Final Flashcards
Transverse fracture
Break occurs at right angles to the long axis of the bone
Spiral fracture
Twisted or circular break that affects the length of bone
Suspicion for child abuse
S-shaped
Longitudinal fracture
Fracture along the length of the bone
Oblique fracture
45 degree angle diagonal or slanting that occurs between horizontal and perpendicular planes of the bone
Comminuted fracture
Splintered into pieces
Impacted fracture
Telescopes or drives one fragment into the other
AKA compression or buckle fracture
Greenstick fracture
Break through the periosteum on one side while only bowing or buckling on the other side
Stress fracture
Fracture on the cortical surface
Can become complete
Avulsion fracture
Small fragment of bone
Complete fracture
Break through the entire bone
Incomplete fracture
Partial break, not completely through the bone
Open fracture
Open wound or break in the skin near the fracture
AKA compound fracture
Closed fracture
No open wound
What is the leading cause of acute and chronic illness in children?
Asthma
Asthma
Chronic inflammatory disorder of bronchial mucosa
Asthma causes 3 things:
- Hyperresponsiveness: inflammation
- Bronchoconstriction
- Reversible airflow obstruction: air can’t get out
Two types of asthma
1. Intrinsic/ non allergic Usually adult onset No hx of allergies Respiratory infections/psychosocial triggers: stress, laughing 2. Extrinsic / allergic Triggers Exercise induced Status asthmaticus: 911
Populations at high risk for asthma
African Americans and Hispanics
Live in inner-city: environmental factors
Premature, low birth weight
Asthma patho: early response
Allergen binds to IgE on mast cells
Mast cells degranulate
Mediators released
Vasodilation, increased permeability, bonchospasm, edema and mucus secretion
Asthma patho: late response
4-8 hours (or immediate if no allergen involved)
Epothelial damage: chemotactic recruitment causes latent release of inflammatory mediators
Accumulation of mucus and cellular debris form plug in airways
Asthma to respiratory failure
Obstruction: impaired expiratory airflow
Air trapping
Hypoxemia
Hyperventilation: increased RR decreases paCO2 which leads to respiratory alkalosis
IF not corrected, tidal volume is decreased: start retaining CO2 = respiratory acidosis
Most common clinical manifestations of asthma
#1 Wheezing Cough Chest tightness Sputum Tachypnea Tachycardia
Severe manifestations of asthma
Cyanosis Retractions, nasal flaring Decreased breath sounds Agitation Pulsus paradoxus
Pulsus paradoxus
Decrease in systolic BP during inspiration
Bronchiolitis: patho
Viral (RSV) attack leads to necrosis of bronchial epithelium
Mucus production = obstruction
Inflammatory exudate
Air trapping = decrease expiratory capacity
Atelectasis: deflated alveoli
Do’s and Don’ts of treating bronchiolitis
DO use inhaled hypertonic saline to keep lung tissue moist
Bronchodilators and steroids NOT recommended
Virchow’s Triad
Vessel wall injury
Circulatory stasis
Hypercoaguable conditions
Clinical manifestations of PE
Restlessness, apprehension, anxiety Dyspnea Chest pain Tachycardia, tachypnea Hemoptysis Progress to heart failure, shock, respiratory arrest
Pulmonary embolism patho
Hypoxic vasoconstriction Decreased surfactant Release of neurohumoral and inflammatory substances Pulmonary edema Atelectosis
Elevated D-dimer
Measure of fibrin degredation factors: trying to break down the clot in a pulmonary embolism
Inflammatory mediators involved in late asthma response
Synthesis of leukotrienes: prolonged smooth muscle contraction
Neuropeptides: increased bronchial hyper-responsiveness: lowers threshold
Eosinophils: direct tissue injury; impaired mucociliary function
Corticosteroids
