Final review 2

Inflammatory Response

• Initiated by cellular injury, complicated by infection
• Involves mast cell degranulation
• Activates three plasma protein systems: complement, clotting, and kinin
• Activates macrophages to release numerous cytokines
• Vascular response: vasodilation (erythema, warmth) and increased capillary permeability (edema)
• Cellular response: cellular infiltration, phagocytosis (pus), and thrombosis (prevents bleeding)
• Nerve ending stimulation causes pain
• Key mediators: histamine, platelet activating factor, prostaglandins, leukotrienes, chemotactants, growth factors, TNF alpha, interleukins, and interferons
• Sequence of events: tissue injury/pathogen invasion; detection/binding of PAMPs/DAMPs to PRRs Activates NF-κB, releases cytokines, initiates vascular/cellular responses
• Leukocytes infiltrate, phagocytosis removes agents
• Complement system activates, opsonizes, and lyses pathogens
• Clotting system forms a blood clot
• Kinin system produces bradykinin, which increases vascular permeability, and causes pain
• Chronic inflammation occurs when acute response is not resolved

Disorders of the Integumentary System: Skin Infections - Causative Organisms

• Bacterial infections are commonly caused by coagulase-positive Staphylococcus aureus and beta-hemolytic streptococci
• Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) is also a significant cause.
• Viral infections include Herpes Simplex Virus type 1 (HSV-1) and type 2 (HSV-2)
• Fungal infections are caused by Candida albicans (yeast) and dermatophytes like Tinea rubrum

Skin Infections - Pathophysiology and Characteristics

• Cellulitis is an infection of the dermis and subcutaneous tissue
• Cellulitis is typically caused by Streptococcus pyogenes or Staphylococcus aureus
• Cellulitis is characterized by an erythematous, warm, edematous, and painful area without distinct borders
• Erysipelas is a superficial skin infection caused by beta-hemolytic streptococci
• Erysipelas presents as firm, red spots that enlarge and coalesce into a clearly circumscribed, bright red, hot lesion with a raised border, also systemic
• Systemic symptoms of erysipelas often precede skin lesions
• Impetigo is a superficial skin infection caused by coagulase-positive S. aureus or alpha-hemolytic streptococci, and is more common in children
• Staphylococcal Scalded-Skin Syndrome (SSSS) is caused by exfoliative toxin-producing Staphylococcus aureus, this leads to desquamation and wrinkling of the skin
• Herpes Simplex Virus (HSV) infections: HSV-1 causes cold sores; HSV-2 typically causes genital lesions, characterized by vesicular lesions
• Candidiasis is a yeast infection caused by C. albicans, affecting skin and mucous membranes
• Tinea Infections are fungal infections such as Tinea capitis, and are characterized by scaly, itchy lesions

Skin Infections - Transmission and Risk Factors

• Bacterial infections usually occur through local invasion of pathogens extending from wounds, ulcers, or skin structures
• HSV is transmitted by direct contact with infected lesions (HSV-1 orally, HSV-2 sexually)
• Fungal infections are transmitted by direct contact with infected lesions or indirect contact with contaminated items
• Risk factors for bacterial skin infections include diabetes mellitus, edema, peripheral vascular disease, skin trauma, insect bites, and immunosuppression
• Transmission of HSV-2 is linked to sexual contact
• Risk factors for candidiasis include moist environments and immunocompromise
• Inappropriate use of topical corticosteroids can worsen fungal infections

Cardiovascular Disorders - Atherosclerosis:

• It begins with injury to endothelial cells lining artery walls, and is an inflammatory disease
• Progressions include: endothelia injury and dysfunction, fatty streak, fibrotic plaque, complicated lesion
• Inflammation, adherence of macrophages, release of inflammatory mediators, oxidation of LDL, and formation of foam cells are involved
• Plaque rupture leads to clot formation, instability, vasoconstriction, which obstruct the lumen
• Risk factors: smoking, hypertension, diabetes, increased LDL, decreased HDL, autoimmunity
• Nontraditional risk factors: increased serum markers for inflammation (e.g., hs-CRP), troponin I, adipokines, infection, and air pollution
• Atherosclerosis leads to vascular remodeling (hyaline sclerosis)
• Consequences of atherosclerosis include myocardial ischemia, myocardial infarction, sudden death (in coronary arteries), stroke, dementia (in cerebral arteries), peripheral artery disease

