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PATH 1000 MIDTERM 2 Exam 2024
Questions & Answers 100%
Correct
Nociceptive Pain - ANSWERSpain receptors in the PNS being stimulated by mechanical, thermal or chemical means Pain Threshold - ANSWERSlowest intensity of pain that a person recognizes Pain Tolerance - ANSWERSgreatest intensity of pain that can be endured Acute Pain - ANSWERSprotective mechanism and sudden onset. Warning of an actual or impending tissue injury
- Presents as increased HR, HTN, diaphoresis and anxiety Somatic Pain - ANSWERSoccurs in connective tissue, muscle, bone and skin Visceral Pain - ANSWERSpain in internal organs and lining of body cavities associated with nausea, vomiting and restlessness Referred Pain - ANSWERSoccurs in an area distant from the point of region
- Visceral sensory fibers enter the spinal cord along with sensory fibers from another point in the body → fibers converge → carry signals to the cerebral cortex Persistent Pain (Chronic Pain) - ANSWERSpain lasting longer than 3 months and may be persistent. Onset can be sudden or develop insidiously
- Leads to physiological adaptation & behavioural and psychological changes Neuralgia - ANSWERSpain in the distribution of a nerve Neuropathic Pain - ANSWERSpain caused by a lesion or dysfunction of the nervous system Phantom Limb Pain - ANSWERSneuropathic pain from nerve trauma or disease
- Occurs in patients who had pain prior to amputation
- Cause:
- Hyperactivity of peripheral nerves
- Scar tissue
- Neuroma formation
Myofascial Pain - ANSWERSpain and inflammation in the fascia that covers muscles due to injury and spams (chronic condition) Thermoregulation - ANSWERSprocess that allows your body to maintain its core internal temperature mediated by the hypothalamus and endocrine system How does aging affect thermoregulation? - ANSWERS- Decreased shivering
- Slowed BMR
- Decreased sweating
- Slowed blood circulation
- Changes to the skin
- Decreased heat producing activities Mechanism of Heat Loss - ANSWERS- Autonomic Nervous system:
- Evaporation & vasodilation
- Relation to environmental temperature:
- Radiation
- Conduction
- Convection - transfer liquids/gases through the air from a warmer environment to a cooler environment Mechanism of Heat Conservation - ANSWERS- Vasoconstriction by sympathetic nervous system Ex: dressing in layers helps with heat conservation as it traps heat in Fever - ANSWERStemporary response to either endogenous or exogenous pyrogens
- Hypothalamus & Brainstem Cause:
- Increased heat production & conservation
- Peripheral vasoconstriction
- Epinephrine release How does fever effect older adults & infants? - ANSWERS- Older Adults
- Limited fever response to infection
- May lead to increased morbidity & mortality
- Infants
- Inability to shiver
- High temps can occur in mild infections
- May develop febrile seizures Hyperthermia - ANSWERSincreased body temperature without hypothalamus trigger.
- Can lead to nerve damage, convulsions & death
Heat Cramps - ANSWERSheat illness due to muscle spasms from loss of large amount of salt and water through exercise Heat Exhaustion - ANSWERSresult of body overheating
- S/S: dizziness, headache, heat sweating, paleness, muscle cramps Heat Stroke - ANSWERSsevere heat illness that results in a body temperature greater than 130°F
- S/S: throbbing headache, unconsciousness, confusion, rapid/strong pulse, red/hot/dry skin (no sweating) Hypothermia - ANSWERScore body temperature falls below 35°C
- Causes:
- Prolonged cold exposure → vasoconstriction, increased blood viscosity, ischemic damage
- Clinical Manifestations:
- Shivering, increased risk of coagulation, ice crystals form in cells causing them to rupture and die Stages of Sleep - ANSWERS- Non Rapid Eye Movement (Non-REM)
- Stage 1: your eyes are closed, but easy to wake you up. Lasts for 5-10 minutes
- Stage 2: you are in light sleep. Heart rate slows and body temperature drops. Body prepares for deep sleep
- Stage 3: deep sleep stage. Body repairs and regrows tissues, builds bone and muscle, and strengthens immune system
- Rapid Eye Movement (REM): happens 90 minutes after you fall asleep. Heart rate and breathing quickens. Intense dreams occur due to hyperactive brain Insomia - ANSWERS(sleeplessness) difficulty falling asleep or staying asleep.
