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Patho Pharm > Final > Flashcards

Final Flashcards

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
Q

Bronchiolitis: patho

A

Viral (RSV) attack leads to necrosis of bronchial epithelium
Mucus production = obstruction
Inflammatory exudate
Air trapping = decrease expiratory capacity
Atelectasis: deflated alveoli

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26
Q

Do’s and Don’ts of treating bronchiolitis

A

DO use inhaled hypertonic saline to keep lung tissue moist

Bronchodilators and steroids NOT recommended

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27
Q

Virchow’s Triad

A

Vessel wall injury
Circulatory stasis
Hypercoaguable conditions

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28
Q

Clinical manifestations of PE

A 
Restlessness, apprehension, anxiety
Dyspnea
Chest pain
Tachycardia, tachypnea
Hemoptysis
Progress to heart failure, shock, respiratory arrest
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29
Q

Pulmonary embolism patho

A 
Hypoxic vasoconstriction
Decreased surfactant
Release of neurohumoral and inflammatory substances
Pulmonary edema
Atelectosis
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30
Q

Elevated D-dimer

A

Measure of fibrin degredation factors: trying to break down the clot in a pulmonary embolism

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31
Q

Inflammatory mediators involved in late asthma response

A

Synthesis of leukotrienes: prolonged smooth muscle contraction
Neuropeptides: increased bronchial hyper-responsiveness: lowers threshold
Eosinophils: direct tissue injury; impaired mucociliary function

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32
Q

Corticosteroids

A 
Glucocorticoids = cortisol like
Mineralocorticoids = aldosterone like
Decrease numbers of inflammatory cells
Decrease cytokines
Affect epithelial cells
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33
Q

Inhaled corticosteroids for asthma treatment

A

Maintenance therapy
Minimal systemic absorption
MDI and nebulizer

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34
Q

Beclomethasone

A 
Inhaled corticosteroid
Asthma treatment
Common AE:
Oropharyngeal candidiasis
Dysphonia
Can promote bone loss
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35
Q

Albuterol

A

Selective beta-2 agonist
Relieves acute bronchospasm
AE: tachycardia, tremor, hypokalemia

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36
Q

Ipratropium

A

Bronchodilator
Blocks muscarinic receptors in bronchi
Short acting anticholingergic

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37
Q

Montelukast

A 
Suppress effects of leukotrienes
Reduce inflammation, bronchoconstriction, airway edema, and mucus production
Treats asthma
Generally well tolerated
Metabolized by CYPP450
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38
Q

Definition of meningitis

A

Inflammation/infection of the meninges and subarachnoid space

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39
Q

Main bacterial cause of meningitis in adults, peds, and newborns

A

Adults: Streptococcus pneumoniae
Peds: Neisseria meningitidis
Newborns: E. Coli and Group- beta strep

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40
Q

Meningitis: patho

A

Neutrophils called to area
Exudate produced: thickens CSF
Causes edema: Increased ICP

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41
Q

3 areas of clinical manifestations for meningitis

A

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

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42
Q

3 main causes of seizures in neonates

A 
#1 infection
Birth defect or injury
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43
Q

Epileptogenic focus

A

Where a seizure starts in the brain

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44
Q

Status epilepticus

A

Can’t get it to stop with traditional meds

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45
Q

Two AED’s also used for bipolar treatment and mood stabilizers

A

Valproic Acid

Carbamazepine

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46
Q

Phenytoin

A

Anti-epileptic
Selective inhibition of sodium channels
Healthy neurons unaffected, only blocks neurons that are hyperactive
Small therapeutic window
AE: Gingivial hyperplasia, rashes, teratogenic

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47
Q

Phenytoin IV

A

Can cause cardiovascular AE: dysrhythmias, hypotension
Purple glove syndrome: extravasation
Must admin slowly with 20 gauge or greater

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48
Q

Fosphenytoin

A

Pro-drug
Only IV
Can infuse faster and has less side effects

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49
Q

Carbamazepine

A

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

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50
Q

Carbamazepine Adverse effect

A

Hyponatremia: promotes ADH secretion and water retention
Monitor sodium levels bc can cause seizures
Lots of drug interactions

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51
Q

Valproic Acid common form

A

Divalproex Sodium: Depakote
Delayed release tablets
Higher compliance

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52
Q

Depakote/ Divalproex

A

Unknown exact MOA

Extensive hepatic metabolism and renal excretion

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53
Q

Divalproex AE

A 
GI disturbance
Hepatoxicity: avoid in under 2 years of age
Pancreatitis
Hyperammonemia
Teratogenic: 4x higher than other AEDs
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54
Q

Levetiracetam

A

Newer AED, possibly safer
Minimally metabolized so minimal drug interactions
Drowsiness is main AE but $$$