Glucocorticoids = cortisol like Mineralocorticoids = aldosterone like Decrease numbers of inflammatory cells Decrease cytokines Affect epithelial cells
Inhaled corticosteroids for asthma treatment
Maintenance therapy
Minimal systemic absorption
MDI and nebulizer
Beclomethasone
Inhaled corticosteroid Asthma treatment Common AE: Oropharyngeal candidiasis Dysphonia Can promote bone loss
Albuterol
Selective beta-2 agonist
Relieves acute bronchospasm
AE: tachycardia, tremor, hypokalemia
Ipratropium
Bronchodilator
Blocks muscarinic receptors in bronchi
Short acting anticholingergic
Montelukast
Suppress effects of leukotrienes Reduce inflammation, bronchoconstriction, airway edema, and mucus production Treats asthma Generally well tolerated Metabolized by CYPP450
Definition of meningitis
Inflammation/infection of the meninges and subarachnoid space
Main bacterial cause of meningitis in adults, peds, and newborns
Adults: Streptococcus pneumoniae
Peds: Neisseria meningitidis
Newborns: E. Coli and Group- beta strep
Meningitis: patho
Neutrophils called to area
Exudate produced: thickens CSF
Causes edema: Increased ICP
3 areas of clinical manifestations for meningitis
Infectious: fever, chills, tachycardia, petechial rash
Neurologic: Decreased LOC, cranial nerve impairment, signs of increased ICP
Meningeal irritation: Nuchal rigidity, Kernig’s sign, Brudzinski’s sign
3 main causes of seizures in neonates
#1 infection Birth defect or injury
Epileptogenic focus
Where a seizure starts in the brain
Status epilepticus
Can’t get it to stop with traditional meds
Two AED’s also used for bipolar treatment and mood stabilizers
Valproic Acid
Carbamazepine
Phenytoin
Anti-epileptic
Selective inhibition of sodium channels
Healthy neurons unaffected, only blocks neurons that are hyperactive
Small therapeutic window
AE: Gingivial hyperplasia, rashes, teratogenic
Phenytoin IV
Can cause cardiovascular AE: dysrhythmias, hypotension
Purple glove syndrome: extravasation
Must admin slowly with 20 gauge or greater
Fosphenytoin
Pro-drug
Only IV
Can infuse faster and has less side effects
Carbamazepine
Used for partial seizures and tonic-clonic
Suppresses high-frequency neuronal discharge in and around seizure foci
Metabolized by liver
Autoinduction: induces body’s enzymes and will metabolize faster
Bone marrow suppression: usually become tolerant
Carbamazepine Adverse effect
Hyponatremia: promotes ADH secretion and water retention
Monitor sodium levels bc can cause seizures
Lots of drug interactions
Valproic Acid common form
Divalproex Sodium: Depakote
Delayed release tablets
Higher compliance
Depakote/ Divalproex
Unknown exact MOA
Extensive hepatic metabolism and renal excretion
Divalproex AE
GI disturbance Hepatoxicity: avoid in under 2 years of age Pancreatitis Hyperammonemia Teratogenic: 4x higher than other AEDs
Levetiracetam
Newer AED, possibly safer
Minimally metabolized so minimal drug interactions
Drowsiness is main AE but $$$
Mannitol
Osmotic diuretic
Treats increased ICP
Glucagon
Hormone that increases amount of glucose in the blood
Insulin
Hormone that decreases the amount of glucose in the blood
Produced by beta cells in the pancreas
Type 1 Diabetes
Absolute insulin insufficiency
Autoimmune attack on beta cells of pancreas
3 P’s of Type 1 Diabetes
Polyuria: increased urine
High glucose in blood brings more water which increases urine output
Polydipsia: increased thirst
Polyphagia: increased hunger
Cells deprived of glucose making brain signal hunger
Blood glucose parameters for Type 1 and 2 diabetes
Random blood glucose >200 with signs and symptoms
Fasting glucose >126
>200 2 hours after oral glucose test
HgA1C > 6.5
Hypoglycemia symptoms