- Day time sleepiness, low energy, irritability, and depressed mood Obstructive Sleep Apnea Syndrome (OSAS) - ANSWERSserious sleep disorder where it causes breathing to repeatedly stops and start during sleep Shift Work Sleep Disorder - ANSWERStrouble sleeping due to working nights or rotating shifts. May also have trouble staying awake or alert during work Restless Leg Syndrome - ANSWERSuncontrollable urge to move your legs due to an uncomfortable sensation Cataract - ANSWERSopaqueness of the ocular lens/thickening of lens due to changes in the lens proteins
- S/S: decreased visual acuity, blurred vision and decreased color perception Glaucoma - ANSWERSvision loss due to damage of the optic nerve resulting in increased pressure within the eye (interocular pressure - IOP). Affects peripheral Vision Open Angle Glaucoma - ANSWERS(most common form) occurs due to blockage of the trabecular network → increased IOP
- Progresses slowly
- Most people are diagnosed once they have lost vision Closed Angle Glaucoma - ANSWERSarea between the cornea and iris has closed, leading to forward displacement of iris towards cornea
- Fluid unable to drain → increased IOP
- Abrupt onset, painful
- Requires immediate medical attention Retinal Detachment - ANSWERStear or break in retina, which causes fluid accumulation in the space between retina & epithelial pigment
- Vitreous gel becomes more liquefied
- Separation deprives retina of oxygen & nutrients
- S/S: floaters, flashes of light Macular Degeneration - ANSWERSdegeneration of the retinal macula
- Usually age related (ARMD)
- Affects central vision Dry (atrophic) Acute Macular Degernation - ANSWERS(most common type) atrophy of retinal epithelial layer
- Drusen thins and dries out macula
- Loss of photoreceptors → loss of central vision
- Can progress to Wet AMD Wet (exudative) Acute Macular Degeneration - ANSWERSabnormal blood vessel growth
- Vessels are leaky and weak → scarring
- Fluid lifts and damages the macula
- Causes rapid loss of vision if untreated and can lead to retinal detachment Conjunctivitis - ANSWERSinflammation or swelling of the conjunctiva ("pink eye") Otitis Externa - ANSWERSinflammation (redness and swelling) of the external ear canal
- Common cause is bacteria (E.coli)
- Occurs after prolonged exposure to moisture
Otitis Media - ANSWERSinfection of the middle ear caused by bacteria
- Common in children
- Can be acute or chronic
- Causes ear pain Reticular Activating System (RAS) - ANSWERSregulates attention & information processing
- Maintains wakefulness/attention (arousal) and helps maintain posture/balance
- Location starts at the top of the spinal cord Alterations of Arousal - ANSWERS- Structural - infections/tumours/injuries
- Metabolic - hypoxia/electrolytes imbalances/hypoglycaemia
- Psychogenic - drugs/psychiatric disorders Five Categories of Neurological Function - ANSWERS1. LOC - determines nervous system function (awareness of person, place, time and arousal)
- Pattern of Breathing -
- Ex: Cheyne-Stokes Respirations
- Pupil Changes - indicates level of brainstem dysfunction (fixed, dilated, pinpoint, sluggish)
- Oculomotor Response - eye movements & reflexes change with brain dysfunction (abnormal movements/absent movements indicate what part of the brain is involved)
- Ex: Doll's Eyes Phenomenon
- Motor Response - evaluates level of brain dysfunction (determines which side of the brain is damaged) Cheyne-Stokes Respirations - ANSWERSabnormal breathing pattern characterized by progressively deeper, sometimes faster, followed by gradual decrease that results in a temporary stop in breathing (apnea)
- Pattern repeats each cycle taking 30 seconds to 2 minutes Cerebral Death - ANSWERSdeath of cerebral hemisphere causing irreversible coma
- Brainstem and cerebellum still function to maintain homeostasis
- Permanent brain damage
- Person does not follow commands, speak or have voluntary movement Brain Death - ANSWERSbrain cannot maintain body's internal homeostasis causing irreversible brain damage
- Absence of cerebral hemisphere function
- Absence of brainstem's vital centers Coma - ANSWERSdeep state of prolonged unconsciousness in which a person cannot be awakened
- Fails to response to painful stimuli, light or sound
- Does not initiate voluntary actions Vegetative State - ANSWERSunawareness of self or environment
- Arousal returns but is sluggish
- Loss of cognitive function
- BP & breathing are maintained
- Brainstem reflexes intact Locked-in Syndrome - ANSWERSpatient is aware but cannot move or communicate verbally due to complete paralysis of nearly all voluntary muscles except for vertical eye movements and blinking Acute Confusional State (Delirium) - ANSWERSacute transient disorder of awareness that affects attention, sleep-wake cycle, and behaviours
- Causes:
- Drug intoxication, ETOH/drug withdrawal, fever, trauma, electrolyte imbalances, head injury, etc.
- Clinical Manifestations:
- Confusion, delusions, hallucinations, loss of concentration, restlessness, irritability, insomnia, poor appetite Dementia - ANSWERSprogressive deterioration of brain function leading to impaired of intellect, memory, language and behaviour
- Clinical Manifestations:
- Memory loss, impaired judgement/learning, hallucinations, sleep disorders, depression, apathy, falls, anxiety Alzheimer's Disease - ANSWERS(leading cause of dementia) brain has neurotic plaques & neurofibrillary tangles in the cerebral cortex & hippocampus
- Unknown cause
- Loss of acetylcholine
- Results in loss of neurons & brain atrophy
- Clinical Manifestations:
- Progression from mild short term memory loss to total loss of cognition, disorientation/confusion, inability to problem solve, dyspraxia (loss of coordination of a learned skill), behavioural changes
