Final ExamSum Flashcards
What is a fracture?
Break in continuity of a bone, an epiphyseal plate, or a cartilaginous joint surface
(Trauma may also occur to adjacent tissue)
What is the healing process of a fracture?
Hematoma- clotting of blood
Fibrous network
Osteoblasts get to work, collagen expands, calcium is deposited
Callus formation-soft start- merges with bone
Remodeling - becomes bone
What are the treatments for a fracture?
Reduction (if bones are not in alignment-internal or external) and immobilization
External immobilization
Surgery
Supportive/comfort care- elevating, ice, non weight bearing, meds
What are the complications of a fracture?
Delayed healing- pain and tenderness longer than expected- 3-6 months after- this is not normal
Compartment syndrome-build up of pressure in soft tissue/fascia compartments, collapse of blood vessels- hypoxia and necrosis
DVT/PE- clotting
Fat emboli syndrome- fat released by long bones, acts as a clot- same symptoms as DVT by anti-coagulation will not work-supportive care
What is malunion?
healing when things are not aligned as they should be.
What is osteomylitis and how is it caused?
Severe pyogenic infection of bone and local tissue
Caused by: Organisms reach bone through bloodstream, adjacent soft tissue or direct introduction of organism into bone
Hematogenous osteomyelitis = most common
What are the treatments for Osteomylitis?
Pharmacological
Surgical
What is osteoporosis? How does it happen?
rate of bone resorption is greater than bone formation
bone mass decreased; fragile bone and fractures-prone to more fractures
-estrogen deficiency, post-menopausal poor calcium intake, lack of use
How do you diagnose osteoporosis? Treatment?
Bone scan
X-rays, CT scan
Treatment – calcium and vit D supp
What is osteoarthritis and how is it caused?
Definition – local degenerative joint disorder- loss of cartilage- bone spurs can occur-osteophytes
Pathogenesis – aging, wear & tear from repetitive stress
What is Rheumatoid arthritis and how is it caused?
Definition – systemic autoimmune inflammatory disease-Granulation tissue over cartilage- pannus –can erode and destroy cartilage
Swelling, enlargement, edema of joint
Damage to tendons and ligaments- contractures of joints
Pathogenesis – genetics,
? environmental, ? Lifestyle, smoking and stress- not 100% sure why
Manifestations of osteoarthritis
Joint pain, crepitus, bony enlargement, stiffness, Heberden and Bouchard nodes
Treatment for osteoarthritis
Exercise, PT, weight loss, medication, complementary therapies, surgery
Manifestations of RA
Pain (diffuse and in joints), malaise, fatigue(autoimmune
Treatment for RA
Medications, biological agents
Gout
disorder of uric acid metabolism leads to deposition of uric acid crystals in joints
hyperuricemia and urate crystal–induced arthritis
Pathogenesis
Greater production of uric acid than the kidney can remove
Treatments for gout
Pharmacological
Non-pharmacological- dietary changes
Alendronate (Fosamax) -Bisphosphonates
Decrease osteoclast activity Causes osteoclast apoptosis Inhibits bone resorption Poor bioavailability Distributes to bone w/lengthy retention time Less frequent dosing
Alendronate (Fosamax) -Bisphosphonates use an d AE
Osteoporosis prevention & treatment Paget’s disease Hypercalcemia of malignancy AE: *Esophagitis Administration info!!! Musculoskeletal pain Ocular inflammation *Osteonecrosis of the jaw- tell dentist** Femur fractures Hyperparathyroidism in Paget’s Disease
Alendronate (Fosamax) -Bisphosphonates administration info
Oral- very important ** AM before breakfast Empty stomach Full glass of water (no other drinks) No food/Drinks x 30 – 60 minutes Upright x 30 minutes
RA Pharmacological Treatment
NSAIDs
Non-Biologic DMARDs
Biologic DMARDs
NSAIDS for RA treatment
Symptomatic relief
Do not prevent joint damage or disease progression
No longer 1st line treatment alone
Non-Biologic DMARDs for RA treatment
Reduce damage & slow progression
Methotrexate (MTX, first line)
Low-dose = Once Weekly
Mechanism of action = Decrease B & T lymphocytes
Adverse Effects: hepatic fibrosis, bone marrow suppression, GI ulceration
Biologic DMARDs for RA treatment
Affect specific processes in development of RA
TNF inhibitors = etanercept (Enbrel)
Adverse Effects: serious infections (fungal, TB); allergic rxns, HF, Cancer, Hematologic abnormalities, hepatotoxicity, CNS demyelinating d/o
Avoid live vaccines, immunosuppressant drugs
What are the differences in the current and evolving paradigm for RA treatment?
