Final Flashcards
(387 cards)
1
Q
What is the role of glucagon in your body?
A
increases the amount of glucose in your blood
2
Q
What is the role of insulin in your body?
A
decreased the amount of glucose in your blood
3
Q
Where is insulin produced?
A
B cells in pancreas
4
Q
What is the pathophysiology of type 1 DM?
A
absolute insulin insufficiency: type 1a caused by autoimmune attack on beta cells of pancreas; B cells are not producing insulin
5
Q
What are the clinical manifestations of type 1 DM?
A
increased blood glucose due to no insulin
6
Q
What are the 3 P’s of Type 1 DM?
A
- polyuria: urination (sugar spills into urine and water follows, increased urine output)
- polydipsia: thirst (body senses hypovolemia, drinking triggers thirst
- polyphagia: hunger (decreased weight due to fluid loss, fat stores broken down, protein broken down; cells need energy)
7
Q
What is the evaluation for type 1 DM?
A
- H and P
- ketones and glucose in urine
- blood glucose
- HgA1c above 6.5
8
Q
What determines diabetes from blood glucose test?
A
- random sampling: blood glucose > 200 mg/dl with classic s/s
- fasting: blood glucose > 126 mg/dl
- 2 hours post 75-g oral glucose load: blood glucose >200 mg/dl
9
Q
What are the treatments for type 1 DM?
A
- insulin therapy
- diet/meal planning
- activity/exercise
- monitoring for complications (acute hyperglycemia, diabetic ketoacidosis, hypoglycemia, chronic changes)
10
Q
What are the s/s of type 1 DM?
A
frequent urination, increased thirst, hunger, weakness, weight loss, blurred vision, nausea, slowed healing time, tingling in hands
11
Q
What are s/s of hypoglycemia?
A
sweating, pallor, irritability, hunger, lack of coordination, sleepiness
12
Q
What are the clinical manifestations of hypoglycemia?
A
TIRED: tachycardia irritability restless excessive hunger diaphoresis, depression
13
Q
What can cause hypoglycemia?
A
increase in exercise, too much insulin
14
Q
What are the causes of diabetic ketoacidosis?
A
not managing insulin, stress; result of increased lipolysis and conversion to ketone bodies (ketones and proteins)
15
Q
what are the clinical symptoms of DKA?
A
metabolic acidosis (adipose -> ketones -> acidic)
16
Q
What are some clinical manifestations of DKA?
A
- hyperkalemia (buffer system H+ -> K; Na-K pump has no insulin so increase in K)
- too much H+: breath deeper and faster (Kussman Respirations)
- fruity breath: acetone
17
Q
Who is most at risk for type 2 DM
A
non Caucasians and elderly
18
Q
what are risk factors for type 2 dm
A
age, sedentary lifestyle, obesity, genetics, metabolic syndrome (pre diabetes: obesity, pre HTN, dyslipidemia)
19
Q
How does type 2 DM work
A
resistant to the action of insulin on peripheral tissues - requirement for more insulin AND lowered glucose utilization
20
Q
Evaluation of type 2 DM
A
- H and P (more subtle)
- glucose in urine
- blood glucose tests
- HbA1C above 6.5
21
Q
treatment for type 2 dm
A
lifestyle - diet, exercise, weight loss (improves glucose tolerance)
medications
monitoring complications (chronic changes)
22
Q
long term consequences of hyperglycemia
A
eyes, kidneys, cardiovascular, cerebrovascular, neuropathy, peripheral vascular infection
23
Q
pathophysiology of gestational diabetes
A
glucose intolerance during pregnancy; thought to occur because placental hormones and weight gain during pregnancy cause insulin resistance and inability to produce the increased amount of insulin needed during pregnancy; glucose tolerance test around 28 weeks
24
Q
treatment of gestational diabetes
A
nutritional counseling and exercise; insulin (if needed)
25
complications of gestational diabetes
baby >4kg, neonatal hypoglycemia, still birth
26
what are the functions of the adrenal cortex
- glucocorticoids (cortisol): energy conversion, immune response, inflammation, stress
- mineralcorticoids (aldosterone): Na/H2O retention
- androgens (sex hormones)
27
What is Addison's disease?
adrenal insufficiency
28
What is Cushing's Disease?
hypercorticolism
29
causes of addison's disease
- destruction of adrenal cortex - decreased secretion of mineralcorticoids, glucocorticoids, and androgens
- removal of adrenal gland, neoplasms, TB, histoplasmosis, CMV (cytomegalovirus), autoimmune disease
30
clinical manifestations of addisions disease
- decreased cortisol: can't make energy (hypoglycemic)
- decreased mineralcorticoids (aldosterone): Na loss, H2O loss, hypotension
- hyperkalemia: acidosis
- decreased androgens: body hair changes
- ACTH suppressed: changes in pigmentation
31
evaluation of addison's disease
- H and P
- lab: plasma cortisol levels
- ACTH stimulation test (normal - rise in cortisol)
- imaging: CT/MRI of adrenal glands
32
treatment of addison's disease
- replace hormones
| - stress dosing (education)
33
causes of cushings disease
pituitary secretion of ACTH, tumor, admin of synthetic glucocorticoids or steroids
34
evaluation of cushings disease
- H and P
- lab: dexamethasone suppression test
- imaging: US, CT, MRI of pituitary or adrenal
35
treatment of cushings disease
surgery or radiation for tumors, pharmacotherapy (anti-HTN, K, diuretics)
36
3 mechanisms that characterize asthma
1. bronchospasm( obstruction)
2. inflammation and edema (mucus)
3. reactivity to variety of stimuli
37
What are 4 classifications of asthma
1. intrinsic/non allergic: usually adult onset, no hx of allergies, respiratory infection/psychological stress
2. extrinsic/allergic (peds population): triggered by pollen, dust, dust mites, cockroach dropping, drugs, chemicals, MS,G, alcohol
3. exercise induced
4. status asthmaticus
38
pathophysiology of asthma early response
inflammation: allergen binds to IgE on mast cells --> degranulate --> mediators released (histamine, leukotrienes, prostaglandin, TNF, IL-1) --> vasodilation, increased permeability, bronchospasm and edema and mucus secretion
39
pathophysiology of asthma late response
chemotactic recruitment causes latent release of inflammatory mediators --> causes bronchospasms, edema and mucus --> synthesis of leukotrienes (prolonged smooth muscle contraction) --> neuropeptides (increased bronchial hyper responsiveness) and eosinophils (direct tissue injury - impaired mucociliary function) --> accumulation of mucus and cellular debris form plug in airways
40
most common clinical manifestations of asthma
wheezing, cough, sputum feeling or chest tightness, tachycardia (hypoxemia), tachypnea
41
severe manifestations of asthma
cyanosis, retractions, nasal flaring, decreased breath sounds, agitation, inability to speak full sentences, pulsus paradoxus (decreased systolic pressure during inspiration)
42
pathophysiology of bronchiolitis
