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238 Cards in this Set
- Front
- Back
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How do many antiviral agents interfere with viral DNA synthesis or transcription?
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Many of the drugs are phosphorylated into triphosphorylated form
This form mimics nucleotide triphosphates The drug is incorporated into synthesis process and blocks further action |
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MOA:
Amantidine |
Antiviral
Impairs uncoating of virus (removal of capsid to allow viral nucleic acid to be released into cell) Binds to M2 matrix protein of influenza A Only effective within 48 hours of symptom onset (similar drug: rimantadine) No longer recommended for use: resistance |
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MOA:
Interferon |
Antiviral
Induces host cell responses to inhibit RNA translation Induces MHC-1 expression DOC for chronic HBV and HCV Used to treat hairy cell leukemia Pegylated form most common (does not require daily dosing) |
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MOA:
Ribavirin |
Antiviral
Phosphorylated to becom ribavirin triphosphate Mimics GTP (guanosine triphosphate) Incorporated into transcription, eventually blocks viral mRNA synthesis DOC for chronic HCV Standard of therapy for HCV: Pegylated interferon alpha PLUS ribavirin |
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MOA:
Acyclovir |
Antiviral
Phosphorylated to acyclovir triphosphate Mimics GTP Is incorporated into DNA and causes inhibition of DNA polymerase Also causes premature DNA chain termination Requires viral thymidine kinase for phosphorylation (only found in select viruses) Selective for HSV-1, HSV-2, VZV (varicella zoster), EBV (Epstein Barr) DOC for HSV-1 and HSV-2 Penetrates BBB Similar drug: Valacyclovir (longer half life, less frequent dosing) |
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MOA:
Vidarabine |
Antiviral
Phosophorylated to imitate ATP Incorporated into DNA, inhibits synthesis Treats all herpes group viruses Especially herpes encephalitis, VZV (varicella zoster) in immunocompromised patients In ointment form, second line (to trifluridine) for herpes keratitis |
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MOA:
Ganciclovir |
Antiviral
Phosphorylated to mimic GTP Incorporated into DNA, inhibits DNA polymerase, causes premature DNA chain termination Similar to Acyclovir but does NOT require viral thymidine kinase DOC for CMV retinitis (in combination with Valganciclovir) Side effect: bone marrow suppression (causes neutropenia or aplastic anemia) |
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MOA:
AZT (Zidovudine) |
Antiviral (anti-retroviral - NRTI [nucleoside reverse transcriptase inhibitor])
Triphosphorylated by human thymidine kinase Mimics TTP Incorporated into DNA and inhibits synthesis Good BBB penetration Treats HIV |
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NRTIs (Nucleoside Reverse Transcriptase Inhibitors)
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Anti-retroviral
AZT (Zidovudine) Didanosine (ddl) Stavudine (d4T) Lamivudine (3TC) |
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MOA:
Protease Inhibitors |
Antiviral
Inhibit cleavage of "giant" protein (gag-pol-env) Cleavage required by HIV to have functional components of the protein Used for HIV Saquinavir Ritonavir Indinavir Nelfinavir Fosamprenavir |
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MOA:
NNRTIs (Non-Nucleoside Reverse Transcriptase Inhibitors) |
Antiviral
Directly inhibit reverse transcriptase Used for HIV Nevirapine Delavirdine Efavirenz |
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MOA:
Fusion Inhibitors |
Antiviral
Prevent fusion between HIV virion and cell Binds to gp41 and prevents fustion with cell membrane Enfuvirtide Increases risk for bacterial pneumonia Most common side effects are insomnia, headache, nausea Severe hypersensitivity reactions possible |
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MOA:
Integrase Inhibitors |
Antiviral
Inhibit HIV viral integrase enzyme Prevents integration and insertion of HIV DNA into human DNA Raltegravir |
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MOA:
Chemokine Co-Receptor Antagonists (CCR5 Antagonists) |
Antiviral
Block CCR5 co-receptor on WBCs targeted by HIV Prevents entry of virus into cell Used in CCR5-topic HIV-1 (R5 virus) that has demonstrated multi-drug resistance Maraviroc Hepatotoxic |
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MOA:
Neuraminidase Inhibitors |
Antiviral
Inhibit influenza virus neuraminidase Used for prophylaxis of influenza A and B in close contacts with infected persons Used to attenuate early disease Zanamivir (not for use in lung disease - causes bronchospasm) Oseltamivir |
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MOA:
Foscarnet |
Antiviral
Direct inhibitor of both DNA polymerase and reverse transcriptase Alternative to ganciclovir for CMV Used for ganciclovir-resistant CMV Used for ganciclovir and acyclovir-resistant VZV and HSV May be useful against HIV but not part of HIV-HAART regimen Nephrotoxic |
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MOA:
Valganciclovir |
Antiviral
Used in combination with ganciclovir for CMV retinitis May cause myelosuppression Contraindicated with ganciclovir allergy |
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MOA:
Trifluridine (Trifluorothymidine) |
Antiviral
Mimics TTP Incorporated into DNA and inhibit synthesis Does not require viral thymidine kinase Active against HSV including emerging thymidine kinase deficient mutants resistant to acyclovir DOC for herpes keratitis (solution form) |
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MOA:
Cidofovir |
Antiviral
Alternative treatment for CMV retinitis DOC for smallpox, severe adenovirus infections Extremely nephrotoxic Can cause Fanconi syndrome at low doses (proximal convoluted tubule destruction) Generally administered with Probenecid to minimize dose/maximize systemic antiviral effect Suppresses viral replication by selective inhibition of viral DNA synthesis Acyclic nucloside phophonate - functions without being phosphorylated (already has mimicry) Very teratogenic |
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Key Features:
Osteogenesis Imperfecta |
Congenital
Disorder of collagen synthesis Fractures Blue, thin sclera |
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Key Features:
Osteopetrosis |
Congenital
Increased density Brittle bones Facial distortion due to bone overgrowth |
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Key Features:
Achondroplasia |
Congenital
Autosomal dominant Defective cartilage synthesis Decreased epiphyseal formatoin Short limbs, normal sized head and torso |
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Key Features:
Osteoporosis |
Acquired
Thinned cortical bone Enlarged medullary cavity Normal Ca, phosphate Normal alkaline phosphatase Decreased bone mass Estrogen deficiency Immobilization Cushing's syndrome |
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Key Features:
Osteomalacia |
