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Internal Medicine > Immuno > Flashcards

Immuno Flashcards

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
Q

Name the organisms cover by Killed or inactivated vaccine

A

Hepatitis A
Typhoid (Vi polysaccharide, intramuscular), Rabies
Influenza
Polio (SalK)

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26
Q

How Hyperacute rejection presents?

A

Widespread thrombosis of graft vessels—-> ischemia and fibrinoid necrosis

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27
Q

How hyperacute rejection occurs?

A

Pre-existing recipient antibodies react to donor antigen (type II hypersensitivity reaction)
activate complement

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28
Q

How acute rejections occurs?

A

If humoral antibodies developed after transplantation

If Cellular—> CD8+ T cells and/or CD4+ T cells activated against donor MHCs (type IV hypersensitivity reaction)

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29
Q

how acute rejections presents ?

A

Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate
Prevent/reverse with immunosuppressants

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30
Q

How chronic rejection occurs?

A

CD4+ T cells respond to recipient APCs presenting donor peptides, including allogeneic MHC
Both cellular and humoral components (type II and IV hypersensitivity reactions)

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31
Q

Important point

A

For patients who are immunocompromised, irradiate blood products prior to transfusion to prevent GVHD

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32
Q

MOA of MYCOPHENOLATE

A

reversible inhibitor of inosine monophosphate dehydrogenase (IMPDH), which is the ratelimiting enzyme in de novo purine synthesis

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33
Q

What is the main side effect of MYCOPHENOLATE?

A

bone marrow suppression.

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34
Q

MOA of AZATHIOPRINE

A

purine analog that is enzymatically converted to 6-mercaptopurine.
It acts primarily by inhibiting purine synthesis.

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35
Q

What is the side effect of AZATHIOPRINE?

A

The major toxicity of azathioprine is dose-related diarrhea, leukopenia, and hepatotoxicity.

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36
Q

MOA of TACROLIMUS and CYCLOSPORINE

A

inhibiting the transcription of interleukin-2 and several other cytokines, mainly the T-helper lymphocytes.

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37
Q

Side effects of tacrolimus

A

nephrotoxicity and hyperkalemia

does not cause hirsutism or gum hypertrophy

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38
Q

Side effects of CYCLOSPORINE

A

Nephrotoxicity and neurotoxicity
Gingival hypertrophy and hirsutism.
Hypertension ( CCB as a TOC)
Glucose intolerance

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39
Q

Important point

A

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.

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40
Q

How to dx Hereditary angioedema?

A

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
Q

Important point

A 
C1 inhibitor concentrate; a bradykinin antagonist (e.g icatibant)
Kallikrein inhibitor (ecallantide)
42
Q

How MuCcune albright syndrome occurs?

A

Defect in the G-protein cAMP-kinase function in the affected tissue, thereby resulting in autonomous activity of that tissue

43
Q

Triad of MuCcune albright syndrome

A

precocious puberty
pigmentation i.e. café au lait spots (large and irregular borders)
and multiple bone defects (polyostotic fibrous dysplasia)

44
Q

How Kallman syndrome occur?

A

Failure of migration of fetal GnRH and olfactory neurons result low FSH and LH
Also loss of smell

45
Q

Dysmorphic features of Prader Willi syndrome

A

Narrow forehead
Almond shaped eyes
Downturned mouth

46
Q

Name the Complications occur due to Prader Willi syndrome

A

Sleep apnea
DM type 2
Gastric distension/rupture
Death by choking

47
Q

How to dx Prader Willi syndrome?

A

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
Q

At what age DUCHENE and becker muscular dystrophy occur?

A

DUCHENE:::. 2-3 years of age
Becker::: 5-15 years of age

49
Q

Triad of Myotonic muscular dystrophy

A

Occur in 12-30 years of age
Facial weakness with dysphagia
Handgrip Myotonia

50
Q

What are the complications of Myotonic muscular dystrophy?

A

Arrthymia
Cataract
Balding
Testicular atrophy/infertility

51
Q

How to dx DUCHENE muscular dystrophy?

A

Dx is confirmed by genetic testing (gold standard)
biopsy shows muscle replacement by fat and fibrosis
and absent dystrophin on immunochemistry staining

52
Q

Important point

A

Myopathic pattern on electromyography (myotonic pattern in myotonic muscular dystrophy)

53
Q

Triad of CONGENITAL CONTRACTURAL ARACHNODACTLY

A

Due to mutation in fibrillin gene 2
Tall stature with arachnodactyly
multiple contractures involving large joints

54
Q

Important point (very very important)

A

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
Q

Screening test of dyslipidemia

A

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
Q

What are the causes of ACUTE URINARY RETENTION IN ELDERLY MEN?

A

BPH or prostatic CA

neurogenic bladder or detrusor muscle inactivity

57
Q

Important point

A

Spinal cord compression in lumbar region bowel/bladder incontinence (rather than retention)

58
Q

Triad of Acute bacterial PROSTATITIS

A

Tender prostate with systemic symptoms

Pyuria with positive urine culture

SxS of lower urine tract like retention of urine, dysuria and pelvic pain

59
Q

Triad of Chronic PROSTATITIS

A

Tender prostate without systemic symptoms

LUTS with pyuria

Due to Recurrent UTI

60
Q

Triad of NON-INFLAMMATORY CHRONIC PROSTATITIS

A

LUTS without fever

Mild tender prostate

Negative Urine DR and culture

61
Q

Triad of INFLAMMATORY CHRONIC PROSTATITIS

A

LUTS without fever

Mild tender prostate

Negative Urine DR and culture

62
Q

D/f b/w NON-INFLAMMATORY CHRONIC PROSTATITIS AND INFLAMMATORY CHRONIC PROSTATITIS

A

-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
Q

Triad of Chronic pelvic pain syndrome

A

LUTS with pain on ejaculation

Hematospermia with negative culture

Pain at pelvic and reproductive areas

64
Q

How to manage Chronic pelvic pain syndrome?

