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IPT: GI/Resp > Block 2 > Flashcards

Block 2 Flashcards

1
Q

What is the cause of hepatic encephalopathy?

A

Accumulation of substances that cant be cleared via liver

Changes in astrocytes which causes brain edema

Substances: Ammonia, glutamate, benzodiazepine receptor AGONISTS, manganese

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2
Q

What is Grade I HE?

A

Day/Night Inversions

MILD confusion

Irritability

Tremors

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3
Q

What is Grade II HE?

A

Lethargy

Disorientation

Inappropriate behavior

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4
Q

What is Grade III HE?

A

Somnolence

SEVERE confusion

Aggressive behavior

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5
Q

What is Grade IV HE?

A

Coma

Also the only one that DOESN’T have asterixis

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6
Q

What dietary changes can you make for HE?

A

Limiting protein intake to 10-20g/day

Max is 0.8-1g/kg/day or 40g/day

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7
Q

What causes the constipation in HE patients?

A

Not eliminating ammonia

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8
Q

What causes the hypokalemia and acidosis in HE pts?

A

Diuretics and diarrhea

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9
Q

What are the pharmacologic Tx for HE (just non-Abxs)?

A

Lactulose (nonabsorbable disaccharide)

Initially: 15-45mL every 1-2hrs until BM

Continue at 15-45mL 2-4x a day and titrate to 3-5 BMs/day

Enema: 300mL in 700mL water and retain for 1 hr

Watch for signs of dehydration

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10
Q

What are the Abx used for HE?

A

Flagyl

Neomycin

Rifaximin

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11
Q

What is the dose and AE of Flagyl for HE?

A

Flagyl 250mg every 8-12hrs

**dont use for long-term due to peripheral neuropathy

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12
Q

What is the dose and AE of Neomycin for HE?

A

Neomycin 500-1000mg every 6hrs or 1% solution enema in 100-200mL NS

**risk for ototoxicity and nephrotoxicity with an increased risk in renal damaged pt

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13
Q

What is the dose and AE of Rifaximin for HE?

A

Rifaximin 550mg 2x or 400mg 3x a day

**nausea and peripheral edema

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14
Q

What are the main causes of cirrhosis?

A

EtOH

Hepatitis B, C, D

Nonalcoholic diseases due to diabetes or metabolic syndrome

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15
Q

What are the less common causes of cirrhosis?

A

Autoimmune hepatitis

Primary cholangitis

AAT deficiency

Hemochromatosis

Wilson disease

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16
Q

What Rx cause cirrhosis?

A

I MAMBAS

Isoniazid

Methyldopa

Amiodarone

Methotrexate

Black cohosh

APAP

anabolic Steroids

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17
Q

What are the lab values for cirrhosis?

A

Decreased albumin

Decreased cholesterol

Increased PT/INR

Increased bilirubin

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18
Q

What are the signs of compensated cirrhosis?

A

Fatigue, weakness, wt loss (>50%)

40% are asymptomatic

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19
Q

What are the signs of decompensated cirrhosis?

A

RUQ pain

Ascites, variceal bleed, jaundice, encephalopathy

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20
Q

What gives pt 1 point for cirrhosis?

A

No encephalopathy or ascites

<2 bilirubin

> 3.5 albumin

PT = 1-4

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21
Q

What gives pt 2 points for cirrhosis?

A

Mild/moderate encephalopathy

Slight ascites

2-3 bilirubin

Albumin 2.8-3.5

PT = 4-6

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22
Q

What gives pt 3 points for cirrhosis?

A

Severe encephalopathy or coma

Moderate ascites

> 3 bilirubin

<2.8 albumin

> 6 PT

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23
Q

What is class A cirrhosis?

A

5-6 points

100% 1 yr survival
85% 2 yrs survival

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24
Q

What is class B cirrhosis?

A

7-9 points

81% 1 yr survival
57% 2 yrs survival

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25
Q

What is class C cirrhosis?

A

10-15 points

45% 1 yr survival
35% 2 yrs survival

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26
Q

What is the MELD score used for in cirrhosis?

A

Transplant listing

Higher score = sicker and will receive transplant sooner

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27
Q

What should be screened for patients who have cirrhosis?

A

Hepatocellular carcinoma with liver ultrasound and alpha fetoprotein every 6 months

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28
Q

What causes portal HTN?

