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N398 > Final > Flashcards

Final Flashcards

1
Q

What is the role of glucagon in your body?

A

increases the amount of glucose in your blood

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2
Q

What is the role of insulin in your body?

A

decreased the amount of glucose in your blood

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3
Q

Where is insulin produced?

A

B cells in pancreas

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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

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5
Q

What are the clinical manifestations of type 1 DM?

A

increased blood glucose due to no insulin

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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)
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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
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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
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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)
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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

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11
Q

What are s/s of hypoglycemia?

A

sweating, pallor, irritability, hunger, lack of coordination, sleepiness

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12
Q

What are the clinical manifestations of hypoglycemia?

A 
TIRED:
tachycardia
irritability
restless
excessive hunger
diaphoresis, depression
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13
Q

What can cause hypoglycemia?

A

increase in exercise, too much insulin

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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)

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15
Q

what are the clinical symptoms of DKA?

A

metabolic acidosis (adipose -> ketones -> acidic)

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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
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17
Q

Who is most at risk for type 2 DM

A

non Caucasians and elderly

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18
Q

what are risk factors for type 2 dm

A

age, sedentary lifestyle, obesity, genetics, metabolic syndrome (pre diabetes: obesity, pre HTN, dyslipidemia)

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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

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20
Q

Evaluation of type 2 DM

A
  • H and P (more subtle)
  • glucose in urine
  • blood glucose tests
  • HbA1C above 6.5
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21
Q

treatment for type 2 dm

A

lifestyle - diet, exercise, weight loss (improves glucose tolerance)
medications
monitoring complications (chronic changes)

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22
Q

long term consequences of hyperglycemia

A

eyes, kidneys, cardiovascular, cerebrovascular, neuropathy, peripheral vascular infection

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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

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24
Q

treatment of gestational diabetes

A

nutritional counseling and exercise; insulin (if needed)

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25
Q

complications of gestational diabetes

A

baby >4kg, neonatal hypoglycemia, still birth

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26
Q

what are the functions of the adrenal cortex

A
  • glucocorticoids (cortisol): energy conversion, immune response, inflammation, stress
  • mineralcorticoids (aldosterone): Na/H2O retention
  • androgens (sex hormones)
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27
Q

What is Addison’s disease?

A

adrenal insufficiency

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28
Q

What is Cushing’s Disease?

A

hypercorticolism

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29
Q

causes of addison’s disease

A
  • destruction of adrenal cortex - decreased secretion of mineralcorticoids, glucocorticoids, and androgens
  • removal of adrenal gland, neoplasms, TB, histoplasmosis, CMV (cytomegalovirus), autoimmune disease
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30
Q

clinical manifestations of addisions disease

A
  • 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
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31
Q

evaluation of addison’s disease

A
  • H and P
  • lab: plasma cortisol levels
  • ACTH stimulation test (normal - rise in cortisol)
  • imaging: CT/MRI of adrenal glands
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32
Q

treatment of addison’s disease

A
  • replace hormones

- stress dosing (education)

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33
Q

causes of cushings disease

A

pituitary secretion of ACTH, tumor, admin of synthetic glucocorticoids or steroids

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34
Q

evaluation of cushings disease

A
  • H and P
  • lab: dexamethasone suppression test
  • imaging: US, CT, MRI of pituitary or adrenal
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35
Q

treatment of cushings disease

A

surgery or radiation for tumors, pharmacotherapy (anti-HTN, K, diuretics)

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36
Q

3 mechanisms that characterize asthma

A
  1. bronchospasm( obstruction)
  2. inflammation and edema (mucus)
  3. reactivity to variety of stimuli
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37
Q

What are 4 classifications of asthma

A
  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
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38
Q

pathophysiology of asthma early response

A

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

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39
Q

pathophysiology of asthma late response

A

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

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40
Q

most common clinical manifestations of asthma

A

wheezing, cough, sputum feeling or chest tightness, tachycardia (hypoxemia), tachypnea

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41
Q

severe manifestations of asthma

A

cyanosis, retractions, nasal flaring, decreased breath sounds, agitation, inability to speak full sentences, pulsus paradoxus (decreased systolic pressure during inspiration)

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42
Q

pathophysiology of bronchiolitis

A

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
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43
Q

changes to breathing mechanisms with bronchiolitis

A
  1. air trapping = hyper inflammation
  2. decreased compliance = atelectasis
  3. increased WOB
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44
Q

clinical manifestations of bronchiolitis

A
  • rhinorrhea and tight cough
  • decreased appetite, lethargy, fever
  • tachypnea and respiratory distress (retractions)
  • abnormal auscultory sounds (wheezing, rhonchi)
  • xray (hyperexpanded lungs, infiltrates, atelectasis)
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45
Q

tx of bronchiolitis

A
  • supplemental O2
  • increase hydration
  • inhaled hypertonic saline
  • NO bronchodilators, steroids, or ABX
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46
Q

Virchow’s Triad of PE

A
  • vessel wall injury
  • circulatory statis
  • hypercoaguable conditions
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47
Q

clinical manifestations of a PE

A

restlessness, apprehension, anxiety, DYSPNEA, chest pain, tachycardia, tachypnea, hemoptysis?, progression to heart failure, shock and respiratory arrest

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48
Q

Dx of PE

A
  • H and P: DVT, pulse ox, RR
  • chest xray
  • ABG (respiratory alkalosis)
  • elevated d-dimer
  • CT
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49
Q

tx of PE

A
  • prevention - ROM, low dose meds
  • respiratory support
  • thrombolytic therapy and heparin
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50
Q

med priorities for asthma vs COPD

A

Asthma: anti-inflammatory and bronchodilators
COPD: bronchodilators and anti-inflammatorys

