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Final Flashcards

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1
Q

Transverse fracture

A

Break occurs at right angles to the long axis of the bone

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2
Q

Spiral fracture

A

Twisted or circular break that affects the length of bone
Suspicion for child abuse
S-shaped

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3
Q

Longitudinal fracture

A

Fracture along the length of the bone

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4
Q

Oblique fracture

A

45 degree angle diagonal or slanting that occurs between horizontal and perpendicular planes of the bone

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5
Q

Comminuted fracture

A

Splintered into pieces

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6
Q

Impacted fracture

A

Telescopes or drives one fragment into the other

AKA compression or buckle fracture

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7
Q

Greenstick fracture

A

Break through the periosteum on one side while only bowing or buckling on the other side

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8
Q

Stress fracture

A

Fracture on the cortical surface

Can become complete

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9
Q

Avulsion fracture

A

Small fragment of bone

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10
Q

Complete fracture

A

Break through the entire bone

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11
Q

Incomplete fracture

A

Partial break, not completely through the bone

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12
Q

Open fracture

A

Open wound or break in the skin near the fracture

AKA compound fracture

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13
Q

Closed fracture

A

No open wound

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14
Q

What is the leading cause of acute and chronic illness in children?

A

Asthma

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15
Q

Asthma

A

Chronic inflammatory disorder of bronchial mucosa

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16
Q

Asthma causes 3 things:

A
  1. Hyperresponsiveness: inflammation
  2. Bronchoconstriction
  3. Reversible airflow obstruction: air can’t get out
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17
Q

Two types of asthma

A 
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
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18
Q

Populations at high risk for asthma

A

African Americans and Hispanics
Live in inner-city: environmental factors
Premature, low birth weight

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19
Q

Asthma patho: early response

A

Allergen binds to IgE on mast cells
Mast cells degranulate
Mediators released
Vasodilation, increased permeability, bonchospasm, edema and mucus secretion

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20
Q

Asthma patho: late response

A

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

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21
Q

Asthma to respiratory failure

A

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

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22
Q

Most common clinical manifestations of asthma

A 
#1 Wheezing
Cough
Chest tightness
Sputum
Tachypnea
Tachycardia
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23
Q

Severe manifestations of asthma

A 
Cyanosis
Retractions, nasal flaring
Decreased breath sounds
Agitation
Pulsus paradoxus
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24
Q