3As

A

Alpha blocker like tamsuloin
Abx like cipro
5Alpha reductase inhibitors finasteride

65
Q

Triad of Testicular cancer

A

U/L painless testicular node

Radical orchiectomy and then biopsy

Firm ovoid mass on examination

66
Q

How to dx Testicular cancer

A

Scrotal US

Tumor markers viz Alpha feto protein / Beta HCG

67
Q

What are the risk factor of testicular cancer?

A

Family history

Cryptosporidium

68
Q

Triad of steroid

A

Athlete with small testis

Low GnRH, LH and FSH/ normal testosterone

Aggression

69
Q

Side effect of 5 alpha reductase Inhibitors

A

Decrease libido

Erectile dysfunction

70
Q

Side effects of Phosphodiesterase Inhibitors

A

Low BP if taken with other anti-HTN
Painful erection

Blue discolouration of eye
Non-arteritic anterior ischemic optic neuropathy

71
Q

How to t/m EPIDIDYMITIS?

A

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
Q

How EPIDIDYMITIS presents?

A

U/L testicular pain

Epididymal pain

Dysuria and frequency

73
Q

Important of Germ cell tumors

A

Non Seminoma Germ cells have increased B-HCG and alpha feto protein

Seminoma Germ cells have increased only B-HCG

74
Q

Important point of Stromal testicular tumors

A

Leydig—>which produce Estrogen or testosterone

Steroli cell tumor which occasionally associated with increased estrogen

75
Q

Important point of Germ cell Tumor

A

Leydig tumor doesn’t have elevated alpha feto.protein and b hcg

76
Q

Triad of Testicular torsion

A

Tender erythematous swell scrotum

Absent cremasteric reflex

Horizontal testicular lie with elevated testis

77
Q

How to DX Testicular torsion?

A

US doppler which shows no blood flow

78
Q

How to manage testicular torsion?

A

Surgical detorsion and fixation with exploration of the C/L side

Or

Manual detorsion if surgery not available

79
Q

What is the basic d/f b/w Testicular torsion and Epididymitis?

A

If elevation of testis decrease pain—> Epididymitis (+ve phren sign)

If elevation of testis doesn’t decrease pain —> Testicular torsion

80
Q

Important point of Spermatogenesis

A

Cryptorchidism, Varicocele

Or Bath in hot tub, laptop computing cause infertility by increasing testicular temperature

81
Q

Difference between Klinefelter syndrome and anabolic steroid

A

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
Q

How to manage Acute bacterial prostatitis?

A

6 weeks TMP-SMX or Quinolones

83
Q

Important point of Acute bacterial prostatitis

A

Avoid doing cystoscopy and Foley catheter as it will lead to rupture of prostate and septic shock

84
Q

How Hereditary angioedema occur?

A

Due to C1 inhibitor deficiency or dysfunction leads to excessive bradykinin

85
Q

Triad of Hereditary angioedema

A

Facial swelling with airway obstruction

No pruritis or urticaria

Colicky abdominal pain with vomiting

86
Q

How to DX hereditary angioedema?

A

Low C4 level

Low C1 inhibitor protein or dysfunction

87
Q

How Penile fracture occur?

A

Rupture of fibrous tunica albuginea that envelopes the corpus cavernosum

Seen in blunt trauma like erect penis during Intercourse

88
Q

Triad of Penil fracture

A

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
Q

How to manage Penile fracture?

A

Dx clinically and need surgical repaired

If associated with uretheral injury Do Retrograde uretherography

90
Q

What are the risk Factor of Male Breast cancer?

A

BRCA1/2

Condition increase Estrogen to androgen ratio—>klinefelter syndrome, Obesity, cirrhosis and marijuana use

91
Q

How Male breast cancer present?

A

Sub areolar mass
Dumpling of skin and nipple
Induration and ulceration

92
Q

How to dx and manage Male breast cancer?

A

Mammography and Bx

93
Q

How to d/f Gynecomastia and breast cancer?

A

Gynecomastia::
Central located with respect to nipple
Indistinct margins with surrounding fat

Breast cancer::
Eccentric to nipple
Well define or spiculated margins

94
Q

How to dx and Treat common variable immunodeficiency?

A

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
Q

What are the chronic manifestation of Common variable immunodeficiency?

A

In lungs::
Sinusitis , pneumonia and otitis
Fibrosis and bronchiectasis

GIT::
Chronic diarrhoea and IBD like condition

Autoimmune::
RA and thyroid disease

96
Q

Difference b/w True and Pseudogynecomastia

A

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
Q

What are the typical features of Edward syndrome?

Face—>Hands—>thorax—->Abdomen—->Lower limb

A

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
Q

What are the typical features of Patau syndrome?

Face—>Hand–>thorax with abdomen—>lower limb

A

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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