Evolving says to reduce the use of DMARDS and to use monotherapy with biologics
What drugs are used for short term gout therapy?
NSAIDs = 1st line agents (commonly indomethacin)
Glucocorticoids
Avoid in pts prone to hyperglycemia
Colchicine
What drug is used for long-term gout therapy?
Long-term = urate-lowering
> 3 times/year
Allopurinol
Colchicine
inhibition of leukocyte infiltration
used for: Gouty attack
Prophylaxis against attacks (at lower doses)
Aborts impending attacks
AE of colchicine
GI (25%) = N/V/Diarrhea, pain = stop therapy Myelosuppression Myopathy (rhabdomyolysis with long term tx)
What are the goals of therapy for hyperuricemia?
Dissolve urate crystals Prevention of crystal formation Prevention of disease progression Reduce frequency of attacks Reduce risk of nephropathy Improve quality of life ** NOT for gouty attack
What are the two ways drugs target hyperuricemia?
Inhibit uric acid formation: Allopurinol (Zyloprim) &Febuxostat (Uloric)
Increase uric acid excretion (uricosuric): Block renal reabsorption of uric acid & Probenacid (Benemid)
Allopurinol (Zyloprim)
Mechanism of action: inhibition of xanthine oxidase Effects: Decreases production of uric acid Lowers risk of crystal precipitation Use Chronic gout Hyperuricemia due to cancer chemotherapy
AE of Allopurinol
Hypersensitivity syndrome
Initial treatment may precipitate gouty attack (start in combo with an NSAID)
Nausea
What are the three steps on the analgesic ladder?
mild pain–> non-opioid- NSAID, acetaminophen, aspirin
mild to moderate –> opioid- codene, tramadol
Severe –> opiod- morphine, fentanyl
What medications are opioid agonists?
Morphine – Gold standard Hydrocodone Oxycodone Hydromorphone Fentanyl
opioid toxicity
respiratory depression, urine retention, N/V, constipation
What are our drugs used for Parkinson’s?
Levodopa + Carbidopa
Ropinrole
Phenelzine
What are our drugs used for Alzheimer’s?
Donepezil
Memantine
What is the goal for Parkinson’s pharm therapy?
**No drugs to prevent neuronal damage or reverse damage already done
Improve patient’s ability to carry out activities of daily life
Help with bradykinesia, gait disturbances, postural instability
What are the two approaches to Parkinson’s pharm therapy?
Dopaminergic agents (activation of DA receptors) Anticholinergic agents (block ACh)
What two types of metabolism does dopamine go through?
– COMT & MOA-B
Which drug is our dopamine replacement?
Levodopa/Carbidopa
What drug is our dopamine agonist?
Nonergotamine: Ropinirole
What is our MOA-B inhibitor?
Selegiline
Levodopa + Carbidopa
increases synthesis of DA –> turns into dopamine
Enters brain- update into few dopaminergic nerve terminals that remain
Only a small amount reaches the brain ** carbidopa enhances effects of levodopa
Levodopa with and without carbidopa
70% of levodopa excreted out- 2-3% to brain without carbidopa
With carbidopa= about 10% to brain instead of 2-3%
Levodopa + Carbidopa response
quick response an gradual loss of effect
“off-on” phenomenon regardless of dosing
AE of Levodopa + Carbidopa
N/V, postural hypotension, Head bobbing, tics, grimacing, tremors, psychosis, Darken sweat and urine
Activate malignant melanoma
What are the drug interaction categories for Levodopa + Carbidopa?
