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Bloc F - Defense > Clinical > Flashcards

Clinical Flashcards

1
Q

Principles of vaccination?

A
  • Stimulate immunity: need to activate appropriate immune response that will induce protection
  • Active immunity (alive or dead virus Þ active response) or passive immunity (antibodies from another person Þ limited life)
  • Whole virus or part of the virus
  • The toxin produced by the virus
  • Conjugated/multiple vaccines
  • Stimulate memory: only effective if vaccinee is protected upon subsequent exposures
  • Herd Immunity: for vulnerable population
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2
Q

Who do we vaccine?

A
  • Those at risk:
  • Children under the age of 1 and elderly are particularly vulnerable
  • Adults facing chemotherapy or transplant also vulnerable
  • Patients with immunodeficiencies
  • Travelers
  • Family contacts
  • Health professionals
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3
Q

Benefits of vaccination?

A
  • Herd immunity
  • Costs (prevention)
  • Contributes to general population health
  • Prevents morbidity and mortality
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4
Q

Side effects of vaccination?

A
  • Side effects: fever, irritability, rash, pain, headache
  • NO EFFECT on autism, sudden death, and brain damage
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5
Q

Criteria for febrile neutropenia?

A
  • Fever: 38oC for more than 1 hour or Þ 38.5 (>100.4oF)
  • Neutropenia: <500 neutrophils/μL
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6
Q

Pathogenesis of febrile neutropenia?

A
  1. Breeches in host defense related to underlying malignancy and treatment:
  • MUCOSITIS: effect of chemo on mucosal barriers (causes MAJORITY of febrile neutropenia)
  • Tumor itself
  • Surgery
  1. Immune defect –> can’t react optimally
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7
Q

Criteria to be a high risk neutropenic febrile patient?

A
  1. Patient-related predictors
    • Age ≥65yrs
    • Poor nutritional status
    • Poor performance based on active comorbidities
  2. Disease-related predictors
    • Advanced stage of cancer
    • Bone marrow failure due to marrow involvement
  3. Anti-cancer treatment-related predictors
    • High dose chemo
    • Absence of growth factor support with high dose chemo
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8
Q

General rules in management of neutropenic fever?

A
  • Most do not have documentable infection but MUST be promptly evaluated and receive empiric broad spectrum antibiotics
  • Infection can progress rapidly to death; hard to distinguish
  • Initiate antibiotics after blood cultures, before other investigations: <60 min
  • Attenuated signs and symptoms due to lack of inflammatory reaction: fever may be ONLY sign
  • Immediately evaluate for evidence of sepsis syndromes
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9
Q

Steps in management of neutropenic fever?

A
  1. HIstory: if chemotherapy in the last 6 weeks Þ SUSPECT NEUTROPENIA
  2. Physical exam
  3. Vitals but NO rectal exam
  4. Culture: blood, urine, stool, sputum, skin, CSF, ascites, pleural fluid
  5. Imaging: CXR for all patients, CT sinuses, abdomen prn
  6. Admitted patients: daily ROS, CBC, examination, blood cultures
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10
Q

Algorith of management of febrile neutropenia?

A
  1. Determine the risk (IDSA)
  2. Empiric antibiotics (< 1 hour)
  3. HIGH RISK: hospital admission and IV antibiotics, INITIATE MONOTHERAPY WITH ANTI-PSEUDOMONAL β-LACTAM ANTIBIOTICS, include G+ and anaerobic coverage if signs of it
  4. LOW-RISK: usually outpatient with oral antibiotics Þ Fluoroquinolone + β-Lactam
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11
Q

Criterias to stop febrile neutropenia treatment?

A
  1. Neutrophils to > 500 cells/μL and rising
  2. Afebrile 48 hrs
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12
Q

What are the 3 effectors of inflammatory allergic reaction?

A
  1. mast cells
  2. basophils
  3. eosinophils
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13
Q

What are the 2 components that explain the increase of allergic diseases?

A
  • GENETIC: there is some genetic predisposition to allergic reactions
  • ENVRIVONMENT: increasing prevalence of allergic diseases in economically advanced regions of the world
  • -> “Hygiene hypothesis”: infections that evoke a TH1 response early in life might reduce the likelihood of TH2 response later in life and vice versa + Infections might protect against devlpm atopy by driving the production of TReg cytokines
  • -> Other possibilities that explain the increase in atopic disease include climate, ovesity, western diet and housing
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14
Q

What are the 4 types of hypersensitivity reactions?

A

A-B-C-D

Type 1 hypersensitivity - IgE - Allergic Anaphylaxis Atopy

Type 2 hypersensitivity - mediated cytotoxicity (ADCC) antiBody

Type 3 hypersensitivity - Immune Complex mediated (IgM, IgG)

Type 4 hypersensitivity – T cell Delayed

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15
Q

Pathophysiology of type 1 hypersensitivity?

