Oral Boards Pathophysiology

• S. Pneumoniae attaches to and then colonizes on nasopharyngeal cells and when aspirated in bronchioles or alveoli, it causes inflammation.
• Occurs when there is a deficit in host’s pulmonary defense mechanism (cough, mucocilliary clearance, etc.)
• May follow a prior upper respiratory tract infection or occur in patients with chronic pulmonary conditions

• H. Flu attaches to and then colonizes on nasopharyngeal cells and when aspirated in bronchioles or alveoli, it causes inflammation.
• Occurs when there is a deficit in host’s pulmonary defense mechanism (cough, mucocilliary clearance, etc.)
• May follow a prior upper respiratory tract infection or occur in patients with chronic pulmonary conditions

• Legionella is aspirated from a contaminated water source such as an airconditioning system or grocery produce mister 2-10 day incubation period
• It attaches to and then colonizes on nasopharyngeal cells and when aspirated in bronchioles or alveoli, it causes inflammation.
• Few bacteria and PMNs (polymorphonuclear leukocytes) seen in tissue sample or sputum smear
• Multifocal pneumonia with patchy lobular inflammation and can progress to extensive multilobar consolidation has been observed.
• Occurs when there is a deficit in host’s pulmonary defense mechanism (cough, mucocilliary clearance, etc.)
• May follow a prior upper respiratory tract infection or occur in patients with chronic pulmonary conditions

• Klebsiella attaches to and then colonizes on nasopharyngeal cells and when aspirated in bronchioles or alveoli, it causes inflammation.
• Hematogenous spread of bacteria from extra pulmonary infections.
• Occurs when there is a deficit in host’s pulmonary defense mechanism (cough, mucocilliary clearance, etc.)
• May follow a prior upper respiratory tract infection or occur in patients with chronic pulmonary conditions

• Mycoplasma pneumonia attaches to and then colonizes on nasopharyngeal cells and when aspirated in bronchioles or alveoli, it causes inflammation
• Incubation period of 2-3 weeks.
• Produces hydrogen peroxide and causes injury to host cells

Excessive secretion of bronchial mucus results in airflow obstruction and air trapping results in hyperinflation.

• Excessive lysis of elastin and other structural proteins in the lung matrix by elastase and other proteases derived from lung neutrophils, macrophages, and mononuclear cells.
• Persistent reduction in forced expiratory flow rates is the most typical finding in COPD.
• Increases in the residual volume and the residual volume/total lung capacity ratio, nonuniform distribution of ventilation, and ventilation-perfusion mismatching also occur

• Hypertrophy of bronchial smooth muscle and mucous glands with subsequent plugging of small airways with thick mucus.
• This airway inflammation underlies disease chronicity and contributes to airway hyperresponsiveness, airflow limitation, and respiratory symptoms
• The airway mucosa is infiltrated with activated eosinophils and T lymphocytes, and there is
• activation of mucosal mast cells.
• Airway epithelium shedding and fibrosis of basement
• membrane with subsequent thickening also occurs

• An increase in cardiac output or an increase in resistance will increase blood pressure.
• Blood pressure is regulated by four different pathways.
• BP = CO x PR
• Baroreceptors- located on arterial wall and they sense a change in pressure.
• Renin-angiotensin-aldosterone system
• Electrolyte and Fluid Balance
• If pathology in one of the above regulatory mechanisms, HTN may result

• Increasing size of plaque results in narrower corridor of blood flow.
• Thus, with exertion requires increased blood flow and less blood flow to myocardium during time of increased need and the myocardium becomes ischemic.
• Faster forming, newer plaques rupture more easily (break in the integrity of the vessel wall, activating the clotting cascade)

• Prolonged imbalance between myocardial oxygen supply and demand leads to the death of myocardial tissue.
• Cardiac work exceeds the ability of the narrowed coronary artery to supply nutritive perfusion.
• Due to ischemic heart disease with coronary atherosclerosis and plaque rupture and thus an
• increases in the amount of luminal impingement by the stenotic lesion.

