
60
Triad of NON-INFLAMMATORY CHRONIC PROSTATITIS
LUTS without fever Mild tender prostate Negative Urine DR and culture
61
Triad of INFLAMMATORY CHRONIC PROSTATITIS
LUTS without fever Mild tender prostate Negative Urine DR and culture
62
D/f b/w NON-INFLAMMATORY CHRONIC PROSTATITIS AND INFLAMMATORY CHRONIC PROSTATITIS
-If Expressed prostatic secretions show a normal no. leukocytes and negative culture—-> non inflammatory --if Expressed prostatic secretions show a WBC more than 10 WBCs/H PF and negative culture
63
Triad of Chronic pelvic pain syndrome
LUTS with pain on ejaculation Hematospermia with negative culture Pain at pelvic and reproductive areas
64
How to manage Chronic pelvic pain syndrome? | 3As
Alpha blocker like tamsuloin Abx like cipro 5Alpha reductase inhibitors finasteride
65
Triad of Testicular cancer
U/L painless testicular node Radical orchiectomy and then biopsy Firm ovoid mass on examination
66
How to dx Testicular cancer
Scrotal US | Tumor markers viz Alpha feto protein / Beta HCG
67
What are the risk factor of testicular cancer?
Family history | Cryptosporidium
68
Triad of steroid
Athlete with small testis Low GnRH, LH and FSH/ normal testosterone Aggression
69
Side effect of 5 alpha reductase Inhibitors
Decrease libido | Erectile dysfunction
70
Side effects of Phosphodiesterase Inhibitors
Low BP if taken with other anti-HTN Painful erection Blue discolouration of eye Non-arteritic anterior ischemic optic neuropathy
71
How to t/m EPIDIDYMITIS?
If Occur due to STI and in less than 35 yrs——-> ceftriaxone and doxycycline If Occur due to coliform and in more than 35 years——>Levofloxacin
72
How EPIDIDYMITIS presents?
U/L testicular pain Epididymal pain Dysuria and frequency
73
Important of Germ cell tumors
Non Seminoma Germ cells have increased B-HCG and alpha feto protein Seminoma Germ cells have increased only B-HCG
74
Important point of Stromal testicular tumors
Leydig--->which produce Estrogen or testosterone Steroli cell tumor which occasionally associated with increased estrogen
75
Important point of Germ cell Tumor
Leydig tumor doesn't have elevated alpha feto.protein and b hcg
76
Triad of Testicular torsion
Tender erythematous swell scrotum Absent cremasteric reflex Horizontal testicular lie with elevated testis
77
How to DX Testicular torsion?
US doppler which shows no blood flow
78
How to manage testicular torsion?
Surgical detorsion and fixation with exploration of the C/L side Or Manual detorsion if surgery not available
79
What is the basic d/f b/w Testicular torsion and Epididymitis?
If elevation of testis decrease pain---> Epididymitis (+ve phren sign) If elevation of testis doesn't decrease pain ---> Testicular torsion
80
Important point of Spermatogenesis
Cryptorchidism, Varicocele Or Bath in hot tub, laptop computing cause infertility by increasing testicular temperature
81
Difference between Klinefelter syndrome and anabolic steroid
Both condition have gynecomastia and low testicular size & volume Anabolic steroid---> There will increase libido and no sparse of facial or body hair Klinefelter---> Decrease libido and sparse facial or body hair
82
How to manage Acute bacterial prostatitis?
6 weeks TMP-SMX or Quinolones
83
Important point of Acute bacterial prostatitis
Avoid doing cystoscopy and Foley catheter as it will lead to rupture of prostate and septic shock
84
How Hereditary angioedema occur?
Due to C1 inhibitor deficiency or dysfunction leads to excessive bradykinin
85
Triad of Hereditary angioedema
Facial swelling with airway obstruction No pruritis or urticaria Colicky abdominal pain with vomiting
86
How to DX hereditary angioedema?
Low C4 level | Low C1 inhibitor protein or dysfunction
87
How Penile fracture occur?
Rupture of fibrous tunica albuginea that envelopes the corpus cavernosum Seen in blunt trauma like erect penis during Intercourse
88
Triad of Penil fracture
Sudden onset pain with snapping sound Hematoma of penis leads to swelling and ecchymosis Sometime unable to pass urine which indicates injury to urethera
89
How to manage Penile fracture?
Dx clinically and need surgical repaired If associated with uretheral injury Do Retrograde uretherography
90
What are the risk Factor of Male Breast cancer?
BRCA1/2 Condition increase Estrogen to androgen ratio--->klinefelter syndrome, Obesity, cirrhosis and marijuana use
91
How Male breast cancer present?
Sub areolar mass Dumpling of skin and nipple Induration and ulceration
92
How to dx and manage Male breast cancer?
Mammography and Bx
93
How to d/f Gynecomastia and breast cancer?
Gynecomastia:: Central located with respect to nipple Indistinct margins with surrounding fat Breast cancer:: Eccentric to nipple Well define or spiculated margins
94
How to dx and Treat common variable immunodeficiency?
Dx:: * CBC = normal WBC count * Quantitative Immunoglobulin panel like low All immunoglobulins esp IgG * No use of flow cytometry Tx:: * Treat the recurrent infection * Immunoglobulin replacement therapy * No response to vaccination
95
What are the chronic manifestation of Common variable immunodeficiency?
In lungs:: Sinusitis , pneumonia and otitis Fibrosis and bronchiectasis GIT:: Chronic diarrhoea and IBD like condition Autoimmune:: RA and thyroid disease
96
Difference b/w True and Pseudogynecomastia
Pseudo—-> Occur in obese patient with excessive deposition of fat in the breast w/o “distinct margin” Rx is weight loss only True—->enlargement of glandular breast tissue with “Distinct margins” and tenderness
97
What are the typical features of Edward syndrome? | Face--->Hands--->thorax---->Abdomen---->Lower limb
Face shows small jaw with prominent occiput and low set Ears Clenched hands with Overlapping fingers Heart and Renal defects Limited hip abduction and Rocker bottom feet
98
What are the typical features of Patau syndrome? | Face--->Hand-->thorax with abdomen--->lower limb
Face shows small eye with small head Or holoprosencephaly Hands shows more than 5 fingers Cardiac with Renal defects and Umbilical hernia / Omphalocele Rocker bottom feet

Internal Medicine (14 decks)

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