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55
Q

Mannitol

A

Osmotic diuretic

Treats increased ICP

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56
Q

Glucagon

A

Hormone that increases amount of glucose in the blood

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57
Q

Insulin

A

Hormone that decreases the amount of glucose in the blood

Produced by beta cells in the pancreas

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58
Q

Type 1 Diabetes

A

Absolute insulin insufficiency

Autoimmune attack on beta cells of pancreas

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59
Q

3 P’s of Type 1 Diabetes

A

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
Q

Blood glucose parameters for Type 1 and 2 diabetes

A

Random blood glucose >200 with signs and symptoms
Fasting glucose >126
>200 2 hours after oral glucose test
HgA1C > 6.5

61
Q

Hypoglycemia symptoms

A 
Tachycardia
Irritable
Restless
Excessive hunger
Diaphoresis, depression
62
Q

Diabetic Ketoacidosis

A

Prolonged hyperglycemia with metabolic acidosis

63
Q

Causes of DKA

A

Illness

Liver turns fatty acids into ketone bodies: an acid, increases acidity of blood

64
Q

Clinical symptoms of DKA

A

Kussmaul respirations: deep, labored breathing trying to reduce C02 to decrease acidity
Fruity smelling breath
Hyperkalemia (insulin needed for sodium-potassium pump)

65
Q

Treatment for DKA

A

Hydration
Insulin
Manage electrolytes

66
Q

Difference between Type 1 and Type 2 diabetes

A

Type 2 body is resistant to action of insulin on peripheral tissues
Requires more insulin
Lowered glucose utilization

67
Q

Risk factors for Type 2 diabetes

A 
Old age
Obesity at any age
Sedentary lifestyle
HTN
Genetic component
Metabolic syndrome
68
Q

Type 2 diabetes: patho

A

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
Q

Long term consequences for type 1 and 2

A

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
Q

Adrenal cortex controls

A

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
Q

Addison’s disease

A

Adrenocortical insufficiency

Caused by destruction of adrenal cortex

72
Q

Cortisol deficiency causes:

A

Decreased liver capacity: decreases gluconeogenesis
Leads to hypoglycemia
Higher levels of ACTH promotes pigmentation of skin (bronze)

73
Q

Aldosterone deficiency causes:

A

Increased loss of sodium and reabsorption of K

Losing more water: leads to hypotension

74
Q

Androgen deficiency causes:

A

Decreased hair growth: axillary and pubic

Decreased libido

75
Q

Main symptoms of Addison’s Disease

A 
Bronze skin
Hypotension
Hypoglycemia
Body hair changes
Weakness
Weight loss
GI disturbance
76
Q

Cushing’s Disease

A

Hypercortisolism

Cluster of clinical abnormalities caused by excessive adrenocortical hormones or related corticosteroids

77
Q

Clinical manifestations of Cushing’s

A 
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
Q

Four types of insulin separated by time of action

A

Short duration: rapid acting (Lispro)
Short duration: slower acting (Regular insulin)
Intermediate duration: NPH
Long duration: Insulin glargine (Lantus)

79
Q

How to mix insulins

A

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
Q

How to treat hypoglycemia (PO, IM, IV)

A

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
Q

Metformin

A

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
Q

Glipizide (Sulfonylureas)

A 
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
Q

Pioglitazone

A

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
Q

Repaglinide

A

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
Q

Incretin mimetics

A 
New class of antidiabetic drug
GLP-1 and GIP: hormones important for glucose absorption
86
Q

Sitagliptin (Incretin mimetic)

A

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
Q

Liraglutide (Incretin mimetic)

A

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
Q

Autosome

A

Name for an ordinary paired chromosome, not a sex chromosome

89
Q

Carrier

A

Person that transmits a genetic condition but suffers no symptoms

90
Q

Heterozygous

A

Having dissimilar pairs of genes (Aa)

91
Q

Homozygous

A

Have the same pairs of genes (AA or aa)

92
Q

Genotype

A

Genetic makeup of an organism

93
Q

Phenotype

A

Appearance of an organism resulting from the interaction of the genotype and environment

94
Q

Chromosome

A

Structure of DNA molecules that consists of 2 strands that wind around each other (double helix)

95
Q

Gene

A

Basic physical unit of inheritance that is passed from parents to offspring

96
Q

Meiosis

A

Cell division used in gamete formation

97
Q

Mutation

A

Change in DNA sequence that results from copy mistakes or exposure to radiation, chemicals or infections

98
Q

Mendel

A

Austrian monk who worked out basic laws of inheritance

99
Q

Inherited

A

Trait that is genetically determined

100
Q

Pedigree

A

Genetic representation of a family tree

101
Q

Punnett Square

A

Diagram used to predict probability outcome of a genetic cross

102
Q

Probability

A

Likelihood of an occurrence

103
Q

Allele

A

Different forms of the same gene

104
Q

Epigenetics

A

How genes are turned on or off by their environment

105
Q

4 broad types of genetic disorders

A

Chromosomal anomalies - abnormal number
Chromosomal anomalies - abnormal structure
Mendelian single-gene disorder - autosomal dominant/ recessive
Mendelian single-gene disorder - x-linked

106
Q

Euploidy

A

“normal”