Acquired
Diffuse radiolucency Low Ca, phosphate High alkaline phosphatase Impaired mineralization Lack of vitamin D Chronic renal insufficiency |
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Key Features:
Paget's Disease |
Acquired
Bones enlarged and radiolucent Extremely high alkaline phosphatase Excessive bone resorption with replacement Gradual enlargement and deformation of bones (osteitis deformans) Increased osteoclast and osteoblast activity Characteristic mosaic pattern of bone on X-ray |
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Hyaline Cartilage
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Type II collagen
Found in: Joints Developing bones Trachea/larynx Nose |
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Elastic Cartilage
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Elastin
Found in: Ear |
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Fibrocartilage
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Type I collagen
Found in: Intervertebral disks Menisci |
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Osteochondroma
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Benign tumor of cartilage
Developmental defect Exostosis at metaphyseal projections |
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Enchondroma
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Benign tumor of cartilage
May develop into chondrosarcoma (malignant) Cartilage within bone |
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Chondroblastoma
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Benign tumor of cartilage
Femur, tibia, humerus epiphysis |
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Chondrosarcoma
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Malignant tumor of cartilage
Spine, pelvic bones Slower growing than osteosarcoma |
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Osteoma
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Benign bone tumor
Skull |
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Osteoid Osteoma
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Benign bone tumor
Painful Tibia or femur (diaphysis) |
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Osteoblastoma
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Benign bone tumor
Like osteoid osteoma Larger but painless May be malignant |
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Osteosarcoma
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Highly malignant bone tumor
Metaphysis of long bone (knee) Codman's triangle |
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Ewing's Sarcoma
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Malignant bone tumor
Very aggressive Young males Pelvis, long bones Within marrow cavity "Onion skin" appearance |
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What is Codman's triangle?
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Triangular area of new subperiostal that is created when a tumor raises the periosteum from the bone
Usually found in osteosarcoma |
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Duchenne Muscular Dystrophy
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X linked
Absent dystrophin protein Most severe of muscular dystrophies Pelvic girdle weakness Pseudohypertrophy of calves (fatty and fibrous infiltration of calf muscles) Gower's sign Usually boys age 3-7 Proximal muscle weakness with waddling gait Increased serum CPK |
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Becker Muscular Dystrophy
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X linked
Abnormal dystrophin protein Less severe than Duchenne May walk until age 20-25 |
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Limb Girdle Muscular Dystrophy
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Autosomal recessive
Late onset |
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Facioscapulohumeral Muscular Dystrophy
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Autosomal dominant
Late onset |
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Myotonic Muscular Dystrophy
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Autosomal dominant
Late onset Distal limb involvement Inability to voluntarily relax muscle |
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What is Gower's Sign?
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When trying to stand up, child uses its hands to "climb" up his/her own body
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Neural Tube Brain Tumors
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Astrocytoma
Glioblastoma Medulloblastoma Oligodendroblastoma |
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Astrocytoma
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Neural tube
Slow growing M > F |
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Glioblastoma
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Neural tube
Always fatal M > F |
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Medulloblastoma
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Neural tube
Children M > F |
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Oligodendroblastoma
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Neural tube
Rare M = F Slow growing Seizures |
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Neural Crest Brain Tumors
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Meningioma
Schwannoma Neurofibroma |
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Meningioma
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Neural crest
From arachnoid Benign F > M Whorling pattern Psammoma bodies |
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Schwannoma
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Neural crest
Acoustic neuroma F > M Associated with Von Recklinghausen's |
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Neurofibroma
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Neural crest
Fibroblasts and Schwann cells Benign Associated with Von Recklinghausen's |
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Ectoderm Brain Tumors
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Craniopharyngioma
Pituitary Adenoma |
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Craniopharyngioma
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Ectoderm
Most common supratentorial tumor in children Compresses optic nerve |
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Pituitary Adenoma
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Ectoderm
60% prolactin (chromophobe) 10% growth hormone (eosinophil) 10% ACTH (basophil) |
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Mesoderm Brain Tumors
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Lymphoma
Lipoma Hemangioblastoma |
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Lymphoma
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Mesoderm
B Cells Periventricular |
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Lipoma
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Mesoderm
Egg shell appearance |
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What is the most common degenerative disease of the CNS?