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51
Q

What are MDIs

A

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

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52
Q

What are DPIs

A

dry powder inhaler delivered directly into lungs; no propellant used; breath activate d; doesn’t require hang-lung coordination; delivers ~20% dose to lungs

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53
Q

How do nebulization

A

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

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54
Q

most common AEs of beclomethasone

A
  • 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
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55
Q

prototype of inhaled corticosteroids

A

beclamethasone

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56
Q

prototype of inhaled bronchodilators

A

albuterol, ipratropium

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57
Q

MOA of albuterol

A

selective beta-2 agonist

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58
Q

use of albuterol

A

relieving acute bronchospasm and prevention of exercise induced bronchospasm

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59
Q

action duration of albuterol

A

immediate benefit, lasts 30-60 minutes

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60
Q

AEs of albuterol

A

tachycardia, tremor, hypokalemia (K will come back out of cell once tx stopped)

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61
Q

MOA of ipratropium

A

block muscarinic receptors in bronchi = bronchodilation

short-acting anticholinergic

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62
Q

use of ipratropium

A

relieve bronchospasm; increased dose won’t do much once muscarinic receptors saturated

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63
Q

onset of ipratropium

A

30 seconds, lasts 6 hours

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64
Q

AEs of ipratropium

A

minimal systemic effects - dry mouth, pharyngeal irritation

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65
Q

MOA of montelukast

A

suppresses effects of leukotrienes (can be used for seasonal allergies)

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66
Q

use of montelukast

A

reduce inflammation, bronchoconstriction, airway edema, mucus production

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67
Q

administration of montelukast

A

orally once daily (2 hours before exercise)

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68
Q

AEs of montelukast

A

generally well tolerated; metabolized by CYP450 - use with phenytoin may decrease levels of montelukast

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69
Q

where does UC affect?

A

mucosa of rectum and colon

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70
Q

patho of UC

A

inflammation at base of crypts of Lieberkuhr –> inflammation –> abscess formation –> abscess coalesce –> ulcer formation –> repair, but fragile and highly vascular tissue

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71
Q

clinical manifestations of UC

A
  • progress variable
  • diarrhea (inability of colon to absorb water
  • increased chance of rectal bleeding r/t ulcers
  • abdominal pain
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72
Q

dx of UC and crohns

A

H&P, biopsy

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73
Q

tx of UC and crohns

A
  • 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
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74
Q

affected areas of crohns

A

inflammation of GI tract extends through all layers of intestinal wall mouth to anus

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75
Q

cardinal feature of crohns

A

granulomas

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76
Q

patho of crohns

A

blockage of GI lymphoid and lymphatic structures –> engorgement and inflammation –> deep linear ulcers (granulomas) –> thickened by fibrous score, deep fistulas (leakage)

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77
Q

clinical manifestations of crohns

A
  • incapable of adequately absorbing nutrients (weight loss, malnutrition, change in ht/wt peds)
  • “skipping lesions”
  • perianal fissures, fistulas, abscesses
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78
Q

inflammation UC vs Crohns

A

UC: mucosal layer only
C: entire intestinal wall

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79
Q

granulmoas UC vs Crohns

A

UC: rare
C: cobblestone appearance

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80
Q

Ulcers UC vs Crohns

A

present in both

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81
Q

anal and perianal fissures UC vs Crohns

A

UC: rate
C: common

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82
Q

abdominal pain UC vs Crohns

A

UC: mild to severe
C: moderate to severe

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83
Q

diarrhea UC vs Crohns

A

UC: common
C: may or may not

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84
Q

bloody stools UC vs Crohns

A

UC: common
C: less common

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85
Q

weight loss UC vs Crohns

A

UC: less common
C: more common

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86
Q

malabsorption UC vs Crohns

A

UC: none
C: common

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87
Q

clinical course of UC vs Crohns

A

remission and exacerbations for both

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88
Q

what is GERD

A

gastroesophageal refluc disease - backflow of gastric contents into esophagus through lower esophageal sphincter

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89
Q

3 causes of GERD

A
  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
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90
Q

clinical manifesations of GERD

A
  • heartburn, regurgitation chest pain, dysphagia

- no symptoms - physiologic reflex (infants)

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91
Q

2 complications of GERD

A
  1. highly acidic gastric contents in esophagus –> strictures (narrowing) of esophagus
  2. aspiration –> impacts respiratory system –> asthma, cough, laryngitis
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92
Q

tx of GERD

A
  • dietary and behavior modifications (low fat, decrease caffeine/alcohol, no smoking, decrease weight
  • antacids and histamine blockers
  • proton pump inhibitors
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93
Q

peds specific GERD risks

A
  • 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)
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94
Q

tx of GERD

A
  • small, frequent feedings and burbing
  • thickened feeding with rice
  • positioning
  • medications
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95
Q

common presenting GERD symptoms (infants)

A
  • feeding refusal
  • recurrent vomiting
  • poor weight gain
  • irritability
  • sleep disturbance
  • respiratory symptoms
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96
Q

common presenting GERD symptoms (older children)

A
  • abdominal pain/heartburn
  • recurrent vomiting
  • dysphagia
  • asthma
  • recurrent pneumonia
  • upper airway problems (chronic cough, hoarse voice)
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97
Q

what is osteomyelitis?