46 chromosomes

107
Q

Aneuploidy

A

Anything other than 46 chromosomes

108
Q

Monosomy

A

Deficiency of a chromosome

109
Q

Polysomy/ trisomy

A

Too many chromosomes

110
Q

Monosomy vs. polysomy

A

Monosomy usually worse

111
Q

Types of abnormal chromosome structures

A

Deletion
Duplications
Inversions
Translocations

112
Q

Point mutations

A

Substitution of a single base pair

Happens often, might not have consequences

113
Q

Frameshift mutations

A

Addition or deletion of 1 or 2 nucleotides
All codons after are incorrect
More severe consequences

114
Q

2 examples of Autosomal recessive disorders

A

Cystic fibrosis

Sickle cell

115
Q

Example of autosomal dominant disorder

A

Huntington’s Disease

Delayed onset, usually > 40

116
Q

X-linked recessive inheritance

A

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
Q

2 examples of x-linked recessive disorder

A

Duchenne Muscular Dystrophy

Hemophilia A

118
Q

Polygenic traits

A

Result from several genes acting together

Environment doesn’t affect outcomes

119
Q

Multifactorial traits

A

Genes make an individual susceptible
Environment can trigger
E.g. HTN, weight, mental health, asthma

120
Q

Penetrance

A

% in which gene is expressed

% of individuals with a given genotype who exhibit the phenotype associated

121
Q

Expressivity

A

Level of expression

Extent of variation in phenotype associated with a particular genotype

122
Q

3 Types of Down Syndrome

A

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
Q

Duchenne Muscular Dystrophy

A

X-linked recessive: affects only males

Muscle cells deficient in protein dystrophin -> weak cell membrane

124
Q

What causes muscle degeneration in Duchenne MD?

A

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
Q

Clinical manifestations of Duchenne Muscular Dystrophy

A

Large calves: muscle replaced by fat
Gower’s sign
Loss of ability to ambulate 8-13
Muscle weakness progresses -> respiratory weakness -> premature death

126
Q

Sickle Cell Disease

A

Autosomal recessive

Point mutation on chromosome 11: codes for different amino acids: changes hemoglobin molecule HbS

127
Q

Hemoglobin molecule HbS

A

When O2 is low, HbS undergoes polymerization and causes hemoglobin to change into sickled shape

128
Q

Triggers for Sickle Cell

A 
Dehydration
Infection
Hypoxemia
Acidosis
Cold exposure
129
Q

Effects of sickling

A

Occlusion of small arteries
Tissue damage due to lack of blood
Pain

130
Q

Clinical manifestations of Sickle Cell

A 
Chronic anemia
Pallor
Jaundice
Fatigue
Delayed growth and puberty
Infections: most common cause of death
131
Q

Vaso-occlusive sickle cell crisis

A 
Blocked blood flow
Extremely painful - joint or bone pain
Lasts days to weeks
Acute chest syndrome
Hand and foot syndrome
132
Q

Acute sequestration sickle cell crisis

A 
911
6 mo - 4 y.o.
Blood pools causing enlargement
Hypovolemic shock
Spleen, liver and lungs
133
Q

Aplastic sickle cell crisis

A

Increased destruction or decreased production
Profound anemia
Associated with viral infections, fever

134
Q

Treatment for Sickle Cell

A 
Stem cell transplant
Education to prevent crisis
Vaccines
Penicillin prophylaxis
Transfusions
Splenectomy
Pain management, hydration and oxygenation
135
Q

S I C K L E

A 
Strokes, Swelling of hands/feet/spleen
Infections, Infarctions
Crisis, Chest syndrome, Cardiac problems
Kidney disease
Liver and Lung 
Eyes/ Erection
136
Q

Ulcerative Colitis

A

Inflammatory disease of the mucosa of the colon and rectum

137
Q

Crohn’s Disease

A

Inflammation of GI tract that extends through all layers of intestinal wall “cobblestones”
Skip lesions: areas of healthy GI tract

138
Q

Major differences between UC and Crohn’s

A

UC: bloody stool, mucosal layer only, diarrhea

Crohn’s: entire intestinal wall, pain, weight loss/malabsorption

139
Q

GERD

A

Backflow of gastric contents into the esophagus through the lower esophageal sphincter

140
Q

GERD in peds

A

Infants can have poor weight gain, respiratory symptoms

Older children: heartburn, vomiting, asthma, pneumonia, upper airway symptoms

141
Q

Osteomyelitis

A

Severe infection of bone and local tissue

142
Q

High risk groups for osteomyelities

A 
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
Q

Compartment Syndrome

A 
Accumulation of pressure in a fracture
Surgical emergency
5 P's:
Pain (out of proportion)
Parasthesia (decreased sensation)
Pallor
Pulselessness
Paralysis
144
Q

Ranitidine (Zantac)

A

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
Q

Omeprazole (Prilosec)

A

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
Q

Sucralfate

A

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
Q

Magnesium hydroxide and Calcium carbonate

A

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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