Oral Boards Etiology

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  1. Pneumococcal pneumonia
    Caused by Streptococcus Pneumoniae, gram (+) cocci
  2. H. flu pneumonia
    gram (-) aerobic and anaerobic pleomorphic coccobacillus bacteria
  3. Legionella Pneumonia
    Gram (-) aerobic bacilli Legionella pneumophila associated with contaminated water sources.
  4. Klebsiella pneumonia
    encapsulated rod that is ubiquitous.
  5. Mycoplasma pneumonia
    Infection of Mycoplasm pneumoniae

    Mycoplasmas are the smallest free-living organisms known, are prokaryotes that are bounded only by a plasma membrane.

    They lack a cell wall and can invade upper and lower respiratory tract
  6. Chronic bronchitis
    • Respiratory infections
    • Occupational exposures to coal mining, gold mining, and cotton textile dust
    • Airway hyperresponsiveness
    • Deficiency of 1-antiprotease
    • Cigarette smoking
    • air pollution
    • Passive or secondhand smoking exposure
  7. Emphysema
    • Cigarette smoking
    • Exposures to environmental tobacco smoke, occupational dusts and chemicals, and indoor air pollution from biomass fuel used for cooking and heating in poorly ventilated buildings
    • Deficiency of 1-antiprotease
  8. Asthma
    Probable hereditary allergy (genetic)

    Atopy- concomitant conditions- atopic dermatitis, allergic rhinitis

    • GERD
    • Exercise
    • Drugs: Beta Blockers, asprin, NSAIDs
    • Infection
    • Environmental factors
    • Allergens
    • Occupational exposure

    Obesity is risk factor
  9. HTN
    Patients with no definable cause are said to have primary, essential, or idiopathic hypertension, 95% of cases.

    A number of environmental factors have been implicated in the development of HTN, including salt intake, obesity, occupation, alcohol intake, family size, and crowding.

    Secondary hypertension, results from other systemic diseases such as renal insufficiency, Cushing’s Syndrome, Pheochromocytoma, CAD, Hyperparathyroidism, Pregnancy,
  10. Angina
    • COCAS
    • CAD
    • Outflow Obstruction
    • Clot, anemia, hypovolemia
    • Aortic Stenosis or Regurgitation
    • Spasm - Prinzmetal’s Angina/cocaine
  11. MI
    Prolonged imbalance between myocardial oxygen supply and demand leads to the death of myocardial tissue.

    CAD, embolus, cocaine use resulting in vasospasm
  12. CHF
    • Systolic dysfunction: impaired myocardial
    • contractility
    • Due to MI, dilated cardiomyopathies, or chronic HTN
    • Diastolic dysfunction: increased ventricular stiffness
    • or impaired myocardial relaxation (relatively normal LVEf)
    • o M.C. cause is LVH resulting from HTN
    • Hypertrophic, restrictive, infiltrative cardiomyopathies (amyloidosis, sarcoidosis), pericardial effusion
    • Diastolic failure now referred to as HF with normal or preserved Ef
    • High Output HF
    • Anemia, hyperthyroidism, A-V fistula with shunting, beriberi (thiamine deficiency) or Paget's disease

    • Low-Output HF (more common than high output)
    • Chronic HTN and ischemic heart disease, cardiomyopathies, valvular heart disease (VHD), dysrhythmias

    • Right-sided HF - M.C. cause of R-sided HF if
    • L-sided HF
    • Pulmonary disease (cor pulmonale is RV hypertrophy and eventual failure resulting from pulmonary disease)
    • Pulmonary
    • HTN, Right ventricular infarction, mitral stenosis (MS)

    • Left-Sided HF
    • Systemic HTN and MI with left ventricular infarction = common causes
    • Other causes = cardiomyopathy, endocarditis, aortic valve disease and mitral regurgitation

    • Cardiac abnormalities: obstructive or regurgitant
    • valvular dz, intracardiac shunting, disorders of HR & rhythm
  13. IDA
    Conditions that increase demand for iron, increase iron loss, or decrease iron intake) or absorption can produce iron deficiency hemoglobinuria.