A

severe infection of bone and local tissue

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98
Q

3 ways osteomyelitis can reach the blood

A
  1. bloodstream (from elsewhere)
  2. adjacent soft tissue injury
  3. direct introduction of organism into bone
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99
Q

high risk groups for osteomyelitis

A
  • surgery
  • open fractures or penetrating wounds
  • IV drug users
  • peds and older adults
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100
Q

2 most common organisms for osteomyelitis

A
  1. staphylococcus aureus

2. streptococcus pneumoniae

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101
Q

clinical manifestations of osteomyelitis

A
  • pain, increased fever (high), muscle spasms, swelling, refusal to use limb
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102
Q

patho of osteomyelitis

A
  1. bacteria enters
  2. inflammation
  3. pus formation - spreads inward
  4. abscess forms
  5. interrupted blood supply = necrosis
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103
Q

dx of osteomyelitis

A
  • xray (may take longer to show up)

- increased WBC, CRP

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104
Q

tx of osteomyelitis

A
  • 4-6 weeks IV antibiotics or IV to PO
  • debridement
  • removal of prosthesis or othe rmaterials
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105
Q

3 pediatric bone differences

A
  1. less brittle, higher collagen to bone ration (+)
  2. stronger periosteum (+)
  3. presence of epiphyseal plate (-)
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106
Q

healing of cortical bone

A
  1. bleeding starts
  2. hematoma
  3. osteoblasts and calcium
  4. callus formation, new bone built, old bone destroyed
  5. callus reabsorbed
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107
Q

clinical manifestations of a fracture

A
  • pain, tenderness
  • impaired sensation
  • decreased mobility
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108
Q

dx of fractures

A

H and P, 2 view xray (may repeat in 1-2 weeks)

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109
Q

tx of fractures

A
  • Ice and elevation
  • reduction (manual or surgical)
  • immobilization/retention (cast or splint)
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110
Q

complications of fractures

A
  • delayed healing
  • nonunion or malunion
  • osteonecrosis
  • osteomyelitis
  • compartment syndrome
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111
Q

5 Ps of compartment syndrome

A

Pain Paralysis Paresthesia (sensation) Pallor Pulses

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112
Q

classification of ranitidine

A

histamine2-receptor antagonist

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113
Q

MOA of ranitidine

A

suppresses the secretion of gastric acid by selectively blocking H2 receptors in parietal cells lining stomach

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114
Q

AEs of ranitidine

A
  • caution in pregnancy
  • drug interactions (CYP450 inhibitor)
  • doses adjusted in renal function
  • rare: thrombocytopenia
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115
Q

classification of omeprazole

A

proton pump inhibitor

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116
Q

MOA of omeprazole

A

irreversible inhibition of H+, K+-ATPase (proton pump) –> blocks gastric production

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117
Q

AEs of omeprazole

A
  • 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)
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118
Q

classification of sucralfate

A

mucosal protectant

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119
Q

transverse fracture

A

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

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120
Q

spiral fracture

A

twisted or circular break that affects the length (suspicion for child abuse), s shaped

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121
Q

longitudinal fracture

A

fracture along the length of the bone

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122
Q

oblique fracture

A

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

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123
Q

comminuted fracture

A

splintered into pieces

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124
Q

impacted fracture

A

telescopes or drives one fragment into the other (may be referred to as compression or buckle fracture)

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125
Q

greenstick fracture

A

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

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126
Q

stress fracture

A

fracture on the cortical surface - can be complete

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127
Q

avulsion fracture

A

ssmall fragment of bone fragments

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128
Q

complete fracture

A

break through the entire bone

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129
Q

incomplete fracture

A

partial break, not completely through bone

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130
Q

open fracture

A

open wound or break in the skin near the fracture (may also be referred to as a compound fracture)

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131
Q

MOA of sucralfate

A

acidic environment changes sucralfate into a thick substance that adheres to an ulcer for up to 6 hours and protects ulcer from further injury

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132
Q

AEs of sucralfate

A
  • constipation
  • caution in pregnancy
  • use cautiously in renal failure (minimal absorption of aluminum salt which will accumulate)
  • interferes with med absorption
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133
Q

classification of magnesium hydroxide and calcium carbone

A

antacids
magnesium hydroxide - milk of magnesia
calcium carbonate - tums

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134
Q

MOA of antacids

A

neutralize gastic acid and inactivate pepsin –> potential mucosal protection due to stimulation of production of prostaglandins

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135
Q

AEs of antacids

A
  • constipation (CC)
  • diarrhea (MH)
  • caution in pregnancy
  • avoid with GI perforation or obstruction
  • caution in renal failure - salts
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136
Q

5 tx for IBD

A
  • 5-aminosalicylates (antiinflammatory)
  • glucocorticoids (steroids)
  • immunosuppressants
  • immunomodulators
  • antibiotics
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137
Q

UC severe tx

A

colectomy, Infliximab, cyclosporine, experimental rx

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138
Q

UC moderate tx

A

Infliximab, immunomodulators, corticosteroids

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139
Q

UC mild tx

A

probiotics, PO/topical amninosalicylates

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140
Q

crohns severe tx

A

surgery, Adalimumab, clinical trials

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141
Q

crohns moderate tx

A

Infliximab, Immunomodulators, corticosteroids

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142
Q

crohns mild tx

A

ABX, aminosalicylates, PO corticosteroids, alternate therapies (fish oil, probiotics)

