226 Notes PDF

lOMoARcPSD|30352485 WEEK 1: ENDOCRINE & DIABETES Physiology: ​fatty acids can’t cross BBB so brain has to use glucose, w/o glucose body breaks fatty acids into ketones which can cause acidosis, glucose can pass easily into BBB without insulin but other cells need insulin to transport glucose inside...

lOMoARcPSD|30352485 WEEK 1: ENDOCRINE & DIABETES Physiology: ​fatty acids can’t cross BBB so brain has to use glucose, w/o glucose body breaks fatty acids into ketones which can cause acidosis, glucose can pass easily into BBB without insulin but other cells need insulin to transport glucose inside ● Liver ​stores glucose as glycogen, converts products to glucose to store as glycogen, breaks down glycogen releasing glucose into blood, fat catabolized into glycerol, protein into amino acids, aerobic carbs into glucose, anaerobic carbs into lactic acid ● Pancreas ​around stomach & small intestine, Islet’s of Langerhan cells, alpha produce glucagon and beta produce insulin, delta creates growth hormone inhibiting hormone (somatostatin) ○ Insulin usually blocks ketone production ○ Somatostatin: blocks insulin and glucagon secretion, promotes lipolysis of adipose tissue, decreases glucose uptake in muscles resulting in increased BGL ● Hypothalamus: ​small, central region of brain, various functions,​ ​link between endocrine & nervous system (main function is homeostasis), produces releasing & inhibiting hormones including corticotropin-releasing hormone, dopamine, GHRH, somatostatin, gonadotropin releasing hormone, thyrotropin releasing hormone ● Pituitary gland: ​behind hypothalamus, master gland as hormones it produces control so many different bodily processes, senses body’s needs and sends signals to organs and glands throughout body to regulate function, secretes essential hormones (GH, ACTH, FSH, LH, TSH, prolactin (PRL)) ● Thyroid gland: ​anterior region of neck below Adam’s apple, produces thyroxine, triiodothyronine, calcitonin, regulates iodine and calcium, main function is to produce thyroxine & triiodothyronine (regulate metabolism, growth, temperature, energy) ● Parathyroid gland: ​4 small glands around/behind thyroid, continuously monitor and regulate blood calcium, releases PTH, affects bones & kidneys, maintains blood calcium ● Adrenal gland: ​on top of kidneys, produce glucocorticoids, mineralocorticoids (aldosterone), cortisol, fight or flight hormones ○ Adrenal medulla: ​adrenaline & noradrenaline, increases BP, HR, pupil dilation, ​pheochromocytoma​ is a rare, non-cancerous tumour that develops in adrenal gland​, can cause panic attacks when agitated, glucagon causes it to release vast amounts of adrenaline resulting in​ adrenal crisis ○ ○ Adrenal cortex: ​aldosterone, cortisol Addison’s disease: ​adrenal glands ​don’t produce enough cortisol​ and sometimes aldosterone, weight loss, muscle weakness, hypotension, sometimes dark skin ○ Cushing’s disease:​ ​hypercortisolism, may be due to tumor or excess growth of pituitary gland causing too much ACTH therefore excess cortisol release from adrenal glands, most commonly due to use of steroid drugs ○ Aldosterone: ​main mineralocorticoid produced by adrenal cortex, essential for sodium conservation in kidney, causes an increase in salt and water resorption into bloodstream ● ● ● ● Gluconeogenesis: ​glucose from fats / proteins Glycolysis: ​breakdown of glucose for energy Glycogenesis: ​convert excess glucose to glycogen for storage Glycogenolysis: ​breakdown of stored glycogen for glucose lOMoARcPSD|30352485 Pathophysiology Hypoglycemia: 1. Glucagon and adrenaline travel through liver > convert glycogen > increase BGL (RAPIDLY RAISE BGL) 2. GH released > increases lipolysis of fat into glycerol > travels to liver > gluconeogenesis into glucose, GH also decreases glucose uptake by muscles (SLOWLY RAISE BGL) 3. Cortisol released from adrenal medulla > increases lipolysis > increased glycerol > gluconeogenesis > increased BGL, cortisol also catabolizes muscle to create AA in severe starvation, AA’s travel to liver and undergo gluconeogenesis (SLOWLY RAISE BGL) 4. Thyroxine can also increase intestinal absorption of carbohydrates to raise BGL Hyperglycemia: 1. Pancreas releases insulin 2. Thyroid hormones increase metabolism (thyroxine, triiodothyronine) T1DM: ​autoimmune, immune cells attack beta producing cells of pancreas, little or no insulin, children & young people, need daily insulin injections or lethal, ​polydipsia, blurred vision, bedwetting, polyuria, lethargy, polyphagia, sudden weight loss T2DM: ​initial inability to respond to insulin (resistance), hormone is ineffective so more is produced, develops over time, inadequate production can result due to failure of pancreatic cells to keep up with demand, usually starts in adulthood, ​less dramatic presentation, may be asymptomatic, can lead to retinopathy, lower-limb ulcers that fail to heal, common oral pharmacology: acarbose, metformin, sulphonylureas, glitazones More likely to present first thing in morning after not eating overnight and taking insulin or using up glucose stores = hypoglycemic Gestational diabetes: ​diagnosed for first time during pregnancy, affects how body uses sugar, causes high BSL that can affect pregnancy & baby, at higher risk of developing T2DM later in life, placenta produces hormones that cause glucose to build up in blood Hypoglycemia symptoms: ​shaky, sweating, confusion, irritability, anxious, tachycardia, dizzy, hungry Hyperglycemia symptoms: ​3 P’s, dry skin, n/v, abdominal pain, sweet breath, SOB, confusion, weakness Hyperglycemia and acidosis cause fluid and potassium to shift out of cells into blood circulation because H+ ions (acids) displace K, causes blood hyperkalemia, gradually diuresed then causing total body hypokalemia, affects heart Symptoms: ● Polyuria due to osmotic diuresis ● Polyphagia due to low intracellular glucose ● Polydipsia due to polyuria / dehydration ● Dryness, tachycardia, hypotension due to dehydration ● Weight loss due to dehydration lOMoARcPSD|30352485 ● Abdominal pain, nausea, vomiting due to hyperosmolar state ● Visual deficits due to hyperglycemic effect on CNS Inadequate perfusion for hyperglycemia: HR>100, BP<100 Hyperglycemic hyperosmolar nonketotic syndrome (HHNS) ● High BGL, no ketones b/c enough insulin in T2DM to suppress ketogenesis ● Pancreas worn out but still producing some insulin ● Can be caused by infection, illness, medication non-compliance ● Common to T2DM ● Hyperosmolar, blood full of sugar, body attempts to excrete it ● Usually occurs after period of hyperglycemia in which fluid intake is inadequate to prevent extreme dehydration due to osmotic diuresis ● Elderly ● BGL>50, BGL gets so high