Pulsus paradoxus

A

Decrease in systolic BP during inspiration

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25
Bronchiolitis: patho
Viral (RSV) attack leads to necrosis of bronchial epithelium Mucus production = obstruction Inflammatory exudate Air trapping = decrease expiratory capacity Atelectasis: deflated alveoli
26
Do's and Don'ts of treating bronchiolitis
DO use inhaled hypertonic saline to keep lung tissue moist | Bronchodilators and steroids NOT recommended
27
Virchow's Triad
Vessel wall injury Circulatory stasis Hypercoaguable conditions
28
Clinical manifestations of PE
``` Restlessness, apprehension, anxiety Dyspnea Chest pain Tachycardia, tachypnea Hemoptysis Progress to heart failure, shock, respiratory arrest ```
29
Pulmonary embolism patho
``` Hypoxic vasoconstriction Decreased surfactant Release of neurohumoral and inflammatory substances Pulmonary edema Atelectosis ```
30
Elevated D-dimer
Measure of fibrin degredation factors: trying to break down the clot in a pulmonary embolism
31
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
32
Corticosteroids
``` Glucocorticoids = cortisol like Mineralocorticoids = aldosterone like Decrease numbers of inflammatory cells Decrease cytokines Affect epithelial cells ```
33
Inhaled corticosteroids for asthma treatment
Maintenance therapy Minimal systemic absorption MDI and nebulizer
34
Beclomethasone
``` Inhaled corticosteroid Asthma treatment Common AE: Oropharyngeal candidiasis Dysphonia Can promote bone loss ```
35
Albuterol
Selective beta-2 agonist Relieves acute bronchospasm AE: tachycardia, tremor, hypokalemia
36
Ipratropium
Bronchodilator Blocks muscarinic receptors in bronchi Short acting anticholingergic
37
Montelukast
``` Suppress effects of leukotrienes Reduce inflammation, bronchoconstriction, airway edema, and mucus production Treats asthma Generally well tolerated Metabolized by CYPP450 ```
38
Definition of meningitis
Inflammation/infection of the meninges and subarachnoid space
39
Main bacterial cause of meningitis in adults, peds, and newborns
Adults: Streptococcus pneumoniae Peds: Neisseria meningitidis Newborns: E. Coli and Group- beta strep
40
Meningitis: patho
Neutrophils called to area Exudate produced: thickens CSF Causes edema: Increased ICP
41
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
42
3 main causes of seizures in neonates
``` #1 infection Birth defect or injury ```
43
Epileptogenic focus
Where a seizure starts in the brain
44
Status epilepticus
Can't get it to stop with traditional meds
45
Two AED's also used for bipolar treatment and mood stabilizers
Valproic Acid | Carbamazepine
46
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
47
Phenytoin IV
Can cause cardiovascular AE: dysrhythmias, hypotension Purple glove syndrome: extravasation Must admin slowly with 20 gauge or greater
48
Fosphenytoin
Pro-drug Only IV Can infuse faster and has less side effects
49
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
50
Carbamazepine Adverse effect
Hyponatremia: promotes ADH secretion and water retention Monitor sodium levels bc can cause seizures Lots of drug interactions
51
Valproic Acid common form
Divalproex Sodium: Depakote Delayed release tablets Higher compliance
52
Depakote/ Divalproex
Unknown exact MOA | Extensive hepatic metabolism and renal excretion
53
Divalproex AE
``` GI disturbance Hepatoxicity: avoid in under 2 years of age Pancreatitis Hyperammonemia Teratogenic: 4x higher than other AEDs ```
54
Levetiracetam
Newer AED, possibly safer Minimally metabolized so minimal drug interactions Drowsiness is main AE but $$$
55
Mannitol
Osmotic diuretic | Treats increased ICP
56
Glucagon
Hormone that increases amount of glucose in the blood
57
Insulin
Hormone that decreases the amount of glucose in the blood | Produced by beta cells in the pancreas
58
Type 1 Diabetes
Absolute insulin insufficiency | Autoimmune attack on beta cells of pancreas
59
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
60
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
61
Hypoglycemia symptoms
``` Tachycardia Irritable Restless Excessive hunger Diaphoresis, depression ```
62
Diabetic Ketoacidosis
Prolonged hyperglycemia with metabolic acidosis
63
Causes of DKA
Illness | Liver turns fatty acids into ketone bodies: an acid, increases acidity of blood
64
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)
65
Treatment for DKA
Hydration Insulin Manage electrolytes
66
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
67
Risk factors for Type 2 diabetes
``` Old age Obesity at any age Sedentary lifestyle HTN Genetic component Metabolic syndrome ```
68
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
69
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
70
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
71
Addison's disease
Adrenocortical insufficiency | Caused by destruction of adrenal cortex
72
Cortisol deficiency causes:
Decreased liver capacity: decreases gluconeogenesis Leads to hypoglycemia Higher levels of ACTH promotes pigmentation of skin (bronze)
73
Aldosterone deficiency causes:
Increased loss of sodium and reabsorption of K | Losing more water: leads to hypotension
74
Androgen deficiency causes:
Decreased hair growth: axillary and pubic | Decreased libido
75
Main symptoms of Addison's Disease
``` Bronze skin Hypotension Hypoglycemia Body hair changes Weakness Weight loss GI disturbance ```
76
Cushing's Disease
Hypercortisolism | Cluster of clinical abnormalities caused by excessive adrenocortical hormones or related corticosteroids
77
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 ```
78
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)
79
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
80
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