- Treatment:
- Use of memory aids, improving hygiene/nutrition/health, use of cholinesterase inhibitors to stop breakdown of acetylcholine Parkinson's Disease - ANSWERSchronic neurodegenerative disorder that degenerates the basal ganglia (affects extrapyramidal system)
- Causes tremors and stiffness/slowing of movement
- Dopamine deficit
- Lewy bodies present
- Treatment:
- Symptomatic to aid with mobility and autonomic symptoms, dopamine modulation medications, deep brain stimulation Seizures - ANSWERSepisode of abnormal electrical activity in the brain due to excessive stimulation
- Clinical Manifestations:
- Repetitive movements, repetitive jerking of a body part, possible unconsciousness, abnormal posturing, eye rolling, excessive salivation Convulsions - ANSWERSspasmodic contractions of any or all muscles in the body Epilepsy - ANSWERSchronic, recurrent patter of seizures (no cause) Status Epilepticus - ANSWERSmultiple seizures with continuous electrical activity without recovery resulting in brain damage and death (medical emergency) Types of Seizures - ANSWERS1. Aura - manifests as the perception of a strange light, an unpleasant smell, or confusing thoughts or experiences
- Prodromal - (occurs hours or days before a seizure) includes mood changes, sleep disturbances, light-headedness, anxiety, irritability, difficulty concentrating and ecstatic feeling
- Tonic Phase - muscle stiffness, rigidity
- Clonic Phase - jerking of the body or parts of the body
- Postictal State - altered state of consciousness after an epileptic seizure (lasting between 5-30 mins) characterized by drowsiness, confusion, nausea, hypertension, headache or migraine Four Stages of Intracranial Pressure (ICP) - ANSWERS- Stage 1 & Stage 2 = compensation is occurring
- Stage 3 = decomposition and loss of autoregulation with changes to mental status, pupils, breathing, V/S (brain cannot function)
- Stage 4 = herniation occurs as brain tissue shifts to hypoxia and ischemia (severe/fatal) Hypotonia - ANSWERSdecreased muscle tone due to decreased excitability of neurons leading to decreased muscle activity
- Causes:
- Cerebellar damage, spinal cord injury, CVA Hypertonia - ANSWERSincreased muscle to caused by upper motor neuron damage
- Involuntary muscle contraction or spasticity
- Muscles are enlarged and firm Hypokinesia - ANSWERSloss of voluntary movement with an intact nervous system
- Can involve akinesia or bradykinesia
- Voluntary movements are difficult to initiate Hyperkinesia - ANSWERSexcessive purposeless movements on the face, lips, tongue or extremities
- May be repetitive or non repetitive movements, twisting movements Upper Motor Syndrome - ANSWERSincludes spasticity hypertonia & hyperreflexia
- Involves paresis (weakness) and paralysis (loss of motor function) Lower Motor Syndrome - ANSWERSincludes impaired voluntary/involuntary movement & flaccid paralysis
- Involves paresis (weakness) and paralysis (loss of motor function) Spinal Shock - ANSWERScomplete cessation of spinal cord following a spinal cord injury/lesion
- Motor paralysis & loss of sensation occurs
- Reflexes below the level of injury are absent
- Temporary or lasts days to months Pyramidal Tract Syndrome - ANSWERSreturn of reflexes resulting in motor dysfunction with muscle over activity, clonus & spasms Types of Paralysis - ANSWERS1. Hemiplegia - paralysis of upper/lower extremities on one side
- Diplegia - paralysis of both sides of the body
- Paraplegia - paralysis of lower extremities
- Quadriplegia - paralysis of all 4 extremities Traumatic Brain Injury - ANSWERSalteration in brain function caused by an external force
- Causes:
- MVA, falls, sports injuries, assaults
- Classified as closed or open blunt force trauma
- Damage occurs through primary or secondary injury Closed Head Injury - ANSWERS(most common type) head strikes a hard surface or an object
- Dura mater remains intact, brain tissue is not exposed Focal Brain Injury - ANSWERSinjury occurs at a specific site
- Compression of the skull and rebound effects
- Includes Coup (point of impact) or Countercoup injuries (brain hits back of the skull) Contusion - ANSWERSblood leaking from an injured vessel
- Most common in the frontal lobe
- Brain edema forms around damaged neural tissue → increased ICP
- Effects occur 18-36 hours post injury Epidural Hematoma - ANSWERSbleeding from artery between dura mater and skull
- Loss of consciousness at injury
- Severe headaches
- Vomiting, drowsiness, confusion, seizures Subdural Hematoma - ANSWERSbleeding from a vein
- Most common cause of Motor Vehicle Accident (MVA)
- Classified as:
- Acute - develop rapidly
- Subacute - develop over 48 hours to 2 weeks
- Chronic - found in alcoholism Intracerebral Hematoma - ANSWERSbleeding within brain (associated with contusions)
- Increased ICP, compression of brain tissues, edema, decreased LOC Diffuse Injury - ANSWERSwidespread areas of the brain are damaged
- Damage to axonal fibres & white matter
- Occurs in whiplash & rotational injuries or concussions
- Axonal damage → decreased speed of information processing & attention span Concussion - ANSWERSmild brain injury
- No loss of consciousness
- Confusion lasts 1 minute to several minutes
- May complain of headache Classic Cerebral Concussion - ANSWERSloss of consciousness lasting < 6 hours
- Retrograde Amnesia: cannot remember memories prior to injury
- Brief period of bradycardia & hypotension (< 30 sec) Spinal Cord Trauma - ANSWERSspinal injury due to hyperextension, fractures, dislocations or rotational forces
- Classified as:
- Primary Injury - initial mechanical trauma * immediate tissue destruction