A

Fibrosis due to cirrhosis causes resistance to blood flow in portal vein

Increased vasoconstriction by decreasing NO, and increased endothelin-1 and ATH

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29
Q

How is portal HTN diagnosed?

A

Pressure gradient >10mmHg between portal vein and inferior vena cava (normal = 3)

Clinical complications: esophageal and gastric varices

Imaging

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30
Q

What kind of BB are used in portal HTN? How does that work?

A

Nonspecific BB

B-1: decreases cardiac output

B-2: prevents splanchnic vasodilation

Unopposed alpha-1: splanchnic vasoCONSTRICTION

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31
Q

Tx of portal HTN

Include Rx and dose

A

Nadolol 20mg daily

Propranolol 10mg 3x day

Titrate to 20-25% reduction in resting HR or absolute HR of 55-60 or until no longer tolerated

**increases risk of hepatorenal syndrome

**same dose for varices as well

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32
Q

What are varices?

A

Gastric/esophageal vessels are enlarged due to increased intrahepatic pressure

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33
Q

How is varices diagnosed?

A

Endoscopy (gold standard)

Grade 1: <5mm

Grade 2:>5mm

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34
Q

Primary prophylaxis and varices?

A

Screen EGD in all cirrhotic pt

No varices present? No pharm. ppx

Varices present w/ HIGH risk for bleed (B or C), use nonselective BB

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35
Q

What happens if there is a bleed in varices?

A

d/c BB in acute setting

Manage airway, fluid resuscitation (make sure Hgb>8)

Then endoscopic exam with pharm. agents

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36
Q

What form of endoscopy is preferred for bleeding varices?

A

Endoscopic band ligation over injection sclerotherapy

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37
Q

What are the Rx used for bleeding varices?

A

Somatostatin OR octreotide

Vasopressin AND Nitroglycerin

Cipro, norfloxacin, or ceftriaxone

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38
Q

What are the vasoactive drugs used for bleeding varices? Dose?

A

Somatostatin OR octreotide

Somatostatin 250mcg IV bolus then 250-500mcg/hr for 3-5days

Octreotide 50-100mcg IV bolus then 25-50mcg/hr for 3-5 days

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39
Q

Vasoactive drug MOA for bleeding varices?

A

Reduces splanchnic blood flow by inhibiting glucagon (and other vasoactive peptides) and direct local vasoconstriction

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40
Q

Vasopressin and nitroglycerin dose for bleeding varices? AE?

A

Vasopressin 0.2 - 0.4 u/min
Max of 0.8u/min

Nitroglycerin 40mcg/min to a max of 400mcg.min for 24 hrs

AE of Nitroglycerin and why only 24hrs = ischemia, arrhythmias, HTN

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41
Q

Abx used for bleed varices? Dose?

A

Cipro 400mg IV every 12hrs

Norfloxacin 400mg PO every12hrs x7 days

Ceftriaxone 1g/day if FQ resistant

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42
Q

Secondary prophylaxis and varices?

A

Propranolol 20mg TID

Nadolol 20-40mg PO daily

Titrate to 20-25% reduction in resting HR or absolute HR of 55-60

If BB is not working, add isosorbide MONOnitrate (but not recommend due to AE)

TIPS if medically unresponsive

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43
Q

What is ascites?

A

> 25 mL of lymph fluid in peritoneal cavity due to:

  1. cirrhosis (liver cant make albumin)
  2. low albumin (lymph fluid leaks OUT of cells into peritoneal cavity)
  3. Portal HTN (nitric oxide is released, activates RAAS, sodium and water retention and vasoconstriction)
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44
Q

SAAG score and Ascites?

A

> 1.1 = fluid accumulation due to portal HTN

<1.1 = other cuase

Serum albumin - albumin in ascetic fluid; found via paracentesis

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45
Q

Diet and ascites?

A

Abstinence from alcohol

Restrict sodium to <2g/day

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46
Q

What happens if you remove a lot of fluid found in ascites?

A

Circulatory collapse, encephalopathy, and renal failure

If >5L of fluid is removed, add 5-8g of albumin/L

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47
Q

How do you Tx ascites?

A

Mild: Spironolactone

Moderate-severe: Furosemide 40mg PO QAM + spironolactone 100mg PO QAM

Doses can be increased PRN but maintain 40:100 ratio

Max Lasix = 160
Max Spironolactone = 400

If spironolactone w/ painful gynecomastia, consider amiloride or triamterene

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48
Q

What is the goal of Tx in ascites with the use of diuretics?