viral attack leads to necrosis of bronchial epithelium (RSV or influenza) --> mucus production obstruction -->
1. inflammatory exudate
2. release chemical mediators (constriction)
3. inflammation - fibrosis and narrowing
43
changes to breathing mechanisms with bronchiolitis
1. air trapping = hyper inflammation
2. decreased compliance = atelectasis
3. increased WOB
44
clinical manifestations of bronchiolitis
- rhinorrhea and tight cough
- decreased appetite, lethargy, fever
- tachypnea and respiratory distress (retractions)
- abnormal auscultory sounds (wheezing, rhonchi)
- xray (hyperexpanded lungs, infiltrates, atelectasis)
45
tx of bronchiolitis
- supplemental O2
- increase hydration
- inhaled hypertonic saline
- NO bronchodilators, steroids, or ABX
46
Virchow's Triad of PE
- vessel wall injury
- circulatory statis
- hypercoaguable conditions
47
clinical manifestations of a PE
restlessness, apprehension, anxiety, DYSPNEA, chest pain, tachycardia, tachypnea, hemoptysis?, progression to heart failure, shock and respiratory arrest
48
Dx of PE
- H and P: DVT, pulse ox, RR
- chest xray
- ABG (respiratory alkalosis)
- elevated d-dimer
- CT
49
tx of PE
- prevention - ROM, low dose meds
- respiratory support
- thrombolytic therapy and heparin
50
med priorities for asthma vs COPD
Asthma: anti-inflammatory and bronchodilators
COPD: bronchodilators and anti-inflammatorys
51
What are MDIs
metered dose inhalers; pressurized device that delivers dose with each actuation; wait 1 minute between puffs; only ~10% reaches lungs; requires hand-lung coordination and spacers
52
What are DPIs
dry powder inhaler delivered directly into lungs; no propellant used; breath activate d; doesn't require hang-lung coordination; delivers ~20% dose to lungs
53
How do nebulization
small machine that converts drug solution into a mist; inhalation achieved through face mask or mouth piece; several minutes to deliver dose; not any better than MDI
54
most common AEs of beclomethasone
- oropharyngeal candidiasis (thrush) - wash out mouth
- dysphonia (crackly voice) - can switch to different MDI
- can promote bone loss - some systemic absorption; calcium efflux from bone
55
prototype of inhaled corticosteroids
beclamethasone
56
prototype of inhaled bronchodilators
albuterol, ipratropium
57
MOA of albuterol
selective beta-2 agonist
58
use of albuterol
relieving acute bronchospasm and prevention of exercise induced bronchospasm
59
action duration of albuterol
immediate benefit, lasts 30-60 minutes
60
AEs of albuterol
tachycardia, tremor, hypokalemia (K will come back out of cell once tx stopped)
61
MOA of ipratropium
block muscarinic receptors in bronchi = bronchodilation
| short-acting anticholinergic
62
use of ipratropium
relieve bronchospasm; increased dose won't do much once muscarinic receptors saturated
63
onset of ipratropium
30 seconds, lasts 6 hours
64
AEs of ipratropium
minimal systemic effects - dry mouth, pharyngeal irritation
65
MOA of montelukast
suppresses effects of leukotrienes (can be used for seasonal allergies)
66
use of montelukast
reduce inflammation, bronchoconstriction, airway edema, mucus production
67
administration of montelukast
orally once daily (2 hours before exercise)
68
AEs of montelukast
generally well tolerated; metabolized by CYP450 - use with phenytoin may decrease levels of montelukast
69
where does UC affect?
mucosa of rectum and colon
70
patho of UC
inflammation at base of crypts of Lieberkuhr --> inflammation --> abscess formation --> abscess coalesce --> ulcer formation --> repair, but fragile and highly vascular tissue
71
clinical manifestations of UC
- progress variable
- diarrhea (inability of colon to absorb water
- increased chance of rectal bleeding r/t ulcers
- abdominal pain
72
dx of UC and crohns
H&P, biopsy
73
tx of UC and crohns
- corticosteriods, immunosuppressants, immunomodulating agents
- nutritional management
- ABX is systemic toxicity and hospitalized
- risk for colon cancer increased - biopsy and endoscopy
- consider colectomy if high grade dysplasia
74
affected areas of crohns
inflammation of GI tract extends through all layers of intestinal wall mouth to anus
75
cardinal feature of crohns
granulomas
76
patho of crohns
blockage of GI lymphoid and lymphatic structures --> engorgement and inflammation --> deep linear ulcers (granulomas) --> thickened by fibrous score, deep fistulas (leakage)
77
clinical manifestations of crohns
- incapable of adequately absorbing nutrients (weight loss, malnutrition, change in ht/wt peds)
- "skipping lesions"
- perianal fissures, fistulas, abscesses
78
inflammation UC vs Crohns
UC: mucosal layer only
C: entire intestinal wall
79
granulmoas UC vs Crohns
UC: rare
C: cobblestone appearance
80
Ulcers UC vs Crohns
present in both
81
anal and perianal fissures UC vs Crohns
UC: rate
C: common
82
abdominal pain UC vs Crohns
UC: mild to severe
C: moderate to severe
83
diarrhea UC vs Crohns
UC: common
C: may or may not
84
bloody stools UC vs Crohns
UC: common
C: less common
85
weight loss UC vs Crohns
UC: less common
C: more common
86
malabsorption UC vs Crohns
UC: none
C: common
87
clinical course of UC vs Crohns
remission and exacerbations for both
88
what is GERD
gastroesophageal refluc disease - backflow of gastric contents into esophagus through lower esophageal sphincter
89
3 causes of GERD
1. issues with LES - closure strength and efficacy; ex. high fat diet, caffeine, alcohol, smoking, obese, meds
2. increase in intrabdominal pressure; ex. pregnancy, constipation, overfed
3. delayed gastric emptying; ex. infants
90
clinical manifesations of GERD
- heartburn, regurgitation chest pain, dysphagia
| - no symptoms - physiologic reflex (infants)
91
2 complications of GERD
1. highly acidic gastric contents in esophagus --> strictures (narrowing) of esophagus
2. aspiration --> impacts respiratory system --> asthma, cough, laryngitis
92
tx of GERD
- dietary and behavior modifications (low fat, decrease caffeine/alcohol, no smoking, decrease weight
- antacids and histamine blockers
- proton pump inhibitors
93
peds specific GERD risks
- reflux normal in newborns
- other risks: cerebral palsy, head injury, neuro issues (affects signal to LES)
- highes in premies and decreases in 6-12 months (LES matures ~6mo)
94
tx of GERD
- small, frequent feedings and burbing
- thickened feeding with rice
- positioning
- medications
95
common presenting GERD symptoms (infants)
- feeding refusal
- recurrent vomiting
- poor weight gain
- irritability
- sleep disturbance
- respiratory symptoms
96
common presenting GERD symptoms (older children)
- abdominal pain/heartburn
- recurrent vomiting
- dysphagia
- asthma
- recurrent pneumonia
- upper airway problems (chronic cough, hoarse voice)
97
what is osteomyelitis?