- Secondary Injury - begins minutes after injury with inflammation, ischemia, edema, etc. ➢ Severity = leads to cord swelling → increased dysfunction
Neurogenic Shock - ANSWERS(vasogenic shock) imbalance between SNS & PNS resulting in massive vasodilation Autonomic Hyperreflexia (Dysreflexia) - ANSWERSdue to stimulation of the SNS caused by distended bladder or rectum
- S/S: sudden HTN, bradycardia, pounding headache, blurred vision Brain Tumour - ANSWERSabnormal growth of cells in brain
- Classified as:
- Primary - originate within brain substances
- Extracerebral - originate outside substances of brain but are part of CNS
- Metastatic (secondary) - originate from an organ outside of the brain but travel to brain
- Clinical Manifestations:
- Seizures, visual disturbances, unstable gait Astrocytes - ANSWERSstar shaped cells that surrounds blood vessels in brain
- Fill spaces between neurons
- Aid in synaptic function
- Aid in blood flow to BBB Astrocytoma - ANSWERS(type of brain cancer) common primary glioma of CNS
- Grade 1-2 = slow growing
- Grade 3-4 = malignant
- S/S: headache, behavioural changes, increased ICP → increased symptoms Meningioma - ANSWERSbenign/slow growing primary extracerebral tumour that originates from the meninges
- Clinical Manifestations present once the tumour is large → focal seizures Spinal Cord Tumour - ANSWERSrare tumour growth that develops within neural tissue (intramedullary) or outside the spinal cord (extramedullary)
- S/S: pain, paresthesias, impaired sensation, cramping, fasciculation, absent tendon reflexes Cerebral Vascular Accidents (CVA) - Stroke - ANSWERSocclusion of cerebral artery leading to impairment of cerebral circulation
- Result of: hemorrhagic (cerebral haemorrhage) and Ischemic (TIA/thrombotic/embolic/lacunar)
- Risk Factors:
- HTN (greatest risk), atherosclerosis, diabetes, smoking, high cholesterol levels, high sodium intake, atrial fibrillation, polycythemias, etc.) Transient Ischemia Attack (TIA) - ANSWERStransient episode of neurological dysfunction (lasts less than 1 hour)
- Result of focal cerebral ischemia
- Sudden focal loss of neurologic function
- S/S: weakness, confusion, loss of balance, visual disturbances, sudden headache
- Warning sign of an impending stroke
- Cause:
- Carotid plaque Intracranial Aneurysm - ANSWERSweak, bulging areas of arterial vessel walls
- Due to arteriosclerosis, trauma and inflammation
- Can be unilateral or bilateral Arteriovenous Malformation - ANSWERSrare congenital lesions that can cause hemorrhagic strokes
- Clinical Manifestations:
- Headache, possible seizure disorder, intracerebral bleeding Subarachnoid Hemorrhage - ANSWERSblood escapes from injured vasculature into the subarachnoid space
- Cerebral blood flow and perfusion decrease
- Blood irritates meninges and other neural tissue
- Risk Factors:
- Intracranial aneurysms, AVM, HT, head injuries
- Clinical Manifestations:
- Explosive headache, transient changes to LOC, nausea/vomiting, stiff neck, photophobia, low grade fever, positive kernig & brudzinski sign Migraine - ANSWERSmoderate to severe headaches lasting from 4 hours to 3 days Clinical Phase of Migraine - ANSWERS1. Premonitory Phase - can occur hours to days before the headache onset
- May experience neck pain, tiredness, irritability, food cravings
- Migraine Aura - can last one hour or longer; present as visual or sensory (not all experience aura)
- Headache Phase - symptoms may last from 4-72 hours (throbbing pain spreading to entire head, fatigue, nausea, vomiting)
- Recovery Phase - can occur from several hours to days (irritability, fatigue or depression) Cluster Headache - ANSWERSextremely painful headaches for a period of days and in short durations (most common in men)
- Clinical Manifestations:
- Severe unilateral tearing/burning, pain around one eye or temporal pain, pain lasting 30 mins - 2 hours, drooping eyelid, nasal congestion Tension Type Headache - ANSWERSmild to moderate headaches causing sensation of pressure around the head that may last several hours or days
- Most prevalent type of headache
- Not aggravated by physical activity
- Can be due to stress, anxiety, poor posture Meningitis - ANSWERSinflammation of the meninges of the brain & spinal cord caused by either a bacteria, virus or fungi Encephalitis - ANSWERSinflammation of the brain due to viral infection from mosquitoes, ticks or live vaccination
- Affects meninges & degenerates nerve cells
- S/S: increased ICP, headache, nausea, vomiting, fever, delirium, seizures, paresis, paralysis Lyme Disease - ANSWERSbacterial infection in the CNS & PNS spread through a tick bite Stages of Lyme Disease - ANSWERS- Stage 1 - bulls-eye red rash with circular margins
- S/S = flu-like symptoms, fever
- Stage 2 - disseminated infection
- S/S = redness, myalgias, arthralgias, headache, meningeal inflammation, neuritis
- Stage 3 - chronic stage (late persistent infection)
- S/S = arthritis, encephalitis, parasthesias, heart failure Multiple Sclerosis - ANSWERSchronic inflammatory disease which causes degeneration of myelin, scarring & loss of axons
- Autoimmune response
- Unknown cause
- Clinical Manifestations:
- Parasthesias face/trunk/limbs, impaired vision, inflammation/swelling of optic disc, stiffness/slowness/weakness in muscles, impaired gait, bowel/bladder incontinence
Guillain Barre Syndrome - ANSWERSautoimmune disorder triggered by a preceding bacterial or viral infection, in which the immune system attacks healthy nerve cells in the PNS
- Recovery can occur over weeks to years depending on level of cell body damage
- Clinical Manifestations:
- Numbness, pain, parasthesias, weakness of limb, may experience paralysis of limbs/respiratory muscles, facial weakness affecting swallowing/chewing/coughing Amytrophic Lateral Sclerosis (ALS) - ANSWERSprogressive degenerative disorder or upper & lower motor neurons
- Cause of death = progressive muscle weakness leading to respiratory failure (no cure)
- Death of neurons, axon degeneration and demyelination
- Clinical Manifestations:
- Affects coordination/speech/swallowing, hypotonia, muscle paresis, loss of diaphragm control, does not affect thought or cognition Syndrome of Inappropriate Antidiuretic Hormones (SIADH) - ANSWERScondition in which the body makes too much ADH
- Causes:
- Ectopic secretion by tumour cells, CNS disorders, Pulmonary disorders, medications
- Clinical Manifestations:
- Thirst, loss of appetite, SOBOE, fatigue, abdomen cramps, vomiting, confusion, lethargy, seizures Diabetes Insipidus (DI) - ANSWERSinsufficiency of ADH that either leads to polyuria (frequent urination) or polydipsia (frequent drinking) - results in the decreased ability to concentrate urine Two Types of Diabetes Insipidus - ANSWERS1. Neurogenic Diabetes Inspidus: most common form, insufficient amounts of ADH, and has an abrupt onset
- Causes:
- Tumours, lesions, aneurysms, infections
- Nephrogenic Diabetes Insipidus: renal tubules does not respond to ADH, has a gradual onset, and can be classified as either acquired or genetic
- Causes:
- Disorders/drugs that affect the renal tubule Type 1 Diabetes Mellitus - ANSWERSautoimmune destruction of pancreatic islet cells (beta cells) - chronic inflammatory response occurs which results in the further destruction of beta cells; absolute insulin deficiency
- 10% of people have type 1 diabetes (under 12 years old)
- Clinical Manifestations:
- Polyuria, polydipsia, weight loss, fatigue, nocturia (excessive urination at night)
- Treatment:
- Control of blood glucose levels, exogenous insulin via injection/pump Type 2 Diabetes Mellitus - ANSWERSresistance to insulin in the peripheral tissues (decreased use of insulin)
- 90% of people have type 2 diabetes
- Risk Factors:
- Obesity, age, physical inactivity, family history, hypertension
- Clinical Manifestations:
- Symptoms are insidious - may present with polydipsia, polyuria, recurrent infections What are some acute complications of diabetes? - ANSWERS- Hypoglycemia, diabetic ketoacidosis (DKA type 1), hyperglycemic hyperosmolar nonketotic syndrome (HHNKS type 2) What are some chronic complications of diabetes? - ANSWERS- Microvascular, diabetic retinopathy, diabetic neuropathy, nephropathy, distal symmetric polyneuropathy, macrovascular Somogyi Effect - ANSWERSlow blood glucose during the night caused by counterregulatory hormones Dawn Phenomenon - ANSWERShigh blood sugar levels early in the morning caused by nocturnal elevations in growth hormone Hyperthyroidism (Grave's Disease) - ANSWERSexcessive stimulation of T3 and T resulting to increased metabolic rate and decreased TSH levels
- Clinical Manifestations:
- Weight loss, mood changes, increased appetite, increased sweating, heat intolerance, exophthalamus, restless, goiter Hypothyroidism - ANSWERSlow amount of T3 and T4 produced resulting to increased amounts of TSH Three Types of Hypothyroidism - ANSWERS1. Primary Hypothyroidism - (most prevalent) loss of functional thyroid tissue
- Autoimmunity (Hashimoto's) - T cells destroys pituitary gland
- Iatrogenic
- Iodine Deficiency
- Congenital Hypothyroidism (Cretinism) - thyroid deficiency (absent) present at birth
- TH needed for brain development; symptoms may not evident until 4 months old
- Clinical Manifestations:
- Fatigue, cold intolerance, weight gain, severe constipation, bradycardia, goiter, myxedema
- Myxedema Coma: severe form of hypothyroidism (medical emergency)
- Clinical Manifestations:
- Bradycardia, hypothermia, hypotension, hypoventilation, hypoglycaemia, altered LOC Cushing's Disease - ANSWERSoverproduction of ACTH causing increased cortisol, glucocorticoids, mineralcorticoids and androgens
- S/S: weight gain (moon face, buffalo hump, truncal obesity), hyperglycemia (diabetes mellitus), arrhythmias/hypertension, hirsutism, osteoporosis, increased risk for infections, weak skin (striae), muscle weakness Addison's Disease - ANSWERShypoactivity of the adrenal gland
- Primary = autoimmune (most common)
- Secondary = prolonged admin of exogenous glucocorticoids
- Clinical Manifestations:
- Hypoglycaemia, weakness, fatigue, hyperpigmentation (tanned skin), hypotension, arrhythmias, poor stress response (no cortisol), decreased hair growth Anemia - ANSWERSa deficient number or concentration of erythrocytes (RBCs) causing blood to not carry as much O2 as required
- Clinical Manifestations:
- Fatigue/weakness, SOBOE, dizziness/fainting, pallor (skin, mucous membranes, nails), increased heart rate and palpitations Iron Deficiency Anemia - ANSWERSinsufficient iron in the blood decreasing hemoglobin production
- Cells are microcytic and hypochromic
- Clinical Manifestations:
- Weakness/fatigue, pallor (earlobes, palms), SOB, stomatitis, fingernails brittle and concave
- Treatment:
- Change diet to include Fe rich foods, iron supplements for 2 years, blood transfusion Three Stages of Iron Deficiency Anemia - ANSWERS1. Body iron stores are depleted
- Iron transport to bone marrow is decreased leading to iron deficient erythropoiesis
- Small Hb deficient cells center circulation
Folate Deficiency Anemia - ANSWERSlack of folic acid in the blood leading to Megaloblastic Anemia (decreased rate of RBC production)
- Cells are macrocytic and normochromic
- Clinical Manifestations:
- Severe cheliosis, stomatitis, painful mouth ulcers, dysphagia, diarrhea
- Treatment:
- Oral folate administration, increase folate in diet Pernicious Anemia - ANSWERSdecrease in RBCs that occurs when the intestines cannot properly absorb vitamin B12. (More common in females)
- Clinical Manifestations:
- Pallor, lethargy/fatigue, nausea/vomiting, stomatitis, loss of appetite, abdominal pain, dyspnea, parasthesia
- Treatment:
- Oral vitamin B12 or B12 injections (lifelong), diet with increased B12 and folic acid Aplastic Anemia - ANSWERSbody stops producing enough new blood cells (damage to bone marrow erythropoiesis)
- Cells are normocytic and normochromic
- Primary = (idiopathic) 75% of all cases
- Secondary = chemical agents (15% of cases)
- Clinical Manifestations (are insidious):
- Petichiae, ecchymosis (bruising), pallor, weakness, infections, SOB, arrhythmias
- Treatment:
- Blood transfusions, bone marrow transplant, medications to stimulate bone marrow, suppress immune system and prevent/treat infections Anemia of Chronic Disease - ANSWERSanemia that affects people who have chronic diseases (AIDS, rheumatoid arthritis, lupus, chronic renal failure) that cause inflammation
- Develops after 1-2 months of disease activity
- Cells are normocytic and normochromic Sickle Cell Anemia - ANSWERSinherited disease from both parents resulting in a distorted sickled shape of the haemoglobin when exposed to low oxygen
- Cells are normocytic and normochromic
- Clinical Manifestations:
- Pallor, jaundice, fatigue, pain, swelling of extremities, dyspnea, risk for infections
Posthemorrhagic Anemia - ANSWERScondition in which a person quickly loses a large volume of circulating hemoglobin Hemolytic Anemia - ANSWERSdisorder in which RBCs are destroyed faster than they can be made Polycythemia Vera - ANSWERSslow-growing blood cancer in which your bone marrow makes too many RBCs, WBC and platelets (stem cell disorder)
- Clinical Manifestations:
- Enlarged spleen → abdominal pain, hypercoagulability → thrombosis & occlusion, plethora, hypertension (risk for angina), hepatomegaly (portal hypertension) Leukocytosis - ANSWERSincreased number of WBCs, especially during an infection Leukopenia - ANSWERSdecreased number of WBCs (leukocytes) Granulocytosis - ANSWERSincreased number of granulocytes in the peripheral blood Neutrophilia - ANSWERSincrease in circulating neutrophils above the expected in a healthy individual ( > 7.5 x 109/L) Neutropenia - ANSWERSlow concentration of neutrophils in the blood Granulocytopenia - ANSWERSdecrease of peripheral blood granulocytes below lower limit of normal range ( < 0.5 x 109/L) Arganulocytosis - ANSWERSserious/life threatening condition where the absolute neutrophil count is less than 100 per microliter of blood Eosinophilia - ANSWERSincrease number of eosinophil's in the blood, occurring in response to some allergens, drugs, and parasites Eosinopenia - ANSWERSlow number of eosinophil (eosinopenia can be a predictor of bacterial infection, and induced by stress reactions, cushing's syndrome or use of steroids Basophilia - ANSWERScondition of having greater than 100 basophils/microliter in the peripheral blood Basopenia - ANSWERSlow level of basophils (may be caused by infections, severe allergies or an overactive thyroid gland) Monocytosis - ANSWERSincrease number of monocytes circulating in the blood (monocytes are WBCs that give rise to macrophages and dendritic cells in the immune system)
Monocytopenia - ANSWERSlow levels of monocytes Lymphocytosis - ANSWERShigh amounts of lymphocytes Lymphocytopenia - ANSWERSabnormally low levels of lymphocytes in the blood Infectious Mononucleosis - ANSWERSacute self-limiting viral infection of B lymphocytes caused by Epstein-Barr Virus (EBV) - herpes viruses
- Transmitted by saliva or other mucosal secretions
- Clinical Manifestations:
- Sore throat, fever, malaise, joint pain, lymphadenopathy, thick exudate in pharynx, fatigue Acute Leukemia - ANSWERScreates undifferentiated/immature cells resulting in overcrowding in the bone marrow
- Abrupt onset; short survival time
- Clinical Manifestations:
- Fatigue (anemia), bleeding (thrombocytopenia - bruising), fever, infection, weight loss/anorexia, lymphadenopathy Chronic Leukemia - ANSWERScells are more differentiated but have impaired function
- Slow onset; longer life expectancy
- Clinical Manifestations:
- Fatigue (anemia), bleeding (thrombocytopenia - bruising), fever, infection, weight loss/anorexia, lymphadenopathy Leukemia - ANSWERScancer of the body's blood-forming tissues (bone marrow and lymphatic system)
- Uncontrolled proliferation in the bone marrow
- Unknown cause Multiple Myeloma - ANSWERSmalignant cancer that forms in a plasma cell causing cancer cells to accumulate in the bone marrow and decreases antibody production Malignant Lymphoma - ANSWERSspread of cancer in the body's lymphatic system Lymphoma - ANSWERSmalignant tumour of the lymphoid tissues
- Based on cells involved - B cell neoplasms, T cell/NK cell neoplasms, Hodgkins/Non- Hodgkins Hodgkin's Lymphoma - ANSWERSmalignant lymphoma that progresses from one lymph node to another
- Presence of Reed-Sternberg cells (infected with EBV) Non-Hodgkin's Lymphoma - ANSWERStumours developing from the lymphocytes
- Lacks Reed-Sternberg cells
- Proliferation of B or T or NK cell neoplasms that become immortal
- Caused by chromosomal translocations