Increase beneficial effects of levodopa
Decrease beneficial effects of levodopa
Increase levodopa toxicity
What are the drugs that increase the beneficial effects of levodopa?
Carbidopa, entacapone, tolcapone, apomorphine, bromocritpine, amantadine, anticholinergic drugs
What are the drugs that decrease the beneficial effects?
Antipsychotic drugs
What drugs increase levodopa toxicity?
MAO inhibitors
Which dopamine agonists are preferred?
Non-Ergotamine-ropinirole
Ropinirole (Requip)
Highly selective
Can be used early in diagnosis
monotherapy or as adjunct to levodopa-carbidopa
Dosed 3 x day
AE of Ropinirole (Requip)
Common adverse effects: nausea, dizziness, somnolence, hallucinations, insomnia
Selegiline
MAO-B inhibitor - can reduce “wearing off” effect
Hepatic metabolism and renal excretion
AE//drug interactions of Selegiline?
AE: hypertensive crisis (remember tyramine)
Intensifies levodopa
Meperidine (stupor, rigidity, agitation, hyperthermia, death) due to serotonin syndrome
Fluoxetine (reports of fatalities with nonselective MOA-Is)
What is our Cholinesterase Inhibitors for Alzheimer’s Disease ?
Donepezil (Aricept)
Donepezil
Approved for mild, moderate and severe AD
Modest improvements in cognition, behavior, and function
Prevent breakdown of ACh by AChE
AE of donepezil
GI effects: nausea, vomiting, dyspepsia, diarrhea = If it’s bad, stop therapy and reassess
Neuro: dizziness and headache
Pulmonary: can see bronchoconstriction (use caution in severe COPD)
CF: symptomatic bradycardia
Drug interactions with donepezil?
watch anticholinergic agents like antihistamines, TCAs and antipsychotics
Memantine (Namenda)
NMDA (N-methyl-D-aspartate) antagonist
Modulates effect of glutamate (major excitatory CNS transmitter
* fairly new
AE of memantine// drug interactions
Dizziness, headache, confusion, constipation
Taking with alkanizing drugs could lead to increased levels of memantine
Sodium bicarbonate, aluminum hydroxide, magnesium hydroxide (Think Antacids)
What are the three mechanisms of brain injury?
Primary brain
Secondary injury
Adenosine triphosphate (ATP) depletion
What is primary brain injury?
direct result of insult- acute-irreversible with tissue necrosis
What is Secondary brain injury?
Development of further injury after primary-more gradual- apoptosis
What is brain injury due to ATP depletion?
shared factor of primary and secondary- ischemia or hypoxia –if ATP drops quickly or a lot= necrosis. Gradual or less significant=apoptosis *can be reversible
What are the Neuron energy needs?
oxygen and glucose – 5-10 mins of ischemia or hypoxia before permanent damage
Calcium- intracellular – during ischemia//hypoxia=not enough energy to move the calcium-
What are 4 Additional mechanisms of brain injury?
Reperfusion Injury
Abnormal Autoregulation
Cerebral Edema
Increased Intracranial Pressure (ICP)
What is reperfusion injury?
sudden improvement in oxygen – free radicals and inflammation
What are the two abnormal autoregulations?
hypotension
hypertension
What are the two types of cerebral edema?
Vasogenic
Cytotoxic
What is vasogenic and cytotoxic cerebral edema?
Vasogenic-blood vessels leak fluid
Cytotoxic- ischemic tissue swell (both can happen together)
What three things would you test for manifestations of brain injury?
Level of Consciousness
Glasgow Coma Scale
Cranial Nerves
What three things does glasgow coma scale check for?