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143
Q

classification of sulfasalzaine

A

5-aminosalicylates (5-ASA)

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144
Q

mode of sulfasalazine

A

PO or rectal (topical)

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145
Q

MOA of sulfasalazine

A

decreases inflammation by inhibiting prostaglandin synthesis

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146
Q

AEs of sulfasalazine

A

blood disorders ( decreased RBCs, platelets), anemia, contains sulfa (drug allergy)

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147
Q

4 types of genetic disorders

A
  1. chromosomal anomalies (mutations) - abnormal # or structure
  2. mendelian signle-gene disorders - autosomal dominant/recessive, x-linked
  3. polygenic/multifactorial disorders
  4. other
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148
Q

4 types of abnormal # genome mutations

A
  • euploidy: 46 chromosomes
  • aneuploidy: not 46 chromosomes
  • monosomy: deficiency of chromosome
  • polysomy: too many chromosomes
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149
Q

disorders involving sex chromosomes

A

most common, less debilitating

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150
Q

ex of autosomal recessive

A

cystic fibrosis

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151
Q

patterns of autosomal recessive

A
  • males and females equally affected
  • carrier may transmit to offspring
  • may delay on onset, incomplete penetrance, variable expressivity
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152
Q

ex of autosomal dominant

A

huntingtons disease (fatal, delayed onset)

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153
Q

pattens of autosomal dominant

A
  • males and females equally affected
  • affected individuals usually have affect parents - no generation skipped
  • carriers/unaffected do not transmit
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154
Q

patten of x-linked recessive

A
  • 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
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155
Q

ex of x-linked recessive

A

Duchenne muscular dystrophy, hemophilia a

156
Q

ex of polygenic traits

A

height, weight, IQ

157
Q

penetrance

A

% 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
Q

expressivity

A

level of expression; extent of variation in phenotype associated with a particular genotype (not uniformed; other gene influences)

159
Q

patho of down syndrome

A
  • 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
Q

characteristics of down syndrome

A

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
Q

duchenne muscular dystrophy overview

A

x-linked recessive, affects only males, apparent by age 3

162
Q

patho of duchenne muscular dystrophy

A
  • 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
Q

clinical manifesations of duchenne muscular dystrophy

A
  • 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
Q

dx of duchenne muscular dystrophy

A
  • H and P
  • elevated creatinine kinase initially
  • muscle biopsy
  • genetic testing
165
Q

overview of sickle cell

A
  • autosomal recessive
  • chromosome 11 point mutation (changes hgb stability)
  • homozygous inheritance 1 in 635
  • heterozygous inheritance (carrier) - 1 in 12
166
Q

patho of sickle cell

A
  • genetic mutation causes defective hemoglobin molecule

- when O2 is low, hgb5 undergoes polymerization and causes it to change to sickle shape

167
Q

triggers for sickling

A

dehydration, infection, fever, acidosis, hypoxia, exposure to cold

168
Q

2 problems caused by sickle cell

A
  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
Q

clinical manifestations of sickle cell

A
  • 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
Q

3 types of sickle cell crises

A
  1. vaso-occlusive
  2. acute sequesterization
  3. aplastic anemia
171
Q

vaso-occlusive crisis

A
  • 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
Q

acute sequesterization

A

6mo-4y, blood pools causing enlargement (hypovolemic shock), emergency, potential locations: spleen, liver, lungs

173
Q

aplastic anemia

A

increased destruction or decreased production of hgb, profound anemia, associated with viral infections, fever

174
Q

tx of sickle cell

A
  • 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
Q

complications of sickle cell

A

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
Q

cystic fibrosis patho

A

defect in a membrane transporter for chloride ions in epithelial cells; results in production of abnormally thick secretions in glandular tissues

177
Q

cystic fibrosis overview

A
  • most common single-gene disorder
  • autosomal recessive
  • chromosome 7 (1300 mutations)
  • caucasian American
178
Q

which neurotransmitters are monoamines

A

adrenaline/epinephrine
noradrenaline/norepinephrine
dopamine

179
Q

What is serotonin responsible for

A

mood

- feeling of well being, sleep, appetite, memory, sexual desire/fxn

180
Q

what is dopamine responsible for?

A

cognitive fxn, motivation, interest and attention, pleasure, euphoria, movement

181
Q

what is norepinephrine responsible for?

A

stress hormone, attention, flight/fight, anxiety

182
Q

what do norepi, serotonin, and dopamine have in common

A

mood, cognitive function

183
Q

prevalence of depression

A

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
Q

risk factors for depression

A

genetics, school failure, stressors, chronic illness, poor coping, SDOH (abuse, neglect, lower ed, lower SES), ADD, learning disabilities

185
Q

what is depression

A

a clinically and etiologically heterogeneous disorder

186
Q

what is the monoamine deficiency theory

A

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
Q

how is depression dx

A

screening tools:

  • patient Health questionnaire 9
  • Epidemiological Studies Depression Scale
  • Pediatric Symptom Checklist
188
Q

how is depression managed

A
  • sleep, nutrition, exercise
  • psychotherapies: cognitive behavioral therapy, interpersonal therapy
  • pharmacotherapy
  • safety plan
189
Q

what is anxiety

A

necessary physiologic response, helps protect us in dangerous situations

190
Q

what are fears

A

emotional response to threat, normal part of development

191
Q

what are worries

A

cognitive manifestations of fear and anxiety

192
Q

what are anxiety disorders

A

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
Q

anxiety disorders in peds

A
  • 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
Q

risk factors for anxiety disorders

A

genetic predisposition, temperament, modeling, physiologic factors and exposure to psychosocial and environmental stressors all contribute
- high rate of comorbidity with depression

195
Q

fight of flight anxiety manifestions and patho

A
  • 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
Q

anxiety disorder manifestations and patho

A
  • 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
Q

dx of anxiety disorders

A

screening:

  • Multidimensional Anxiety Scale for children
  • Screen for Child Anxiety Related Emotional Disorders
  • Spense Children’s Anxiety Scale
198
Q

tx of anxiety disorders

A

education, coping strategies, cognitive (worry), behavioral (relaxation), exposure

199
Q

what may happen if anxiety disorders are not treated?