A
  • An allergic reaction induced by specific antigen (allergen)
  • Provoked by re-exposure to the same antigen
  • Mediated by specific IgE antibodies (Antibody-mediated): IgE is tightly bound to FceRI at the surface of mast cells and basophils –> will release inflammatory mediators such as Histamine, platelet-activating factor, leukotreins, bradykinins, prostaglandins, and cytokines that contribute to inflammation when bound to an antigen
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16
Q

Diseases associated with type 1 hypersensitivity?

A

The most common type (20% of the population)

  • Asthma
  • Rhino-conjunctivitis
  • Dermatitis
  • Food allergy
  • Urticaria
  • Drug allergy
  • Other chronic diseases
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17
Q

Pathophysiology of type 2 hypersensitivity?

A

Antibody-dependent cell mediated cytotoxicity (ADCC) (IgG, IgM) made against intrinsic Ag (normal self-antigens)

  • Failure in immune tolerance
  • Cross reactivity foreign antigen with self molecule on the surface of host cells
  • Opsonization of the host cells (phagocytosis)
  • Complement activation (MAC lysis of the host cells)
  • NK cell activation: destruction of host cells by the release of pergorins and grazymes
  • Activation or blockage of important cell receptors
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18
Q

Diseases associated with type 2 hypersensitivity?

A
  • Penicillin allergy: the RBCs absorbs the drug and express it at its surface Þ it creates MAC complex (membrane attack complex) Þ the body attacks RBCs
  • AB and Rh blood group incompatibilities (Transfusion reactions)
  • Autoimmune diseases: Myastenia gravis, Idiopathic Thrombocytopenic Purpura, Goodpasture’s, Graves’
  • Some drugs
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19
Q

Pathophysiology of type 3 hypersensitivity?

A

Caused when soluble antigen-antibody (IgG or IgM) complexes, which are normally removed by macrophages in the spleen and liver, form in large amounts and overwhelm the body These small complexes lodge in the capillaries, pass between the endothelial cells of blood vessels - especially those in the skin, joints, and kidneys - and become trapped on the surrounding basement membrane beneath these cells The antigen/antibody complexes then activate the classical complement pathway This may cause:

  1. Massive inflammation: due to complement protein C5a
  2. Influx of neutrophils: due to complement protein C5a, resulting in neutrophils discharging their lysosomes and causing tissue destruction and furthers inflammation c. MAC lysis of surrounding tissue cells, due to the membrane attack complex, C5b6789n; and
  3. Aggregation of platelets: resulting in more inflammation and the formation of microthrombi that block capillaries
  4. MAC lysis
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20
Q

Diseases associated with type 3 hypersensitivity?

A
  • Serum Sickness (ex: Ceclor)
  • Immune Complex Glomerulonephritis
  • Extrinsic Allergic Alveolitis (Farmer’s lung)
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21
Q

Pathophysiology of type 4 hypersensitivity?

A
  • Mediated by TH1 cells by a series of phases that each take several hours: exposure to antigen –> presentation through APC –> activation of TH2 –> production of IgE (in the tissues)
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22
Q

Diseases associated with type 4 hypersensitivity?

A
  • Immunized TB: Purified Proteine Derivative (PPD) test
  • Poison ivy
  • Contact dermatitis (cosmetics, solvents…)
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23
Q

Treatement of allergic reaction?

A

Epinephrine IM

Alpha 1 adrenergic receptor

  • Increase peripheral vascular resistance by promoting vasoconstriction = decreases ski perfusion
  • Reduces angioedema
  • Improves coronary perfusion
24
Q

10 Warning Signs of Imm-Def?

A
  1. 8 or more new ear infections within a year
  2. 2 or more serious sinus infection within a year
  3. 2 or more months of antibiotics with little effect
  4. 2 or more pneumonias within a year
  5. Failure of infant to gain weight or grow normally
  6. Recurrent skin or organ abscess
  7. Persistent thrush in mouth or elsewhere on skin, after age 1
  8. Need for IV antibiotics to clear infections
  9. 2 or more deep seated infections
  10. Family history of primary immunodeficiency
25
Q

Signs of suspected B cell deficiency?

A
  • Multiple/Severe Bacterial infections
  • Respiratory Tract bacterial Infections (Streptococcus, Haemophilis)
  • Usually seen after 6 months when maternal antibodies lost
26
Q

Signs of suspected T cell deficiency?

A
  • Opportunistic infections (Candida sp, Pneumocystis jiroveci)
  • Fungal, viral, intra-cellular infections
  • Diarrhea/Malabsorption
  • Poor Growth/Failure to Thrive
27
Q

Signs of suspected phagocytes deficiency?