81
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
82
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 ```
83
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)
84
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
85
Incretin mimetics
``` New class of antidiabetic drug GLP-1 and GIP: hormones important for glucose absorption ```
86
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
87
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
88
Autosome
Name for an ordinary paired chromosome, not a sex chromosome
89
Carrier
Person that transmits a genetic condition but suffers no symptoms
90
Heterozygous
Having dissimilar pairs of genes (Aa)
91
Homozygous
Have the same pairs of genes (AA or aa)
92
Genotype
Genetic makeup of an organism
93
Phenotype
Appearance of an organism resulting from the interaction of the genotype and environment
94
Chromosome
Structure of DNA molecules that consists of 2 strands that wind around each other (double helix)
95
Gene
Basic physical unit of inheritance that is passed from parents to offspring
96
Meiosis
Cell division used in gamete formation
97
Mutation
Change in DNA sequence that results from copy mistakes or exposure to radiation, chemicals or infections
98
Mendel
Austrian monk who worked out basic laws of inheritance
99
Inherited
Trait that is genetically determined
100
Pedigree
Genetic representation of a family tree
101
Punnett Square
Diagram used to predict probability outcome of a genetic cross
102
Probability
Likelihood of an occurrence
103
Allele
Different forms of the same gene
104
Epigenetics
How genes are turned on or off by their environment
105
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
106
Euploidy
"normal" | 46 chromosomes
107
Aneuploidy
Anything other than 46 chromosomes
108
Monosomy
Deficiency of a chromosome
109
Polysomy/ trisomy
Too many chromosomes
110
Monosomy vs. polysomy
Monosomy usually worse
111
Types of abnormal chromosome structures
Deletion Duplications Inversions Translocations
112
Point mutations
Substitution of a single base pair | Happens often, might not have consequences
113
Frameshift mutations
Addition or deletion of 1 or 2 nucleotides All codons after are incorrect More severe consequences
114
2 examples of Autosomal recessive disorders
Cystic fibrosis | Sickle cell
115
Example of autosomal dominant disorder
Huntington's Disease | Delayed onset, usually > 40
116
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
117
2 examples of x-linked recessive disorder
Duchenne Muscular Dystrophy | Hemophilia A
118
Polygenic traits
Result from several genes acting together | Environment doesn't affect outcomes
119
Multifactorial traits
Genes make an individual susceptible Environment can trigger E.g. HTN, weight, mental health, asthma
120
Penetrance
% in which gene is expressed | % of individuals with a given genotype who exhibit the phenotype associated
121
Expressivity
Level of expression | Extent of variation in phenotype associated with a particular genotype
122
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%)
123
Duchenne Muscular Dystrophy
X-linked recessive: affects only males | Muscle cells deficient in protein dystrophin -> weak cell membrane
124
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
125
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
126
Sickle Cell Disease
Autosomal recessive | Point mutation on chromosome 11: codes for different amino acids: changes hemoglobin molecule HbS
127
Hemoglobin molecule HbS
When O2 is low, HbS undergoes polymerization and causes hemoglobin to change into sickled shape
128
Triggers for Sickle Cell
``` Dehydration Infection Hypoxemia Acidosis Cold exposure ```
129
Effects of sickling
Occlusion of small arteries Tissue damage due to lack of blood Pain
130
Clinical manifestations of Sickle Cell
``` Chronic anemia Pallor Jaundice Fatigue Delayed growth and puberty Infections: most common cause of death ```
131
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 ```
132
Acute sequestration sickle cell crisis
``` 911 6 mo - 4 y.o. Blood pools causing enlargement Hypovolemic shock Spleen, liver and lungs ```
133
Aplastic sickle cell crisis
Increased destruction or decreased production Profound anemia Associated with viral infections, fever
134
Treatment for Sickle Cell
``` Stem cell transplant Education to prevent crisis Vaccines Penicillin prophylaxis Transfusions Splenectomy Pain management, hydration and oxygenation ```
135
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 ```
136
Ulcerative Colitis
Inflammatory disease of the mucosa of the colon and rectum
137
Crohn's Disease
Inflammation of GI tract that extends through all layers of intestinal wall "cobblestones" Skip lesions: areas of healthy GI tract
138
Major differences between UC and Crohn's
UC: bloody stool, mucosal layer only, diarrhea | Crohn's: entire intestinal wall, pain, weight loss/malabsorption
139
GERD
Backflow of gastric contents into the esophagus through the lower esophageal sphincter
140
GERD in peds
Infants can have poor weight gain, respiratory symptoms | Older children: heartburn, vomiting, asthma, pneumonia, upper airway symptoms
141
Osteomyelitis
Severe infection of bone and local tissue
142
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 ```
143
Compartment Syndrome
``` Accumulation of pressure in a fracture Surgical emergency 5 P's: Pain (out of proportion) Parasthesia (decreased sensation) Pallor Pulselessness Paralysis ```
144
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
145
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)
146
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
147
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

Patho Pharm (2 decks)

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