A
  • major depressive disorder and substance misuse

- long term physiologic effects of stress cause GI, CV later in like

200
Q

what is insulin

A

natural hormone synthesized by beta cells of pancreas with Islets of Langerhans; proinsulin = precursor

201
Q

short duration: rapid acting

A

lispro (humalog)
aspart (NovoLog)
glulisine (Apidra)

202
Q

short duration: slower acting

A

regular insulin (humalin R, Novolin R)

203
Q

intermediate duration

A

NPH

204
Q

long duration insulin

A

glargine (lantus)

205
Q

SEs of insulin

A

hypoglycemia, hypokalemia, allergic rxn

206
Q

metformin use

A

initial drug choice for type 2 DM (pancreas still working)

207
Q

metformin MOA

A
  • 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
Q

PK of metformin

A

slowly absorbed from small intestine, excreted unchanged in kidneys, NOT worries about hypoglycemia

209
Q

common SEs of metformin

A

GI related (decreased appetite, N/D)

210
Q

toxicity of metformin

A

lactic acidosis; caution with renal function due to accumulation and lactic acidosis
- dont give to pts with increased creatinine levels

211
Q

class of metformin

A

biguanides

212
Q

class of glipizide

A

sulfonylureas

213
Q

moa of glipizide

A

stimulates release of insulin from pancreatic islets - doesn’t work if pancreas doesn’t work

214
Q

use of glipizide

A

solo or in combo (metformin)

215
Q

AEs of glipizide

A

hypoglycemia

216
Q

precautions of glipizde

A

dose reduced in elderly, renally eliminated (toxicity - hypoglycemia), avoid in pregnancy (fetal hypoglycemia)

217
Q

pioglitazone class

A

thiasolidinediones (glitazones)

218
Q

pioglitazone MOA

A

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
Q

considerations for pioglitazone

A

metabolized by CYP2C8

220
Q

AEs of pioglitazone

A

most common: RTI, HA, sinusitis, myalgia

most important: fluid retention, hypoglycemia

221
Q

class of repaglinide

A

meglitinides (glinides)

222
Q

moa of repaglinide

A

stimulates insulin release (like sulfonylureas)

223
Q

dosing of repaglinide

A

4x a day

224
Q

metabolism of repaglinide

A

by liver with short half life ( hour)

225
Q

AEs of repaglinide

A

rapidly absorbed by GI - patient needs to eat no later than 30 minutes after admin

226
Q

class of sitagliptin

A

gliptins (DPP-4 inhibitor)

227
Q

moa of sitagliptin

A

blocks DPP-4 - sends GLP and GIP down pancreas pathway - stimulates glucose-dependent release of insulin, suppresses postprandial release of glucagon

228
Q

SEs of sitagliptin

A

common: URIs, HA, inflammation of nasal passages and throat
serious: hypoglycemia, pancreatitis, hypersensitivity (anaphylaxis, SJS)

229
Q

class of liraglutide

A

incretin mimetics

230
Q

moa of liraglutide

A

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
Q

use of liraglutide

A

solo or combined (reduce dose of sulfonylureas to avoid hypoglycemia(

232
Q

admin of liraglutide

A

SQ injection daily

233
Q

AEs of liraglutide

A

dose-related GI (N/D/C), rare: pancreatitis

234
Q

most common bacterial meningitis adults

A

streptococcus pneumoniae (2nd most common in peds)

235
Q

most common bacterial meningitis peds

A

Neisseria meningitidis

236
Q

most common bacterial meningitis in newborns

A

E.Coli and GBBHS

237
Q

patho of meningitis

A
  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
Q

clinical manifestations of meningitis

A
  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
Q

eval of meningitis

A
  • 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
Q

tx of meningitis

A
  • IV antibiotics for bacterial
  • antiviral and steroids - viral
  • manage complications (seizures, increased ICP)
  • supportive
    prevention: immunizations, screenings
241
Q

most common causes of increased ICP

A

adults: stroke, trauma, tumors
peds: tumor, structural malformation, infections

242
Q

3 etiologies of increased ICP

A
  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
Q

clinical manifestations of increased ICP

A
  • 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
Q

eval o increased ICP

A
  • H and P
  • imaging
  • LP
245
Q

tx of increased ICP

A
  • underlying cause
  • continuoys monitoring and alleviating pressure
  • cerebral oxygenatino
  • pharm
246
Q

what are seizures

A

alteration in membrane potential that makes certain neurons abnormally hyperactive and hypersensitive to change

247
Q

seizures across lifespan

A

neonates: infection, birth defects, injury
children: genetics, trauma, febrile seizures
adults: cerebral vascular disease