Cardiovascular Disorders - Hypertension:

• Features multiple mechanisms, including changes in the SNS, RAAS, and natriuretic peptides
• Inflammation, endothelial dysfunction, obesity-related hormones, and insulin resistance play a role
• Increased vascular volume from decreased renal salt excretion contributes to sustained hypertension.
• Genetic and environmental factors interact to cause neurohumoral dysfunction and promote inflammation
• Numerous genetic vulnerabilities with environmental risks (obesity, adipokines, insulin resistance, dysfunction of the SNS and RAAS) are risk factors
• Consequences of sustained hypertension include blood vessel sclerosis and damage to the retina, kidney, heart, and brain
• More complications include left ventricular hypertrophy, myocardial ischemia, heart failure, accelerated atherosclerosis, renal disease (nephrosclerosis), stroke, hypertensive crisis

Cardiovascular Disorders - Heart Failure:

• Inflammation occurs in the Pathophysiology of cardiovascular disease, which can lead to heart failure
• Sustained hypertension due to increased workload can lead to left ventricular hypertrophy and heart failure
• Myocardial ischemia and infarction resulting from atherosclerosis can also cause heart failure
• Infections, such as viral myocarditis, can lead to cardiomyopathy and heart failure

Respiratory Disorders - Asthma:

• Chronic inflammatory disease characterized by bronchial hyperreactivity and reversible airflow obstruction
• Airway epithelial exposure to antigen in sensitized individuals initiates both innate and adaptive immune responses (type I hypersensitivity)
• Involves dendritic cells, Th2 lymphocytes, B lymphocytes, mast cells, neutrophils, eosinophils, basophils
• These cells contribute to persistent inflammation of the bronchial mucosa and airway hyperresponsiveness
• Early and late asthmatic responses occur
• Viral infections, allergens, inhaled irritants, obesity, acetaminophen, and GERD can trigger or exacerbate asthma
• Airway dysbiosis is linked to allergen sensitization and asthma development
• Genetic predisposition, allergen exposure, viral infections, exposure to irritants, obesity, and possibly microbiome dysbiosis are risk factors
• Reversible airflow obstruction, bronchial hyperreactivity, and airway inflammation cause dyspnea, wheezing, and coughing

Respiratory Disorders - Chronic Obstructive Pulmonary Disease (COPD):

• Chronic irritant exposure (e.g., smoking) recruits neutrophils, macrophages, and lymphocytes to the lung
• Progressive damage results from inflammation, oxidative stress, extracellular matrix proteolysis, and cell death
• Frequent infectious exacerbations and lung senescence contribute to disease progression
• This leads to airway obstruction and loss of surface area for gas exchange.
• Although the primary cause of irritants is chronic inflammation in COPD, bacterial and viral infections are common causes of exacerbations
• Cigarette smoking is the primary risk factor for COPD
• Other factors include air pollution, occupational exposure, and genetic predisposition
• Signs and symptoms: airway obstruction, air trapping, loss of surface area for gas exchange, frequent exacerbations, dyspnea, cough, hypoxemia, and hypercapnia

Restrictive Lung Disorders - Acute Respiratory Distress Syndrome (ARDS):

• Acute lung inflammation and diffuse alveolocapillary injury result from direct pulmonary injury or severe systemic inflammation
• Damage to lungs leads to activation of neutrophils, macrophages, and platelets, with the release of inflammatory cytokines
• Increased capillary membrane permeability causes fluid, protein, and blood cells to leak into the interstitium and alveoli (pulmonary edema)
• Surfactant production decreases, this leads to atelectasis
• Predisposing factors include sepsis, pneumonia (bacterial, viral, with COVID-19), trauma, burns, aspiration, systemic inflammation
• COVID-19 can lead to ARDS via a hyperinflammatory state
• Acute onset of bilateral infiltrates on chest radiograph
• Additional S&S: persistent hypoxemia despite supplemental oxygen and decreased lung compliance.