severe infection of bone and local tissue
98
3 ways osteomyelitis can reach the blood
1. bloodstream (from elsewhere)
2. adjacent soft tissue injury
3. direct introduction of organism into bone
99
high risk groups for osteomyelitis
- surgery
- open fractures or penetrating wounds
- IV drug users
- peds and older adults
100
2 most common organisms for osteomyelitis
1. staphylococcus aureus
| 2. streptococcus pneumoniae
101
clinical manifestations of osteomyelitis
- pain, increased fever (high), muscle spasms, swelling, refusal to use limb
102
patho of osteomyelitis
1. bacteria enters
2. inflammation
3. pus formation - spreads inward
4. abscess forms
5. interrupted blood supply = necrosis
103
dx of osteomyelitis
- xray (may take longer to show up)
| - increased WBC, CRP
104
tx of osteomyelitis
- 4-6 weeks IV antibiotics or IV to PO
- debridement
- removal of prosthesis or othe rmaterials
105
3 pediatric bone differences
1. less brittle, higher collagen to bone ration (+)
2. stronger periosteum (+)
3. presence of epiphyseal plate (-)
106
healing of cortical bone
1. bleeding starts
2. hematoma
3. osteoblasts and calcium
4. callus formation, new bone built, old bone destroyed
5. callus reabsorbed
107
clinical manifestations of a fracture
- pain, tenderness
- impaired sensation
- decreased mobility
108
dx of fractures
H and P, 2 view xray (may repeat in 1-2 weeks)
109
tx of fractures
- Ice and elevation
- reduction (manual or surgical)
- immobilization/retention (cast or splint)
110
complications of fractures
- delayed healing
- nonunion or malunion
- osteonecrosis
- osteomyelitis
- compartment syndrome
111
5 Ps of compartment syndrome
Pain Paralysis Paresthesia (sensation) Pallor Pulses
112
classification of ranitidine
histamine2-receptor antagonist
113
MOA of ranitidine
suppresses the secretion of gastric acid by selectively blocking H2 receptors in parietal cells lining stomach
114
AEs of ranitidine
- caution in pregnancy
- drug interactions (CYP450 inhibitor)
- doses adjusted in renal function
- rare: thrombocytopenia
115
classification of omeprazole
proton pump inhibitor
116
MOA of omeprazole
irreversible inhibition of H+, K+-ATPase (proton pump) --> blocks gastric production
117
AEs of omeprazole
- long term use increases risk of osteoporosis (increased fracture risk r/t decreased absorption of calcium)
- increased risk of: pneumonia, c.diff, dementia, kidney injury
- drug interactions: inhibition of CYP2C19 --> Clopidogrel (Plavix) - prevents conversion of prodrug to active form (anti-platelet drug)
118
classification of sucralfate
mucosal protectant
119
transverse fracture
break occurs at right angles to the long axis of the bone
120
spiral fracture
twisted or circular break that affects the length (suspicion for child abuse), s shaped
121
longitudinal fracture
fracture along the length of the bone
122
oblique fracture
45 degree angle diagonal or slanting that occurs between horizontal and perpendicular planes of the bone
123
comminuted fracture
splintered into pieces
124
impacted fracture
telescopes or drives one fragment into the other (may be referred to as compression or buckle fracture)
125
greenstick fracture
break through the periosteum on one side while only bowing or buckling on the other side
126
stress fracture
fracture on the cortical surface - can be complete
127
avulsion fracture
ssmall fragment of bone fragments
128
complete fracture
break through the entire bone
129
incomplete fracture
partial break, not completely through bone
130
open fracture
open wound or break in the skin near the fracture (may also be referred to as a compound fracture)
131
MOA of sucralfate
acidic environment changes sucralfate into a thick substance that adheres to an ulcer for up to 6 hours and protects ulcer from further injury
132
AEs of sucralfate
- constipation
- caution in pregnancy
- use cautiously in renal failure (minimal absorption of aluminum salt which will accumulate)
- interferes with med absorption
133
classification of magnesium hydroxide and calcium carbone
antacids
magnesium hydroxide - milk of magnesia
calcium carbonate - tums
134
MOA of antacids
neutralize gastic acid and inactivate pepsin --> potential mucosal protection due to stimulation of production of prostaglandins
135
AEs of antacids
- constipation (CC)
- diarrhea (MH)
- caution in pregnancy
- avoid with GI perforation or obstruction
- caution in renal failure - salts
136
5 tx for IBD
- 5-aminosalicylates (antiinflammatory)
- glucocorticoids (steroids)
- immunosuppressants
- immunomodulators
- antibiotics
137
UC severe tx
colectomy, Infliximab, cyclosporine, experimental rx
138
UC moderate tx
Infliximab, immunomodulators, corticosteroids
139
UC mild tx
probiotics, PO/topical amninosalicylates
140
crohns severe tx
surgery, Adalimumab, clinical trials
141
crohns moderate tx
Infliximab, Immunomodulators, corticosteroids
142
crohns mild tx
ABX, aminosalicylates, PO corticosteroids, alternate therapies (fish oil, probiotics)
143
classification of sulfasalzaine
5-aminosalicylates (5-ASA)
144
mode of sulfasalazine
PO or rectal (topical)
145
MOA of sulfasalazine
decreases inflammation by inhibiting prostaglandin synthesis
146
AEs of sulfasalazine
blood disorders ( decreased RBCs, platelets), anemia, contains sulfa (drug allergy)
147
4 types of genetic disorders
1. chromosomal anomalies (mutations) - abnormal # or structure
2. mendelian signle-gene disorders - autosomal dominant/recessive, x-linked
3. polygenic/multifactorial disorders
4. other
148
4 types of abnormal # genome mutations