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Alzheimer's
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Alzheimer's Disease
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Diffuse cortical atrophy
Senile plaques (beta-amyloid protein) Neurofibrillary tangles (cytoplasmic deposit of tau protein) Most common degenerative disease of CNS |
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Pick's Disease
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CNS degenerative disease
Lobar atrophy Mainly frontal and temporal |
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Parkinson's Disease
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CNS degenerative disease
Bradykinesia, rigidity, resting tremor Dopamine depletion (caudate, putamen) Lewy bodies (spherical inclusions in melanin-depleted neurons of substantia nigra) |
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ALS
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CNS degenerative disease
Rapidly progressive Degeneration of corticospinal tract (UMN) Degeneration of alpha-motorneurons (LMN) |
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Huntington's Disease
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CNS degenerative disease
Chorea, athetoid movements Atrophy of caudate, putamen, frontal cortex Autosomal dominant |
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Friedreich's Ataxia
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CNS degenerative disease
Pes cavus Loss of proprioception Tremors Babinski reflex Spinal cord atrophy (spinocerebellar, corticospinal, posterior columns) Autosomal recessive |
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Upper motor neuron lesions cause:
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Spasticity
Increased tendon reflexes |
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Lower motor neuron lesions cause:
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Paralysis
Fasciculations Absent tendon reflexes |
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Multiple Sclerosis
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Demyelinating disease of CNS
Onset at age 20-40 Associated with cool, temperate climate Oligoclonal bands on CSF electrophoresis (multiple monoclonal gamma globulins - characteristic but not entirely specific) |
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Devic's Disease
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Demyelinating disease
Like MS but limited to spinal cord and optic nerve |
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Guillan-Barre Syndrome
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Demyelinating disease of PNS
Mainly peripheral motor nerves Autoimmune (often follows viral infection) |
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Adrenoleukodystrophy
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Demyelinating disease
Accumulation of long chain cholesterols Blindness, ataxia Latent adrenal insufficiency X linked |
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Schilder's Disease
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Demyelinating disease
Focal to brain Children Visual, auditory, motor defects Variant of adrenoleukodystrophy |
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Hyperfunction of Anterior Pituitary:
Eosinophile Cells |
Prolactin:
Male: decreased libido, impotence Female: galactorrhea, amenorrhea, infertility Growth Hormone: Prepubertal: giantism Adults: acromegaly |
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Hyperfunction of Anterior Pituitary:
Basophile Cells |
ACTH:
Cushing's disease |
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Sheehan's Syndrome
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Pituitary hypofunction
Panhypopituitarism Caused by ischemic necrosis (often postpartum) Hypothyroidism Hypogonadism Hypoadrenalism |
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Dwarfism
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Pituitary hypofunction
Growth hormone deficiency or lack of receptors |
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Eunuchoid Pituitary Hypofunction
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Hypogonadism
Primary amenorrhea Gonadotropin deficiency (common) |
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What are the two parts of the adrenal gland? What do they produce?
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Cortex - Steroids
Medulla - Epinephrine, Norepinephrine |
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Adrenal Adenoma
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Cortex
Most do not produce steroids Conn (increased mineralocorticoids) Cushing (increased glucocorticoids) Virilization (increased androgens) |
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Adrenal Carcinoma
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Cortex
Much rarer than adenomas Usually produce hormones |
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Pheochromocytoma
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Adrenal medulla
10% extra-adrenal 10% bilateral 10% malignant |
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Adrenal Neuroblastoma
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Common in children under 5
From medulla or sympathetic chain ganglia |
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Conn Syndrome
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Adrenal adenoma (cortex)
Increased mineralocorticoids Hypernatremia Hypervolemia High BP Potassium loss -> muscle weakness |
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Cushing's Syndrome
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Adrenal adenoma (cortex)
"Moon face" "Buffalo hump" Truncal obesity Skin striae Osteoporosis Low glucose tolerance |
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What are the three zones of the adrenal cortex? What do they produce?
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Zona Glomerulosa - Mineralocorticoids
Zona Fasciculata - Glucocorticoids Zona Reticularis - Androgens |
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What are the two cell types in the thyroid gland? What do they produce?