    • MIMICD
    • Menstrual bleeding
    • intravascular hemolysis
    • Malabsorption of iron
    • Inadequate dietary iron intake
    • chronic blood loss
    • Dialysis fistula
    • Diversion of iron to fetal and infant erythropoesis during pregnancy and lactation
  14. Megaloblastic anemia
    • · Most megaloblastic anemias due to deficiency of cobalamin (vitamin B12) and/or folic acid.
    • · Vitamin B12 deficiency - poor dietary intake of vitamin B12, pernicious anemia (autoimmune destruction of parietal cells), ileal disease or resection resulting in malabsorption of vitamin B12, tropical sprue, fish tapeworm.
    • · Folate deficiency- most common in alcoholics; many iatrogenic causes; poor intake, defective absorption, pregnancy, people who do not eat fresh fruits and vegetables and those who overcook their food,and hemolytic anemias
  15. Hemolytic anemia
    • · RBC destruction may be extravascular- premature removal from circulation by liver and spleen or intravascular- disruption of RBC membranes during circulation and obvious sign is hemoglobinuria
    • · Inherited hemolytic anemias may be due to RBC membrane defects such as hereditary spherocytosis (autosomal dominant), RBC enzyme defects such as G6PD deficiency (x linked recessive enzyme deficiency), or hemoglobinopathies such as sickle cell disease (autosomal recessive trait).
    • · Acquired forms may be immune or non-immune related
  16. Thalassemia
    • Hereditary autosomal dominant disorder
    • Genetic disorder resulting in decreased amounts of functional hemoglobin
    • α-Thalassemia: deletion of a-globin genes results
    • in an excess of b-globin chains.
    • b-Thalassemia: point mutation of b-globin gene (s) results in an excess of a-globin chains.
  17. Alpha thalassemia
    • 1 or more of the 4 a chain genes deleted leading to reduced
    • a globin chain synthesis
  18. Beta thalassemia
    Usually caused by point mutations in Chromosome 11
  19. Viral Hep
    • HAV: RNA hepatovirus A, incubation period 2-6 weeks, avg 30 days
    • HBV: DNA virus B, Transmitted via inoculation of infected blood or body fluids—transfusions, unprotected intercourse, needle sharing
    • Incubation period—6 weeks to 6 months
    • HCV: RNA virus HCV is transmitted primarily
    • through large or repeated percutaneous (i.e.,
    • passage through the skin) exposures to infectious blood, such as:
    • IVDU –m.c. in the US
    • Receipt of donated blood, blood products, and organs –now rareo
    • Needlestick injuries in healthcare settings
    • Birth to an HCV-infected mother
  20. Crohns
    Unknown, infectious and immunologic mechanisms have been proposed.

    Genetic link identified.

    Associated with smoking
  21. Ulcerative Colitis
    • · Idiopathic
    • · Genetic associations in MHC locus HLA class II alleles, interleukin-1 family of genes, and the multidrug resistant gene MDR1.
    • · Relationship between ulcerative colitis and bacterial flora, in there is an increase in Bacteroids and Enterobacteriaceae have been found in the inflamed bowel segments.
    • · An appendectomy before age 20 is associated with a reduced risk of developing ulcerative colitis.
    • May have autoimmune component, which is B27
  22. Obesity
    • Psychosocial behavior
    • Environmental Factors
    • Genetic Association
    • Sedentary lifestyle plus chronic ingestion of excess calories
    • Secondary causes:
    • -Cushing's syndrome
    • -Hypothyroidism
    • -Insulinoma
    • -Mental Retardation syndromes
    • -PCOD
    • Medications: DAMPS
    • Antidiabetes
    • antidepressants
    • Mood stabilizers
    • antipsychotics
    • steroids

    • OCPs
    • Eating disorders
    • Smoking cessation
    • Leptin receptor mutations--rare
  23. TIA
    • Result of small emboli, and the risk of additional emboli causing permanent deficits is high
    • Cardiac origin (AFIB, mitral valve dz)
    • Inflammatory Origin – SLE, ArteritisVascular (ulcerated atherosclerotic plaque, fibromuscular dysplasia, arteritis, subclavian steal syndrome)
    • In the absence of atrial fibrillation, 90% of these emboli originate from proximal internal carotid artery Hematological causes include P. vera, sickle cell, and hyperviscosity
  24. CVA
    Ischemic strokes- 80% of all strokes

    • oCerebral thrombosis = lacunar and large vessel
    • thrombosis

    § Commonly due to atherosclerosis

    oCardiac emboli: A-fib, MI, mural thrombus, bacterial endocarditis

    oHypercoagulable states: polycythemia vera, pregnancy, OCPs, sickle cell, Factor V Leiden mutation

    oVascular etiologies: temporal arteritis, vaculitis

    oOther causes: Transient Ischemic Attacks (TIA)

    • ·Hemorrhagic strokes- 20%
    • Generally caused by AVMs or aneurysms à result in SAH or Intercerebral hemorrhage
  25. Strep pharyngitis
    GABHS, gm(+)
  26. Acute OM
    • Following URI
    • Virus: RSV, influenza, rhinovirus, enterovirus
    • Bacteria: S. pneumo, H flu, M catarrhalis, S. pyogenes
  27. Chronic OM
    • Recurrent otitis media: >3 episodes within 6 months, or 4 episodes within 12 months
    • Following disease or trauma
    • Pathogens: p aeruginosa, proteus, s aureus
  28. Serous OM
    • Prolonged blockage of auditory tube, resulting in transudate fluid
    • Following URI or barotrauma
  29. Acute sinusitis
    • Viral: MOST COMMON CAUSE: rhinovirus
    • Bacterial: Strep pneumoniae
    • Nosocomial caused by Staph & Gm (-)
    • Fungal and atypical organisms in immunocompromised hosts.