- euploidy: 46 chromosomes
- aneuploidy: not 46 chromosomes
- monosomy: deficiency of chromosome
- polysomy: too many chromosomes
149
disorders involving sex chromosomes
most common, less debilitating
150
ex of autosomal recessive
cystic fibrosis
151
patterns of autosomal recessive
- males and females equally affected
- carrier may transmit to offspring
- may delay on onset, incomplete penetrance, variable expressivity
152
ex of autosomal dominant
huntingtons disease (fatal, delayed onset)
153
pattens of autosomal dominant
- males and females equally affected
- affected individuals usually have affect parents - no generation skipped
- carriers/unaffected do not transmit
154
patten of x-linked recessive
- more often in males
- can skip generations via female carrier
- never passed father to son (father passes y)
- passed from affected father to all daughters (affected or carrier daughters based on mom's x)
- males: no other x to act as dominant
155
ex of x-linked recessive
Duchenne muscular dystrophy, hemophilia a
156
ex of polygenic traits
height, weight, IQ
157
penetrance
% in which gene is expressed; % of individuals with a given genotype who exhibit the phenotype associated with that genotype (heterozygous trait may present one of the other and skip generations)
158
expressivity
level of expression; extent of variation in phenotype associated with a particular genotype (not uniformed; other gene influences)
159
patho of down syndrome
- trisomy 21 caused by nondisjunction (95%) - pair of 21st chromosome fails to separate in meiosis
- translocation (4%) - full or partial copy of chromosome 21 attaches to another chromosome
- mosaicism (1%) - some cells have 46 and some have 47 chromosomes
160
characteristics of down syndrome
cognitive disability, low set ears, wide nasal bridge, protruding tongue, upward slant to eyes, epicanthal folds, single palmar crease, small stature, nuchal changes, hypotonia, increased risk for CHD, leukemia, respiratory problems
161
duchenne muscular dystrophy overview
x-linked recessive, affects only males, apparent by age 3
162
patho of duchenne muscular dystrophy
- muscle cells are deficient in protein dystrophin - weak cell membrane
- leaks creatinine kinase and takes in calcium
- proteases and inflammatory processes activated
- leads to muscle fiber necrosis and muscle degeneration
163
clinical manifesations of duchenne muscular dystrophy
- presents with muscel weakness, difficulty walking
- progressive
- large calves: normal fiber replaced with fat and CT
- gradual loss of ability to ambulate by 8-13 years
- Gower's sign: way to get from floor to standing
- scoliosis - progressive s/s
- osteoporosis, fractures
- weakness of muscle progresses -> respiratory weakness --> premature death
164
dx of duchenne muscular dystrophy
- H and P
- elevated creatinine kinase initially
- muscle biopsy
- genetic testing
165
overview of sickle cell
- autosomal recessive
- chromosome 11 point mutation (changes hgb stability)
- homozygous inheritance 1 in 635
- heterozygous inheritance (carrier) - 1 in 12
166
patho of sickle cell
- genetic mutation causes defective hemoglobin molecule
| - when O2 is low, hgb5 undergoes polymerization and causes it to change to sickle shape
167
triggers for sickling
dehydration, infection, fever, acidosis, hypoxia, exposure to cold
168
2 problems caused by sickle cell
1. sickling - occlusion of small arteries (no O2 to tissues/organs), tissue damage, pain
2. anemia - shorter life span due to hemolysis; hyperbilirubinemia (bili byproduct of RBC breakdown)
169
clinical manifestations of sickle cell
- present around 4-6 months d/t fetal hgb carrying more O2
| - chronic anemia, pallor, jaundice, fatigue, delayed growth/puberty, infections (most common cause of death)
170
3 types of sickle cell crises
1. vaso-occlusive
2. acute sequesterization
3. aplastic anemia
171
vaso-occlusive crisis
- sickled cells and vasospasm block blood flow
- thrombosis and infarction
- lasts days-weeks
- potential locations: joint or bone pain, acute chest syndrome (lungs), dactylitis (hand foot syndrome), priapism (penis), cerebrovascular
172
acute sequesterization
6mo-4y, blood pools causing enlargement (hypovolemic shock), emergency, potential locations: spleen, liver, lungs
173
aplastic anemia
increased destruction or decreased production of hgb, profound anemia, associated with viral infections, fever
174
tx of sickle cell
- stem cell transplant
- education to prevent crisis (hydration, exposure to cold, decreased infection, treat fever)
- vaccinations
- penicillin prophylaxis
- transfusions, splenectomy
- pain management, hydration, oxygenation
175
complications of sickle cell
S - strokes, swelling (hands/feet), spleen
I - infections, infarctions
C - crisis, chest syndrome, cardiac problems
K - kidney disease
L - liver and lung problems
E - eyes, erection
176
cystic fibrosis patho
defect in a membrane transporter for chloride ions in epithelial cells; results in production of abnormally thick secretions in glandular tissues
177
cystic fibrosis overview
- most common single-gene disorder
- autosomal recessive
- chromosome 7 (1300 mutations)
- caucasian American
178
which neurotransmitters are monoamines
adrenaline/epinephrine
noradrenaline/norepinephrine
dopamine
179
What is serotonin responsible for
mood
| - feeling of well being, sleep, appetite, memory, sexual desire/fxn
180
what is dopamine responsible for?
cognitive fxn, motivation, interest and attention, pleasure, euphoria, movement
181
what is norepinephrine responsible for?