Restrictive Lung Disorders - Idiopathic Pulmonary Fibrosis (IPF):

• A multifactorial disease involving epithelial damage and innate and adaptive immune responses
• Neutrophils, macrophages, fibroblasts, and T lymphocytes are involved
• Inflammatory cytokines and growth factors lead to a fibrotic process Interstitial and alveolar fibrin deposition, scarring, and honeycombing of lung parenchyma Oxidative stress also contributes
• The exact cause is unknown, but epithelial damage and abnormal immune responses are implicated
• Genetic factors and environmental exposures may play a role
• Progressive scarring of lung tissue, leading to dyspnea, cough, and reduced lung function

Gastrointestinal Disorders - Hepatitis:

• Inflammation of the liver
• Pathologic lesions include hepatic cell necrosis, scarring (with chronic disease), and Kupffer cell hyperplasia
• Cell-mediated immune mechanisms, release of inflammatory mediators, and persistent inflammation promote cellular injury
• Viral infection damages hepatocytes and obstructs bile canaliculi, leading to cholestasis and jaundice
• Primarily caused by hepatitis viruses (A, B, C, D, and E)
• Hepatitis A is typically transmitted through the fecal-oral route
• Hepatitis B, C, and D are usually transmitted through bloodborne or sexual contact
• Hepatitis E is mainly transmitted through the fecal-oral route, often via contaminated water
• Risk factors: exposure to contaminated food/water (HAV, HEV), sharing needles, unprotected sex, mother-to-child transmission (HBV, HCV, HDV)

Inflammatory Bowel Disorders - Ulcerative Colitis (UC):

• Chronic inflammatory disease that begins with inflammation at the base of the crypt of Lieberkühn in the large intestine
• UC starts the rectum and may extend in its entirety
• Lesions are limited to the mucosal epithelium and are not transmural
• Decreased mucin secretion leads to increased mucosal permeability in UC
• Immune response is stimulated by increased passage of pathogens and antigens
• Activation of T cells and dendritic cells triggers the production of pro-inflammatory cytokines
• The exact cause is unknown, but it involves a dysregulated immune response to the gut microbiota in genetically susceptible individuals
• Inflammation and ulceration of the colonic mucosa
• Signs and Symptoms include diarrhea (often bloody), abdominal pain, and urgency

Urinary and Renal Disorders - Urinary Tract Obstructions

• Obstruction of urine flow (e.g., kidney stones, prostatic hypertrophy, tumors, congenital abnormalities) leads to increased pressure within the urinary tract.
• Increased pressure causes distension of the affected structures (e.g., ureter, renal pelvis).
• Prolonged obstruction can impair blood flow, leading to ischemia and damage to renal tissue.
• Stasis of urine increases the risk of urinary tract infections (UTIs).
• Obstructions themselves are not caused by organisms, but they are a risk factor for UTIs.
• Common uropathogens: Escherichia coli, Staphylococcus saprophyticus, Klebsiella, Proteus, and Pseudomonas.
• Risk factors: kidney stones, enlarged prostate, tumors, congenital abnormalities, and conditions causing strictures. Symptoms vary depending on location/severity.
• Obstructions include flank pain, changes in urination (frequency, urgency, decreased output), UTI symptoms (dysuria, fever).

Urinary and Renal Disorders - Acute Kidney Injury (AKI)

• There is not enough information provided to summarise Urinary Incontinence
• AKI results from ischemic injury, nephrotoxic exposure, sepsis, or obstructive processes
• Injured renal tissues initiate a complex inflammatory immunopathophysiological response
• This leads to microcirculatory disturbances, functional impairment, and cell death
• Activation of innate immunity components (leukocytes, coagulation factors, complement) drives kidney inflammation and damage
• Gram-negative bacteremia (sepsis) is a major cause of AKI; infections like postinfectious glomerulonephritis and endocarditis also lead to AKI
• Risk factors involve hypovolemia, reduced cardiac output, renal hypoperfusion, exposure to nephrotoxic agents (medications, contrast), systemic inflammation.
• The defining characteristics to detect a sudden decline in kidney function are: Increased serum creatinine and blood urea nitrogen; also look for Oliguria and electrolyte imbalances