- Affects middle age > 50 years old Thrombocytopenia - ANSWERSdecreased platelets in circulation due to decreased production of platelets or increased consumption (most common) Immune Thrombocytopenia (ITP) - ANSWERSmost common type of thrombocytopenia Acute Immune Thrombocytopenia - ANSWERSlarge amounts of antigens in blood that leads to formation of immune complexes which binds to platelets and destroyed by the spleen ➢ Affects children; lasts 1-2 months ➢ Treatment: o Self limiting once source of the antigen is resolved Chronic Immune Thrombocytopenia - ANSWERSantibody mediated destruction of platelet antigens (Type 2 hypersensitivity) ➢ Affects adults ➢ Treatment: o Treatment is palliative not curative, goal to prevent platelet destruction, medications used include glucocorticoids, splenectomy Thrombocythemia - ANSWERSincreased platelet count Vitamin K - ANSWERSessential for production of clotting factors VII/IX/X and prothrombin (coagulation)
- Synthesized in the large intestine and obtained through diet Disseminated Intravascular Coagulation (DIC) - ANSWERSunregulated release of thrombin & fibrin formation at the same time → bleeding and clotting
- May lead to organ failure
- Diagnosis:
- Protein fragment from the breakdown of blood clot (via D-dimer test) - Protein not present in blood until coagulation is activated
- Treatment:
- Eliminate underlying condition, control ongoing thrombosis, maintain organ function
Thrombus - ANSWERSblood clot that forms and remains in a vessel Emboli - ANSWERSblood clot lodged in a blood vessel and blocks the flow of blood in that location depriving tissues of normal blood flow and oxygen Chronic Venous Insufficiency - ANSWERScondition when the venous wall/valves in the leg are not working effectively, making it difficult for blood to return to the heart from the legs (cause blood to pool - stasis and tissue hypoxia) Deep Vein Thrombosis (DVT) - ANSWERSclot formation in the large veins of the lower extremities
- Untreated DVT will increase the risk of thromboembolization Hypertension - ANSWERSelevated blood pressure ( > 140/90)
- Primary (essential) Hypertension - multifactorial disease; increase peripheral resistance & blood volume. No known cause
- Risk factors: family history, age, gender, race, dietary sodium, smoking, obesity, ETOH consumption
- Secondary Hypertension - secondary to underlying disease process or other. Direct cause identified
- Causes: renal/endocrine/vascular disorders, pregnancy, medications (BCP/corticosteroids/antihistamines)
- Malignant Hypertension - rapidly progressive (diastolic > 140 mm/Hg)
- Results in - encephalopathy, cerebral edema, organ damage Orthostatic Hypotension - ANSWERSdecrease in BP within 3 minutes of moving or standing
- Results in blood pooling and low arterial pressure
- Causes:
- Medications, prolonged immobility, dehydration, venous pooling (pregnancy/varicosities)
- S/S: dizziness, blurring or vision loss, syncope Aneurysm - ANSWERSlocalized dilation or outpouching of a vessel wall & can occur in any blood vessels
- Occur due to arteriosclerosis or hypertension
- Most commonly occur in the thoracic or aortic abdominal area True Aneurysm - ANSWERSinvolves all layers of the arterial wall resulting in weakening of the vessel wall (can be fusiform or saccular)
False Aneurysm - ANSWERS(pseudoaneurysm) collection of blood leaking from an artery or vein that is contained by surrounding tissue - extravascular hematoma Aortic Aneurysm - ANSWERSabnormal bulge that occurs in the wall of the aorta - typically asymptomatic until rupture
- S/S with rupture: severe pain and hypotension Arterial Thrombus Formation - ANSWERSany condition (atherosclerosis, aneurysms, endocarditis, septic shock, inflammation, injury) that activates the coagulation cascade
- Thrombus can occlude artery → ischemia in tissues supplied by artery
- Thrombus can dislodge → thromboembolism
- Risk Factors = cigarette smoking, obesity, hypertension, sedentary lifestyle, dyslipidemia, diabetes Myocardial Ischemia - ANSWERSoccurs when blood flow to your heart is reduced, preventing the heart muscle from receiving enough oxygen
- Imbalance between coronary supply & myocardial demand
- Causes: tachycardia, exercise, hypertension, hypertrophy, coronary spasm, dysrhythmias, atherosclerotic plaques (most common cause)
- Clinical Manifestation
- Angina Acute Coronary Syndrome - ANSWERStotal obstruction of one/more coronary arteries, which decreases O2 to the heart (irreversible hypoxic injury) leading to myocardial cell death
- STEMI - transmural infarct (full thickness) with complete blockage of a coronary artery
- NSTEMI - partial thickness infarct; non-occlusive; can lead to serious heart damage
- Clinical Manifestations:
- Persistent chest pain, pallor, diaphoresis, nausea/vomiting, rapid pulse
- Complications: dysrhythmias, organic brain syndrome Stable Angina - ANSWERS(angina pectoris) gradual narrowing/hardening of arterial walls Unstable Angina - ANSWERS(dangerous type of angina) signals the atherosclerotic plaque has ruptured → sign of an impending infarction
Prinzmetal Angina - ANSWERS(vasospastic) unpredictable transient ischemia occurring at rest (occurs with or without atherosclerosis) Types of Embolism - ANSWERS1. Venous/Arterial Thromboembolism - vascular obstruction from a dislodged thrombus
- Can be associated with abnormal rhythms (A-fib or A-flutter)
- Air Embolism - blood vessel blockage caused by one or more bubbles of air/gas in the circulatory system
- Fat Embolism - piece of intravascular fat that lodges within a blood vessel and causes a blockage of blood flow. Most commonly occurs after fractures to the long bones of the lower body (femur/tibia/pelvis) Atherosclerosis - ANSWERSinflammatory disease in which plaque builds up inside the arteries (hardening/thickening of vessels) due to high cholesterol levels and the accumulation of lipid-laden macrophages
- Results in ischemia
- Leading cause of CAD & CVD (high risk for heart attack and stroke) Coronary Artery Disease - ANSWERSoccluded coronary arteries most commonly caused by atherosclerosis
- Leads to low blood supply of myocardial cells → ischemia