A

Weight loss of 0.5kg/day (no edema) to 1kg/day (edema)

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49
Q

Besides diet and diuretics, what else can you do for ascites?

A

d/c drugs that retain sodium and water like NSAIDs

TIPS (Transjugular Intrahepatic Portosystemic Shunt) ***for those not responsive to diuretics and sodium restriction

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50
Q

What are the most common ways to cause Spontaneous Bacterial Peritonitis?

A

Intestinal bacterial overgrowth (cirrhosis)

Bacterial translocation from lumen to peritoneal cavity

Can spread to mesenteric lymph nodes and into blood

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51
Q

What medications cause Spontaneous Bacterial Peritonitis?

A

PPIs and non-selective BB

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52
Q

Risk factors of Spontaneous Bacterial Peritonitis?

A

Ascetic fluid protein <1

Bilirubin >2.5

Variceal hemorrhage**

Prior episode of Spontaneous Bacterial Peritonitis**

**More common in child pugh class C

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53
Q

What lab findings confirm Spontaneous Bacterial Peritonitis?

A

> 250 PMNs/mL in ascetic fluid

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54
Q

What is the empiric Abx Tx of Spontaneous Bacterial Peritonitis?

A

Ceftriaxone 1-2g IV daily

Cefotaxime 2g IV q8h

or

FQs PO only if they never had exposure to Rx, no vomit, no shock, no grade II to IV HE, and if dont have SCR>3

Then give Ofloxacin 400mg PO q12h

Duration for all Tx = 5 days

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55
Q

Other Tx besides Abx for Spontaneous Bacterial Peritonitis?

A

Albumin 1.5g/kg on day 1

Then 1g/kg on day 3

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56
Q

Who is placed on primary prophylaxis on Spontaneous Bacterial Peritonitis?

A

Inpatients w/ cirrhosis and other complications that put them at risk for Spontaneous Bacterial Peritonitis (history, GI bleed, ascitic fluid protein <1g)

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57
Q

Who is placed on secondary prophylaxis on Spontaneous Bacterial Peritonitis?

A

Everyone whos had it before, and they get it forever unless they get a liver transplant or full resolution of ascites

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58
Q

What meds are used for secondary prophylaxis on Spontaneous Bacterial Peritonitis?

A

Norfloxacin 400mg PO daily

Cipro 750mg PO qWeekly

Bactrim 1 tab PO 5x week

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59
Q

What causes hepatorenal syndrome?

A

Portal HTN causes splanchnic blood pool

Vasodilation

Low circulating blood activates SNS, RAAS, release of vasopressin

Leads to increased CO and retention of Na/Water but kidneys dont get blood due to vasoconstriction

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60
Q

What is type I hepatorenal syndrome?

A

Acute (<2wks) onset unresponsive to volume expansion

Doubles SCr >2.5 or reduces CrCl by 50% to <20

Survival: 1 month

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61
Q

What is type II hepatorenal syndrome?

A

Slower progression vs I; aka diuretic resistant ascites

Survival: 6 months

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62
Q

What are the general Tx recommendations for hepatorenal syndrome?

A

Albumin 1g/kg up to 100g/day

Hemodialysis or CRRT until transplant

Liver transplant or TIPS may be required

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63
Q

What Pharm. Tx are used in hepatorenal syndrome?

A

Dopamine + albumin

Preferred: Albumin + Octreotide + Midodrine

Norepi + albumin (if they cant PO and must be in ICU)

Vasopressin + terlipressin

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64
Q

What are the doses of Albumin + Octreotide + Midodrine for hepatorenal syndrome?

A

Albumin 10-20g IV qd for 20 days

Octreotide up to 200mcg SQ TID

Midodrine up to 12.5-15mg PO TID to allow 15mmHg BP increase

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65
Q

What is the purpose of the liver?

A

To produce more polar metabolites aka more hydrophilic

Phase 1: oxidative, CYP

Phase 2: conjugation, glucuronyl transferases, etc

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66
Q

What are the common Rx that can cause DILI?

A

Abx

Anti-epileptics

NSAIDs

IBD Rx

Allopurinol, amiodarone, chlorpromazine

Herbal stuff

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67
Q

Differences between the characteristics of DILIs

A

Intrinsic - dose dependent, short onset

Idiosyncratic - not dose dependent, latency period

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68
Q

Characteristics of hepatocellular injury?