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Follicle cells - T3/T4
Parafollicular C-cells - Calcitonin |
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Graves' Disease
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Hyperthyroidism
Diffuse Toxic Goiter Lymphocytes Small follicles Little colloid |
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Plummer's Disease
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Hyperthyroidism
Nodular Toxic Goiter Hyperplasia Hypertrophy Colloid accumulation |
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Diffuse Simple Goiter
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Hypothyroidism
Iodine deficiency Hyperplasia Hypertrophy |
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Hashimoto's Thyroiditis
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Hypothyroidism
Lymphocytes Plasma cells Atrophic follicles Little colloid |
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Riedel's Thyroiditis
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Hypothyroidism
Fibrous replacement |
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De Quervain's Thyroiditis
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Euthyroid
Viral Leakage of colloid Granulomas |
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Sick Euthyroid Syndrome
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Low T3/T4 but no clinical signs of hypothyroidism
TSH normal Caused by severe illness, trauma, stress |
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Follicular Thyroid Adenoma
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Benign
Very common Most are cold nodules |
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Papillary Thyroid Cancer
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Malignant
Younger patients Associated with radiation exposure Psammoma bodies More common than follicular carcinoma |
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Follicular Thyroid Cancer
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Malignant
Adenomatous pattern More aggressive than papillary carcinoma |
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Anaplastic Thyroid Cancer
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Malignant
Undifferentiated Poor prognosis |
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Medullary Thyroid Cancer
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Malignant
Parafollicular (C-cells) Often associated with MEN type II |
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What are the parathyroid glands derived from?
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3rd and 4th pharyngeal pouches
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What do parathyroids produce?
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PTH (parathyroid hormone)
Acts on bone osteoclasts to mobilize calcium |
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Causes:
Hyperparathyroidism |
Primary - adenoma (most common)
Secondary - chronic renal failure, vitamin D deficiency |
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Causes:
Hypoparathyroidism |
Thyroidectomy (most common)
DiGeorge's Syndrome PTH low Calcium low |
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Causes:
Pseudohypoparathyroidism |
Receptor defect
Short stature Short metacarpal bones PTH high Calcium low |
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Pseudopseudohypoparathyroidism
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Same physical appearance as in pseudohypoparathyroidism
PTH normal Calcium normal |
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Renal Osteodystrophy
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Chronic renal failure leads to:
Decreased phosphate excretion Phosphate binds ionized calcium in serum Hypocalcemia Increased PTH Bone demineralization TX: Aluminum (to bind phosphate) |
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What is the most common endocrine disease?
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Diabetes Mellitus
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IDDM
Type I Diabetes Mellitus |
Primary diabetes
Less common Juvenile onset Prone to ketoacidosis Possible viral etiology? Weak genetic predisposition (HLA DR3, DR4) Auto-immune - anti-islet cell antibodies Decreased number of beta islet cells |
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NIDDM
Type II Diabetes Mellitus |
Primary diabetes
Very common Adult onset Not prone to ketoacidosis Strong genetic predisposition Inadequate insulin secretion Obesity, insulin resistance Hyalinization of islet cells |
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Maturity Onset Diabetes of the Young
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Primary diabetes
Rare Juvenile onset Glucokinase defect (glucose sensor) |
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Diabetes Mellitus associated with Hemochromatosis
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Secondary diabetes
"Bronze diabetes" |
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Diabetes Mellitus associated with Chronic Pancreatitis, Pancreas Carcinoma
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Secondary diabetes
Islet cell destruction due to associated disease causes diabetes |
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Gestational Diabetes
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1-3% of women
Induces excessive fetal insulin secretion Increases risk of birth trauma (increased fetal weight) Glucose tolerance usually returns to normal after birth 30% of women will develop overt DM within 5 years |
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What is MEN?
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Multiple endocrine neoplasia
Autosomal dominant Inherited disorder with variable penetrance Type 1 - due to loss of tumor suppressor gene Neoplasia arises when second (healthy) allele mutates |
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MEN Type 1
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Adrenal cortex
Pituitary Parathyroid Pancreas (gastrinoma) "pity-para-pan" Clinical presentations: Primary hyperparathyroidism (90%) -> hypercalcemia Gastrin (70%) -> Zollinger-Ellison Syndrome -> peptic ulcers Pituitary tumors (60%) -> visual disturbances (sometimes also produce GH -> acromegaly) |
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MEN Type 2A
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Adrenal medulla
Thyroid medulla Parathyroid "para-medullary-medulla" Clinical presentations: Medullary carcinoma of thyroid (bilateral) (100%) -> early diagnosis is essential Benign pheochromocytoma (bilateral) (50%) -> hypertensive crisis (headache, sweating, palpitations) Primary hyperparathyroidism (20%) -> hypercalcemia |
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MEN Type 2B
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Adrenal medulla
Thyroid medulla Mucosal neuromas Marfanoid features |
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What is the most common cancer in the US?