that fluid intake and excretion is increased ● 3 poly’s, hyperosmolarity, possible focal neuro deficits, delirium ● No ketotic smell, no kussmaul’s respirations ● Slower onset (days) Diabetic ketoacidosis (DKA) ● High BGL, ketones present ● Stimulates mitochondria to convert free fatty acids into ketones, normally insulin blocks ketone production but in DKA pts have no insulin ● 11-30 BGL ● Glucosuria leads to osmotic polyuria > cellular dehydration and sodium/potassium alterations ● Onset over hours ● Kussmauls’ respirations, acetone breath, 3 poly’s, ACS, dehydration, abdominal pain, nausea, vomiting ● Potassium imbalance, increased hydrogen ions in blood displace K+ ions, K+ lead to hyperkalemia, gradually diuresed resulting in total body hypokalemia, heart vulnerable to failure during Na/K balance disruption ● Occurs subsequent to stressed state e.g. infection, something that uses up glucose ● Absolute insulin deficiency ● Common to T1DM Ketones: ​can cross BBB barrier, strong organic acids that cause generalized acidosis, ketoacids break down into acetone (sweet breath odour) Thiamine: ​vitamin B1, helps cells turn carbs into energy Alcoholic ketoacidosis ● Not necessarily associated with insulin deficiency ● Chronic alcohol use and insufficient nutrition (alcohol + starvation) + dehydration - alcohol diminishes hepatic gluconeogenesis and leads to decreased insulin secretion (w/o insulin ketone production is not inhibited), increased lipolysis, impaired fatty acid oxidation and subsequent ketogenesis, counter-regulatory hormones increased and may further inhibit insulin secretion ● Euglycemic ● No three poly’s, ACS due to intoxication, abdominal pain ● Break down fats and proteins into glycerol and AA’s > converted to glucose ● Dehydration due to suppression of ADH by alcohol, vomiting also leads to dehydration ● Presents 1-2 days after binge drinking lOMoARcPSD|30352485 Acute pancreatitis: ​inflammatory disease of pancreas, abdominal pain in RUQ that may last for days and radiate to back, nausea, vomiting, tenderness, fever, tachycardia, pain worse after eating, generally mild, local & systemic complications, gallstone migration into bile duct and alcohol abuse most frequent causes, increased serum concentrations of amylase & lipase WEEK 2: TOXICOLOGY Management principles: ​histories unreliable, search for clues, always suspect polypharmacy, safety priority, airway protection, rx hypotension with fluid, seizures with benzos, misted cooling for hyperthermia, MICA etc. Autonomic nervous system toxidromes Cholinergic Produce, alter or release acetylcholine Examples: CNS depressants: anti-anxiety / muscle relaxants / antiepileptics / pre-anaesthetic meds Pharmacology: excess acetylcholine in synapse, constant stimulation, occurs by inactivating cholinesterase inhibitors Presentation: SLUUDGE: salivation, lacrimation, unresponsive, urinary incontinence, diaphoresis, GI upset, emesis + pinpoint pupils + fasciculations (muscle twitch Rx: anti-cholinerage e.g. pralidoxime (2-PAM), atropine for supraventricular bradycardias, has to be administered right away for toxic nerve agents but organophosphates have longer window, fluid Anticholinergic Block acetylcholine​ (aCH binds to muscarinic or nicotinic receptors) Examples: antipsychotics, antispasmodics, cyclic antidepressants, antihistamines, sleep aids, cold preparations Pharmacology: block effects of acetylcholine through too much binding blocking parasympathetic side, SNS more dominant Presentation: ● Mad as a hatter: hats used to have mercury to cure felts causing confusion when they enter skin ● Blind as a bat: dilated pupils ● Dry as a bone: blocked salivary & sweat glands ● Red as a beet: due to hyperthermia ● Hot as a desert: blocked sweat glands ● Full as a flask: urethral sphincter unable to open, no urination Rx: prepare for seizures, take any plants or pills with you for analysis Over-the-counter drugs Paracetamol / panadol Analgesic, most common OD Hepatotoxicity likely to occur with single ingestion > 250mg/kg or greater than 12g in 24 hours, nearly all pts with >350mg/kg develop severe liver toxicity, absorbed in stomach/colon/small intestine GI upset, minor hematemesis or completely asymptomatic for 24 hrs (toxic time bomb) Rx: n-acetylcysteine if given within 8 hours Aspirin (acetylsalicylic acid) Commonly in pain relief creams, rapidly absorbed through stomach, used as wart remover Weak acid, damaging, travels through BBB to affect CNS, fatal after 10-30g in adults and 3g in children Progressive onset (maybe not evidence after 6-12hrs), nausea, vomiting, diarrhoea, tinnitus (ringing in ears), hyperventilation, respiratory alkalosis (from hyperventilation) metabolic acidosis, ACS, rapid deterioration Rx: supportive measures, dextrose for pts w/ ACS lOMoARcPSD|30352485 NSAIDS For musculoskeletal pain and fever Difficult to OD on NSAIDS other than ASA, below 100mg/kg unlikely, severe clinical toxicity at >400mg/kg Presentation non-specific, depends on pts condition Poisons Paraquat Dermal exposure limited injury, high fatality with ingestion, causes toxic reactions to many parts of body, concentrates in cells, hyperoxia can intensify damage >30mL (a mouthful or two) of 20-24% concentrate is lethal, 10mL can cause significant illness Painful mouth, pain w/ swallowing, nausea, vomiting, abdominal pain, respiratory complaints indicate systemic poisoning, heart/kidney/liver failure Rx: remove clothing, don’t touch, soap & water, monitor RR and SpO2, avoid O2 unless hypoxic, ACS rare to explore other causes Cyanide Binds to tissue, affects cytochrome oxidase, interferes with oxygen use, blocks ETC, can’t recharge ATP aerobically, cellular hypoxia especially in CNS Fires, ingestion or exposure to sodium nitroprusside Presentation depends on route/duration/exposure, CNS and cardiovascular dysfunction Rx: full PPE, high flow O2 regardless of SpO2, hydroxocobalain (B12) directly binds with cyanide and resultant molecule is inert Carbon monoxide Odorless, tasteless, colorless, non-irritating gas formed by incomplete hydrocarbon combustion, heating systems, fuel burning devices, kerosene heaters, charcoal grills, camping stoves, gas powered electrical generators, motor vehicles in poorly ventilated areas (all poorly functioning), underground electrical cable fires produce CO which seeps into buildings & homes Binds to Hb with 240x affinity, impaired O2 tx & utilization Silent killer, variable & non-specific presentation, all people in household who complain of similar symptoms suggests CO, ventilate building & find source, moderate: intoxicated symptoms, headache, malaise, nausea, dizzy, severe: neurologic symptoms, seizures, syncope, coma, cardiovascular/metabolic