A
  • Infections of the skin, Liver, GI Tract, gingivitis/periodontitis
  • Abscesses NO PUS
  • Delayed separation of the umbilical cord and wound healing
28
Q

Signs of suspected complement deficiency?

A

C1-C4 deficiency

  • Associated with Rheumatic Disorders
  • Pyogenic Infections

C5-C9 Complement deficiency

  • Susceptibility to Encapsulated organisms (Pneumococcus, Meningococcus, H. flu)
29
Q

What test do we order when a immune deficiency is suspected?

A

It depends on the age at onset, distribution of PID, site and types of infections… not just “the usual immunology work-up” DEPENDS ON THE PRESENTATION!!

  • Number and function always
  • DNA sequencing
  • Specific work-up related to the suspected deficiency
30
Q

Characteristics of Di George syndrome?

A
  • Involves submicroscopic deletion of specific part of chromosome 22 (22q11), most common microdeletion syndrome
  • Dysmorphic features
  • Heart malformations
  • Parathyroid and calcium deregulation
  • Thymus hypoplasia –> leas to immune deficiency
  • Failure of development of 3rd & 4th pharyngeal pouches
  • Variable loss of T-cell mediated immunity
  • Psychiatric disorders in adulthood –> schizophrenia, anxiety, depression
  • Autoimmune disease such as autoimmune cytopenia, thrombocytopenia, and juvenile rheumatoid arthritis are most common. Autoimmune thyroid disease, autoimmune uveitis (inflammation of middle layer of the eye that can lead to serious visual consequences), and selective IgA deficiency may occur as well. Severe eczema and asthma are also seen.
  • ORDER A FISH (Fluorescence in situ hybridization)
  • Autosomal dominant inheritance but can happen de novo (50/50 to transmit it)
31
Q

Familial Mediterranean Fever characteristics?

A
  • Hereditary inflammatory disorder
  • Characterized by recurrent attacks of fever, peritonitis, pleurisy, painful, swollen joints (arthralgia and occasionally arthritis), and a characteristic ankle rash, starts in the 20s.
  • Amyloidosis, which can lead to renal failure, is the most severe complication
  • Caused by mutations in MEFV gene, locus is at 16p13.3 (tip of short arm of chromosome 16): assists in controlling inflammation by deactivating the immune response Þ inappropriate or prolonged inflammatory response.
  • Most cases autosomal recessive (AR) (25% chances to pass it to child)
  • Do molecular genetic testing
  • Suspect if family member with renal failure, episodes of fever and ethnic origin
  • For acute episodes, mainly supportive, including IV saline for hydration and use of NSAIDs, paracetamol, or dipyrone for pain relief;
  • Lifelong treatment with colchicine (1-2 mg/day orally in adults and 0.5-1 mg/day in children) prevents painful inflammatory attacks and the deposition of amyloid
  • Routine treatment of end-stage renal disease, including live related-donor renal transplantation.
32
Q

What is Sicca symptom?

A

Dry eyes and dry mouth

33
Q

Scleroderma (limited or diffuse)?

A
  • Uncontrolled severe fibrosis of the skin, blood vessels and other affected organs
  • Organs most affected are the skin, lungs, blood vessels, GI tract and kidneys
  • Most patients have Raynaud’s and a positive ANA
34
Q

What is Sjögren’s Syndrome?

A
  • Affects the exocrine glands: dry mouth (Xerostomia) and dry eyes (Xerophthalmia) also called Sicca symptoms
  • Associated with the anti-Ro (SSa) and anti-La (SSb) autoantibodies
35
Q

What is Mixed Connective Tissue Disease (MCTD)?

A
  • SLE
  • scleroderma
  • inflammatory myositis
36
Q

Systemic symptoms of autoimmune Connective Tissue Diseases?

A
  • Weight loss
  • Poor appetite
  • Fever
37
Q

Non-specific symptoms of autoimmune Connective Tissue Diseases?

A
  • Raynaud’s
  • Sicca: dry eyes and dry mouth
  • Diffuse lymphadenopathy
38
Q

Manifestations autoimmune Connective Tissue Diseases?

A

INFLAMMATION IS THE KEY

  • Arthritis
  • Certain types of skin rashes
  • Mucosal ulcers
  • Ocular symptoms
  • Lung involvement
  • Renal function
  • Peripheral nerve defect
39
Q

Work-up of autoimmune connective tissue disease?

A
  • Complete Blood Count (CBC)
  • Renal function (Creatinine)
  • Liver function tests
  • Urine analysis
  • Urine protein measurement
  • Inflammatory tests: C-Reactive Protein (CRP) and Erythrocyte Sedimentation Rate (ESR) but NOT specific
  • Auto-antibodies: a lot of false positive and false negative
  • TISSUE BIOPSY IS THE BEST WAY TO KNOW
40
Q

Clinical manifestations of lupus?