stress hormone, attention, flight/fight, anxiety
182
what do norepi, serotonin, and dopamine have in common
mood, cognitive function
183
prevalence of depression
by 17 years, lifetime prevalence of MDD is 13-15%; higher in girls and older children; leading cause of global disability; directly related to suicide which is 3rd leading cause of death
184
risk factors for depression
genetics, school failure, stressors, chronic illness, poor coping, SDOH (abuse, neglect, lower ed, lower SES), ADD, learning disabilities
185
what is depression
a clinically and etiologically heterogeneous disorder
186
what is the monoamine deficiency theory
no regular/usual amount of monoamines in synaptic space; causes: decreased baseline number, overactive re-uptake, enzymes eating up before getting to postsynaptic, not enough transporters
187
how is depression dx
screening tools:
- patient Health questionnaire 9
- Epidemiological Studies Depression Scale
- Pediatric Symptom Checklist
188
how is depression managed
- sleep, nutrition, exercise
- psychotherapies: cognitive behavioral therapy, interpersonal therapy
- pharmacotherapy
- safety plan
189
what is anxiety
necessary physiologic response, helps protect us in dangerous situations
190
what are fears
emotional response to threat, normal part of development
191
what are worries
cognitive manifestations of fear and anxiety
192
what are anxiety disorders
fears, worries or anxiety occur outside range of normal developmental responses, are extreme, cause significant distress, impair function (social and school)
PERSISTENT, EXCESSIVE, AND UNREALISTIC WORRY
193
anxiety disorders in peds
- most common psych illness in children and adolescents (8-10%)
- can start in preschool, usually doesn't cause impairment until school age
- girls 2x more likely
194
risk factors for anxiety disorders
genetic predisposition, temperament, modeling, physiologic factors and exposure to psychosocial and environmental stressors all contribute
- high rate of comorbidity with depression
195
fight of flight anxiety manifestions and patho
- regulated through limbic system: sensory input (thalamus), context and memory (hippocampus), emotional regulation (amygdala)
- activated under stress and danger
- prefrontal cortex helps to modulate
196
anxiety disorder manifestations and patho
- dysregulation
- activated in situations that are not a treat (or an exaggerated response to a threat)
- involvement of neurotransmitters: norepi, serotonin, dopamine, GABA
- release of stress hormones and adrenaline without regulation
197
dx of anxiety disorders
screening:
- Multidimensional Anxiety Scale for children
- Screen for Child Anxiety Related Emotional Disorders
- Spense Children's Anxiety Scale
198
tx of anxiety disorders
education, coping strategies, cognitive (worry), behavioral (relaxation), exposure
199
what may happen if anxiety disorders are not treated?
- major depressive disorder and substance misuse
| - long term physiologic effects of stress cause GI, CV later in like
200
what is insulin
natural hormone synthesized by beta cells of pancreas with Islets of Langerhans; proinsulin = precursor
201
short duration: rapid acting
lispro (humalog)
aspart (NovoLog)
glulisine (Apidra)
202
short duration: slower acting
regular insulin (humalin R, Novolin R)
203
intermediate duration
NPH
204
long duration insulin
glargine (lantus)
205
SEs of insulin
hypoglycemia, hypokalemia, allergic rxn
206
metformin use
initial drug choice for type 2 DM (pancreas still working)
207
metformin MOA
- inhibit glucose production in liver
- slightly reduces glucose absorption in gut
- sensitizes insluin receptors in target tissues (fat and skeletal muscle)
- does NOT stimulate insulin release
208
PK of metformin
slowly absorbed from small intestine, excreted unchanged in kidneys, NOT worries about hypoglycemia
209
common SEs of metformin
GI related (decreased appetite, N/D)
210
toxicity of metformin
lactic acidosis; caution with renal function due to accumulation and lactic acidosis
- dont give to pts with increased creatinine levels
211
class of metformin
biguanides
212
class of glipizide
sulfonylureas
213
moa of glipizide
stimulates release of insulin from pancreatic islets - doesn't work if pancreas doesn't work
214
use of glipizide
solo or in combo (metformin)
215
AEs of glipizide
hypoglycemia
216
precautions of glipizde
dose reduced in elderly, renally eliminated (toxicity - hypoglycemia), avoid in pregnancy (fetal hypoglycemia)
217
pioglitazone class
thiasolidinediones (glitazones)
218
pioglitazone MOA
reduces insulin resistance and decreases glucose production - activates PPAR Gamma ( peroxisome proliferator-activated receptor) --> turns on insulin-responsive genes that help regulate carb and lipid metabolism)
219
considerations for pioglitazone
metabolized by CYP2C8
220
AEs of pioglitazone
most common: RTI, HA, sinusitis, myalgia
| most important: fluid retention, hypoglycemia
221
class of repaglinide
meglitinides (glinides)
222
moa of repaglinide
stimulates insulin release (like sulfonylureas)
223
dosing of repaglinide
4x a day
224
metabolism of repaglinide
by liver with short half life ( hour)
225
AEs of repaglinide
rapidly absorbed by GI - patient needs to eat no later than 30 minutes after admin
226
class of sitagliptin
gliptins (DPP-4 inhibitor)
227
moa of sitagliptin
blocks DPP-4 - sends GLP and GIP down pancreas pathway - stimulates glucose-dependent release of insulin, suppresses postprandial release of glucagon
228
SEs of sitagliptin
common: URIs, HA, inflammation of nasal passages and throat
serious: hypoglycemia, pancreatitis, hypersensitivity (anaphylaxis, SJS)
229
class of liraglutide
incretin mimetics
230
moa of liraglutide
analog of human GLP-1 that causes direct activation of GLP-1 receptors - slows GI emptying time, stimulates glucose-dependent insulin release, inhibits postprandial release of glucagon
231
use of liraglutide
solo or combined (reduce dose of sulfonylureas to avoid hypoglycemia(
232
admin of liraglutide
SQ injection daily
233
AEs of liraglutide
dose-related GI (N/D/C), rare: pancreatitis
234
most common bacterial meningitis adults
streptococcus pneumoniae (2nd most common in peds)
235
most common bacterial meningitis peds
Neisseria meningitidis
236
most common bacterial meningitis in newborns
E.Coli and GBBHS
237
patho of meningitis
1. invading organism
2. inflammatory response: neutrophils to fight - CSF clogged, thick from exudate - blocks CSF flow