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Skin cancer
Directly related to exposure 80% basal cell carcinomas with very low metastatic potential |
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Seborrheic Keratosis
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Benign skin tumor
Brownish/gray Scaly Greasy |
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Keratocanthoma
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Benign skin tumor
Rapidly growing pink papules Looks like squamous cell carcinoma but is benign |
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Actinic Keratosis
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Benign skin tumor
Crusty red papule Premalignant |
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Basal Cell Skin Carcinoma
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Malignant skin tumor
Pearly gray papule |
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Squamous Cell Skin Carcinoma
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Malignant skin tumor
Erythematous, scaly, or oozing ulcer Bowen's disease - squamous carcinoma in situ |
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Skin Melanoma
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Malignant skin tumor
Brown, black, red, white, purple Irregular borders Lentigo maligna - grows horizontally Nodular melanoma - grows vertically "ABC": Asymmetric lesion Borders irregular Color variations Diameter increasing |
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Pemphigus
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Vesicles on mucosa
Autoantibodies against intercellular junctions of keratinocytes |
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Pemphigoid
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Like pemphigus but larger bullae on abdomen and groin
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Impetigo
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Honey colored crust
Superficial skin infection Staphylococcus or beta-hemolytic Streptococci |
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Pityriasis
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Viral cause?
Herald patch that then spreads along flexural lines |
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Rosacea
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Large red nose
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Pemphigus
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Vesicles on mucosa
Autoantibodies against intercellular junctions of keratinocytes |
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Pemphigoid
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Like pemphigus but larger bullae on abdomen and groin
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Impetigo
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Honey colored crust
Superficial skin infection Staphylococcus or beta-hemolytic Streptococci |
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Pityriasis
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Viral cause?
Herald patch that then spreads along flexural lines |
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Rosacea
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Large red nose
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Xanthoma
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Hyperlipidemia
Foamy histocytes |
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Capillary Hemangioma
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"Salmon patches" and stork bites
Spontateously regress Strawberry hemangiomas Initially grow, later regress |
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Cavernous Hemangioma
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Port wine stain
Assosciated with Sturge-Weber Does not resolve spontaneously |
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Cafe-au-Lait Spots
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Associated with Von Neurofibromatosis
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Vitiligo
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Irregular depigmentation
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Pathology Associated With Toxin:
Cadmium |
Honeycomb pneumonia
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Pathology Associated With Toxin:
Cobalt |
Cardiomyopathy
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Pathology Associated With Toxin:
Chromium |
Lung cancer
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Pathology Associated With Toxin:
Lead |
Inhibits heme synthesis
Renal tubular acidosis |
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Pathology Associated With Toxin:
Mercury |
Neurotoxic (Minamata disease)
Proximal tubular necrosis |
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Pathology Associated With Toxin:
Arsenic |
Lung cancer
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Pathology Associated With Toxin:
Asbestos |
Mesothelioma
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Pathology Associated With Toxin:
Aromatic Amines |
Bladder cancer
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Pathology Associated With Toxin:
Benzene |
Leukemia
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Pathology Associated With Toxin:
Vinyl Chloride |
Liver angiosarcoma
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Pathology Associated With Toxin:
Alpha-Amanitin |
Fulminant hepatitis
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Pathology Associated With Toxin:
Carbon Monoxide (CO) |
Forms carboxyhemoglobin
Do not confuse with methemoglobin, which contains oxidized Fe+3 |
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Pathology Associated With Toxin:
Cyanide |
Inhibits mitochondrial cytochromes
Loss of O2 utilization |
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Microscopic Findings:
Amyloid |
Birefringence
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Microscopic Findings:
Reed-Sternberg Cells |
Hodgkin's Disease
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Microscopic Findings:
Barrett's Esophagus |
Metaplasia
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Microscopic Findings:
Granulomas |
Caseating: TB
Non-Caseating: foreign body |
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Microscopic Findings:
Teratoma |
Skin, teeth, neural tissue, etc
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Microscopic Findings:
Kidney Immunofluoresence |
Linear: Goodpasture's
Granular: Membranous GN Mesangial: IgA Nephropathy |
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Microscopic Findings:
Alzheimer's Disease |
Neurofibrillary tangles
Plaques |
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Microscopic Findings:
Parkinson's Disease |
Depigmentation of substantia nigra
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What structures comprise the bony thorax?
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Thoracic spine
Ribs Sternum |
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Name the facets of the thoracic vertebrae and their articulations:
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Costal facets - Rib heads and tubercles (same number rib/vertebra)
Articular facets (Zygophphyseal facets), superior and inferior - Superior and inferior vertebrae |
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What is the "rule of threes" in the thoracic spine?
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T1-T3 = transverse process located on same horizontal plane as spinous process of given vertebra
T4-T6 = transverse process located halfway between that vertebra's spinous process and the spinous process of the vertebra above it T7-T9 = transverse process located on horizontal plane corresponding with spinous process of vertabra directly above it T10 = T7-T9 T11 = T4-6 T12 = T1-T3 |
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What are the features of typical ribs? Which are the typical ribs?
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Head
Neck Tubercle Angle Shaft (Must have all 5) Ribs 3-10 |
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What are the features of atypical ribs? Which are the atypical ribs and why?