manifestations Rx: remove from environment, high flow O2 (SpO2 inaccurate), ECG to rule out myocardial ischemia, hyperbaric oxygen (tx to appropriate hospital) Psychodepressants Alcohol Also in mouthwash, perfume, cocaine extracts, OTC meds Enhances and inhibits various NT’s: euphoria, lowered social inhibitions, decreasing LOC in OD, increases GABA (inhibitory NT), LT effects: ataxia, peripheral neuropathy, easy bruising, abnormal heart rate & rhythm, heart failure, HTP, liver damage, hepatitis, esophageal variances, confusion, loss of coordination, depression Also consider head trauma, hypoglycemia, hypothermia, co-poisonings etc. ● BAC 0.01-0.10: euphoria, mild coordination deficits ● BAC 0.10-0.20: coordination & psychomotor deficits, decreased attention, ataxia, slurred speech, mood changes ● BAC 0.20-0.30: lack of coordination, incoherent thoughts, confusion, nausea, vomiting ● >0.030: stupor, LOC, coma, respiratory depression, lethal Rx: ensure euglycemia, airway mx, investigate other injuries/toxins, benzos to sedate if violent Opioids Work at opioid receptors, opioids come from opium poppy plant, for pain relief Narcotics​ = drugs such as opiates or oxycodone which can relief pain Morphine, heroin, fentanyl, codeine, oxycodone Interact at opioid receptors (g-coupled protein receptors which accept morphine as a ligand, receptors in CNS and GI tract), safe in short term, euphoria, pain relief Hypotension, respiratory depression, pinpoint pupils, sedation Rx: naloxone for narcotic OD: blocks opioid receptors preventing their activation by agonists, lasts just under an hour, limited adverse effects and no contraindications, monitor for re-sedation as half life of many opioids exceed naloxone, 0.4-2mg IV/IM/IN repeat prn for adults, slowly administer until pupils enlarge, get them stable but still relatively sedated going to hospital Sedative hypnotics Synthetic analogs = artificial compounds differing from natural compound in structure, resemblance and function CNS depression, slurred speech, ataxia, normal vitals except GHB, hallucinogens @ high doses, only benzos have an antidote 1. Benzos: ​fairly safe alone, relaxation, induces sleep, anticonvulsant, anti-anxiety, high addiction potential, OD rare, antidote = flumazenil (attach to GABA receptors on chloride ion channels in CNS increasing intracellular chloride making them negative and harder to fire) 2. GHB: ​synthetic analog of GABA, precursor to GABA/glutamate, OD leads to coma with abrupt onset and resolution, weak agonist at GABA receptor, reduces alcohol elimination rate 3. Ketamine: ​generally safe, can cause psychotic delirium, wide TI, hallucinogenic/dissociative effects as illicit drug, antagonist at acetylcholine receptors, facilitates GABA inhibition, antianxiety, muscle relaxant, anti-seizure lOMoARcPSD|30352485 Sympathomimetic toxicity (stimulates sympathetic nerves) (amphetamines, speed, cocaine, pseudoephedrine, ritalin, meth, MDMA): ​dilated pupils, hyperthermia, agitation, tachycardia, sweating, tremor, aggression Serotonin toxicity: from combining drugs that increase serotonin causing excess nerve cell activity, potentially life-threatening, ​hyperreflexia, increased muscle tone, hyperthermia, agitation, tachycardia, tremor, diaphoresis Alcohol withdrawal: ​lasts 2 hrs - 4 days from stopping drinking, symptoms include tremor, anxiety, headache, seizure, hallucinations, nausea WEEKS 3-5: ECG (see powerpoint) WEEK 6: CNS ASSESSMENT & CRANIAL NERVES 12 cranial nerves, sensory or motor or both, PNS components, connect brain to head/neck/trunk 1. smell 2. sight 3/4/6: eye movement (pupillary constriction) 5/7: face (sensory & motor) 8. hearing 9-12: swallowing, tongue, moving head Papilledema: ​serious medical condition where optic nerve at back of eye becomes swollen - visual disturbances, headaches, nausea, occurs with buildup of pressure in or around the brain causing optic nerve to swell Tracts ● Sensory ascending tract: sends sensory info to brain ● Pyramidal tracts: ​there are ​two,​ modulate ​facial movement, ​from brain to large voluntary muscles and ​control body movement ● Extrapyramidal tracts: ​control ​involuntary motor responses​, posture, walking, complicated movements in hands, there are ​several ○ EP symptoms: ​serious neurological symptoms due to antipsychotic medication, acute dystonia, akinesia, akathisia, tardive dyskinesia, can rx acute dystonic rxns with midazolam but otherwise we don’t treat these Acetylcholine: ​NT in motor axons in each muscle, broken down by acetylcholinesterase CNS assessment: ​AVPU, GCS, eyes, neck, movement ● Pain assessment:​ nail-bed pressure or trap squeeze ● GCS issues: ​components more important than actual score, same score predicts different TBI mortality depending on components, doesn't incorporate brain-stem reflexes, motor score doesn't factor in unilateral pathology, unreliable in pts in middle range 9-12, subject to language barriers, children, drugs/alcohol, variation in verbal scores, intubation, unvalidated in toxicology, ideal for bedside use in hospital to assess neurological functions, not TBI ● Memory:​ distant, recent and incident, retrograde amnesia is before incident and anterograde is after lOMoARcPSD|30352485 ● Dizziness/balance/falling = vertigo ● Pupil assessment: ​PEARL, do it in dark environment, miosis = constriction, mydriasis = dilation, direct response is pupil receiving light constricting, consensual response is when the other constricts too, after stimulation should return to normal size, difference between pupil size >1mm = anisocoria (genetic, head trauma, stroke, medication to eye), bilateral dilated (midbrain injury, sympathetic stimulation, oxytocin), irregular pupils (trauma), dysconjugate gaze (congenital, frontal lobe lesion), pinpoint (age, pontine injury, narcotics, nicotine, antipsychotics, ondansetron, MAO inhibitors, organophosphates), nystagmus (uncontrolled, involuntary eye movements due to congenital, inner ear problems, eye problems, CNS problems, meds or alcohol) ● Check hx of neuro problems, check medications ● Neck stiffness / nuchal rigidity: meningitis WEEK 7: NEUROLOGICAL PATHOPHYSIOLOGY Differential dx of ACS: 8 S’s 1. Smashed (trauma) 2. Sugar 3. Salt (electrolytes) 4. Substances (drugs) 5. Stroke 6. Syncope 7. Severe hypothermia 8. Severe hyperthermia Brain walls ● Disease infiltration: ​herpes, encephalitis, meningococcal meningitis, external bacteria / viruses ○ Encephalitis: ​inflammation of the brain, most commonly caused by a viral infection, mild asymptomatic or flu-like symptoms, severe can be lethal, immediate attention required for confusion, hallucinations, seizures, weakness and loss of sensation ○ Herpes: ​virus travels through a nerve to the skin causing a cold sore, in rare cases can travel to the brain = form of encephalitis, usually affects temporal lobe (memory and speech) ● Trauma to brain walls, CNS injury, hemorrhage Brain’s ability to stretch ● ● Swelling: TBI / hydrocephalus ​(accumulation of CSF causing increased pressure) Intraparenchymal intrusion: ​space occupying lesions or hemorrhage, coning (downward cerebellar herniation, move downward through foramen magnum possibly compressing lower brainstem and upper spinal cord), cushing’s reflex (systolic HTP (eventually diastolic hypotension), bradycardia, cheyne-stokes irregular respirations): classic sign of intracranial HTP & warning sign of brain herniation or coning, cheyne-stokes breathing is abnormal breathing that is progressively deeper and sometimes faster followed by gradual decrease resulting in temporary apnea then it repeats, seen in pts with TBI, tumours, heart failure, strokes or hyponatremia ● CPP = MAP - ICP Brain nutrients ● AKA / alcoholism ● Hypoglycemia (<4) / hyperglycemia (>10) / DKA / HHS ● Electrolytes ○ Hypernatremia​ = increased sodium, hyponatremia = low sodium, dehydration ○ Syndrome of inappropriate ADH secretion (SIADH)​ due to pneumonia, brain disease, cancer, thyroid problems, meds etc > cells dehydrated and BP increases lOMoARcPSD|30352485 ○ Hypokalemia​ may be due to vomiting, diarrhoea, laxatives, furosemide, DKA, chronic alcohol, chronic kidney disease, prednisone, congenital, presents with muscle weakness, aches, cramps & palpitations ● Malnutrition ● GI absorption diseases ● Food needs to be free from poisons or drugs, liver failure causes toxins to be retained, symptoms depend on substance: decreased GCS, agitation, respiratory depression, anxiety, dissociation, paralysis, nausea, odd posturing / movements Oxygen supply to brain ● Hypoxia / hypoperfusion ● CO2 excretion impaired by hypoperfusion or hypoventilation Fluid pressure in brain ● Blocked (embolytic) or burst vessels (hemorrhagic) (CVA’s) ● Dilated vessels (high BP), painful headache, neurogenic shock ● Sufficient perfusion required (CPP = MAP - ICP) Electricity: ​seizures Temperature ● Hypothermia: ​decreased vascular volume, CNS depression, unstable cardiac rhythms common, osborn waves on ECG, bradycardia + osborn waves + not shivering + ALOC would be moderate hypothermia around 30 degrees, shivering generally stops when insulin is no longer available for glucose transfer, antidepressants may impair pts response to hypothermia ○ ○ Temp ranges ■ Normal 36.5-37.5 ■ Early hypothermia 32-35 ■ Loss of shivering 30 ■ Deep hypothermia 28 Rx with gentle handling, don’t actively warm but prevent further heat loss, chemical heat packs, commence CPR w/o pulse, if VF or pulseless VT after 3 defibs cease defib & continue CPR, double interval time between meds ● Hyperthermia: ​cells shrink, lose sodium to vascular volume which heightens threshold for depolarization = diminished reflexes, ACS & weakness, greater increase in heat causes loss of intracellular water, distortion of cell membranes, mitochondria swell, collapse of cytoskeleton, red blood cells deform, hypoxia causes agitation / delirium, excessive heat can precipitate sickle cell crisis, core temp >42 incompatible w/ cell integrity (denature), pt who is hot to touch and not sweating is dying, rx: cool immediately w/ evaporative cooling, next best is ice pack, fluid replacement, keep skin wet, fan pt ○ Heat fatigue: weakness, lack of coordination ○ Heat exhaustion: same as above but decreased LOA, increased HR & RR ○ Head cramps due to sodium imbalance ○ Heat stroke: frank confusion / delirium, temp >41 degrees, classically in sustained high ambient temp environments with high ambient humidity ○ Anhydrosis: loss of sweating ○ Exertional rhabdomyolysis: breakdown of muscle from extreme physical exertion, death of muscle fibres, release their contents (damaging proteins) into blood > renal failure, presents w/ dark/red urine, decreased urination, weakness, muscle aches Shocking situations / imagery: ​psychogenic syncope Neurological anatomy ● CSF: ​supports brain so it floats in skull, transports nutrients / chemical messengers / waste, reduces brain weight, colorless, 80% glucose, replaced approx every 8 hrs in adults lOMoARcPSD|30352485 ● BBB: ​protects neurons from changes within environment, allows stable physiology in brain, interface between capillary walls & neural tissue, endothelial cells restrict diffusion of microscopic agents (bacteria) into CSF, selective barrier, allows glucose, AA’s, electrolytes, ineffective against fat-soluble molecules that cross plasma membranes ● ● Gyri and sulci increase surface area of brain: ​ridge / folds between clefts on cerebral surface in brain Limbic system: ​functional group of nuclei that regulate emotions and memory ○ Regulates autonomic or endocrine function in response to emotional stimuli, also involved in reinforcing behaviour ○ Sensory, motor and association areas of cortex enable complex actions from which the desire to perform these actions comes from limbic system ● Blood supply ○ Internal common carotid arteries: supply 80% of cerebrum ○ Vertebral arteries ○ Drained by sinus system into jugular veins ○ Circle of Willis: ​connects anterior and posterior blood supply in brain allowing CBF to be maintained where one vessel is blocked and equalizes BP in anterior & posterior brain regions ● ● Four lobes ○ Frontal: voluntary motor control, judgement, decision making, language, personality ○ Parietal: sensory, conscious perception ○ Temporary: auditory, olfactory, memory ○ Occipital: perception of visual stimuli Layers encasing brain & spinal cord ○ ○ Subdural space ○ Arachnoid mater: ​smooth epithelial membrane w/ villi, blood vessels poorly protected in this layer due to thin / elastic tissue ○ ○ ● Dura: ​periosteal and inner meningeal layers, tough, fibrous, layers sandwich thin section containing blood vessels & fluid Subarachnoid space Pia mater: ​thin, delicate tissue, accompanies blood vessels as they enter cerebral tissue Main components of brain ○ Cerebrum: ​left & right hemispheres divided by longitudinal fissure and connected by ​corpus callosum, contralateral function​, white & grey matter ■ ○ ○ Cerebellum: ​motor movement, balance, muscle tone, compares arriving sensations with past permitting repetition e.g. walking Diencephalon ■ ■ ○ Cerebral cortex: ​conscious mind, communication, voluntary movement, intellect Hypothalamus: ​pituitary gland, homeostatic regulation, autonomic functions, ADH & oxytocin, endocrine link Thalamus: ​emotion, behavioural drives, relay station of ascending sensory info Brain stem ■ ■ ■ Mesencephalon: midbrain: ​auditory and visual reflexes Pons: ​bridge from cerebellum to brainstem, carry & relay sensory motor info, ascending/descending/transverse tracts Medulla oblongata: ​contains all relay between spinal cord and brain, autonomic nuclei controlling visceral activities, sensory and motor nuclei lOMoARcPSD|30352485 WEEK 8: NEUROLOGICAL CONDITIONS: HEADACHE & STROKE Five primary headache syndromes: ​migraine, cluster, tension-type, normal, chronic paroxysmal hemicrania (severe, debilitating unilateral headache usually affecting area around the eye, usually multiple severe yet short headache attacks affecting only one side of cranium - similar to cluster) Migraine Vasoconstriction then rebound vasodilation, pts often used to having them, prodromal symptoms (early s&s) Slow to rapid onset of pulsating / throbbing pain, worse w/ activity, moderate-severe intensity, nausea and or vomiting, photophobia and or phonophobia, usually on one side of head Cluster Release of vasoactive mediators, pain pathways initiated via trigeminal nerve activation Begins w/o warning, 30 mins - 2 hrs, lacrimation on affected side, congestion of nasal mucosa, ptosis of ipsilateral eye (drooping on same side), usually concentrated around one eye Tension-type Hypersensitivity of trigeminal nerve and afferent nerves in cranial / facial muscles, doesn’t usually have prodromal symptoms Mild-moderate pain, tight band or pressure around head, location varies, gradual onset, not aggravated by physical activity USE DOLORS TO DESCRIBE THESE Rx with paracetamol & anti-emetics, opioids of limited benefit, ​if pain persists after 15 minutes can give fentanyl Considerations for assessing headache: SNOOP 1. 2. Systemic symptoms, ​illness or condition e.g. fever, weight loss, cancer, pregnancy, immunocompromised Neurological symptoms ​or abnormal signs e.g. confusion, impaired alertness, seizures, papilledema, meningismus (a group of similar symptoms to meningitis - stiff neck, reaction to light and headache - without inflammation of meningeal layer) lOMoARcPSD|30352485 3. 4. Onset is new: ​particularly age > 40 or sudden (thunderclap), 55-65 females are more likely to have big brain bleeds Other associated symptoms ​or features e.g. head trauma, illicit drug use, toxic exposure, headache awakens from sleep, worse with valsalva, precipitated by cough / exertion / sex 5. Previous headache hx: ​with headache progression or change in attack frequency, severity or clinical features Life threatening causes of secondary headaches: ​trauma to head or neck, CVA, cerebral vasculitis (inflammation of vessel wall in brain or spinal cord), tumor, seizure, increased ICP, medications, poisons, infections (meningitis, encephalitis), HTP, dehydration, renal or thyroid problems ● Secondary headache: due to an underlying medical condition Rx for headaches: ​gentle handling, low lights, no noise, non-narcotic analgesia (paracetamol), antiemetic (prochlorperazine), raise stretcher head to 30 degrees to decrease ICP, tx to neuro centre if pt has red flags Increasing ICP: ​normal is 5-15mmHg, ICP derived from pressure of brain matter, blood & CSF, cranium can’t expand so change in one requires changes in other to maintain ICP (monro-kellie), body can handle fluid changes of about 100mL w/o changing ICP, CPP = MAP - ICP, compression of brain contents leads to CNS herniation (coning = worst case TBI) ● Recognition: Cushing’s triad: HTP, bradycardia + irregular respiratory rate (cheyne-stokes)​, pupillary changes, speech changes, ALOC, headache, seizure, posturing, vomiting (versus shock would be hypotension, tachycardia and tachypnea) ● Herniations ○ ○ Falx cerebri: ​fold of meningeal layer of dura, separates L&R cerebral cortex, called a ​subfalcine herniation Tentorium: ​extension of dura mater that separates cerebellum from lower brain, called a ​transtentorial herniation - midbrain pushed through tentorial notch upward ○ ● Tonsilar: ​compression of pons and medulla damages vital centres for respiratory and cardiac function eventually resulting in cardiorespiratory arrest, ​brainstem herniation Rx: tx, airway control, intubation, antiemetics, rx seizures w/ benzos ​(stopping seizures necessary b/c they use up glucose), ​avoid hypothermia, stretcher head @ 30 degrees Neuromuscular diseases 1. Parkinsons: ​reduction in dopamine due to interference in dopamine producing parts of motor centres in brain, movement disorders, often have falls, pts take ledopa and carbidopa which aid normal dopamine conversion in brain), akinesia, bradykinesia, rigid, stooped, shuffling gait, tremor etc., may be called to falls, problems w/ swallowing or psychiatric issues 2. Acute dystonic reactions​: involuntary sustained muscle contractions causing abnormal posture and repetitive twisting motions, can be genetic or drug induced (antipsychotics, antiemetics), laryngospasm and failure of respiratory muscles most concerning acute issues 3. Amyotrophic lateral sclerosis (ALS): ​type of motor neuron disease (MND), steady, progressive and irreversible degeneration of upper & lower motor neurons, progressive muscle weakness leading to failure & death within 2-5 years of disease onset (up to 5-10), progression of primary muscle atrophy caused by disuse secondary to nerve innervation 4. Multiple sclerosis: ​steady, progressive and irreversible degeneration of myelin sheath primarily in CNS, unknown cause possibly autoimmune, most frequent cause of permanent disabilities in young adults (20-40) aside from trauma 5. Myasthenia gravis: ​caused by autoimmune destruction of nicotinic aCH receptors, causes respiratory muscle depression, episodic muscle weakness, may worsen with activity and decrease with rest Stroke ​(paramedics don’t dx, need CT) 1. 2. 