3. cerebral changes: s/s of ICP, disrupts blood flow (ischemia), continues to exacerbate inflammatory response
238
clinical manifestations of meningitis
1. infectious: fever, tachycardia, chills, petechial rash
2. neurologic: decreased LOC, cranial nerve involvement, seizures, irritability, delirium (ICP_
3. meningeal irritation: throbbing headache, photophobia, nuchal rigidity
239
eval of meningitis
- H and P
- Lumbar puncture: culture and gram stain, increased pressure, CSF (high WBC, high neutrophils, high protein, low glucose - bacterial, normal glucose - viral)
240
tx of meningitis
- IV antibiotics for bacterial
- antiviral and steroids - viral
- manage complications (seizures, increased ICP)
- supportive
prevention: immunizations, screenings
241
most common causes of increased ICP
adults: stroke, trauma, tumors
peds: tumor, structural malformation, infections
242
3 etiologies of increased ICP
1. cerebral edema - vasogenic (interstitial edema), cytotoxic edema (intracellular edema), often occur together
2. spce occupying process - tumors, hematomas, abscess
3. hydrocephalus - excessive accumulation of CSF - malformations, space-occupying processes
243
clinical manifestations of increased ICP
- HA, changes in LOC, pupils, vomiting
- Cushing's Triad: increased systolic BP, decreased pulse, altered RR
- seizures, decreased motor functino, posturing
infants: bulgin fontanels, increased HC, high pitched cry, poor feeing, sun-setting eyes
244
eval o increased ICP
- H and P
- imaging
- LP
245
tx of increased ICP
- underlying cause
- continuoys monitoring and alleviating pressure
- cerebral oxygenatino
- pharm
246
what are seizures
alteration in membrane potential that makes certain neurons abnormally hyperactive and hypersensitive to change
247
seizures across lifespan
neonates: infection, birth defects, injury
children: genetics, trauma, febrile seizures
adults: cerebral vascular disease
248
generalized seizures
```
entire brain involved; involvement of thalamys and reticular activing system results in lsos of consciousness:
- absence: staring
- myoclonic: single/several jerks
- atonic: drop attacks
- tonic/clonic: jerking of many muscles
post-ictal
```
249
partial seizures
limited to one hemisphere
- simple: no change in LOC; motor, sensory, and/or autonomic
- complex: similar, lose/change consciousness
- secondary generalization: begins partial but then involves both hemispheres (conscious to lose consciousness)
250
dx of seizures
H and P
neuro exam
EEG, labs, imaging
251
tx of seizures
safety, airway, document, underlying cause, meds, avoid triggers
252
febrile seizures
seizure accompanied by fever (>100.4) without central nervous system involvement (no infection necessary); 6mo-5y
253
traditional AEDs
older, more experience, more data, significant AEs, lots of drug interactinos, cheaper
254
newer AED agents
les SEs and drug interactions, better tolerability, generally safer in pregnancy, more expensive
255
moa of phenytoin
selective inhibition of Na channels:
- slows recovery of Na channels from inactive to active state
- entry of Na into neurons inhibited = suppression of action potentials
- Na blockade limited to neurons that are hyperactive (healthy neurons unaffected)
256
PK of phenytoin
saturable - half life dependent on dose; metabolized by liver (capacity)
257
doseing of phenytoin
- loading dose weight based IV or PO
- maintenance dose by plasma[ ]
- NTI
- toxic: >20mcg/mL - nystagmus, sedation, ataxia, diplopia, seizures
258
AEs of phenytoin
gingival hyperplasia, derm (most common): mortibilliform rash, SJS, TEN
IV admin: dysrhythmias, hypotension, purple glove syndrome
259
route fosphenytoin
IV only
260
moa fosphenytoin
prodrug to liver --> phenytoin
261
admin and SE of fosphenytoin
easier admin, less AEs (no purple glove, decreased incidence of hypotension)
262
considerations for fosphenytoin
may be infused faster but doesn't work faster than phenytoin
263
moa of carbamazepine
suppresses high-frequency neuronal discharge in and around seizure foci - likely due to delayed recovery of Na channels from inactivated state (like phenytoin)
264
PK of carbamazepine
- metabolized by liver: drug interactions
- causes autoinduction: induces liver to increase metabolism - can't give larger or more rapid dose (titrate over weeks) - as therapy continues, half life decreases
265
AEs of carbamazepine
CNS: nystagmus, blurred vision, ataxia, vertigo, unsteadiness (tolerance)
hematologic: bone marrow suppression (leukopenia, anemia, thrombocytopenia, fatal aplastic anemia), decreased RBC, WBC, plt
Teratogen: risk spina bifida
Hyponatremia: promotes ADH secretion
Derm: morbilliform rash, photosensitivity, SJS, TEN
266
class of divalproex
valproic acid
267
MOA od divalproex
- suppression of high-frequency neuronal firing through Na channel blockade
- suppresses Ca influx through T-type Ca CHannels
- augment inhibitory influence of GABA
268
PK of divalproex
extensive hepatic metabolism and renal excretion
269
AEs of divalproex
GI, hepatotoxicity (avoid in <2yo), pancreatitis, hyperammonenemia, teratogenic 1st trimester
Drug interactions: phenobarbital, phenytoin
270
MOA levetiracetam
unknown - does not bind to GABA or other NT
271
routel evetiracetam
IV or PO
272
PK levetiracetam
minimally metabolized, renally eliminated
273
SEs of levetiracetam
mild/moderate: drowsy, asthenia
274
class of mannitol
osmotic diuretic
275
MOA od mannitol
crosses BBB to get fluid out (cerebral edema)
276
SEs of mannitol
dehydration, hypotension, decreased electrolytes
277
considerations of mannitol
- sugar molecule crystallizes - inspect bag and use filter needle
- monitor serum osmolarity for stability
278
4 fetal circulation shunts
- ductus venosus: shunts away from liver
- ductus arteriosus: PA to aorta
- foramen ovale: RA to LA
- high pulmonary vascualr resistance
279
causes of CHD
- chromosomal disorders (6% downs)
- intrauterine infections
- maternal metabolic disorders, drug exposure, alcohol exposure
- increased maternal age
- prematurity
280
acyonotic disorders and their effects
- increased pulmonary blood flow: ASD, VSD, PDA
| - obstruction to blood flow from ventricles: coarctation of aora
281
cyanotic disorders and their effects
- decreased pulmonary blood flow: tetrology of fallot
| - mixed blood flow: transposition of great arteries
282
3 main effects of CHD
1. pressure gradients: birth (systemic to pumonic), L side to R side