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Any rib that does not have all five features of a typical rib
Rib 1 - no angle, head only articulates with T1 (most articulate with two vertebrae) Rib 2 - Extra tuberosity on shaft Ribs 11, 12 - No neck or tubercle, head that only articulates with one corresponding vertebra Rib 10 sometimes considered atypical - head only articulates with corresponding vertebra |
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What are true ribs?
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Connected directly to sternum by costal cartilage
Ribs 1-7 |
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What are false ribs?
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Not directly connected to sternum
Ribs 8-10 - connect by costal cartilage to rib superior to them Ribs 11, 12 also false ribs (although classified as floating ribs) - do not connect to sternum at all |
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What are floating ribs?
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Do not connect to sternum at all
Ribs 11,12 |
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What is the broadest and most curved rib?
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Rib 1
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What are the functions of the ribs?
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Motion
Support Protection |
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What is the primary motion of the thoracic spine?
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Rotation
Order of ease for thoracic motion: Rotation > Flexion/Extension > sidebending |
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What is special about the motion of T11 and T12?
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More akin to lumbar vertebrae
Order of ease: Flexion/Extension > Sidebending > Rotation |
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What are the three types of rib motion?
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Pump handle (ribs 1-5)
Bucket handle (ribs 6-10) Caliper (ribs 11, 12) |
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What are the muscles of inspiration?
|
Primary:
Diaphragm Intercostals (external, internal, innermost, subcostal) Secondary: Scalenes Pectoralis minor Latissimus dorsi Quadratus lumborum Serratus anterior and posterior |
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Explain the actions of the diaphragm in respiration:
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Contracts with inspiration
Relaxes with expiration Contraction/relaxation causes pump-like action to aid in return of lymph and venous blood back to thorax Attachments: Ribs 6-12 bilaterally Bodies and intervertebral discs of L1-L3 Xyphoid process Innervation: phrenic nerve (originates from C3-C5 nerve roots) |
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Explain the use of the intercostal muscles in respiration:
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Lift ribs with inhalation
Prevent retractions during inspiration |
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Inhalation Somatic Dysfunction (Ribs)
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Exhalation restriction
Engaged as if in inhalation ("stuck up") Key rib: lowest in group (bottom) |
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Exhalation Somatic Dysfunction (Ribs)
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Inhalation restriction
Engaged as if in exhalation ("stuck down") Key rib: highest in group (top) |
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Thoracic level of sternal notch:
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T2
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Thoracic level of spine of scapula:
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T3
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Thoracic level of sternal angle (angle of Lous):
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T4
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Thoracic level of inferior angle of scapula:
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T7
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What cell type does HIV destroy?
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CD4 T cells
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What are the two types of HIV?
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Serotypes:
HIV-1 (predominant) HIV-2 (mainly in Africa) |
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How is HIV transmitted?
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Blood
Semen Vaginal secretions Breast milk |
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What are the three stages of HIV infection?
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Acute:
3-4 wks to develop antibodies (may take months) Symptomatic with "generalized viral symptoms" Latent Period: Asymptomatic NOT latent in reproduction of HIV, but in symptoms Advanced Symptomatic Infection (AIDS): Defined by clinical parameters |
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What are the clinical parameters to define AIDS?
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Positive HIV test PLUS one of the following
1) <200 CD4 T cells/uL 2)AIDS defining opportunistic infections (Pneumocystis pneumonia, Toxoplasmosis, CMV retinitis, Mycobacterium avium complex, progressive multifocal leukoencephalopathy, cryptococcal meningitis) 3) AIDS associated malignancies (Kaposi's sarcoma, brain lymphoma, invasive cervical cancer, some non-Hodgkin's lymphomas) 4) HIV complicating infections (HIV dementia/encephalopathy, extrapulmonary TB, chronic isosporiasis or cryptosporidosis, disseminated histoplasmosis, chronic or pulmonary HSV, disseminated coccidiomycosis, esophageal or respiratory candidiasis) |
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What are direct effects/complications of HIV infection?
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Fever
Weight loss Cachexia Night sweats |
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What are the two methods of clot formation?
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Platelet activation and aggregation
Clotting cascade activation |
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What does a bleeding time test?
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Platelet function
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What does a PT (prothrombin time) test?
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Extrinsic and common pathways of clotting cascade
Factors I, II, V, VII |
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What does a PTT (partial thromboplastin time) test?
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Intrinsic and common pathways of clotting cascade
All factors except VII, XIII |
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What does TT (thrombin time) test?