3. TIA: ​stroke-like condition that lasts <24 hrs, usually <1 hr, warning sign for full on stroke Reversible ischemic neurological deficit (RIND): ​stroke-like condition, 24-72 hrs, similar to TIA but lasts longer CVA: ​lasting neurological syndrome caused by hypoperfusion that lasts >72 hrs, infarcted part of brain tissue results lOMoARcPSD|30352485 Cerebral perfusion: two internal carotid arteries (R&L) (80% of CBF) and two vertebral arteries (R&L) (20% of CBF), most strokes occur in middle cerebral artery (MCA)​: hemiplegia in face and body on same side sparring forehead,​ posterior cerebral artery (PCA) strokes ​have hemiplegia in face & body on contralateral sides w/o forehead sparing, less common, face side affected is ipsilateral to CVA Ischaemic stroke: ​clot blocks BF to area of brain, more common, surrounding area in danger of imminent tissue death (penumbra is the salvable tissue with treatment), clot creates a core dead affected area (infarcted umbra), most occur in MCA presenting with middle cerebral artery syndrome which is very different to presentations for anterior/posterior/basilar cerebral arteries Hemorrhagic stroke: ​bleeding inside or around brain tissue, various presentations b/c global lesions Neurological exam: ​use MASS and​ ​ACT FAST to determine if pt is + and can be taken to hospital for ECR, screening exam + history help decide which components of exam must be conducted in more detail, exams must be expanded when asymmetry or abnormality is found, should also be expanded to focus on pts specific complaints e.g. memory loss needs thorough mental status testing ● Mental status: ​orientation to TPP, make sure they can follow at least one complicated demand (two moves) without nonverbal cues, if responses are appropriate no further mental status testing is required (unless they have cognitive complaints) ● Cranial nerves: ​test visual fields in one eye, both pupillary responses to light, eye movements in all directions, facial strength and hearing to finger rub ● ● ● Motor system: ​test strength in bilateral muscles, observe gait Reflexes Sensation: ​test light touch sensation in all four distal limbs Important neurological symptoms to note: ● Vertigo (brainstem or cerebellar) ● Diplopia (double vision) ● Restricted ocular motion (H test) ● Dysarthria (difficulty speaking) ● Dysphasia (language difficulties) ● Dysphagia (difficulty swallowing) ● Ataxia (difficulty coordinating movement) lOMoARcPSD|30352485 ● Limb hemiplegia / hemiparesis Stroke mimics: ​toxic metabolites (BGL, hypernatremia, hyponatremia, hepatic encephalopathy), ingestions (drugs, meds), post ictal (after a seizure = ​todd’s paresis​ = temporary paralysis after a focal seizure), migraine, neurological disorders (MS, leukoencephalopathy (swelling of white matter), bell’s palsy (temporary, unilateral paralysis of face usually due to trauma or infection to facial nerve), syncope, sepsis Stroke rx: ​airway control, fast tx to appropriate facility, fast identification is key, fibrinolytics can occur in hospital up to 4.5 hrs after the stroke (not given by paramedics b/c we don’t know if ischemic or hemorrhagic w/o CT) Reading: delirium & confusional states: ​more common in elderly, many complex underlying medical conditions, encephalopathy and acute confusional state often used synonymously w/ delirium, confusion indicates a problem with coherent thinking and is essential component of delirium, ​delirium is a special type of confusional state characterized by increased vigilance, with psychomotor and autonomic overactivity; pt displays agitation, excitement, tremulousness, hallucinations, fantasies and delusions, ​aCH has a key role, anticholinergic drugs can cause delirium when given to healthy volunteers, conditions that decrease acH synthesis such as hypoxia & hypoglycemia can cause delirium, commonly identified risk factors are underlying brain diseases like dementia, stroke or Parkinsons, precipitating factors: polypharmacy, infection, dehydration, malnutrition, bladder catheters, etc., family members will often say pt “isn’t acting quite right”, early manifestation is change in level of awareness and ability to focus, sustain or shift attention, pt will be drowsy, lethargic or even semiconscious, perceptual disturbances, cognitive & perceptual problems, often a prodromal phase (fatigue, sleep disturbance, depression, anxiety etc.), hard if you don’t know pts baseline levels (e.g. dementia pts) 5 key features of delirium: ​disturbance in attention & awareness, disturbance over a short period of time and tends to fluctuate, additional disturbance in cognition, disturbances not better explained another pre-existing disorder or in the context of reduced arousal such as coma, evidence of disturbance caused by medical condition, intoxication, withdrawal or medication, additional features: psychomotor behavioural disturbances, variable emotional disturbances Most common causes of delirium: ​fluid & electrolyte imbalances, infection, drug or alcohol toxicity or withdrawal (specifically barbiturates, benzos, SSRI’s), metabolic disorders (hypoglycemia, hypercalcemia, uremia, liver failure, thyrotoxicosis), low perfusion states (shock, heart failure), postoperative states, ​less common causes: ​hypoxemia, hypercarbia, encephalopathy, adrenal failure, CNS infection, seizures, trauma Intracranial hemorrhage ● Extradural or epidural ​(on or around the dura mater)​: ​usually due to trauma = torn meningeal artery, arterial blood between dura & skull, may or may not lose consciousness transiently​, after injury regain normal LOC​ (lucid interval)​, ongoing​ severe headache​ (stripping of dura from bone by expanding hemorrhage causes pain), over next few hours may gradually lose consciousness + headache, drowsy, ● nausea, vomiting, ​enlarged pupil in one eye, prognosis good if clot is evacuated Subdural: ​usually due to trauma especially in elderly & alcoholics (cerebral atrophy), ​often from sudden velocity changes ​(shaken baby syndrome), blood pools between dura and arachnoid, usually caused by tear in vein rather than artery so lower pressure = ​slower ● symptom progression (weeks after trauma), ​nausea, vomiting, slurred speech, ​vision changes, ​confusion, drowsiness, ​hemiparesis Subarachnoid: ​extreme extra pressure on vessels e.g. from exertion causing a burst in a weak vessel, typically​ thunderclap headache, meningism ​(nuchal rigidity, photophobia),​ quickly unconscious, double vision, stroke-like symptoms: focal neurological deficit​s often present either at same time as headache or soon after ○ Thunderclap headache: ​extremely painful, sudden onset, reaches most intense pain within 1 minute, lasts at least 5 mins, can be due to dissection, rupture or blockage, n/v, fainting, headache pain including neck or lower back ● Intraparenchymal or intracerebral: ​about 10% of hemorrhages, very fatal, hard to get to this part of brain to repair, substantial displacement of brain parenchyma may cause ICP elevation and fatal herniation syndromes​, clinical manifestations determined by size & location, headache, LOC, seizure, HTP, fever, cardiac arrhythmias, anisocoria, nystagmus etc. ● Rx: ​transport to neuro centre, airway control, intubation, antiemetics, rx seizure w/ benzo, avoid hypothermia, stretcher head @ 30 degrees lOMoARcPSD|30352485 Reading: stupor & coma: ​clinical states w/ impaired responsiveness to external stimulation, either difficult to arouse or unarousable, coma = unarousable unresponsiveness, stupor/lethargy/obtundation = states between alertness & coma, alteration in arousal represents acute life-threatening emergency, mostly due to trauma, cerebrovascular