Urinary and Renal Disorders - Chronic Kidney Disease (CKD)

• CKD results from progressive loss of nephron function over time from various underlying causes
• There is persistent inflammation, also hypoxia, and oxidative stress contribute to the development of renal fibrosis
• Chronic inflammation is a significant contributor to oxidative stress in CKD
• Proteinuria and angiotensin II activity are key factors in the progression of renal injury
• CKD is less commonly caused by direct infection but recurrent pyelonephritis (kidney infection) can cause scarring and lead to CKD, as well as systemic infections leading to conditions like postinfectious glomerulonephritis
• Risk Factors include diabetes mellitus, hypertension, glomerulonephritis, polycystic kidney disease, and obstructive uropathy
• The Characteristics involve a gradual decline in kidney function, often with few early symptoms
• Later indications include azotemia, uremia (accumulation of toxins), fluid and electrolyte imbalances, anemia, hypertension, and systemic effects affecting multiple organ systems

Module 7 - Diabetes Mellitus

• Diabetes mellitus (DM) is a group of disorders characterized by chronic hyperglycemia and glucose intolerance.
• Type 1 Diabetes Mellitus: caused by a defect or failure of the beta cells in the pancreas
• This failure leads to impaired insulin production
• Hyperglycemia may not be evident until 80-90% of beta cell function is lost
• Type 1A DM involves an autoimmune mechanism
• Type 2 Diabetes Mellitus: characterized by insulin resistance and impaired insulin secretion
• This leads to reduced glucose uptake and storage
• Insulin resistance is a reduced sensitivity to the effects of insulin and may result from:
• an abnormal insulin molecule
• high amounts of insulin antagonists
• downregulation of the insulin receptor
• altered glucose transporter (GLUT) proteins
• Gestational Diabetes Mellitus: Glucose intolerance diagnosed during pregnancy
• Chronic hyperglycemia in diabetes leads to oxidative stress (increased production of reactive oxygen species) and glycation (covalent binding of glucose to proteins and lipids, forming advanced glycation end- products - AGEs)
• These processes damage nerves, vasculature, and glomeruli.
• Glycation products can also activate immune cells, causing inflammation and stimulating reactive oxygen species production.
• Type 1A diabetes has an autoimmune basis, but it is not directly caused by an infecting organism
• Characteristics: Chronic hyperglycemia and glucose intolerance.
• Acute complications: Hypoglycemia (especially in Type 1 due to inappropriate insulin dosage) and diabetic ketoacidosis (due to insulin deficiency leading to fatty acid metabolism and ketone body production).
• Chronic complications: Oxidative stress, microvascular diseases (retinopathy, nephropathies, neuropathies), and macrovascular disease.
• Diabetic retinopathy leads to blindness.
• Diabetic nephropathy involves progressive changes in the kidney and is a common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD).
• Risk Factors: Age, obesity, hypertension, physical inactivity, family history, and metabolic syndrome including high triglyceride levels, low HDL cholesterol level, high blood pressure, and high fasting glucose concentration

Module 7 - Diabetes Insipidus

• A state of hypofunction of the posterior pituitary gland.
• DI involves insufficient ADH action or secretion
• This leads to an inability of the kidneys to conserve water.
• Etiology: Not mentioned
• Characteristics: Not detailed in the provided sources.
• Risk Factors: Not listed; though hypopituitarism, including DI, can be caused by damage or tumor presence in the pituitary gland.