248
Q

generalized seizures

A 
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
Q

partial seizures

A

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
Q

dx of seizures

A

H and P
neuro exam
EEG, labs, imaging

251
Q

tx of seizures

A

safety, airway, document, underlying cause, meds, avoid triggers

252
Q

febrile seizures

A

seizure accompanied by fever (>100.4) without central nervous system involvement (no infection necessary); 6mo-5y

253
Q

traditional AEDs

A

older, more experience, more data, significant AEs, lots of drug interactinos, cheaper

254
Q

newer AED agents

A

les SEs and drug interactions, better tolerability, generally safer in pregnancy, more expensive

255
Q

moa of phenytoin

A

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
Q

PK of phenytoin

A

saturable - half life dependent on dose; metabolized by liver (capacity)

257
Q

doseing of phenytoin

A
  • loading dose weight based IV or PO
  • maintenance dose by plasma[ ]
  • NTI
  • toxic: >20mcg/mL - nystagmus, sedation, ataxia, diplopia, seizures
258
Q

AEs of phenytoin

A

gingival hyperplasia, derm (most common): mortibilliform rash, SJS, TEN
IV admin: dysrhythmias, hypotension, purple glove syndrome

259
Q

route fosphenytoin

A

IV only

260
Q

moa fosphenytoin

A

prodrug to liver –> phenytoin

261
Q

admin and SE of fosphenytoin

A

easier admin, less AEs (no purple glove, decreased incidence of hypotension)

262
Q

considerations for fosphenytoin

A

may be infused faster but doesn’t work faster than phenytoin

263
Q

moa of carbamazepine

A

suppresses high-frequency neuronal discharge in and around seizure foci - likely due to delayed recovery of Na channels from inactivated state (like phenytoin)

264
Q

PK of carbamazepine

A
  • 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
Q

AEs of carbamazepine

A

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
Q

class of divalproex

A

valproic acid

267
Q

MOA od divalproex

A
  • suppression of high-frequency neuronal firing through Na channel blockade
  • suppresses Ca influx through T-type Ca CHannels
  • augment inhibitory influence of GABA
268
Q

PK of divalproex

A

extensive hepatic metabolism and renal excretion

269
Q

AEs of divalproex

A

GI, hepatotoxicity (avoid in <2yo), pancreatitis, hyperammonenemia, teratogenic 1st trimester

Drug interactions: phenobarbital, phenytoin

270
Q

MOA levetiracetam

A

unknown - does not bind to GABA or other NT

271
Q

routel evetiracetam

A

IV or PO

272
Q

PK levetiracetam

A

minimally metabolized, renally eliminated

273
Q

SEs of levetiracetam

A

mild/moderate: drowsy, asthenia

274
Q

class of mannitol

A

osmotic diuretic

275
Q

MOA od mannitol

A

crosses BBB to get fluid out (cerebral edema)

276
Q

SEs of mannitol

A

dehydration, hypotension, decreased electrolytes

277
Q

considerations of mannitol

A
  • sugar molecule crystallizes - inspect bag and use filter needle
  • monitor serum osmolarity for stability
278
Q

4 fetal circulation shunts

A
  • ductus venosus: shunts away from liver
  • ductus arteriosus: PA to aorta
  • foramen ovale: RA to LA
  • high pulmonary vascualr resistance
279
Q

causes of CHD

A
  • chromosomal disorders (6% downs)
  • intrauterine infections
  • maternal metabolic disorders, drug exposure, alcohol exposure
  • increased maternal age
  • prematurity
280
Q

acyonotic disorders and their effects

A
  • increased pulmonary blood flow: ASD, VSD, PDA

- obstruction to blood flow from ventricles: coarctation of aora

281
Q

cyanotic disorders and their effects

A
  • decreased pulmonary blood flow: tetrology of fallot

- mixed blood flow: transposition of great arteries

282
Q

3 main effects of CHD

A
  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
Q

PDA patho

A
  • 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
Q

clinical manifestatinos of PDA

A
  • heart failure
  • machine-like murmor
  • widening pulse pressure
  • bounding pulses
  • cardiac enlargement
285
Q

Eval and tx of PDA

A
  • echocardiogram
  • manage HF
  • Inodomethacin - closes ductus artiosus
  • cardiac cath or surgery
286
Q

patho of ASD

A
  1. pressure from LA to RA
  2. acyanotic
  3. increased load on r side (more blood to pump) - R sided HF
287
Q

clinical manifestatinos of ASD

A
  • depends on size
  • fatigue, dyspnea on exertion (SOB)
  • recurrent resp infections - fluid on R side
  • systolic murmor
  • HF develops young adulthood
    newborns: exertion
288
Q

eval and tx of ASD

A
  • echocardiogram
  • spontaneous closure if possible
  • manage HF
  • cardiac cath or surgery
289
Q

patho of VSD

A
  1. pressure LV to RV
  2. acyanotic
  3. workload R side - r sided HF, r sided V hypertophy
290
Q

clinical manifestatinos of VSD

A
  • r/t size
  • murmor (loud, harsh systolic)
  • HF
291
Q

eval and tx of VSD

A
  • may close on own
  • meds: digoxin, diuretics, ACE-I
  • manage HF
  • cardiac cath or surgery
292
Q

patho of coarctation of aorta

A
  1. pressure increased behind defect and decreased pressure after
  2. acyanotic
  3. workload L side - LV hypertrophy, pulmonary edema (backs up)
293
Q

clinical manifestations coarctation of aorta

A
  • murmur (systolic with ejection click)
  • poor LE perfusion
  • difference in UE and LE pulses and BP
  • initially L side HF
294
Q