Tachycardia Irritable Restless Excessive hunger Diaphoresis, depression
Diabetic Ketoacidosis
Prolonged hyperglycemia with metabolic acidosis
Causes of DKA
Illness
Liver turns fatty acids into ketone bodies: an acid, increases acidity of blood
Clinical symptoms of DKA
Kussmaul respirations: deep, labored breathing trying to reduce C02 to decrease acidity
Fruity smelling breath
Hyperkalemia (insulin needed for sodium-potassium pump)
Treatment for DKA
Hydration
Insulin
Manage electrolytes
Difference between Type 1 and Type 2 diabetes
Type 2 body is resistant to action of insulin on peripheral tissues
Requires more insulin
Lowered glucose utilization
Risk factors for Type 2 diabetes
Old age Obesity at any age Sedentary lifestyle HTN Genetic component Metabolic syndrome
Type 2 diabetes: patho
Insulin resistance causes body to produce more insulin: hyperinsulinemia
Over time, beta cells lose function in pancreas: leads to hypoinsulinemia
Leads to increase in glucagon: leads to type 2 diabetes
Long term consequences for type 1 and 2
Eyes: visual acuity, blurred vision, cataracts
Kidneys: end stage renal failure from HTN
Heart disease and HTN
Stroke
Neuropathy
Poor peripheral perfusion
Increased risk of infection
Adrenal cortex controls
Cortisol: suppression of CRH and ACTH
Glucocorticoids: play role in immune system, inflammatory process and convert food into energy
Mineralcorticoids: aldosterone - sodium and K, BP, fluid status
Androgens: male sex hormones
Addison’s disease
Adrenocortical insufficiency
Caused by destruction of adrenal cortex
Cortisol deficiency causes:
Decreased liver capacity: decreases gluconeogenesis
Leads to hypoglycemia
Higher levels of ACTH promotes pigmentation of skin (bronze)
Aldosterone deficiency causes:
Increased loss of sodium and reabsorption of K
Losing more water: leads to hypotension
Androgen deficiency causes:
Decreased hair growth: axillary and pubic
Decreased libido
Main symptoms of Addison’s Disease
Bronze skin Hypotension Hypoglycemia Body hair changes Weakness Weight loss GI disturbance
Cushing’s Disease
Hypercortisolism
Cluster of clinical abnormalities caused by excessive adrenocortical hormones or related corticosteroids
Clinical manifestations of Cushing’s
Personality changes Hyperglycemia Moon face: fat deposits on face and shoulders CNS irritability NA and fluid retention (edema) GI distress Osteopororsis Thin skin/ extremities
Four types of insulin separated by time of action
Short duration: rapid acting (Lispro)
Short duration: slower acting (Regular insulin)
Intermediate duration: NPH
Long duration: Insulin glargine (Lantus)
How to mix insulins
Draw up short acting first
Do not want long acting mixed in a vial of short acting
Short acting and long acting mixed together
How to treat hypoglycemia (PO, IM, IV)
PO if A and O x4: OJ or sugar tabs
IV dextrose for patients who can’t do PO
IM dextrose would cause muscle damage
IM glucagon possible
Metformin
Oral med for Type 2 DM
MOA: inhibits glucose production in liver
Sensitizes insulin receptors in target tissue
NO Hypoglycemia bc does NOT stimulate insulin
AE: GI disturbance
Can cause lacticacidosis in renal dysfunction
Glipizide (Sulfonylureas)
First PO antidiabetic MOA: stimulates release of insulin from pancreatic cells * Pancreas must be functional Commonly used with metformin Avoid in renal dysfunction and pregnancy
Pioglitazone
MOA: reduces insulin resistance and decreases glucose production
Not a monotherapy
Metabolism: CYP2C8 (drug interactions)
AE: respiratory infections, HA, sinusitis, fluid retention (imp in cardiac disease)
Repaglinide
MOA: stimulates insulin release (if sulfonylurea doesn’t work, this won’t either)
Very short half life
AE: hypoglycemia - must eat 30 min after taking