Eye opening
Verbal response
Motor response
What two parts of the brain effect speech?
Broca’s area
Wernicke’s area
You have a patient who is having a lot of trouble understanding what you are saying to them, which part of the brain would they most likely have damage to?
Wernicke’s area
When someone has damage to the Broca’s area, what would they have trouble with in language?
Making or expressing language
What two types of strokes are there?
Ischemic and Hemorrhagic
Ischemic strokes are caused by what two things?
Thrombotic and Embolic
What two places do hemorrhagic strokes occur?
intracerebral and subarachnoid
What is the circle of willis?
where major arteries connect in brain
What is a TIA?
transient ischemic accident- symptoms only last short time
What are two ways ischemic strokes occur?
Atherosclerosis
Arterial clots
What are the two types of treatments for ischemic strokes?
Thrombolytic
Save the penumbra!
What is the penumbra?
hurting but not yet dead- function can be regained
Intracerebral hemorrhage ?
Same clinical manifestation of hemorrhagic- acute-headache
Severe chronic HTN
May recover but mortality is more common if they don’t recover
Treatments: manage BP- can’t be too low because we need blood flow- permissive hypertension
ICP? Blood-monitor
What are two types of Subarachnoid Hemorrhage?
Primary injury
Secondary injury
Vasospasm
Hydrocephalus
What is an Aneurysm? What happens when it’s ruptured?
weakening or out-pouching of blood vessel
-blood spreads into cerebral spinal fluid- meningeal irritation – blood can plug and cause hydrocephalus – headache, vasospasms-obstructed blood flow- can lead to second ischemic stroke
What can cause an aneurysm? What are some treatments?
High BP, cocaine use, acute alcohol intoxication can cause a rupture – stroke
Can clip, or embolize – preventative treatment for vasospasms – manage BP
What is Arteriovenous Malformation? What happens with rupture? What are some treatments?
blood vessels not formed right- large and fragile ball of blood vessels- seizure and stroke with rupture
Treatment:removal- kill off a little of them at a time, radiation, embolization,
What are stroke complications?
Motor and sensory deficits
Language deficits
Cognitive deficits
What are the motor manifestations of Parkinson’s?
Tremor Rigidity-cogwheel, halting Bradykinesia Postural changes Shuffling Decreased facial expression Micrographia
What are the non-motor manifestations of Parkinson’s?
Depression Personality changes Cognitive dysfunction, dementia Sleep disturbance Urinary retention
What is multiple sclerosis?
demyelination anywhere in the central nervous system, caused by autoimmune process
What is are the clinical manifestations of multiple sclerosis?
Fatigue Visual impairment/changes Depression Spasticity Sexual dysfunction Neuropathic pain Ataxia and tremor Cognitive dysfunction Dizziness and vertigo Bladder, bowel dysfunction
What are some treatments for multiple sclerosis?
interrupting the autoimmune process with medications, symptomatic/supportive treatment. some small doses of chemo
What are the four types of MS subtypes: Symptom patterns?
Relapsing-remitting
Secondary progressive
Primary progressive
Progressive -relapsing
How would relapsing-remitting pattern be described?
Drastic increases with drastic decreases and some coming back down to base-line, some don’t
Esophageal pain–> Heartburn and Chest pain
When people com in for chest pain they want to make sure it’s not heart issue
Acidic gastric fluid come up- muscular spasms from reflux- can radiate to neck or throat. Can be similar to angina–> esophageal spasm
What are the differences in Visceral, Somatic, and Referred abdominal pain
Visceral diffused, not localized, cramping or irritation and inflammation- gnawing or burning
Somatic Sharp intense pain, more localized, from injury to specific place.
Referred feels like it’s in a different area than it is.
What are causes of emesis?
Coordinated sequence of abdominal muscle contraction with reverse esophageal peristalsis
Alterations in the integrity of GI tract wall (gastroenteritis)
Alterations in motility (obstruction)
What is intestinal gas and how is it caused?