disease, intoxications, infections, seizures & metabolic derangements, when assessing arousability pay attention to vocalization, eye opening and limb movement, trap squeeze or pressing on supraorbital nerve most common, coma is a transitional state that rarely lasts more than several weeks except in cases of ongoing sedative therapies WEEK 9: SEIZURES & NEUROLOGICAL SYNDROMES Seizures: ​chaotic electrical brain activity, transient, abnormal excessive synchronous neuronal activity in brain, most are self-terminating and <5 mins, only treat as paramedics if ​>5 mins or multiple discrete seizures w/o full return to consciousness still >5 mins total​ ​(status epilepticus),​ first time seizures can last >30 mins in 10% of pts, seizures use 250% ATP in brain (energy) and extra 60% oxygen, CBF increases dramatically, causes may be ​genetic, structural, metabolic or unknown (tuberous sclerosis, cortical dysplasia (congenital), stroke, trauma, infection, immune based (acquired)) Status epilepticus: ​results from either failure of mechanisms responsible for seizure termination or from the initiation of mechanisms which lead to abnormally prolonged seizures, can have LT consequences including neuronal death, neuronal injury and alteration of neuronal networks depending on type and duration of seizures, most extreme form of seizure, at least half of pts with SE don’t have epilepsy, prognosis of SE worsens with increasing duration Non-convulsive status epilepticus: ​underrecognized, requires EEG for detection, no classic ictal features, features show possibility of seizures: bilateral facial twitching, unexplained nystagmoid eye movements during obtunded periods, hippus (restless mobility of pupil), automatisms, acute aphasia (impaired language) etc. Seizure vocabulary ● ● ● ● ● ● Tonus: ​sustained muscle contraction Atonic: ​muscle flaccidity Clonic: ​muscle jerking, sustained Tonic-clonic: ​sustained contraction then jerking, previously known as tonic-clonic Focal: ​isolated to one part of the body Absence: ​momentary (<60 s) loss of situational awareness, “absent stare” not synonymous with absence seizure since arrest activity also occurs in other seizure types ● ● ● Myoclonus: ​a quick, involuntary muscle jerk, unsustained Eyelid myoclonia: ​upward jerking of eyelids Jacksonian march: ​orderly progression of seizure activity from distal part of limb toward one side of body due to activity in primary motor complex ● Todd’s paresis: ​focal weakness / paralysis in a part of body (typically unilaterally in appendages) after a seizure, may be misdiagnosed as stroke, may affect gaze, speech or vision Stages of seizure 1. 2. 3. 4. Prodromus: ​period of time from first symptom to full seizure development (hrs - days), e.g. time from diplopia to seizure Aura: ​initial alterations in perception, usually seconds-mins before seizure Ictus: ​seizure Post-ictal: ​state of confusion, mins-hrs, after seizure (not always present), exhausted, sweaty, lethargic, hypoxic Dangers of seizures: hypoxia, use up glucose, acidosis SE that continues subsequent to benzos described as ​refractory Children prone to ​febrile convulsions: ​seizure in children 6 months - 5 years when they have a temperature, usually in first day of fever, a few seconds up to 15 mins, usually harmless lOMoARcPSD|30352485 Epilepsy: ​having two or more unprovoked seizures Types of seizures: ​earliest prominent onset manifestation defines seizure type Focal onset = starts in one area of body ● Awareness ○ ○ Focal aware = aware of self and environment during seizure ​(elements of consciousness = awareness, memory, responsiveness, sense of self)​, ​doesn’t always require hospital, “focal aware with maintained awareness” Focal unaware = didn’t know what was happening during event, confused, ​if awareness is impaired for any portion of seizure is defined as impaired awareness, all generalized seizures are impaired by definition ● ○ Some start focal unilateral and become bilateral tonic-clonic, “focal to tonic-clonic” ○ Focal behaviour arrest seizure shows arrest of behaviour as the prominent feature of the entire seizure Motor or non-motor, ​“focal non-motor seizure with impaired awareness,” motor and/or non-motor signs & symptoms at onset, if both are present motor signs will usually dominate unless non-motor are prominent (e.g. sensory) ○ ○ Motor: ​physical activity including atonic, automatisms, clonic, epileptic spasms or hyperkinetic, myoclonic or tonic activity Non-motor: ​autonomic, behaviour arrest, cognitive, emotional or sensory dysfunction, eyelid myoclonia Generalized onset = bilateral (refers to propagation patterns), whole body, ​awareness not used as a classifier for generalized seizures as vast majority have impaired awareness, generalized motor are bilateral from onset ● ● Motor: ​tonic-clonic, clonic, tonic, epileptic spasms, atonic etc., Non-motor (absence): ​sudden cessation of awareness and activity, typically in children, eyes open, fixated gaze, sudden start and stop, usually less complex automatisms (lip smacking, hand movements) (automatisms are actions performed w/o conscious thought or intention), can be prominent myoclonic activity or eyelid myoclonia, absence refers to sudden cessation of activity and awareness & tend to occur in younger age groups and have more sudden start and termination Unknown onset = if no one saw it start, can be motor or non-motor, further descriptive explanation can be offered, ​can still be classified as motor, non-motor tonic-clonic, epileptic spasms or behaviour arrest Tonic seizures of epileptic spasms can be focal or generalized onset Bilateral = tonic clonic seizures that propagate to both hemispheres versus generalized = apparently originate simultaneously in both hemispheres lOMoARcPSD|30352485 Assessment: ​aura, personal or family hx, compliance w/ anti-seizure meds, triggers (exhaustion, overstimulation, illness), description, physical exam (head trauma, oral trauma, rhinorrhea, otorrhea (ear drainage), otorrhagia, rhinorrhea (ear or nose hemorrhage)), incontinence, meningism (fever, stiff neck), focal neuro deficits (do CVA neuro exam) Differential dx: ​syncope, metabolic conditions (sugar abnormalities), meds, migraine, vascular (CVA, TIA, RIND), sleep disorders (narcolepsy), movement disorders, GI conditions, psychiatric conditions (panic attacks, pseudo seizures, breath holding spells), traumatic cause (TBI) Rx: ​don’t hold them down! make area safe, loosen clothing, time seizure, cushion head, turn on side, ensure airway patent, midazolam 5 or 10mg repeat @ 5 or 10 mins IM if SE, can t&r for adults with epilepsy if they meet criteria Neurological syndromes: Neurogenic shock: ​shock w/ normal blood volume and increased vascular volume (normovolemic hypotension), a type of distributive shock, vascular volume in wrong place, often related to SCI, damage to spinal column usually above T4, lack of sympathetic stimulation allowing adrenaline and vasoconstriction and inability to speed HR (lack of adrenal response) ● s&s: lower body paralysis & anaesthesia, hypotension, possible sweat line (pale, sweaty above and dry and vasodilated below), absence of pain and presence of unexpected calmness, absence of tachycardia (unless AD) ● Rx: spinal precautions, conservative fluid challenge (increase BP but don’t fluid overload), vasopressor Neuroleptic malignant syndrome: ​severe drug rxn to neuroleptic drugs (antipsychotics, major tranquilizers) ● s&s: ACS, motor abnormalities, hyperthermia, autonomic hyperactivity (tachycardia, arrhythmias, tachypnea, labile HTP (fluctuating BP)) ● Rx: stop causative drug (hospital needs to change meds), aggressively cool, tx Malignant hyperthermia: ​life-threatening response to meds, usually triggered by combination of inhalational anaesthetic and depolarizing neuro-muscular blocker so often happens during surgery ● s&s: muscle rigidity (lockjaw), tachycardia, dysrhythmias, tachypnea, acidosis, shock, hyperthermia, hypercapnia may be early sign ● Rx: stop causative drug, aggressively cool, tx Autonomic dysreflexia: ​affects individuals with pre-existing SCI above T6, can result in hypertensive crisis causing seizure, cardiac arrhythmia or intracranial hemorrhage (life-threatening), widespread reflex activity of SNS triggered by an ascending sensory (usually painful (noxious)) stimulus below level of injury ● Below SCI: ​overactive sympathetic response uncontrolled due to lack of response from normal regulation vasomotor centres in the brainstem, results in severe vasoconstriction below SCI (skin pallor, piloerection, sudden rise in BP, headache, cold) ● Above the SCI: ​parasympathetic activity below SCI occurs when increased BP is sensed by baroreceptors in aortic arch and carotid bodies resulting in compensatory bradycardia via vagus nerve, flushed skin (dilation), profuse sweating above injury but not satisfactory to control HTP due to massive SNS vasoconstriction of splanchnic bed ● General symptoms: pounding headache, anxiety, nausea, blurred vision, nasal obstruction, bradycardia common but sometimes tachycardia, SOB, anxiety, BP elevated at least 20mmHg above normal systolic (BP for individuals w/ high paraplegia or tetraplegia may usually be low (90-100) therefore may be symptomatic with normal BP for population), severity ranges from asymptomatic HTP to hypertensive crisis complicated by profound bradycardia and cardiac arrest or intracranial hemorrhage and seizure ● Common causes: distended bladder, UTI, stones, constipation, rectal irritation, hemorrhoids, ingrown toenail, burns, tight clothing, distended stomach, menstrual cramping etc. ● Rx by treating cause of noxious stimuli (loosen clothing, check bladder drainage, avoid pressing bladder), elevate head and lower legs, if symptoms persist pharmacological treatment with short-acting anti-hypertensive med: GTN for severe headache and/or BP>160 given 10 minutely until symptoms resolve, BP<160 or side effects, no patch There are 12 thoracic nerves (T1 descending to T12) MY EXTRA NOTES lOMoARcPSD|30352485 Drugs to start recalling Clonazepam, temazepam, midazolam Common benzodiazepines Sertraline, citalopram, escitalopram, paroxetine, fluoxetine, fluvoxamine Antidepressants Gliclazide T2DM medication Sulphonureas Class of oral medications that treat diabetes by increasing insulin release from pancreas Metformin 1st line T2DM medication especially for obese pts Acarbose T2DM medication Novorapid, lantus Insulin Amitriptyline A TCA drug Astrix Low dose aspirin Furosemide Diuretic, treats fluid retention, edema, CHF, liver disease, kidney disorders Prednisolone Steroid for allergies, cancer, autoimmune or inflammatory conditions Prednisone Corticosteroid to suppress immune system and decrease inflammation in asthma, COPD and rheumatologic diseases, also treats hypercalcemia Simvastatin (zocor), atorvastatin (lipitor), rosuvastatin (crestor) Statins treat high cholesterol / abnormal lipid levels to prevent cardiovascular disease Coloxyl Stool softener, treats constipation Sotalol hydrochloride For abnormal heart rhythms, e.g. atrial fibrillation Perindopril (coversyl) ACE inhibitor, treats HTP and prevents heart attack in people with CAD Esomeprazole (nexium) Reduces stomach acid, treats heartburn, difficulty swallowing and persistent cough Metoprolol Beta-blocker (beta-adrenergic blocking agents), affects heart and circulation, treats angina and HTP, reduce effects of adrenaline Nitrolingual Treats angina, nitrate that dilates blood vessels, ​nitrates work by leading to an increase in cCMP leading to decreased available calcium in smooth muscle (relaxes vessels - less contraction) Digoxin (lanoxin) Treats various heart conditions such as atrial flutter or fibrillation or heart failure Chronotropic drugs Affect heart rate by altering electrical conduction system of heart, eg. digoxin is a negative chronotrope (decreases HR) Telltale signs & symptoms for specific conditions ● Signs ○ Dusky appearance - chronic pulmonary disease ○ Jaundice - hepatic failure ○ Needle tracks - drug abuse ○ Cherry-red lips - possible CO poisoning ○ Sweet ketotic breath - ketosis lOMoARcPSD|30352485 ○ Bitten tongue, possible fracture-dislocation of shoulder - convulsive seizure ○ Fever - infection, heat stroke, anticholinergic intoxication ○ Cheyne-Stokes respirations - impaired cardiac output, cerebral dysfunction ○ Hypotension - circulatory failure from sepsis, hypovolemia, cardiac failure, certain drugs ○ Bruises - trauma ○ Raccoon’s eyes (periorbital ecchymosis) - head trauma ○ Battle’s sign (bruising over mastoid) - basal skull fracture ○ Sweaty - fever, hypoglycemia ○ CSF rhinorrhea - skull fracture ○ Asymmetries of movement and reflexes - hemiplegia of the nonmoving side implying a lesion affecting the opposite cerebral hemisphere or upper brainstem ● Symptoms ○ Abrupt loss of consciousness - subarachnoid hemorrhage, seizure ○ Gradual loss of consciousness - brain tumor ○ Fluctuating loss of consciousness - recurring seizures, subdural hematoma, metabolic encephalopathy ○ Headache or vomiting prior to loss of consciousness - intracranial hemorrhage ○ Neurologic episodes - TIA, seizure ○ Increasing headache - expanding intracranial lesion, infection ○ Recent fall - subdural hematoma ○ Recent confusion or delirium - metabolic or toxic cause ○ Transient visual symptoms (e.g. diplopia, vertigo) - ischemia in posterior circulation