2. oxygenation: L side oxygentated, R side unoxygenated
3. workload of heart - upstream and effects
283
PDA patho
- 24-72 hours to close
1. blood to PA due to pressure
2. acyanotic (blood back to lungs)
3. pressure to lungs - pulmonary HTN, R side failutre)
284
clinical manifestatinos of PDA
- heart failure
- machine-like murmor
- widening pulse pressure
- bounding pulses
- cardiac enlargement
285
Eval and tx of PDA
- echocardiogram
- manage HF
- Inodomethacin - closes ductus artiosus
- cardiac cath or surgery
286
patho of ASD
1. pressure from LA to RA
2. acyanotic
3. increased load on r side (more blood to pump) - R sided HF
287
clinical manifestatinos of ASD
- depends on size
- fatigue, dyspnea on exertion (SOB)
- recurrent resp infections - fluid on R side
- systolic murmor
- HF develops young adulthood
newborns: exertion
288
eval and tx of ASD
- echocardiogram
- spontaneous closure if possible
- manage HF
- cardiac cath or surgery
289
patho of VSD
1. pressure LV to RV
2. acyanotic
3. workload R side - r sided HF, r sided V hypertophy
290
clinical manifestatinos of VSD
- r/t size
- murmor (loud, harsh systolic)
- HF
291
eval and tx of VSD
- may close on own
- meds: digoxin, diuretics, ACE-I
- manage HF
- cardiac cath or surgery
292
patho of coarctation of aorta
1. pressure increased behind defect and decreased pressure after
2. acyanotic
3. workload L side - LV hypertrophy, pulmonary edema (backs up)
293
clinical manifestations coarctation of aorta
- murmur (systolic with ejection click)
- poor LE perfusion
- difference in UE and LE pulses and BP
- initially L side HF
294
eval and tx for coarctation of aorta
- echocardiogram
- improve CO - diuretics and digoxin
- prostaglandin E - keeps PDA
- cardic cath and/or surgery
295
defects of tetralogy of fallot
1. VSD
2. overriding aorta (crosses both V to aorta - unO2 blood)
3. pulmonary stenosis
4. RV hypertrophy
296
patho of tetralogy of fallot
1. pressure: washing machine
2. cyanotic - unO2 to aorta
3. workload: R side (pulmonary stenosis)
297
clinical manifestions of tetralogy of fallot
- severity r/t pulmonary stenosis (can't get blood to lungs to oxygenate)
- worsesn after DA closes
- cyanosis, fatigue
tet spells
- murmur (harsh, systolic) and thrill
- boot shaped heart on xray
298
eval and tx of tetralogy of fallot
- echocardiogram
- prostaglanin E
management of tet spells
series of surgeries
299
patho of transposition of GA
RV - aorta - unO2 - body
| LV - PA - O2 - lungs
300
clinical manifestions of transposition of GA
- cyanosis at birh
- hypoxemia with o2 (doesnt help)
- progressive desat and acidosis
- HF
301
eval and tx
- prostaglandin E
| - cardiac cath and surgery
302
CO formula
stroke volume (preload, afterload, contractility) X HR
303
common causes of HF
myocardial ischemia, HTN, cardiomyopathy
304
5 classificatinos of HF
- r sided: ineffective RV functino, blood backs to RA, PERIPHERAL CIRC
- L sided: ineffective LV functino, blood backs to LA, LUNGS
- biventricular: RV and LV not working
- systolic: V dont pump enough blood out, systemic circ (reduced myocardial contractility, low EF)
- diastolic: V dont fill properly, change in stroke volume
305
what are forward backwards effets
backwards effects of L side = forwards effets of R side
306
L sided HF effects
backward: pulmonary congestions
forward: decreased tissue perfusion
307
clinical manifestations of L sided HF
- dyspnea, orthopnea
- cough, crackles
- hemoptysis
- tachycardia, S3 and S4
- cool, pale skin
308
r sided HF effects
backward: systemic congestions
forward: decreased tissue perfusion
309
clinical manifestions of R sided HF effects
- JVD
- hepato-splenomegaly
- weight gain, edema
310
dx of CHF
H and P
chest xray - where is fluid?
ECG, EKG - electrical activity
- echocardiogram
311
tx oc CHF
- manipulate preload, afterload, contractility
- improve CO: digitalis, digoxin
- minimize congestive symptoms: diuretics
- minimize cardiac workload: pacemaker, ACEI, ARBs
312
result of peds CHF
decreased LV systolic funcitno: LA and pulmonary venous HTN, pulmonary venous congestions
313
clinical manifesations of CHF in peds
- impaired myocardial functin
- pulmonary congestion
- general: poor feeing, FTT
314
tx of CHF in peds
- underlying cardiac defect
- fluid balancel increase carolie count, diuretics, decrease volume of feeds
- increase CO
315
4 medical tx goals of HF
1. preload reduction: reduce circulating blood volume
2. afterload reduction: vasodilation
3. myocardial protection: catecholemines and angiotensin 2 have damaging effect on myocardium
4. inotropic support - improves contractility
316
1st line of med for HF and why
diuretics - decrease blood volume
317
3 broad classificatinos of diuretics and prototype
thiazide diuretics - hydrochlorothiazide
loop diuretics - furosemide
potassium-sparing diuretics - spironolactone
318
Hydrochlorothiazide
- thiazide diuretic
- ineffective with low GFR
- for mild diuresis
- AE: hypokalemia
319
Furosemide
- loop diuretic
- produces significant diuresis
- works even with low GFR
- AE: hypokalemia, hypotensino, hypovolemia
- lasts ~6 hours; higher dose does not equal better response
320
spironolactone
- potassium-sparing diuretic
- minimal diuresis
- can be used to prevent hypokalemia with loop diuretics
- AE: hyperkalemia, gynecomastia in med
321
2 categories of drugs that inhibit RAAS and prototypes
- ACE-I: Lisinopril
- ARBs: Losartan
- Aldosterone antagonists: Spironolactone
322
uses of lisinopril
- ACE-I
| - cornerstone of therapy: decrease mortality, improve functino, favor cardiac remodeling
323
benefits of lisinopril
hemodynamic benefits: arteriolar dilation, venous dilation, suppresses aldosterone release
324
AEs of lisinopril
angioedema, hyperkalemia, cough
325
benefits of losartan
improve LV EF, reduce symtpoms, increased exercise tolerance, decrease hospitalizations, enhance QOL, reduce mortality, less cardiac remodeling vs ACEI, similar HD benefits as ACEI
326
AE of losartan
hyperkalemia, less angioedema
327
MOA of spironloactone
blocks aldosterone receptors in hears and vessels; reduces symptoms and decreases hospitalizations, prolongs life
328
aldosterone effects
- promotion of myocardial remodeling (impairs pumping)
- promotion of myocardial fibrosis (increased risk of dysrthythmias)
- activation of SNS
- promotion of vascular fibrosis (decreased arterial compliance)
- promotion of baroreceptor dysfucntion
329
beta blockers added to conventional therapy...