Results from altered motility or lack of digestive enzymes
Normal causes
Swallowing of air
Bacterial and digestive action on intestinal contents
Neutralization of acids by bicarbonate in upper GI tract
What are the clinical manifestations of intestinal gas?
Belching
Abdominal distention
Excessive flatus
What are some causes of constipation?
Dietary (low in fiber); cellulose (preventive)
Lack of exercise
Aging: slowed rate of peristalsis
Pathologic conditions that alter motility (ex: diverticulitis, obstruction)
What are the 4 types of diarrhea?
Osmotic
Secretory
Exudative (mucus, blood, protein)
Motility disturbances
How does osmotic and secretory diarrhea work?
Osmotic- lactose intolerance- increased amount of substances that are not being absorbed well
Secretory- toxin in intestines – an infection – stimulates fluid and inhibits absorption
What is peptic ulcer disease?
Upper GI disorders caused by hydrochloric acid and pepsin
What is PUD associated with?
H. pylori NSAIDs Stress (glucocorticoids) Smoking Genetics
What are destructive aspects of PUD?
Hydrochloric acid
H. pylori
NSAIDs
What are protective aspects to PUD?
Intact mucosal lining
Mucosal regeneration
Why is H. pylori so damaging to the mucosa?
promotes ulcers and prevents healing
What are clinical manifestations of PUD?
Epigastric burning –> relieved with intake of food
Nausea
Abdominal upset
Chest discomfort
Can be asymptomatic and present with complications
What are the complications of PUD?
Perforation
Bleeding
What diagnostic tools are used for PUD?
Upper GI barium contrast radiography
Endoscopy
H. pylori testing (on biopsy)
What is the treatment for PUD?
Focus: Ulcer healing
Medications: PPI, Sucralfate, Antibiotics for H pylori
What are the two main causes of liver disease?
Hepatocellular- cells of liver not working
Portal hypertension- poor or inadequate blood flow/perfusion
Hepatocellular failure
Jaundice Decreased clotting factors Hypoalbuminemia Decrased vitamins D and K (Osteomalacia―vitamin D; poor blood-clotting factor production – vitamin K) Feminization poor BG control
What is jaundice and what are the 3 causes?
dysfunction in process of bilirubin metabolism
Prehepatic
Hepatic
Posthepatic
Prehepatic
Hepatic
Posthepatic
Prehepatic- hemolysis (excessive breakdown of blood cells), hematoma, ineffective erythropoietin
Hepatic - dysfunction of liver cells, ex) newborn jaundice
Posthepatic - mechanical obstruction
What is portal hypertension and what are the clinical manifestations?
Results in varices throughout the GI tract and ascites
* Gastroesophageal varices
Bleeding with varices, vomiting with blood, rectal bleeding, bloody stool, anemia, shock? Loss of blood
What is the treatment for portal hypertension?
Fluid resuscitation Blood replacement Clotting factors Medications Surgical interventions vitamins Balloon tamanade – inflated to apply pressure
Portal systemic encephalopathy
Excessive ammonia – exact cause unknown
Can cause neurologic and psychiatric problems- could look like dementia, psychosis, lethargy, coma
Asterixis – “flapping tremor”
Treatment for portal systemic encephaopathy
lactulose – helps eliminate nitrogenous waste- antibiotics, low protein diet, high fiber
What are some complications of liver disease?
Ascites
Spontaneous bacterial peritonitis
Hepatorenal syndrome
What is Spontaneous bacterial peritonitis?
gut bacteria moves through wall into peritoneal- start can be very vague, can have fever, test peritoneal fluid, positive culture and elevated WBC, antibiotics- poor prognosis
What is hepatorenal syndrome?
acute, progressive- kidneys were normal until the liver is so bad that it effects them
Diagnosing liver disease
AST (aspartate aminotransferase) ALT (alanine aminotransferase) ALP (alkaline phosphatase) Bilirubin Albumin PT (prothrombin time)
What two types of hepatitis are transmitted through food?