Incretin mimetics
New class of antidiabetic drug GLP-1 and GIP: hormones important for glucose absorption
Sitagliptin (Incretin mimetic)
Blocks DPP-4: stimulates glucose-dependent release of insulin; suppresses postprandial release of glucagon
Common AE: URI, HA
Serious: hypoglycemia, pancreatitis, Stevens-Johnson syndrome
Liraglutide (Incretin mimetic)
MOA: analog of human GLP-1 that causes direct activation of GLP-1 receptors
Slows gastric emptying time, stimulates glucose-dependent insulin release, inhibits post-prandial release of glucagon
SQ Injection
AE: GI disturance, rarely pancreatitis
Autosome
Name for an ordinary paired chromosome, not a sex chromosome
Carrier
Person that transmits a genetic condition but suffers no symptoms
Heterozygous
Having dissimilar pairs of genes (Aa)
Homozygous
Have the same pairs of genes (AA or aa)
Genotype
Genetic makeup of an organism
Phenotype
Appearance of an organism resulting from the interaction of the genotype and environment
Chromosome
Structure of DNA molecules that consists of 2 strands that wind around each other (double helix)
Gene
Basic physical unit of inheritance that is passed from parents to offspring
Meiosis
Cell division used in gamete formation
Mutation
Change in DNA sequence that results from copy mistakes or exposure to radiation, chemicals or infections
Mendel
Austrian monk who worked out basic laws of inheritance
Inherited
Trait that is genetically determined
Pedigree
Genetic representation of a family tree
Punnett Square
Diagram used to predict probability outcome of a genetic cross
Probability
Likelihood of an occurrence
Allele
Different forms of the same gene
Epigenetics
How genes are turned on or off by their environment
4 broad types of genetic disorders
Chromosomal anomalies - abnormal number
Chromosomal anomalies - abnormal structure
Mendelian single-gene disorder - autosomal dominant/ recessive
Mendelian single-gene disorder - x-linked
Euploidy
“normal”
46 chromosomes
Aneuploidy
Anything other than 46 chromosomes
Monosomy
Deficiency of a chromosome
Polysomy/ trisomy
Too many chromosomes
Monosomy vs. polysomy
Monosomy usually worse
Types of abnormal chromosome structures
Deletion
Duplications
Inversions
Translocations
Point mutations
Substitution of a single base pair
Happens often, might not have consequences
Frameshift mutations
Addition or deletion of 1 or 2 nucleotides
All codons after are incorrect
More severe consequences
2 examples of Autosomal recessive disorders
Cystic fibrosis
Sickle cell
Example of autosomal dominant disorder
Huntington’s Disease
Delayed onset, usually > 40
X-linked recessive inheritance
More often in males
Can skip a generation via carrier female
Never passed from father to son
Affected father passes to all his daughters
2 examples of x-linked recessive disorder
Duchenne Muscular Dystrophy
Hemophilia A
Polygenic traits
Result from several genes acting together
Environment doesn’t affect outcomes
Multifactorial traits
Genes make an individual susceptible
Environment can trigger
E.g. HTN, weight, mental health, asthma
Penetrance
% in which gene is expressed
% of individuals with a given genotype who exhibit the phenotype associated
Expressivity
Level of expression
Extent of variation in phenotype associated with a particular genotype
3 Types of Down Syndrome
Trisomy 21 caused by nondisjunction (95%)
Translocation: full or partial copy of chromosome 21 attaches to another chromosome (4%)
Mosaicism: some cells have 46 chromosomes and some have 47 (1%)
Duchenne Muscular Dystrophy
X-linked recessive: affects only males
Muscle cells deficient in protein dystrophin -> weak cell membrane
What causes muscle degeneration in Duchenne MD?