  30. Viral rhinitis
    Adenovirus, rhinovirus, coronavirus, RSV (Respiratory Syncytial Virus) – common in Winter.
  31. PUD-Gastric
    • Top three causes: NSAID use, chronic H. pylori infections, acid hypersecretory states (such as Zollinger Ellison syndrome)
    • M/C in the antrum
  32. PUD-Duodenal
    • > 90% occur in duodenal bulb
    • Prevalence of H. pylori infection in duodenal ulcer patients is 75-90%
    • Top 3 causes of PUD: NSAIDs, chronic H. pylori
    • infections, acid hypersecretory states (Zollinger Ellison syndrome)
    • Emotions/Stress do NOT cause PUD
  33. Acute renal failure
    • Pre-renal ARF:
    • o Most Common form of ARF
    • oResults in decreased intravascular volume and CO2
    • Rapidly reversible upon restoration of blood flow
    • BUN:Cr ratio –>20:1
    • Intrinsic ARF:
    • oInside the kidney
    • oExclude pre and post-renal causes first
    • oStructures in kidney are sites of injury
    • Triggered by ischemia or nephrotoxic substance = ATN, AGN, AIN
    • BUN:Cr ratio – 10:1
    • Post-renal ARF:
    • oLeast common
    • oUrinary flow obstruction
    • oBladder neck obstruction – BPH in men, Neurogenic bladder
    • oUreteric Obstruction – Calculi, tumor
    • Anticholinergic drugs
    • BUN:Cr ratio ->20:1
  34. Chronic renal failure
    • May be due to HTN, Polycystic Kidney Disease, Progression of ARF, GN, congenital dz, collagen vascular dz
    • M.C. cause of CKD = diabetic nephropathy
    • Hypertensive nephropathy = common cause of CKD in elderly
    • Over 70% of late-stage CKD cases due to DM or HTN
  35. HIV and AIDS
    • HIV retrovirus uses reverse transcriptase to replicate within host cells
    • Virus transmitted via blood, semen, vaginal secretions, and breast milk
    • Sexual contact, parenterally (IVDU, needle stick, transfusion), vertically from mom to child (vag. delivery, breast feeding)
  36. Tension Headache
    • Can be physical manifestation of psychosocial stress
    • Assoc. with depression, anxiety
    • May be due to cervical muscle contraction and/or temporal muscle contraction, but not proven
  37. Migraine
    • HA can be initiated/amplified by various triggers:
    • glare, bright lights, noise, hunger; excess stress, OCPs, barometric pressure changes, hormonal changes during menses, lack of or excess sleep, ETOH, chocolate, citrus
    • Dopamine Hypersensitivity – most migraine symptoms can be induced by dopaminergic stimulation
    • Neurotransmitter 5-HT (i.e. Serotonin) may play a role in migraine
  38. T1DM
    • 1/3 due to genes (on Chromosome 6 with HLA DR3 or DR4) , and 2/3 due to environmental factors
    • Type 1 is usually due to autoimmune destruction of pancreatic islet B cells à stops insulin production and causes a rise in blood glucose
    • 95% of Type1 DM pts have either HLA DR-3 or HLA DR-4
    • Immune mediated (90%)
    • Destruction of pancreatic islet B-cells
    • Theory it results from infectious (rubella, coxsackie B4) or toxic cause (n-nitroso from smoking)
    • People who are predisposed to developing an autoimmune response
    • Idiopathic (10%)
    • No evidence of pancreatic B-cell autoimmunity o
    • Insulinopenia and ketoacidosiso
    • Subgroup of DM patients is designated as Type 1B--> usually Asian or African origin
  39. T2DM
    • Obesity/visceral fat linked to peripheral insulin resistance and loss of B-cell function à impairs insulin secretion
    • Circulating amt. of glucose prevents ketoacidosis but not hyperglycemia
    • Plasma insulin elevated in early stage; declines in late stage
  40. Hypothyroid disorders
    • Deficiency of thyroid hormones
    • Primary: structural/functional interference w/production of hormone, disease of thyroid gland or lack of pituitary TSH
    • Secondary: DM, pernicious anemia, myasthenia gravis, gonadal failure, medications
    • Iodine deficiency
    • Genetic thyroid enzyme defects
    • Iatrogenic: thyroid ablation
    • Autoimmune: Hashimoto’s (most common)