• o
• Total thrombotic
• occlusion is superimposed on the atherosclerotic plaque- full thickeness Q wave
• infarction

• o
• Absence of total
• thrombotic occlusion- non-Q wave
• infarction

• CAD and MIs lead to loss of functional cardiac muscle and a decrease in myocardial contractility.
• Valvular regurgitation increases preload, and HTN/aortic stenosis leads to increased afterload.
• The muscle undergoes hypertrophy to compensate for the increased volume leading to LVH.
• When the heart can no longer pump the volume of blood entering it, fluid retention occurs and leads to left sided heart failure.
• As left sided gets worse, it causes right sided failure.
• Systolic dysfunction resulting from decrease in myocardial contractility, excess preload or excess afterload.
• Diastolic dysfunction is inability of the ventricle to contract normally and expel sufficient blood is systolic failure and the inability relax and fill normally.

As iron levels decrease, serum iron levels and ferritin storage levels decrease whileTIBC increases. Hemoglobin synthesis becomes impaired and thus iron-deficient erythropoiesis occurs, resulting in hypochromic, microcytic, hypoferremic anemia.

• Deficiency of vitamin B12 or folate results in impaired DNA synthesis leading to large, megaloblastic RBCs.
• Cytoplasmic development is normal
• Pernicious anemia is a lack of intrinsic factor due to destruction of parietal cells and thus an inability to absorb vitamin B12 in gut.

• G6PD: G6PD deficiency is a hereditary enzyme defect that causes episodic hemolytic anemia because of decreased ability of the RBC to deal with oxidative stresses.
• Sickle cell anemia: Hgb S occurs when valine substitutes for glutamine on the β-chain
• Decreased solubility of Hgb S in hypoxic tissues leads to sickle-shaped cells.
• Sickled cells have difficulty passing through small capillaries, leading to blockage and tissue necrosis; sickled cells are destroyed, resulting in hemolytic anemia
• Hereditary spherocytosis: An abnormality in spectrin results in disordered RBC membrance that is sphere shaped.

• α thalassemia disorders – reduction in the synthesis
• of α-globin chains
• β thalassemia disorders - reduction in the synthesis
• of β- globin chains
• Globin synthesis is defect leads to decreased
• hemoglobin
• synthesis leads to damaged RBCs
• Types of Hemoglobin
• HbA - 2 alpha (α) & 2 beta (β)chains
• 95-98%
• HbA2 - 2 alpha (α)& 2 delta(δ)
• chains 2-3%
• HbF (Fetal) -
• 2 alpha (α) & 2 gamma (γ) chains 1%
• Usually HbF becomes HbA at 6-9 mos old

• 1. Silent carrier: missing 1 alpha gene
• 2. Alpha thalassemia minor: missing 2 alpha genes
• 3. Hb H disease: missing 3 alpha genes
• 4. Bart’s Hb: missing all 4 alpha genes
• Aka. Hydrops fetalis - not compatible w/ life

• Damage to liver cells is caused by direct injury from the virus or indirectly as a result of inflammation
• During acute inflammation, swollen hepatocytes are less able to detoxify drugs, produce clotting factors, cholesterol, plasma proteins, bile and glycogen, store fat soluble vitamins and perform other functions

• Damage to liver cells is caused by direct injury from the virus or indirectly as a result of inflammation
• During acute inflammation, swollen hepatocytes are less able to detoxify drugs, produce clotting factors, cholesterol, plasma proteins, bile and glycogen, store fat soluble vitamins and perform other functions

• Damage to liver cells is caused by direct injury from the virus or indirectly as a result of inflammation
• Cell-mediated immune responses and elaboration by T cells of antiviral cytokines contribute to the containment of infection and pathogenesis of liver injury associated with hepatitis C
• During acute inflammation, swollen hepatocytes are less able to detoxify drugs, produce clotting factors,
• cholesterol, plasma proteins, bile and glycogen, store fat soluble vitamins and perform other functions

• Sustained inflammatory response causing ulceration, structuring, fistulas, abscess
• Strongly associated w/ cigarette smoking

Exact pathogenesis is unknown but the current theory is that it is an inappropriate response to exogenous infectious agents or host factors, with or without some component of autoimmunity.