A and E
How are hepatitis B, C, and D transmitted?
Blood
B=sexual contact
How do you treat hepatitis B,C and D?
Immunoglobulins and antiviral
What is chronic persistent hepatitis?
mild and asymptomatic- no treatment needed
What is chronic active hepatitis?
progressive and destructive- can lead to cirrhosis, fatigue, malaise, N, anorexia, ascites, jaundice, abd pain- liver enzymes- treatment based on cause
What is autoimmune hepatitis?
chronic active, diagnosed by antibodies, treated differently
What causes cirrhosis of the liver?
Liver diseases including hepatitis
Biliary cirrhosis
Alcoholic cirrhosis
Clinical manifestations of cirrhosis
All of the symptoms resulting from hepatocellular failure and portal hypertension.
What is cirrhosis?
Fibrotic, nodules- permanent damage – poor blood flow
Which medications eradicate the H Pylori infection?
what are their AE?
Amoxicillin (Amoxil)
Clarithromycin (Biaxin)
Metronidazole (Flagyl)
Nausea and diarrhea
What is our Histamine2-Receptor Antagonists drug?
Ranitidine (Zantac):
How does Ranitidine work?
Suppresses the secretin of gastric acid by selective blocking H2 receptors in parietal cells lining the stomach
What are the AE of ranitidine?
Caution in pregnancy
Multiple drug interactions with cimetidine (P450 inhibitor – avoid with theophylline, warfarin, phenytoin, lidocaine, etc.)
Doses needs to be adjusted in renal insufficiency
What are the AE of Omeprazole?
*Long-term use increases risk of osteoporosis
Increased fracture risk due to decreased absorption of calcium
*Increased risk of:
Pneumonia
Clostridium difficile infection
What drug interactions does omeprazole have?
Clopidogrel (Plavix)
What is motion sickness caused by?
*stimulation of the vestibular system–which has many histaminic (H1) and muscarinic cholinergic receptors
What are the four parts of the brain that affect vomiting?
Chemoreceptor trigger zone (CTZ)
Cerebral cortex
Vestibular system and
GI tract - visceral afferents
When you think motion sickness, you think_____?
vestibular mechanism
What is our serotonin antagonist?
Ondansetron (Zofran):
What does Ondansetron do?
Blocks 5HT3 receptors in CTZ & afferent vagal neurons in the upper GI tract
**prevention of chemo induced and post-op N/V
What are the AE of Ondansetron?
QTc prolongation, headache, dizziness, lightheadedness
What does Promethazine (Phenergan); do?
block dopamine2 receptors in CTZ
What are the AE of promethazine?
respiratory depression, sedation, local tissue injury with extravasation, EPS
What is Metoclopramide (Reglan)
and how does it work?
Prokinetic/Dopamine Antagonists
Controls N/V by blocking dopamine and serotonin receptors
Augments action of acetylcholine, which causes an ↑ in GI motility
Good for gastroparesis (diabetes)
What are the AE of Metoclopramide?
Contraindicated in clinical with GI perforation, bleeding or obstruction
Can cause diarrhea and tardive dyskinesia-EPS
What is normal transit (functional) constipation?
Normal rate of stool passage, but difficulty with stool evacuation from low-residue, low-fluid diet
What is slow-transit constipation?
Impaired colonic motor activity with infrequent bowel movements and straining
What type of laxative is Psyllium (Metamucil)?
Bulk-Forming Laxatives
Psyllium (Metamucil)
Functions like dietary fiber- soften fecal mass and increase mass
Used for diverticulosis and irritable bowel syndrome
**48 – 72 hours for clinical effect
AE:Esophageal obstruction
What type of laxative is Docusate sodium (Colace)?