A
  • Cutaneous Manifestations: malar rash (butterfly), Subacute Cutaneous Lupus Erythematosus (SCLE), Discoid Lupus Erythematosus (DLE)
  • Mucosal Ulcers
  • Arthritis: Jacoud’s arthripathy, erosive polyarthritis, arthralgias, osteonecrosis, osteoporosis, fibromyalgia
  • Lupus Nephritis: 60% will have kidney involvement, SURVEILLANCE
  • Serositis: pleuritis and pericarditis
  • Hematological problems: anemia, thrombocytopenia, leuko and lymphopenia
  • Autoantibodies: Antinuclear Antibodies (ANA), Antiphospholipids Antobodies (anticardioipins, lupus anticoagulant, anti beta-2 glycoprotein
41
Q

Gold standard evaluation of Lupus?

A

Clinical diagnosis is the expert opinion of the clinician based on the presence of clinical signs and symptoms and supported by the presence of appropriate diagnostic tests

42
Q
  • Low CH50
  • Neisserial infection particularly neisseria meningitidis

What’s your diagnosis?

A

Defiency of proteins of the membrane attack complex (C5-8)

43
Q
  • Absent AH50
  • Meningococcal disease

What’s your diagnosis?

A

Properdin deficiency

44
Q
  • omphalitis, leukocytosis and destructive gingivitis, recurrent infections of skin, respiratory tract, bowel and perirectal area
  • Inflammation
  • High WB
A

LAD-1: problems in sticking

–> tests for CD18/CD11 (=LFA1) integrin

45
Q
  • One of “The big 5”: Nocardia species, Burkholderia cepacia, Aspergillus species, Serratia marcesens, Staphylococcus aureus (No BASeS)
  • NO fever

What’s your diagnosis?

A

Chronic granulomatous disease (CGD)

46
Q
  • Respiratory infections (sinusitis, mastoditis, pneumonia…) repeatedly, are severe with incomplete response to therapy
  • Difficulty of heal wounds

What’s your diagnosis?

A

Classical NK deficiency

47
Q

What is the gold standard test for IgE related allergy?

A

Challenge test

48
Q

Yound athlete that had an anaphylaxic shock while doing sport?

A

Food-dependent exercise-induced anaphylaxis

–> Epinephrin IM comme d’hab.

49
Q

How do you calculate the TBSA in a burn injury?

A

The rule of 9 – ADULTS ONLY

  • Head = 9
  • Back = 18
  • Front = 18
  • Legs = 18
  • Arms = 9

Lund-Browder diagram – KIDS

50
Q

What are the Burn center referral criteria?

A
  1. 2nd or 3rd more than 10% TBSA in children and elderly
  2. 2nd or 3rd more than 20% TBSA adults
  3. Face, hands, feet, joints (ADL + esthetical implications)
  4. ANY 3rd degree
  5. Inhalation
  6. Electrical
  7. Circumferential
  8. Any other medical comorbid disorder
51
Q

How do you calculate the amount of fluid rescucitation in a burn victim?

A

The Parkland Formula

  • 4 cc/kg/%TBSA = total in the first 24 hours
  • ½ in the first 8h
  • ½ in the other 16 hours
  • EX: 70 kg 50% = 4 x 70 x 50 = 14L = 7 in 8 hours and 7 in 16h
52
Q

Principles of RBM choosing wisely?

A
  1. Shared decision-making
  2. Harm reduction
  3. Resource stewardship
53
Q

Important questions to prevent overdiagnosis?

A
  1. Do I really need this test?
  2. What are the downsides?
  3. Are there simpler safer options?
  4. What happens if I do nothing?
54
Q
  • Upper or lower respiratory tract symptoms (recurrent)
  • Necrotizing pauci-immune glomerulonephritis
  • Arthritis
  • Purpura
  • Positive cANCA

What’s your diagnosis?

A

Granulomatosis with polyangiitis (GPA)

55
Q

Positive pANCA indicates what?

A
  1. Microscopic polyangiitis (MPA)

or

  1. Eosinophilic granulomatosis with polyangiitis (EGPA)
56
Q

Complications of small vessels vasculitis?

A
  1. stenosis
  2. occlusion
  3. aneurysm formation
57
Q
  1. Allergic rhinitis and asthma X 10 years
  2. Peripheral eosinophilia (>1500) and eosinophilic tissue infiltrates of multiple organs (lungs, GI tract)
  3. Vasculitic disease involving the nerves, lung, heart, GI tract, and kidneys

What’s your diagnosis?

A

Eosinophilic granulomatosis with polyangiitis (EGPA)

Bloc F - Defense (7 decks)

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