eval and tx for coarctation of aorta

A
  • echocardiogram
  • improve CO - diuretics and digoxin
  • prostaglandin E - keeps PDA
  • cardic cath and/or surgery
295
Q

defects of tetralogy of fallot

A
  1. VSD
  2. overriding aorta (crosses both V to aorta - unO2 blood)
  3. pulmonary stenosis
  4. RV hypertrophy
296
Q

patho of tetralogy of fallot

A
  1. pressure: washing machine
  2. cyanotic - unO2 to aorta
  3. workload: R side (pulmonary stenosis)
297
Q

clinical manifestions of tetralogy of fallot

A
  • 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
Q

eval and tx of tetralogy of fallot

A
  • echocardiogram
  • prostaglanin E
    management of tet spells
    series of surgeries
299
Q

patho of transposition of GA

A

RV - aorta - unO2 - body

LV - PA - O2 - lungs

300
Q

clinical manifestions of transposition of GA

A
  • cyanosis at birh
  • hypoxemia with o2 (doesnt help)
  • progressive desat and acidosis
  • HF
301
Q

eval and tx

A
  • prostaglandin E

- cardiac cath and surgery

302
Q

CO formula

A

stroke volume (preload, afterload, contractility) X HR

303
Q

common causes of HF

A

myocardial ischemia, HTN, cardiomyopathy

304
Q

5 classificatinos of HF

A
  • 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
Q

what are forward backwards effets

A

backwards effects of L side = forwards effets of R side

306
Q

L sided HF effects

A

backward: pulmonary congestions
forward: decreased tissue perfusion

307
Q

clinical manifestations of L sided HF

A
  • dyspnea, orthopnea
  • cough, crackles
  • hemoptysis
  • tachycardia, S3 and S4
  • cool, pale skin
308
Q

r sided HF effects

A

backward: systemic congestions
forward: decreased tissue perfusion

309
Q

clinical manifestions of R sided HF effects

A
  • JVD
  • hepato-splenomegaly
  • weight gain, edema
310
Q

dx of CHF

A

H and P
chest xray - where is fluid?
ECG, EKG - electrical activity
- echocardiogram

311
Q

tx oc CHF

A
  • manipulate preload, afterload, contractility
  • improve CO: digitalis, digoxin
  • minimize congestive symptoms: diuretics
  • minimize cardiac workload: pacemaker, ACEI, ARBs
312
Q

result of peds CHF

A

decreased LV systolic funcitno: LA and pulmonary venous HTN, pulmonary venous congestions

313
Q

clinical manifesations of CHF in peds

A
  • impaired myocardial functin
  • pulmonary congestion
  • general: poor feeing, FTT
314
Q

tx of CHF in peds

A
  • underlying cardiac defect
  • fluid balancel increase carolie count, diuretics, decrease volume of feeds
  • increase CO
315
Q

4 medical tx goals of HF

A
  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
Q

1st line of med for HF and why

A

diuretics - decrease blood volume

317
Q

3 broad classificatinos of diuretics and prototype

A

thiazide diuretics - hydrochlorothiazide
loop diuretics - furosemide
potassium-sparing diuretics - spironolactone

318
Q

Hydrochlorothiazide

A
  • thiazide diuretic
  • ineffective with low GFR
  • for mild diuresis
  • AE: hypokalemia
319
Q

Furosemide

A
  • 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
Q

spironolactone

A
  • potassium-sparing diuretic
  • minimal diuresis
  • can be used to prevent hypokalemia with loop diuretics
  • AE: hyperkalemia, gynecomastia in med
321
Q

2 categories of drugs that inhibit RAAS and prototypes

A
  • ACE-I: Lisinopril
  • ARBs: Losartan
  • Aldosterone antagonists: Spironolactone
322
Q

uses of lisinopril

A
  • ACE-I

- cornerstone of therapy: decrease mortality, improve functino, favor cardiac remodeling

323
Q

benefits of lisinopril

A

hemodynamic benefits: arteriolar dilation, venous dilation, suppresses aldosterone release

324
Q

AEs of lisinopril

A

angioedema, hyperkalemia, cough

325
Q

benefits of losartan

A

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
Q

AE of losartan

A

hyperkalemia, less angioedema

327
Q

MOA of spironloactone

A

blocks aldosterone receptors in hears and vessels; reduces symptoms and decreases hospitalizations, prolongs life

328
Q

aldosterone effects

A
  • 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
Q

beta blockers added to conventional therapy…

A
  • improve LV EF
  • increase exercise tolerance
  • slow progression of HF
  • decreased need for hospitalization
  • prolong survival
330
Q

MOA of BBs

A

protecting heart from excessive sympathetic stimulation and protecting against dysrhythmia

331
Q

Metoprolol

A
  • regular and ER salt forms
  • AE: fluid retention and worsening HF, fatigue, hypotension, bradycardia, heart block
  • Watch HR (body more dependent)
332
Q

digoxin class

A

cardiac glycosides

333
Q

digoxin potential effect

A
  • 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
Q

consideations of digoxin

A
  • 2nd line agent
  • NTI
  • adjust for renal dysfunction
  • drug interactions
335
Q

AEs of digoxin

A

very dangerous

  • cardiac dysrhythmias (exacerbated by hypokalemia and elevated digoxin levels)
  • CNS and GI
  • anorexia, N/V, visual disturbances (halo)
  • drug interactions
336
Q

hydralazine class

A

vasodilator

337
Q

hydralazine MOA

A

selective dilation of arterioles (little/no venous effect)