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Common pathway of clotting cascade
Factors I, II |
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Von Willebrand Disease
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Deficiency of Von Willebrand Factor
Also causes factor VIII functional deficiency Autosomal dominant Tx: VWF or humate (purified factor VIII) May include desmopressin (DDAVP) to release factor VIII from endothelial cells Signs and Symptoms: Bleeding from small cuts Easy bruising Increased menstrual bleeding Increased PTT AND bleeding time |
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Hemophilia A
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Lack of factor VIII
Tx: factor VIII X-linked recessive Excessive bleeding Increased PTT Normal PT and bleeding time |
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Hemophilia B
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Christmas Disease
Lack of factor IX Tx: factor IX X-linked recessive Excessive bleeding Increased PTT Normal PT and bleeding time |
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Vitamin K Deficiency
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Results in non-functional factors II, VII, IX, X (need vitamin K to be gamma carboxylated to become activated)
Excessive bleeding May be due to: Fat malabsorption - Vit K is fat soluble (Cystic fibrosis, chronic pancreatitis) Antibiotics (long term or high dose) - destroy gut flora that provide Vit K Newborns - lack gut flora Coumadin/Warfarin - prevent vitamin K activation of factors |
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Disseminated Intravascular Coagulation (DIC)
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Coagulation within blood vessel lumens follwed by mucosal bleeding
Disorder of spontaneous activation of coagulation cascade Results in intravascular coagulation, organ ischemia, consumption of clotting factors to yield mucosal bleeding May be fatal May be initiated by: Bacterial endotoxins Presence of dead tissue Certain forms of acute myelogenous leukemia Initially prolonged PTT with increased d-dimer, then prolonged PT also seen |
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Idiopathic Thrombocytopenic Purpura( ITP)
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Petechiae
Purpura Mucosal bleeding Disorder of decreased platelet numbers Children: acute, post-viral infection, usually self-limiting Adults: often chronice, anti-structural platelet antibodies Tx: corticosteroids |
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Thrombotic Thrombocytopenic Purpura (TTP)
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Unknown specific cause
May be associated with autoimmune-induced inhibition of enzyme responsible for destruction/recycling of VWF Spontaneous platelet aggregation with resulting systemic platelet clot formation and consumption of platelets FATAL if untreated Tx: plasmapheresis Signs and Symptoms: Severe thrombocytopenia Schistocytes, helmet cells, triangular RBCs Evidence of hemolysis (low hemoglobin, high reticulocyte count, polychromasia on blood smear, high LDH [lactate dehydrogenase], ischemic organ damage, fever) |
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Spherocytosis
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Familial spherocytosis, chronic familial icterus, spherocytic anemia
Chronic disease characterized by hemolysis of spheroidal RBCs, anemia, splenomegaly RBCs are functional, but spleen is insulted and hemolyzes them due to shape Causes anemia - can be severe Can be treated by splenectomy Sphere shaped RBCs due to deficiency in spectrin |
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G6PD Deficiency
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X-linked recessive
More common in blacks In RBCs, pentose PO4 pathway is sole means of producing NADH RBCs very sensitive to oxidative damage in G6PD deficiency RBC lysis occurs on exposure to excess radicals Fava beans, sulfa drugs, quinine derivatives, many other sources Most common enzymopathy |
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Sickle Cell Anemia
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Autosomal recessive
Yields HBS instead of normal hemoglobin Most common in blacks - carrier state confers resistance to malaria Single amino acid substitution (valine for glutamate) in beta globin chain at 6th amino acid More prone to crystallization under some circumstances of less than optimal oxygenation - hypoxia, acidosis, dehydration |
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What is a sickling crisis?
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Any sickling event of RBCs
Usually caused by hypoxia, acidosis, dehydration Results in occlusion of vessels by sickled RBCs Repeated events result in autosplenectomy (scarring and resulting self-destruction of spleen) |
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Alpha Thalassemia
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Decreased synthesis of alpha globin chains
Homozygosity is lethal Microcytic anemia and splenomegaly |
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What is unique about the inheritance of the alpha-thalassemia alleles?
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Inherit 2 from each parent
Critical allele, so evolved to make sure that we always have it 1 lost: asymptomatic 2 lost: moderate microcytic anemia 3 lost: severe microcytic anemia 4 lost: lethal |
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Beta Thalassemia
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Decreased synthesis of beta globin chains
Jaundice Leg ulcers Splenomegaly Major = Cooley's anemia (severe microcytic anemia) Minor (moderate microcytic anemia) |
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What is Bart's Hemoglobin?
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4 gamma globin chains
Found in alpha thalassemia FATAL |
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What are the types of autoimmune hemolytic anemia?
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Warm agglutinin
Cold agglutinin Named for temp at which anti-RBCs are most active |
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Risk factors for warm agglutinin disease:
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Drugs (methyldopa, dopa, high dose penicillin or cephalosporin)
Malignancies (leukemia, lymphoma) SLE |
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Risk factors for cold agglutinin disease:
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Mycoplasma pneumonia
Mononucleosis Lymphoma 50% are idiopathic |
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What is the Coombs Test?
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Direct:
Mix rabbit antisera to RBC antibodies with patient's RBCs If RBCs precipitate, RBCs were coated with anti-RBC antibodies Detects immune-mediated hemolysis Detects antibodies directly bound to RBCs Indirect: Mix patient's plasma with normal RBCs Anti-RBC antibody presence in plasma will cause RBCs to precipitate Used to identify free floating antibodies against RBCs Test of choice for isoimmunization in Rh(-) females |
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Megaloblastic Anemia
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Due to defective DNA synthesis
Leukopenia Hypersegmented neutrophils Thrombocytopenia Caused by: Vitamin B12 deficiency (also causes neurologic symptoms) Folate deficiency (no neurologic symptoms) Antineoplastic drugs Microbes or drugs that limit folate or B12 availability |
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What are some causes of Vitamin B12 deficiency?