Surfactant Laxatives
Docusate sodium (Colace)
- Alter stool consistency, water into feces = stool softener
- Stimulate intestinal motility
- Increase quantities of water and electrolytes in the intestinal lumen
- Widely used and abused
Legitimately used for opioid-induced constipation and for constipation from slow intestinal transit
What type of laxatives are Bisacodyl (Dulcolax) & Senna (Senokot)?
Stimulant laxatives
Bisacodyl (Dulcolax) & Senna (Senokot
-selective action on the nerve plexus of intestinal smooth muscle leading to enhanced motility
-Rapid effects, but harsh cramping, depending on dosage ** don’t take with antacids, milk, PPIs
Castor oil is a member of this class (Pregnancy Category X)
What are the AE of laxative salts?
Dehydration: substantial water loss
Renal decline: toxicity
Sodium retention: exacerbated heart failure, hypertension, edema
What are the osmotic laxitives?
Polyethylene glycol (PEG) Lactulose
Polyethylene glycol (PEG)
Miralax, glycolax, Peglax
Nonabsorbable
Effect in 2 -4 days
AE: nausea, bloating, cramping, flatulence
PEG + electrolytes – used for bowel preps
Golytely
Colyte
Lactulose
Semisythethic dissacharide
Galactose + fructose
Metabolized by colonic bacteria to lactic, formic, & acetic acids
Also used for hepatic encephalopathy
Acids exert mild osmotic action
Effect in 1 – 3 days
AE: significant flatulence & cramping
What is the difference between a allergy and autoimmune hypersensitivity?
Allergy – the antigen attacked is foreign
Autoimmune – the antigen attacked is self
What is the Antigenic mimicry theory
theory?
foreign antigen is similar to self so small alterations can look like the antigen= body attacks
What is the Release of sequestered antigens theory?
during fetal development self antigen have not been exposed to lymphocytes and then meet later which causes an attack
What is the T-cell theories
B-cell theories
Mast cell theory?
T-Cell- Suppressor t-cell function altered- something in process that’s not working
B-cells- Same for t cells but for Bcells
Mast cells- Same as t cell for mast
What are some examples of Genetic factors and Environmental triggers for autoimmunity?
Genetic- genes that are associated with autoimmune- women are more likely
Environmental- viruses or bacteria- toxins in soil
Hypersensitivity 1-3 are mediated by what type of cells? What are some examples?
B-cells
1-anaphylactic reaction
2- rheumatic heart disease
3- systemic lupus erythematosis
Hypersensitivity 4 is mediated by what type of cell?
Example
T-cells
4- contact dermatitis
How do you get Type I Hypersensitivity and what does it do?
Genetic
exposure to an antigen, IgE receptors link on mast cell in area of exposure, mast cells release proinflammatory mediators (e.g. histamine) with immediate 15-30 min reaction
Histamine
Increased vascular permeability Vasodilation Urticaria Smooth muscle constriction Increased mucus secretion Pruritus (H1 receptor stimulated) Has different receptors (H1-H4); each receptor causes different responses
What are some local responses for type 1 hypersensitivity?
Urticarial (hives)
Sinusitis
Asthma
What are some systemic responses to type 1 hypersensitivity?
Vasodilation
Bronchoconstriction
Shock
What happens with type 2 hypersensitivity?
Also known as tissue-specific, cytotoxic, or cytolytic hypersensitivity
Often immediate reaction, but some occur over time
Antibodies attack antigens on surface of specific cells or tissues causing lysis
**works on antigens or tissues of another human- blood, transplants
Rheumatic Heart Disease
Group A Beta-hemolytic streptococcal throat infection
Rheumatic fever, inflammation, tissue damage:
Skin
Joints
Heart: endocardium, valves, muscle
Central Nervous System
What would someone present with if they had rheumatic heart disease?
Sore throat Aching joints Fever Swollen lymph nodes Nausea Vomiting Skin nodules Rash
What lab/clinical findings would you find with rheumatic heart disease?