Disorders of the Anterior and Posterior Pituitary Gland

• Disorders are broadly categorized by hyperfunction or hypofunction.
• Anterior Pituitary Hyperfunction (Hyperpituitarism): Often due to a pituitary adenoma. Sources do not elaborate on the specific pathophysiologies of different hyperpituitary conditions.
• Anterior Pituitary Hypofunction (Hypopituitarism): Often due to damage or the presence of a tumor. Sources do not elaborate on the specific pathophysiologies of different hypopituitary conditions.
• Posterior Pituitary Hyperfunction (Syndrome of Inappropriate ADH Secretion - SIADH): Characterized by excessive antidiuretic hormone (ADH) secretion and ADH stimulates water reabsorption in the collecting ducts and distal tubules of the kidney.
• SIADH can lead to hyponatremia.
• Etiology: SIADH can be caused by ADH-secreting tumors and Hypopituitarism can be due to tumors
• Other Features of pituitary disorders (both anterior and posterior) are not detailed in the provided excerpts.
• Risk Factors: The presence of tumors affecting the pituitary gland can lead to both hyper- and hypofunction

Disorders of the Adrenal Cortex

• The adrenal cortex, located on top of the kidney, and is involved in cortisol secretion.
• Cushing Syndrome involves elevated circulating cortisol levels (hypercortisolism)
• This can be primary (due to issues within the adrenal cortex like adenoma, hyperplasia, or carcinoma) or secondary (due to increased ACTH secretion from the anterior pituitary)
• Addison’s Disease involves autoimmune destruction of adrenal cortical cells, adrenal atrophy, or destruction by disease, surgical removal, or inadequate secretion of ACTH by the pituitary gland. Etiology: Not detailed in the excerpts.

Disorders of the Thyroid and Parathyroid Gland- Thyroid Disorders:

• Hyperthyroidism is characterized by excessive thyroid hormone, specifically goiter in Grave's
• Hypothyroidism: Marked by insufficient thyroid hormone production
• Autoimmune basis in Hashimoto's thyroiditis
• Characteristics of Hyperthyroidism: Tachycardia, weight loss, diarrhea, increased appetite, nervousness, restlessness, heat intolerance, goiter (in Grave’s disease), pretibial myxedema, exophthalmos (bulging of eyes), and potential thyrotoxic crisis (acute and severe exacerbation).
• Characteristics of Hypothyroidism: Fatigue, weakness, cold intolerance, constipation, dry skin, brittle hair and nails, and potential myxedematous coma (severe, life-threatening hypothyroid state).
• Risk Factors of Hashimoto’s thyroiditis (hypothyroidism): Autoimmune basis, genetic predisposition and immune system dysregulation.
• The features of primary Hyperparathyroidism are:
• secretion is increased and is not under the usual feedback control mechanisms
• the calcium level in the blood rises due to increased bone resorption and GI absorption of calcium
• Primary hyperparathyroidism is not caused by microorganisms. Approximately 80% to 85% of cases are caused by parathyroid adenomas, another 10% to 15% result from parathyroid hyperplasia, and approximately 1% of cases are caused by parathyroid carcinoma.
• May also be caused by a variety of genetic causes Features: Hallmarks are Hypercalcemia and hypophosphatemia, as well as those related to muscle(fatigue, weakness, myalgia), nervous system issues (headache, depression, anxiety, psychosis, impaired memory, confusion), and GI Systems issues (anorexia, nausea, vomiting, abdominal pain, peptic ulcer disease, constipation)
• Other less common clinical signs are hypertension, arthralgia and arthritis, and rarely pancreatitis Risk factors for primary hyperparathyroidism include parathyroid adenomas, hyperplasia, or carcinoma, Genetic predisposition, also including genes causing multiple endocrine neoplasia.

Secondary Hyperparathyroidism is defined by: the parathyroid glands attempting to compensate in response to chronic hypocalcemia

• Secretion of PTH is elevated, failing to achieve normal calcium levels due to insufficient amounts of activated vitamin D. Causative Organisms: Secondary hyperparathyroidism is not caused by microorganisms. Risk factors for secondary hyperparathyroidism: Decreased activation of vitamin D in individuals with renal failure, Dietary deficiency of vitamin D or calcium, Decreased intestinal absorption of vitamin D or calcium, Ingestion of certain drugs, such as phenytoin, phenobarbital, and laxatives. Tertiary Hyperparathyroidism: can develop after any long- Standing period of hypocalcemia, such as is seen with chronic dialysis, renal transplantation, or GI malabsorption Characteristic Features are: excessive secretion of PTH and may cause hypercalcemia. Risk factors for tertiary hyperparathyroidism: Chronic kidney disease and long-term dialysis, Renal transplantation, Gastrointestinal malabsorption leading to prolonged hypocalcemia.

