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To really know 1 Flashcards

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1
Q

IgE-Mediated Hypersensitivity (type 1), bound to mast cells, and causes

A

Anaphylaxis, seasonal allergy (hay fever), food allergy (peanut, shellfish), hives, eczema

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2
Q

IgG-Mediated Cytotoxic Mediated Hypersensitivity (type 2)

A

Red blood cells detroyed by complement and antibodies during a transfusion of mismatched blood type or during erythroblastosis fetalis

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3
Q

Immune Complex-Mediated Hypersensitivity (type 3)

A

Antigen-antibody comlexes depositions
Glomerulonephritis, rheumatoid arthritis, SLE

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4
Q

Cell-Mediated Hypersensitivity (Type 4)

A

Th1 cells secrete cytokines, which activate macrophages
Contact dermatitis, Tuberculin reaction, autoimmune disease (diabetes mellitus type 1, Multiple sclerosis, rheumatoid arthritis)

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5
Q

Type 1 collagen component (…)
abnormal in (…)

A

Bone and scar
Osteogenesis imperfecta

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6
Q

Type 2 collagen

A

Cartilage

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7
Q

Type 3 collagen

A

Skin, Vessels, and Granulation Tissue

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8
Q

Type 4 collagen

A

Basement membrane

Alport

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9
Q

Fibrillin / Elastin

A

Marfan
Emphysema (Excessive elastase)

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10
Q

Transplant rejection : Hyperacute

Onset
Mechanism
Hypersensitivity

A

Onset: Immediate
Mechanism: Preformed antibodies
Thrombosis and occlusion of graft vessels.
Hypersensitivity: type 2

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11
Q

Transplant rejection : Acute

Onset
Mechanism
Hypersensitivity

A

Onset: Weeks to months
Mechanism: T cell mediated immune response
Inflammation and leukocyte infiltration of graft cells
Hypersensitivity: type 4

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12
Q

Transplant rejection : Chronic

Onset
Mechanism
Hypersensitivity

A

Onset: months to years
Mechanism: T-cell mediated process resulting from the foreign MCH “looking like’’
Intimal thickening and fibrosis of graft vessels, graft atrophy
Hypersensitivity: 3 and 4

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13
Q

Transplant rejection : Graft

Onset
Mechanism
Hypersensitivity

A

Onset: varies
Mechanism: Donor T-cells in the graft proliferate and attack the recipient’s tissue
Bone marrow transplant (++)
Diarrhea, rash, jaundice
Hypersensitivity: 4

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14
Q

Toxoplasmosis (TORCH):
Triad
Clinic
Tx

A

Triad: Intracranial calcifications, Hydrocephaly, Chorioretinitis

Blueberry muffin rash
Seizures, intellectual disabilities, vision impairment

Tx: Pyrimethamine + Sulfadiazine + Leucovorin

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15
Q

Congenital Rubella Syndrome (TORCH)

A

Deafness, Cataracts, Heart disease

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16
Q

Cytomegalovirus (HHV-5) (TORCH)

A

deafness
blueberry muffin rash
Intracranial calcifications , true periventricular

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17
Q

Congenital syphilis (TORCH)

A

Wimberger sign
Rash, jaundice
Snuffles

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18
Q

Late onset syphilis in children

A

Frontal bossing
Interstitial keratitis
Saddle nose
Short maxilla
Protuding mandibles
Hutchinson incisors
Mulberry molars

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19
Q

Parvovirus B19 (TORCH)

A

Anemia
Hydrops fetalis

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20
Q

Congenital Varicella-Zoster Virus (HHV-3) (TORCH)

A

Hypoplastic limbs
Skin & occular lesions
CNS abnormalities

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21
Q

Neonatal Varicella-Zoster Virus (late pregnancy)

A

Vesiculopapular rash
Disseminated infection: pneumonia, hepatitis, encephalitis

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22
Q

What results from the loss of function of:
- BRCA1 / BRCA2
- MSH
- p53
- Rb

A
  • Breast ovarian cancer
  • Hereditary nonpolyposis colon cancer
  • Li-Fraumeni syndrome, human
    papillomavirus infection
  • Retinoblastoma
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23
Q

What results from the gain of function of:
- BCL-2

A
  • Follicular lymphoma
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24
Q

Medications that act on G1 phase:

A
  • Hormonal drugs
  • Antineoplastic enzymes: asparaginase, pegaspargase
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25
Medications that act on M phase:
Vinca alkaloides: vinblastine, vincristine, vinorelbine
26
Medications that act on S phase:
- Tpoisomerase-1 inhibitors: topotecan, irinotecan - 1: Antimetabolites: a. folate analogs: metothrexate b. purines analogs: cladribine, fludarabine, mercaptopurine, pentostatin, thioguanine c. pyrimidines analogs: capecitabine, cytarabine, gemcitabine, floxuridine, fluoruracil - 2 : Hydroxyurea
27
Medications that act on G2 phase:
Bleomycin
28
Medications that act on G2 and M phases:
- Taxanes: docetaxel, paclitaxel - Epipodophyllotoxin derivatives: etoposide, teniposide Bleomycin
29
Gray or milky discharge, fishy odor, positive amine test (whiff test), clue cells, pH > 4.5
Bacterial vaginosis (Gardnerella vaginalis)
30
Yellow-green, frothy discharge; strawberry cervix, foul smelling, flagellated protozoa, elevated pH (> 4.5)
Trichomoniasis ( Trichomonas vaginalis)
31
Thick, white, curd-like discharge (cottage cheese appearance) Pseudohyphae, pH(4.0-4.5)
Yeast infection (Candida albicans )
32
Normal anion gap metabolic acidosis
''USED CRAP'' Ureterostomy Small bowel fistula Extra chloride Diarrhea Carbonic anhydrase Renal tubular acidosis Addison's disease Pancreatic duodenal fistula
33
IgA roles
Dimer. Secreted into mucous, saliva, tears, colostrum. Tags pathogens for destruction. Prevents adherence of bacteria/viruses to mucosa Mucosal immunity, selective IgA deficiency (most common immunodeficiency) ***IgA nephropathy (Berger disease) – hematuria post-URI*** ***Multiple myeloma – ↑ monoclonal IgG or IgA***
34
IgM roles
First antibody produced in immune response Pentamer (efficient at agglutination) Strong complement activator Does not cross placenta Primary response, recent infection ***Waldenström macroglobulinemia – ↑ IgM*** Classical pathway: IgG and IgM activate C1 (C1q binds Fc region)
35
IgE roles
Binds to mast cells/basophils Mediates Type I hypersensitivity (allergies, anaphylaxis) Defense against parasites (helminths)
36
IgD roles
Unclear function Found on naive B cells with IgM Rare in circulation B cell maturation marke
37
IgG roles
Crosses placenta (passive immunity to fetus) Main antibody in secondary response Activates complement, opsonization, neutralization Chronic infection, memory ***Paroxysmal cold hemoglobinuria – IgG-mediated hemolysis *** Classical pathway: IgG and IgM activate C1 (C1q binds Fc region)
38
Classical pathway
Trigger: Antigen–antibody complexes (IgG or IgM) 🔑 “GM makes classic cars” → IgG, IgM activate Classical Key Steps: C1 complex (C1q + C1r + C1s) binds Fc region of IgG or IgM Cleaves C2 and C4 → forms C4b2a (C3 convertase) ***Antibodies (IgG, IgM) = Classical only*** ***Lectin is innate immunity but uses same C2/C4 as Classical***
39
Lectin Pathway
Trigger: Mannose residues on pathogens Uses mannose-binding lectin (MBL) instead of C1 Activates MASP proteins → cleaves C2 and C4 → forms C4b2a (C3 convertase) 🧠 Structurally identical to Classical from C2/C4 on, just different trigger
40
Alternative pathway
Trigger: Spontaneous hydrolysis of C3 or direct contact with pathogen surfaces C3 → C3b (spontaneous or microbial) C3b binds Factor B Factor D cleaves B → forms C3bBb (C3 convertase) Properdin stabilizes C3bBb 🧠 Does NOT require antibodies — part of innate immunity ***Alternative = always on at low levels → amplifies response***
41
MAC (C5-C9) deficiency
Know the MAC deficiency = Neisseria link cold
42
Complement deficiency syndromes