Hx of group A strep throat infection Heat, redness, swelling in large joints Pink-red macular rash on trunk and arms Chorea (rare) Serum c-reactive protein White blood cell count (WBC) Erythrocyte sedimentation rate (ESR)
Type III Hypersensitivity
Possible etiologies: infection, environmental antigen, autoimmune process
Pathogenesis: deposit of antigen-antibody complexes in tissues results in activation of complement and self-sustaining inflammation (ongoing)
Mechanism of injury: the ongoing inflammation causes tissue injury
What is the difference between small and large deposits with type 3 hypersensitivity?
Smaller- can circulate longer in boy which can cause increased immune response but can also be removed by kidneys
Large- phagocytized more readily- if they circulate they can be stuck in kidney
Systemic lupus erythematosus
Occurs more frequently in women (7 to1)
Individual develops antibodies against nuclear antigens such as DNA, DNH, and RNA
Variety of signs and symptoms
Diagnosis may be difficult
Systemic lupus erythematosus and patient reports
Relapsing/remitting symptoms Fatigue Weight loss Fever Dyspnea Chest pain Joint pain Muscle pain Facial rash Bruising
Systemic lupus erythematosus and clinical findings
Serum antinuclear antibody titer ≥ 1:80 Anemia Thrombocytopenia Pleural friction rub Pericardial friction rub
Type IV Hypersensitivity
Delayed hypersensitivity
Pathogenesis: sensitized T cells react with antigen and initiate inflammation and cell destruction – antibodies are not necessary produced
Contact hypersensitivity
Most familiar type (poison ivy)
Epidermal phenomenon
Peaks in 48 to 72 hours
Slow reaction; hapten very small, incomplete antigen; becomes complete antigen when attaches to a carrier
What are our 2 antihistamines-1?
Diphenhydramine
Cetirizine
What is our Beta-adrenergic agonists
?
Epinephrine
What are our Corticosteroids?
Prednisone
Methylprednisolone
Histamine 1 effects
Vasodilation
Increased capillary permeability
Bronchoconstriction
Activation of sensory nerve production of itching and pain
Promotes secretion of mucus
CNS: role in cognition, memory, sleep-wake cycle
Diphenhydramine
Use: Allergic Reactions, Sleep, Motion Sickness, Common Cold
*Injectable, Oral, Topical
Take with food
Interactions-Look for concomitant antimuscarinic agents
Look for concomitant sedating agents
Diphenhydramine AE
Sedation- 1st gen, across BBB CNS - Dizziness, incoordination, confusion, fatigue CNS stimulation Severe: Respiratory depression Severe local tissue injury
Cetirizine
2nd Generation/Non Sedating Antihistamine
Incidence is < 10%…could argue if this is truly “non-sedating”
Advantages:Dosed daily vs. q 4 – 6 hours
Glucocorticoid Pharmacologic Effects
Interrupt inflammatory process via many mechanisms
Inhibit synthesis of mediators: prostaglandins, leukotrienes, histamine
Suppress infiltration of phagocytes
Suppress proliferation of lymphocytes
AE of Glucocorticoid
Adrenal insufficiency, Osteoporosis: suppresses bone formation by osteoclasts, Infection, Glucose intolerance,
Myopathy, Fluid & electrolyte abnormalities, Growth retardation, Psychologic disturbances, Cataracts and glaucoma, Peptic ulcer disease
Epinephrine AE
Hypertension
Dysrhythmias
Angina (increased cardiac work and oxygen demand)
Necrosis following extravasation
Hyperglycemia: activation of beta receptors breaking down glycogen
Epinephrine formulations
1:1000 (0.3) 1 mg/1 mL concentration SC, IM dosing 1:10,000 (3) 1 mg/10 mL IV & intracardiac administration
Epi Pen Counseling Points
Discuss triggers and when to use
Show proper technique with holding pen
Do not put your thumb over the top!!
Inject in outer thigh at a 90 degree angle through clothes and HOLD in place for at least 10 seconds