- improve LV EF
- increase exercise tolerance
- slow progression of HF
- decreased need for hospitalization
- prolong survival
330
MOA of BBs
protecting heart from excessive sympathetic stimulation and protecting against dysrhythmia
331
Metoprolol
- regular and ER salt forms
- AE: fluid retention and worsening HF, fatigue, hypotension, bradycardia, heart block
- Watch HR (body more dependent)
332
digoxin class
cardiac glycosides
333
digoxin potential effect
- positive inotrope (inhibits Na-K-ATPase pump)
- increased CO
- alter electrical activity of heart
- favorable effect on neurohormonal systemis
- decreased HF symptoms
- does NOT have impact on mortality (not given early)
334
consideations of digoxin
- 2nd line agent
- NTI
- adjust for renal dysfunction
- drug interactions
335
AEs of digoxin
very dangerous
- cardiac dysrhythmias (exacerbated by hypokalemia and elevated digoxin levels)
- CNS and GI
- anorexia, N/V, visual disturbances (halo)
- drug interactions
336
hydralazine class
vasodilator
337
hydralazine MOA
selective dilation of arterioles (little/no venous effect)
338
hydralazine in combo with nitrates
- reduce morbidity and mortality in AA pts receiving optimal therapy with ACEI and BBs
- combo also recommended to decrease morbidity/mortality in pts with current ot prior symptomatic HF who cannot get ACE I or aRBS
339
AE of hydralazine
hypotension, tachycardia, lupus-like sydrome
340
nitrate pathway
free nitrite ion --> converted to nitric oxide --> results in vasodilation
341
nitroglycerin forms
SL tabs, topical, spray, transdermal patch, IV
342
MOA of nitroglycerin
dilates veins and decreases venous return (preload) which decreases oxygen demand
343
drug interactions of bitroglycerin
phosphodiesterase Type 5 Inhibitors (Viagra) - leads to excessive vasodilation and drop in BP
344
nitroglycerin considerations
tolerance occurs rapidly; nitrate-free interval
345
classification of paroxetine
selective serotonin reuptake inhibitors (SSRIs)
346
paroxetine route
daily; 1st line
347
paroxetine MOA
inhibits serotonin reuptake
348
paroxetine AEs
most common: GI
| sexual dysfunctnion, weight gain, withdrawal, serotonin syndrome
349
what is serotonin syndrome
muscle rigidity, altered mental status, fever
350
paroxetine considerations
- may take 4-8 weeks for effect
| - drug interactions - antiplatelet agents
351
classification of amitriptyline
tricyclic antidepressants (TCAs)
352
amitriptyline MOA
blocks neuronal reuptake of NE and serotonin
353
amitriptyline AEs
orthostatic hypotension, sedation, anticholinergic effects, cardiac toxicity, seizures
354
amitriptyline considerations
- multiple drug interactions
- lethal overdoses
- low doses used for neuropathic pain and sleep (rarely used for depression)
355
classification of venlafaxine
serotonin-norepinephrine reuptake inhibitors
356
venlafaxine MOA
blocks reuptake of NE and serotonin (effects similar to SSRIs)
357
venlafaxine AEs
weight gain, HA, insomnia, dizziness, sexual dysfunction, serotonin syndrome, hypertension, tachycardia
358
venlafaxine considerations
watch for interactions with NSAIDs and anticoagulants (minor antiplatelet effect)
359
classification of bupropion
atypical antidepressant
360
bupropion forms
immediate, sustained, XL tablets (dosed different # times/day)
361
bupropion MOA
unclear: dopamine blocker, NE reuptake
362
bupropion AEs
common: agitation, HA, dry mouth, constipation, weight loss
serious: seizures
363
bupropion considerations
- good alternative to SSRIs
- drug interactions - metabolized by CYP
- used for smoking cessation
364
classification of alprazolam
benzodiazepine
365
alprazolam route
PO
366
alprazolam MOA
binds to GABA receptor - chloride channel complex; intensifies effects of GABA
367
alprazolam AEs
CNS depression, respiratory depression, anterograde amnesia, withdrawals, hypotension (IV)
368
what are 3 monoamines
epi, norepi, dopamine
369
effects of serotonin
MOOD, feeling of wellbeing, sleep, appetite, memory, sexualy desire
370
effects of dopamine
cognitive function, motivation, interest and attention, pleasure, euphoria, movement
371
effects of norepi
stress hormone, attention, fight/flight, anxiety
372
overlapping effet of norepi, serotonin and dopamine
mood and cognitive function
373
who does depression effect
- higher in girls and older children
- leading cause of global disability
- directly related to suicide (3rd leading cause of death in ages 10-24)
374
risk factors for depression
- 1st degree family member
- school failure
- stressors
- chronic illness
- poor coping
- SDOH - neglect, abuse, lower SES
- ADD, learning disabilities
375
what is the monoamine deficiency theory
no regular/usual amount in synaptic space
376
causes of monoamine deficiency
- decreased baseline #
- reuptake (overactive)
- enzymes eating up before getting to post synapatic
- not enough transporters
377
dx of depression
screening tool:
- patient health q 9
- epidemiologic studies depression scale
- pediatric symptom list
378
management of depression
- sleep, nutrition, exercise
- psychotherapies - cognitive behavioral therapy, interpersonal therapy
- pharmacotherapy
- safety plan
379
what is anxiety
necessary physiologic response, helps protect us in dangerous situations
380
what are fears
emotional response to threat, normal part of development
381
what are worries
cognitive manifestatinos of fear and anxiety
382
what are anxiety disorders
fears, worries, or anxiety occur outside range of normal developmental responses, are extreme, cause significant distress, impair function - PERSISTENT, EXCESSIVE, AND UNREALISTIC WORRY
383
fight or flight response
- regulated through limbic system (sensory input - thalamus; context and memory - hippocampus; emotional regulation - amygdala)
- activated under stress and danger
- prefrontal cortex helps to modulate
384
fight or flight response in anxiety disorders
- dysregulation
- activated in situations that are not a threat (or have an exaggerated response)
- involvement of NTs: norepi, serotonin, dopamine, GABA
- release of stress hormones and adrenaline without regulation
385
dx of GAD
screening:
- Multidimensional Anxiety Scale for children
- Screen for Child Anxiety Related Emotional Disorders
- Spense Children's Anxiety Scale
386
tx of GAD
- education
- coping strategies
- cognitive (worry)
- behavioral (relaxation)
- exposure
387
long term effects of untreated GAD
- major depressive disorder and substance misuse
| - GI, CV issues