    Drugs, radioiodine therapy and external radiation therapy

  41. Hyperthyroidism

    • Graves’s: autoimmune d/o of thyroid causing
    • increased release of thyroid hormones (HLA B8 and DR3)
    • Subacute Thyroiditis, Struma Ovarii
    • Thyrotoxicosis factitia, Thyroid carcinoma. toxic adenoma
    • Amiodarone-induced thyrotoxicosis
    • Post-partum thyroiditis, pituitary tumor
    • Hashimoto's Thyroiditis

    Exogenous iodine induced
  42. Osteoarthritis
    a. No single cause and the exact etiology is unknown

    b. Increased risk: age, hereditary predisposition, female, obesity, articular congenital deformity, joint trauma, high bone mineral density, low estrogen status

    c. These factors may lead to a joint environment that’s susceptible to trauma and external mechanical stressors that are exacerbated by physical activities

    d. Local mechanical factors (periarticular muscle weakness, misalignment and structural joint abnormality) further facilitate disease progression

    e. Internal and external factors lead to a failed joint

    Occupational hx, women=autsomal dominant, men are autosomal recessive

    neuropathic: charcots and diabetes, metabolic: wilsons, pseudogout, hemochromotosis, endocrine disorders
  43. Osteoporosis
    • Reduction and disarray of bone’s collagen matrix -->Makes up 40% of bone mass
    • Compromised bone strength predisposing to increased risk of fracture, especially of the spine and hip

    Secondary: malignancies, corticosteroid use, hormonal imbalances, GI disorders
  44. Disc herniation
    Degeneration of the nucleus pulposus and the annulus fibrosus increases with age and may be asymptomatic or painful

    Trauma is the most common cause

    Any change in pressure: a sneeze, cough, or trivial movement, may cause the nucleus pulposus to prolapse, pushing the frayed and weakened annulus posteriorly

    Movements: repetitive lifting, pulling, pushing, bending sideways, or twisting

    In severe disk disease, the nucleus may protrude through the annulus (herniation) or become extruded to lie as a free fragment in the spinal canal.
  45. Spinal stenosis
    Congenital - characterized by short, thick pedicles that produce both spinal canal and lateral recess stenosis

    ·Acquired - usually due to degenerative diseases (spondylosis, spondylolisthesis, scoliosis), trauma, spine surgery, metabolic or endocrine disorders such as osteoporosis, acromegaly, etc.
  46. Degenerative dementia
    • APEO
    • Alzheimer’s: unknown, possibly genetic, infectious, toxic most common
    • --Diffuse atrophy of the cerebral cortex with secondary enlargement of the ventricles
    • Parkinson’s: unknown, genetic, recreational use of MTPT
    • Environmental factors:
    • aluminum, mercury, viruses, ETOH
    • Other possibilities: elevated homocysteine and cholesterol, HTN

    • Cortical Lewy Body 3rd most common cause
    • Psychiatric: depression, pseudodementia
    • Infectious: syphilis, meningitis, encephalities, Creutzfeldt-Jakob
    • Neoplasma
    • Congenital: Huntingtons, Wilsons
    • Toxocologic: alcohol, drugs, heavy metals
    • Vitamind deficiencies: thiamine, niacin, b12
  47. Vascular dementia
    • MCHAD
    • Multiple small (lacunar) and large strokes
    • CVA, CAD
    • Hyperlipidemia, HTN
    • A. fib
    • DM
  48. Depression
    • No single known cause àcombo of genetic, biochemical, environmental, developmental and psychological factors
    • Clear familial predominance, but no established pattern of inheritance
    • Meds – Anti-HTN drugs, antiarrhythmics, glucocorticoids, analgesics, anti-parkinsonian, & anticonvulsants
    • Chronic disease and medical conditions: hypocalcemia, cardiac pathology, HIV/AIDS, thyroid disease, Parkinson’s, dementia
    • Assoc. with chronic fatigue, fibromyalgia
    • (-) life events, stressful situations, Post-partum, death of a relative, assault, severe marital/relationship problems
  49. Lumbar sprain/strain
    Hx of twisting or lifting, excessive force, flexion or extension of the lower back

    Predisposing factors = repetitive movements of lifting, pushing or pulling or bending
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Oral Boards Etiology
2011-07-20 14:13:32

For oral boards
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