Module 8 - Stress Response

• The hypothalamus–pituitary–adrenal (HPA) axis, the sympathetic nervous system (SNS), and the immune system (IS) becomes active when demand exceeds person’s coping abilities or when there is a perceived or anticipated threat which disrupts homeostasis
• The SNS responds and leads to increased heart rate, dilated pupils and bronchi, and liver glucose release, through the release of catecholamines
• The hypothalamus –pituitary–adrenal (HPA) axis involves the release of cortisol; this supports the effects of catecholamines, suppresses the immune-inflammatory response, delays wound healing, and modulates the reproductive hormone system.
• Also causes release of cytokines
• The stress response itself is not directly caused by microorganisms, instead stressors such as exposure to cold temperatures or psychological e.g., exam deadlines
• Chronic stress-induced activation of these systems has the potential to compromise recovery and predispose individuals to unhealthy coping strategies and illnesses and has the following phases: Alarm phase releases epinephrine, the “fight or flight is triggered In the resistance phase the body adapts and the exhaustion phase uses all resources which may lead to a compromised immune system and stress related illnesses

Module 8 -Eating Disorders

• Aberrant eating Behaviour and weight regulation, as well as disturbed attitudes towards body weight and shape
• This is may be influenced by disturbed serotonin functions as well as Anorexia nervosa which as a result of negative protein and energy balance secondary to reduced food intake and abnormal metabolism.
• This is 10x more prevalent in women, and develops int he mid- to late- adolescence

Module 8 - Schizophrenia

• Debilitating and heterogeneous mental illness characterized by disorganized thoughts
• Neuropathology involves an increase in dopamine release in the mesolimbic system, decreased dopamine release in the mesocortical pathway, decreased levels of GABA and glutamate, and increased density of serotonin receptors within the cerebral cortex.
• The clinical features include hallucinations, delusions, formal thought disorder, bizarre behavior (positive features) flattening affect, alogia, anhedonia, attention deficits, apathy (negative features) and impaired attention, planning and motor

Module 8 - Bipolar Disorders

• Periods major depression followed by periods of mania
• Etiology: Elevated levels of norepinephrine, dopamine, and/or serotonin influence the hypothalamic-pituitary-thyroid (HPT) system and increased ventricular volume
• Clinical features of Bipolar : Mania is an elevated level of euphoria lasting at least 1 week, often accompanied by grandiosity, increased energy, rapid speech, racing thoughts, reduced concentration, increased goal-focused activity, poor judgment, and sometimes delusions and hallucinations.

Module 8 - Depressive Disorders (General Information)

• Characterized by a sustained emotional sate of sadness
• Decreased norepinephrine, serotonin, and/or dopamine levels within the synaptic cleft may be involved
• Stress elevated cortisol secretion as well

Module 8 - Anxiety Disorders (Features and Risk Factors)

• Anxiety disorders involve persistent and uncontrollable states of fear and anxiety; Secondary to Drug Rxns and Physical Illnesses:

• o Panic Disorder: Etiology is currently unknown but has a with genetic influence and increased autonomic sensitivity & decreased benzodiazepine receptors Features panic attacks with intense autonomic intensity, with lightheadedness, tachycardia, etc o Generalized Anxiety Disorder (GAD): Etiology is currently unknown but has a genetic compnent, with Abnormalities BZ binding, and alterations in specific brain regions Like the cingulate cortex and amygdala are reported"

      Features: Excessive and
        persistent worries about life events, often with motor disturbances, etc
                 Irritability, and fatigue
     o   Post-traumatic Stress Disorder (PTSD): Stress induced
         alterations prefrontal cortex, leading to a
         persistent dysregulation  system.
              Symptoms: Recurring thoughts, flashbacks etc
                That lead to: Negative cognitions
               The risk factor here is terror/life-threat
    o    Obsessive-Compulsive Disorder (OCD) is  With the etiologies involving:
        A genetic component, Involves abnormal communication between the basal ganglia and prefrontal
        cortex, increased activity in which prefrontal cortex decreases serotonin
      characterized by obsessions
  