• With an increase in consumption of calories and a lack of activity, adipose is stored in the body
• The adipose cells increase in size and number

• Atherosclerosis leads to luminal narrowing of vessels, plaque ulceration, thromboembolism, or a cardioembolic event which decreases blood flow to the brain and decreases normal neurological function
• Turbulent high BP can cause injury to the endothelium which can activate the thrombogenic cascade-->allows formation of clots which can lodge in small vessels leading to the brain, occluding blood flow to that region
• Degree of decreased blood flow depends on the site of occlusion, the pt’s anatomy, and degree of collateral circulation
• ---Ex. If cerebral blood flow falls to zero, brain tissue will die within 4-10 minutes

• Brain maintains an appropriate cerebral blood flow through autoregulation
• Atherosclerosis can occlude cerebral vessels or break and trigger thrombus formation à occluding vessels and decreasing cerebral perfusion
• Turbulent blood flow due to narrowing of lumen or valvular disease can cause endothelial injury à activates thrombogenic cascade
• Prolonged hypotension dropping pressure below 60 mm/Hg-->occurs in cardiac arrest à leads to infarction
• Causes poorly perfused “watershed” areas between major vascular territories
• Ischemia is caused by decrease in blood flow that lasts longer than a few seconds due to lack of glycogen in neurons and “energy crisis”

Transmission occurs via droplets of infected secretions

Nl: URI nasopharynx pathogen introduced into inflammatory fluid collecting in middle ear

• Chronic: Recurring otitis media infections causes overgrowth of bacteria in ear canal. Often due to
• untreated acute infections

Serous: Auditory tube blocked causing negative pressure and fluid build-up

• Occurs when pus or irritant is trapped behind a closed ostium or the paranasal sinuses have continuous exposure to external environment of ostia of the nose
• Virus, bacteria, or fungus infects sinuses causing inflammation of lining of sinuses and ostia. Inflammation closes the ostia resulting in increase pressure felt by pt as localized pain of throbbing, localized to affected sinuses.
• Most commonly involved is the maxillary sinus; then ethmoid, frontal, sphenoid sinuses

• Virus infects nasal passages.
• Transmission via direct inhalation of virus-laden droplets of mucous secretions of infected patients.

• PUD is caused by an imbalance between
• production of acid (parietal cells) and ability of mucosa to prevent damage (prostaglandins
• and somatostatins) on lesser curvature of stomach

PUD is caused by an imbalance between production of acid (parietal cells) and ability of mucosa to prevent damage (prostaglandins and somatostatins) on lesser curvature of stomach

• Pre-renal ARF:
• o Hypovolemia – decreased MAP
• o Triggered by SNS and renin-angiotensin-aldosterone system
• Norepi and angio II and argenine stimulate vasoconstriction and preserve blood to heart and brain

• Intrinsic ARF
• o Tubular epithelium most commonly affected and takes 1-2 weeks to restore blood flow and regenerate cells

Nephrotoxic substances: radiocontrast, Abx (AGs), APAP, chemo, organic solventsPost-renal ARF:

o One or both kidneys are obstructed

o One kidney has ability to excrete daily nitrogenous wastes (unless B/L obstruction)

Compensated by increased renal blood flow, but constriction causes decreased GFR

• Kidney damage with or without decreased GFR GFR < 60 for > 3 mos with or without kidney damage
• Uncontrolled DM, HTN or long-standing Kidney disease
• ARF
• Pre-renal: vascular dz, arterionephrosclerosis (hypoperfusion)
• Intrinsic: scarring from DM, sclerosis from HTN or drugs like NSAIDs and analgesics
• Post-renal: long-standing obstruction from stones, tumor or prostate

• Dx of HIV depends on demonstration of antibodies to HIV and/or the direct detection of HIV or one of it’s counterparts
• ---Antibodies to HIV generally appear in circulation 2-12 weeks following infection (avg. 6 weeks)
• Hallmark of symptomatic HIV = immunodeficiency caused by continuing viral replication
• HIV virus can infect all cells expressing the T4 (CD4) antigen, which HIV uses to attach to the host cell
• Chemokine co-receptors are required for virus entry
• Once HIV
• enters a cell, it can replicate using reverse transcriptase to transform RNA to
• DNA and integrase to incorporate viral DNA into host cell nucleus

• ·
• Cell
• principally infected is the CD4 Helper T-lymphocyte, which directs other cells
• in the immune network (i.e. B-cells and macrophages); macrophages act as
• reservoir, disseminate to other organ systems

• ·
• CD4 count
• falls, leaving pt more immunocompromised and susceptible to infections

• ·
• HIV virus
• can also lead to release of cytokines and neurotoxins that lead to neuro dysfunction