Muscle cells deficient in protein dystrophin
Weak cell membrane leaks creatinine kinase and takes in calcium
Inflammatory process activated
Leads to muscle fiber necrosis and degeneration
Clinical manifestations of Duchenne Muscular Dystrophy
Large calves: muscle replaced by fat
Gower’s sign
Loss of ability to ambulate 8-13
Muscle weakness progresses -> respiratory weakness -> premature death
Sickle Cell Disease
Autosomal recessive
Point mutation on chromosome 11: codes for different amino acids: changes hemoglobin molecule HbS
Hemoglobin molecule HbS
When O2 is low, HbS undergoes polymerization and causes hemoglobin to change into sickled shape
Triggers for Sickle Cell
Dehydration Infection Hypoxemia Acidosis Cold exposure
Effects of sickling
Occlusion of small arteries
Tissue damage due to lack of blood
Pain
Clinical manifestations of Sickle Cell
Chronic anemia Pallor Jaundice Fatigue Delayed growth and puberty Infections: most common cause of death
Vaso-occlusive sickle cell crisis
Blocked blood flow Extremely painful - joint or bone pain Lasts days to weeks Acute chest syndrome Hand and foot syndrome
Acute sequestration sickle cell crisis
911 6 mo - 4 y.o. Blood pools causing enlargement Hypovolemic shock Spleen, liver and lungs
Aplastic sickle cell crisis
Increased destruction or decreased production
Profound anemia
Associated with viral infections, fever
Treatment for Sickle Cell
Stem cell transplant Education to prevent crisis Vaccines Penicillin prophylaxis Transfusions Splenectomy Pain management, hydration and oxygenation
S I C K L E
Strokes, Swelling of hands/feet/spleen Infections, Infarctions Crisis, Chest syndrome, Cardiac problems Kidney disease Liver and Lung Eyes/ Erection
Ulcerative Colitis
Inflammatory disease of the mucosa of the colon and rectum
Crohn’s Disease
Inflammation of GI tract that extends through all layers of intestinal wall “cobblestones”
Skip lesions: areas of healthy GI tract
Major differences between UC and Crohn’s
UC: bloody stool, mucosal layer only, diarrhea
Crohn’s: entire intestinal wall, pain, weight loss/malabsorption
GERD
Backflow of gastric contents into the esophagus through the lower esophageal sphincter
GERD in peds
Infants can have poor weight gain, respiratory symptoms
Older children: heartburn, vomiting, asthma, pneumonia, upper airway symptoms
Osteomyelitis
Severe infection of bone and local tissue
High risk groups for osteomyelities
Kids under 16, esp. males and older adults due to risk of injury Indwelling devices Instrumentation (rods) Metabolic/vascular disease Diabetes Smoking, alcohol abuse, IV drugs
Compartment Syndrome
Accumulation of pressure in a fracture Surgical emergency 5 P's: Pain (out of proportion) Parasthesia (decreased sensation) Pallor Pulselessness Paralysis
Ranitidine (Zantac)
OTC and Rx, IV and PO
Suppresses the secretion of gastric acid by selectively blocking H2 receptors in parietal cells (acid producers) lining the stomach
Drug interactions: P450 inhibitor
Omeprazole (Prilosec)
OTC and Rx, IV and PO
Proton pump inhibitor: irreversible inhibition of Hydrogen Potassium ATPase: blocks gastrin production
Gastrin hormone helps with GI motility and stomach acid production
AE: long term use increases risk of osteoporosis; increased risk of pneumonia, C. diff, dementia and kidney injury
Inhibits CYP2C19 (Plavix inhibition)
Sucralfate
Acidic environment changes sucralfate into thick substance that adheres to an ulcer for up to 6 hours - protects from further injury
AE: constipation, caution in pregnancy and renal failure, may interfere with absorption of other meds
Magnesium hydroxide and Calcium carbonate
Neutralize gastric acid and inactivate pepsin
Potential mucosal protection due to stimulation of production of prostaglanidns
AE: constipation and diarrhea, caution in pregnancy and renal dysfunction, avoid in GI obstruction/perforation