338
Q

hydralazine in combo with nitrates

A
  • 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
Q

AE of hydralazine

A

hypotension, tachycardia, lupus-like sydrome

340
Q

nitrate pathway

A

free nitrite ion –> converted to nitric oxide –> results in vasodilation

341
Q

nitroglycerin forms

A

SL tabs, topical, spray, transdermal patch, IV

342
Q

MOA of nitroglycerin

A

dilates veins and decreases venous return (preload) which decreases oxygen demand

343
Q

drug interactions of bitroglycerin

A

phosphodiesterase Type 5 Inhibitors (Viagra) - leads to excessive vasodilation and drop in BP

344
Q

nitroglycerin considerations

A

tolerance occurs rapidly; nitrate-free interval

345
Q

classification of paroxetine

A

selective serotonin reuptake inhibitors (SSRIs)

346
Q

paroxetine route

A

daily; 1st line

347
Q

paroxetine MOA

A

inhibits serotonin reuptake

348
Q

paroxetine AEs

A

most common: GI

sexual dysfunctnion, weight gain, withdrawal, serotonin syndrome

349
Q

what is serotonin syndrome

A

muscle rigidity, altered mental status, fever

350
Q

paroxetine considerations

A
  • may take 4-8 weeks for effect

- drug interactions - antiplatelet agents

351
Q

classification of amitriptyline

A

tricyclic antidepressants (TCAs)

352
Q

amitriptyline MOA

A

blocks neuronal reuptake of NE and serotonin

353
Q

amitriptyline AEs

A

orthostatic hypotension, sedation, anticholinergic effects, cardiac toxicity, seizures

354
Q

amitriptyline considerations

A
  • multiple drug interactions
  • lethal overdoses
  • low doses used for neuropathic pain and sleep (rarely used for depression)
355
Q

classification of venlafaxine

A

serotonin-norepinephrine reuptake inhibitors

356
Q

venlafaxine MOA

A

blocks reuptake of NE and serotonin (effects similar to SSRIs)

357
Q

venlafaxine AEs

A

weight gain, HA, insomnia, dizziness, sexual dysfunction, serotonin syndrome, hypertension, tachycardia

358
Q

venlafaxine considerations

A

watch for interactions with NSAIDs and anticoagulants (minor antiplatelet effect)

359
Q

classification of bupropion

A

atypical antidepressant

360
Q

bupropion forms

A

immediate, sustained, XL tablets (dosed different # times/day)

361
Q

bupropion MOA

A

unclear: dopamine blocker, NE reuptake

362
Q

bupropion AEs

A

common: agitation, HA, dry mouth, constipation, weight loss
serious: seizures

363
Q

bupropion considerations

A
  • good alternative to SSRIs
  • drug interactions - metabolized by CYP
  • used for smoking cessation
364
Q

classification of alprazolam

A

benzodiazepine

365
Q

alprazolam route

A

PO

366
Q

alprazolam MOA

A

binds to GABA receptor - chloride channel complex; intensifies effects of GABA

367
Q

alprazolam AEs

A

CNS depression, respiratory depression, anterograde amnesia, withdrawals, hypotension (IV)

368
Q

what are 3 monoamines

A

epi, norepi, dopamine

369
Q

effects of serotonin

A

MOOD, feeling of wellbeing, sleep, appetite, memory, sexualy desire

370
Q

effects of dopamine

A

cognitive function, motivation, interest and attention, pleasure, euphoria, movement

371
Q

effects of norepi

A

stress hormone, attention, fight/flight, anxiety

372
Q

overlapping effet of norepi, serotonin and dopamine

A

mood and cognitive function

373
Q

who does depression effect

A
  • 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
Q

risk factors for depression

A
  • 1st degree family member
  • school failure
  • stressors
  • chronic illness
  • poor coping
  • SDOH - neglect, abuse, lower SES
  • ADD, learning disabilities
375
Q

what is the monoamine deficiency theory

A

no regular/usual amount in synaptic space

376
Q

causes of monoamine deficiency

A
  • decreased baseline #
  • reuptake (overactive)
  • enzymes eating up before getting to post synapatic
  • not enough transporters
377
Q

dx of depression

A

screening tool:

  • patient health q 9
  • epidemiologic studies depression scale
  • pediatric symptom list
378
Q

management of depression

A
  • sleep, nutrition, exercise
  • psychotherapies - cognitive behavioral therapy, interpersonal therapy
  • pharmacotherapy
  • safety plan
379
Q

what is anxiety

A

necessary physiologic response, helps protect us in dangerous situations

380
Q

what are fears

A

emotional response to threat, normal part of development

381
Q

what are worries

A

cognitive manifestatinos of fear and anxiety

382
Q

what are anxiety disorders

A

fears, worries, or anxiety occur outside range of normal developmental responses, are extreme, cause significant distress, impair function - PERSISTENT, EXCESSIVE, AND UNREALISTIC WORRY

383
Q

fight or flight response

A
  • 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
Q

fight or flight response in anxiety disorders

A
  • 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
Q

dx of GAD

A

screening:

  • Multidimensional Anxiety Scale for children
  • Screen for Child Anxiety Related Emotional Disorders
  • Spense Children’s Anxiety Scale
386
Q

tx of GAD

A
  • education
  • coping strategies
  • cognitive (worry)
  • behavioral (relaxation)
  • exposure
387
Q

long term effects of untreated GAD

A
  • major depressive disorder and substance misuse

- GI, CV issues

N398 (2 decks)

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