(recurrent thoughts or urges) and/or compulsions (repetitive behaviors or

Risk & Genetics

• Generalized Anxiety Disorder (GAD):: genetic + exposure to

Module 9- Acquired Brain Injury and Cerebrovascular Disorders

Acquired Brain Injury (ABI) : "Alteration in brain Function or Other Evidence of Brain Pathology Caused". Primary focal (such as Contrecoup) Vs Axnonal injury Causes: Unintentional Falls / motor vehicle injuries Cerebrovascular disease (CVD) leads to ischemia or hemorrhage. Common Etiologies involve Thrombotic (Atherosclerosis / Embolic ( fragments thrombi outside ) Rupture of blood vessels, With Mass and 2nday Ischemia

Module 10 -General Patho and Organisms for Joint Disorders

Meningitis and PD

• Pathophysiology, Signs, Transmission"
• Inflammation as main driver, Signs as common manifestation is a cerebrovascular accident (CVA) or stroke, with sudden and focal symptoms Transmitted: ""bacterial (S. pneumoniae, N. meningitides, H. influenza), Viral, Fungal, Causes - bacteria (eg. S. pneumoniae, N. meningitidis, H. influenza), Viral (eg. enteroviruses, herpes Simplex, west nile) Causes/ Pathology Parkinson's
• Pathophysiology: The pathogenesis of primary PD is unknown Involves nigral Degeneration and Lewy Bodies (Alpha-Synuclein) Causes: None

Module 10 -MS and Myasthenia Gravis

"General Patho, Causative, and Risk Pathophysiology: Autoimmune and Loss Axons

• Cause: Likely from infections (but the antigens remain ""Unknown"")" Myasthenia main thing that effects transmission at the NMJ. Causes : Again autoimune but assoc with thymic abnorms AND Infections

Module 10 - Alzheimers and Joint Disorders

Alz Pathology: Amyloid plaques AND Neurofibrillary Tangles which = problems with intellectual functioning Causes infectious factors have been noted which include (Herpes, Spirochetes Etc) Joint Disease Pathology: Main thing = Damaged synovial AND cartilage Causes: Generally BActiera but like (Bacteria / Mycoplasma / viruses / fungi etc )

Note on causes (some risk factors not always causative) ""Risk"""" in Joint Dis - Genetic factors / Age etc"

Module 10 -Metabolic and Musculoskeletal Disorders

"Patho for Metabolic Bone : ""Abnormal bone Strength vs Turnover Rate : osteoporosis. Causes - genetic and lifestyle""" Musculoskel" Pathophysiology: Trauma and Injuries

• Fractures, dislocations, and etc"""" Causes Trauma"

Module 11 - Blood Disorders (Anemias and Luekemia)

""Pathophysiology for Anemias as main issue or decreased number of erythrocytes in the blood. 3 Main issues=

• Blood Loss
• Impaired Production Increased - Etiology
• B19
• Etc) : Leukemias are malignancy """

Module 11 - Blood Disorders (Lymphomas)

"Pathology Genetic Mutations / Viral Infections HL - Hodjkin / NHL ""EBV linked too hodkin" Causes "EBV link, and some other viruses"""

Module 11 - Blood Disorders Plate

Issue and Cause - ""platelets, Causes e Toxins (E. Coli, Shigella)) as well"

Module 12 - Module 12; Main Risk factor Endometriosis being longer exogenous exposure / Family Hx.

Symptoms main ones to watch our for: Infertility, Pelvic pain. and/ abnormal vaginal bleeding .

Module 12 - Sexually Transmitted Infections General Info

STI causes HIV - Etiology HIV-1 : Retrovirius The most prevalent sti. Can have Asymptomatic - Viral shred Herpes: Direct Contact, sexual relations Symptoms, vesicles. Causes herpes simple virus