• ·
• Within a few
• weeks of being infected with HIV, some people develop flu-like symptoms that
• last for a week or two, but others have no symptoms at all; may appear and feel
• healthy for several years

• ·
• 80% of pts
• with <200 CD4 cells/mcL with develop AIDS within 3 years without use
• of antiretroviral therapy

Unknown

• “probably related to ↓ neurotransmitter serotonin”
• H/A may result from the release of neuropeptides acting as neurotransmitters at the trigeminal nerve
• branches…leading to an inflammatory process
• Another theory is the involvement of the dorsal raphe nucleus

• - It is a catabolic disorder
• -Circulating insulin virtually absent
• -Blood glucose levels rise, plasma glucagon is elevated
• -Glucosuria occurs
• -Osmotic diuresis results in dehydration
• - Pancreatic B cells fail to respond to all insulinogenic stimuli
• -Shift from carbohydrate to fat and protein metabolism
• -Causing a release of ketones into the blood stream, causing ketoacidosis.

• Pancreatic b cells respond poorly to glucose
• Sugar rises, b cells respond less
• Normalizing glucose improves b cell function/tissue
• response to insulin

• Degree of severity ranges from mild and not recognized to severe myxedema
• Primary hypothyroidism produces TSH elevation (lack of negative feedback); serum free-thyroxine levels usually reduced
• Secondary causes characterized by decreased concentration of serum free-thyroxine and TSH levels

• 1° Hyperthyroidism is due to over-functioning thyroid gland
• 2° Hyperthyroidism is due to over-stimulation of the thyroid gland by excessive TSH (aka TSH-dependent hyperthyroidism)
• Production of thyroid hormone is unregulated in both, which causes the sx

• The pathophysiology occurs in 3 stages.
• - 1st phase, there is an increase in cartilaginous water content in the joint, causing it to soften. This causes fissuring and microfractures, which results in sclerosis and bone cysts formation.
• - Phase 2 is characterized by inflammation. The formed bone cysts cause leakage of collagen, cartilage fragments, all which lead to phagocytosis and the release of inflammation mediators.
• -Phase 3 is characterized by repair, as calcification and new bone formation can be seen in the affected joint.

• Imbalance between resorption (osteoclasts) and formation of bone (osteoblasts)
• Process of remodeling interrupted by: decreased Ca+ and Vit. D, decrease in androgens and estrogen, too much PTH, decreased physical activity, meds: glucocorticoids, cigarette smoking
• Primary: in women, decrease estrogen cause increase bone resorption and trabecular bone loss
• Demineralization occurs most often in the spine, hip, pelvis, and wrist

• A change in pressure causes the nucleus pulposus to prolapse pushing the thinning annulus posteriorly which impinges on the spinal cord nerve root
• Inflamm. and production of proinflammatory cytokines within the protruding/ruptured disk can cause back pain
• Nerve root injury (radiculopathy) from disk herniation may be due to compression, inflammation or both

• Narrowing of spinal canal compresses nerve roots à symptoms due to direct compression of the nerve roots
• Can be due to enlarging osteophytes at facet joints, hypertrophy of ligamentum flavum, epidural fat deposition

• AD:
• Decrease Acetylcholine
• Degeneration of cholinergic fibers
• Senile plaques and neurofibrillary tangles
• Cortical atrophy
• Parkinson’s:
• Dopamine production by brain cells in the substantia nigra is diminished

• Multi-infarct dementia:
• Individuals who have had several strokes may develop chronic cognitive deficits
• Strokes may be large or small (sometimes lacunar) and usually involve several different brain regions
• More common in individuals with left-hemisphere lesions
• Diffuse white matter disease:
• Results from chronic ischemia due to occlusive disease of small, penetrating cerebral arteries and arterioles
• (microangiopathy)
• HTN is main cause; any disease-causing stenosis of small cerebral vessels may be a critical underlying factor

• Multifactorial and involves changes in receptor-neurotransmitter relationships in the limbic system.
• ·Serotonin, norepinephrine, and dopamine are the primary neurotransmitters involved

• Tearing of muscle fibers or distal ligamentous attachments of the paraspinal muscles
• Results in inflammation which causes spasm
• When the tissues surrounding the spine are damaged, proprioceptors can be temporarily or permanently damaged leading to reinjuries and chronic pain/problems