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Diphyllobothrium latum (worm)
Poor diet Type A gastritis Megaloblastic anemia AND neurologic symptoms |
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Plummer-Vinson Anemia
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Due to low grade, long term iron deficiency
"Tea and toast" diet Results in esophageal webs - cause dysphagia for solids (but not for liquids) |
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What does it mean if dysphagia only affects solids? Both solids and liquids?
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Solids only:
Anatomic cause Solids and liquids: Neuromuscular cause |
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Fanconi Anemia
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Inability to remove oxygen radicals from bone marrow
Autosomal recessive Clinical findings: Microcephaly Cafe au lait spots Small or absent thumbs Deformed or absent radius bones Recurrent aplastic anemia High risk for leukemia or lymphoma |
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Heinz Bodies
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Denatured hemoglobin visible within RBCs
G6PD deficiency |
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Howell-Jolly Bodies
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Visible nuclear fragments within RBCs
Appear as basophilic (blue) granules Indicative that RBCs are leaving marrow while still immature |
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Basophilic Stippling
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Multiple tiny blue dots within RBCs
Lead poisioning |
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Siderocytes
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Pappenheimer bodies
Extra iron in RBCs Represents iron not bound to hemoglobin Result of iron overload secondary to deranged bone marrow function (not dietary excess) |
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Reticulocytes
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Immature RBCs
Released early from bone marrow in response to hemorrhage or similar events Blue lace-like patterns visible within RBCs - remnants of ribosomal RNA |
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What is neutropenia?
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Low number of neutrophils
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What are the causes of neutropenia?
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Decreased production (bone marrow disease, chemotherapy, HIV infection, VitB12/folate deficiency)
Increased destruction (Felty's syndrome - variant of rheumatoid arthritis involving immune mediated destructio of neutrophils via anti-neutrophil antibodies) |
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What is leukocytosis?
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High number of white blood cells
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What is Neutrocytosis?
|
Neutrophilia
High number of neutrophils Acute inflammation Acute infection (especially bacterial) Certain cancers Leukemia of neutrophils |
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What is Eosinocytosis
|
Eosinophilia
High number of eosinophils Type I hypersensitivity Helminthic infections |
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What is Lymphocytosis?
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High number of lymphocytes
Granulomatous diseases Viral infection Pertussis (toxin prevents lymphocyte entry to lymph nodes, so increased number in blood) |
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What is monocytosis?
|
High number of monocytes
Granulomatous diseases Infectious mononucleosis |
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Explain the difference between leukemia and lymphoma
|
Leukemia: neoplastic WBCs in the blood
Lymphoma: solid tumor of neoplastic lymphocytes |
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Explain what "Acute" and "Chronic" mean in leukemia
|
Acute = immature cells
Chronic = mature cells |
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Acute Lymphocytic Leukemia (ALL)
|
Overabundance of immature lymphoblasts
Most common malignancy of children Lymphadenopathy Impaired bone marrow function |
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Acute Myelogenous Leukemia (AML)
|
Overabundance of immature WBCs (other than lymphoblasts)
All ages, but peaks between 15-39 Impaired bone marrow function Auer rods in myeloblasts (red staining peroxidase positive meedle like structures - evidence of myeloid proliferation) |
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Chronic Myelogenous Leukemia (CML)
|
Overabundance of mature WBCs other than lymphocytes
25-60 years old, peak between 30-40 Insidious onset Impaired bone marrow function Philadelphia chromosome (9:22 chromosomal translocation to create bcr-abl fusion oncogene) Low LAP (leukocyte alkaline phosphatase) |
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Chronic Lymphocytic Leukemia (CLL)
|
Overabundance of mature lymphocytes
Over 50 years, males > females Lymphadenopathy Impaired bone marrow function Variant: Sezary Syndrome (leukemic portion of mycosis fungoides) |
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Hairy Cell Leukemia
|
Mostly in middle aged white men
Rarely hepatomegaly Splenomegaly (#1 sign) Involves only B cells Develop hair-like projections Impaired bone marrow function Positive TRAP (tartrate-R-acid phosphatase CD25 markers present |
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Hodgkin's Disease
|
Leukocytosis of PMNs
Reed-Sternberg cells (high number = worse prognosis) Contiguous spread Nodal involvement 4 subtypes: Lymphocyte predominance (best prognosis) Nodular sclerosis (more common in women, better prognosis than mixed) Mixed cellularity Lymphocyte depletion (worst prognosis) |
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Non-Hodgkin's Lymphoma
|
Widespread adenopathy
Hypercalcemia Hepatosplenomegaly Probably of viral etiology Associated with bcl-2 Spreads to multiple different nodes Neutrocytosis |