C1 esterase inhibitor deficiency → Hereditary angioedema (↑ bradykinin, NO urticaria) C3 deficiency → Recurrent pyogenic infections, ↑ risk of Type III HSR MAC (C5-C9) deficiency → Recurrent Neisseria infections DAF (CD55) deficiency → Paroxysmal nocturnal hemoglobinuria (PNH)
43
Key complement products
C3b Opsonization (b = bind bacteria) C5a Neutrophil chemotaxis (a = attract) C3a, C5a Anaphylaxis (histamine release) C5b–C9 (MAC) Cell lysis of gram-negative bacteria
44
Gs proteins: Stimulatory
Activates: Adenylyl cyclase → ↑ cAMP → ↑ PKA 🔑 "Gs = Stimulate cAMP" Receptors: β1, β2, β3 (adrenergic) D1 (dopamine) H2 (histamine) V2 (ADH → aquaporins in kidney) ***Gs overstimulation: Cholera toxin permanently activates Gs → ↑ cAMP → secretory diarrhea*** ***ADH receptors: V2 = water reabsorption in kidney (Gs)***
45
Gi proteins: Inhibitory
Inhibits: Adenylyl cyclase → ↓ cAMP 🔑 "Gi = Inhibit cAMP" Receptors: α2 (adrenergic) M2 (muscarinic) D2 (dopamine) ***Gi inhibition: Pertussis toxin inhibits Gi → ↑ cAMP → whooping cough***
46
Gq proteins : Calcium & Contraction
Activates: Phospholipase C → IP₃ + DAG → ↑ intracellular Ca²⁺ → PKC activation 🔑 "Gq = Que cuts PIP2 into DAG + IP3" Receptors: HAVe 1 M&M H1 (histamine) α1 (adrenergic) V1 (ADH → vascular smooth muscle) M1, M3 (muscarinic) ***Gq: Often linked with smooth muscle contraction (e.g., α1 = vasoconstriction)*** ***ADH receptors: V1 = vasoconstriction (Gq)***
47
Vitamin A : Retinoic acid
Receptor: Intracellular nuclear receptor Function: Gene transcription regulation in epithelial cell differentiation Clinical: Used in acute promyelocytic leukemia (APL) → all-trans retinoic acid (ATRA) Deficiency: Night blindness, dry skin Toxicity: Teratogenic, pseudotumor cerebri Only A & D use nuclear hormone receptors
48
Vitamin D: Calcitriol
Receptor: Intracellular nuclear receptor Function: Regulates Ca²⁺ and phosphate homeostasis Clinical: Deficiency: Rickets (kids), osteomalacia (adults) Excess: Hypercalcemia Activated in kidney (1α-hydroxylase) Only A & D use nuclear hormone receptors
49
Vitamin E: Tocopherol
Receptor: Not receptor-mediated — acts as an antioxidant (protects RBCs, membranes) Function: Scavenges free radicals Clinical: Deficiency: Hemolytic anemia, spinocerebellar symptoms (similar to B12 but no methylmalonic acid ↑) E = antioxidant (free radical scavenger)
50
Vitamin K
Receptor: Cofactor, not receptor-mediated Function: Activates clotting factors II, VII, IX, X, protein C & S via γ-carboxylation Clinical: Deficiency: Bleeding in newborns (give injection at birth), ↑ PT/INR K = γ-carboxylation cofactor for clotting, no receptor
51
Water-Soluble Vitamins
B-complex & C vitamins mostly act as coenzymes — no specific receptors
52
Vitamin C : Ascorbic acid
Function: Antioxidant, hydroxylation of proline/lysine in collagen Mechanism: Enzyme cofactor – not receptor-mediated Clinical: Deficiency → Scurvy: swollen gums, petechiae Enhances iron absorption (keeps it reduced)
53
Vitamin B1 : Thiamine
Cofactor for dehydrogenases (e.g., PDH, α-KG DH) No receptor – coenzyme Wernicke-Korsakoff, Beriberi
54
Vitamin B2 : Riboflavin
FAD, FMN coenzymes No receptor Cheilosis, corneal vascularization
55
Vitamin B3 : Niacin
NAD⁺, NADP⁺ No receptor – precursor Pellagra: 3 D’s
56
Vitamin B5: Panthotenic acid
CoA synthesis No receptor Fatty acid metabolism
57
Vitamin B6 : Pyridoxine
PLP cofactor for transaminases No receptor INH-induced deficiency
58
Vitamin B7 : Biotin
Cofactor for carboxylation (e.g., pyruvate carboxylase) No receptor Avidin (raw eggs) causes deficiency
59
Vitamin B9 : Folate
DNA/RNA synthesis No receptor – coenzyme Neural tube defects
60
Vitamin B12: Cobalamin
Methyl transfer, odd-chain FA metabolism No receptor Subacute combined degeneration

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