- Complete occlusion of artery → infarction Silet Angina - ANSWERSsymptoms do not present; can be due to stress; more common in women Pericarditis - ANSWERSinflammation of the pericardium due to an infection that commonly occurs after MI
- Clinical Manifestations:
- Fever, severe chest pain that increases with respiration, restlessness, friction rub Pericardial Effusion - ANSWERSaccumulation of fluid in pericardial cavity due to pericarditis Pericardial Tamponade - ANSWERSinterferes with right atrium filling leading to decreased ventricle filling which results in right side heart failure Cardiomyopathy - ANSWERSdisease of the heart muscle that makes it harder for the heart to pump blood to the rest of the body leading to heart failure Types of Cardiomyopathy - ANSWERS- Dilated Cardiomyopathy (DCM): condition in which the heart's ability to pump blood is decreased due to an enlarged/weakened left ventricle
- Hypertrophic Cardiomyopathy (HCM): disease in which the heart muscle (myocardium) becomes abnormally thick making it harder to pump blood
- Restrictive Cardiomyopathy (RCM): wall of the heart becomes rigid, restricting the heart from stretching and filling with blood properly Aortic Stenosis - ANSWERS(most common abnormality) narrowing of the aortic valve opening, which restricts blood flow from the left ventricle to the aorta
- Due to congenital, aging and rheumatic heart disease Mitral Stenosis - ANSWERSnarrowing of the mitral valve opening that blocks blood flow from the left atrium to the left ventricle Aortic Regurgitation - ANSWERSdiastolic flow of blood from the aorta into the left ventricle Mitral Regurgitation - ANSWERSleakage of blood backward through the mitral valve each time the left ventricle contracts Heart Failure - ANSWERSimpaired pumping capacity of the heart resulting in a build up of blood and fluids within the organs and tissues → decreased perfusion of tissues Left Heart Failure - ANSWERSany condition that impairs left ventricle pumping or increases the workload of the left ventricle (hypertension, myocardial ischemia, valvular disorders)
- Systolic Failure - loss of contractible ability (ventricle contracts poorly & empties incompletely)
- Diastolic Failure - stiffness of the ventricles & loss of relaxation (impairs ability to fill with blood between contractions)
- Clinical Manifestations:
- Dyspnea, orthopnea, cyanosis, frothy sputum, fatigue, cough, pulmonary edema, hypertension Right Heart Failure - ANSWERSinability of right ventricle to move deoxygenated blood forward in pulmonary circulation resulting in backward movement of blood into systematic circulation
- Results from left side heart failure
- Clinical Manifestations:
- Peripheral edema, hepatosplenomeagly, ascites, weight gain, JVD Sinus Bradycardia - ANSWERSslow heartbeat of less than 60 beats per minute
Simple Sinus Tachycardia - ANSWERSfaster than normal heart rate of over 100 beats per minute Tricuspid Regurgitation - ANSWERSdisorder in which the tricuspid valve does not close tight enough which causes blood to flow backwards into the right atrium when the right ventricle contracts Mitral Valve Prolapse Syndrome - ANSWERScondition in which the two valves flaps of the mitral valve does not close smoothly or evenly but instead, bulges (prolapse) upward into the left atrium
- Most common in young women
- Regurgitant murmur
- Asymptomatic and does not require medical management Rheumatic Fever - ANSWERSinflammatory disease that can develop when strep throat or scarlet fever isn't properly treated (can affect the heart, joints, brain and skin) Infective Endocarditis - ANSWERSinfection and inflammation of the endocardium
- Bacterial infection caused by staph or streptococcus that results in vegetation's
- Vegetation's accelerate fibrin formation and activate the clotting cascade Atrial Fibtrillation - ANSWERSabnormal heart rhythm characterized by rapid and irregular beating of the atrial chambers Ventricular Fibrillation - ANSWERSrapid heart beat and erratic electrical impulses causing the ventricles to quiver uselessly, instead of pumping blood Shock - ANSWERSoccurs when the CV system is unable to maintain perfusion to tissues, cells and organs resulting in impairment of cell metabolism, tissue function, low O2 & nutrient delivery and low waste removal
- Shock affect O2 delivery and glucose
- Can progress to organ failure & death Cardiogenic Shock - ANSWERSinadequate or ineffective cardiac pumping resulting in decreased blood flow to tissues and organs
- Heart contractility is ineffective → decreased cardiac output Hypovolemic Shock - ANSWERSmedical emergency in which severe blood/fluid loss makes the heart unable to pump enough blood to the body (organs may stop working) Septic Shock - ANSWERSdangerous and life threatening condition that occurs when sepsis results of an infection
- Begins with systemic inflammatory response syndrome which then releases chemical mediators
- Triggered by either a gram (+) or gram (-) bacteria
Multiple Organ Dysfunction Syndrome (MODS) - ANSWERSprogressive dysfunction of 2 more organ systems due to an uncontrollable inflammatory response to a severe illness or injury
- Most common cause is sepsis & shock
- Initial organ injury that results in ischemia or decreased perfusion Neurogenic Shock - ANSWERS(vasogenic shock) imbalance between SNS and PNS resulting in massive vasodilation
- Rare form of shock
- Trauma to spinal cord results in sudden loss of autonomic & motor reflexes Anaphylactic Shock - ANSWERSwidespread hypersensitivity to an allergen (15 mins before you see symptoms)
- Results in vasodilation, peripheral pooling and relative hypovolemia
- Severe shock symptoms developing rapidly