A

Increased in LFTs

Metabolic type: Rx binds covalently to intra. proteins

Immune-med.: haptenization leads to immune response

High risk of death

EX: tylenol

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69
Q

How does hepatocellular injury present and what are the lab abnormalities?

A

Usually occurs within 1 yr of Rx initiation

Ab pain, N/V, jaundice later

ALT greatly increases

LDH and bilirubin also increases

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70
Q

What is cholestasis?

A

Reduction or stoppage of bile flow

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71
Q

How does cholestasis present and what are the lab abnormalities?

A

Pruritus, dark urine, jaundice

Alkaline phosphatase greatly increases

May present with vanishing bile duct syndrome, bilirubin and cholesterol will go up as well

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72
Q

What is steatosis?

A

Accumulation of FA in mitochondria

Microvesicular = tiny fat drops that DONT displace nucleus

Macrovesicular = do displace nucleus

Amiodarone causes this kind of damage

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73
Q

How does immunoallergic DILI present and what are the lab abnormalities?

A

Cholestatic injury + immunoallergic

ALT and alkaline phosphatase both greatly increase

Phenytoin causes this damage via HLA-B*1502

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74
Q

How do you calculate R value?

A

(ALT/55) / (Alk Phos/130)

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75
Q

How do you interpret R value?

A

≥5 = heptaocellular

≤2 = cholestatic

2-5 = mixed

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76
Q

What is RUCAM?

A

Exposure to DILI

-9 to 10; higher = more likely of DILI

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77
Q

What is Hy’s Law?

A

Mortality risk after DILI, usually within 6 months

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78
Q

What are the treatments for overdose on….

APAP
MTX
Valproic acid
Pruritus
Coagulopathy
Immune-mediated
A 
APAP - N acetylcysteine
MTX - Leucovorin
Valproic acid - L carnitine
Pruritus - Cholestyramine/Colestipol
Coagulopathy - Vit. K
Immune-mediated - Corticosteroids
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79
Q

How is APAP metabolized and how does it cause damage?

A

Goes thru glucuronidation or sulfation

or

Metabolized by CYP2E1 as a toxic metabolite (NAPQI)
then can go through glutathione conjugation to become a stable metabolite

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80
Q

How does N-acetylcysteine treat APAP overdose?

A

Works on the glutathione conjugation part

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81
Q

How does Valproic acid overdose work?

A

Mitochondrial toxicity, causes hyperammonemia

Lower carnitine levels, causes mitochondrial dysfunction

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82
Q

When should you rechallenge in DILI cases?

A

Only if DILI is questionable, serious, no other Tx is available, AND they have no signs/symptoms

Reduce dose by 1/2 and titrate up slowly

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83
Q

How do you treat DILI?

A

D/c offending agent, give antidote if possible

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84
Q

Pulmonary Gas Exchange, what goes in/out of alveoli?

A

CO2 in

O2 out (to blood)

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85
Q

What antibody is present in the defenses of the lung?

A

IgA and serum immunoglobulins

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86
Q

What makes up total lung capacity?

A

IRV + TV + ERV/RV

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87
Q

What makes up the lung capacity that we can breathe in/out ourselves?

A

VC (vital capacity)

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88
Q

Tidal volume + IRV = ???

A

IC (inspiratory capacity)

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89
Q

What is FEV1?

A

Volume of air exhaled during the first second of FVC (forced volume capacity)

Diminished by decreased total lung capacity or lack of effort

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90
Q

What is FEV1/FVC?

A

Measure of airway obstruction w/ or w/o restriction

Normally ≥75%

Anything ≤70% suggest OBSTRUCTION (INDEPENDENT of size or TLC)

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91
Q

ERV + RV = ???

A

FRC (functional residual capacity)

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92
Q

What cant the spirometry measure?

A

Anything with RV in the equation

  1. RV
  2. TLC
  3. FRC
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93
Q

Bronchospasm vs Emphysema

Reduced diameter of airways…

A

Bronchospasm

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94
Q

Bronchospasm vs Emphysema

Reduction in elastic recoil/lung elasticity…

A

Emphysema

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95
Q

In obstructive lung disorders, what volumes are increased/decreased?

A

Decreased: VC, IRV, ERV

Increased: RV, FRC, RV, TLC

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96
Q

Pulmonary fibrosis is an example of obstructive/restrictive disease?

A

Restrictive

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97
Q

Restrictive disease and FEV1/FVC, how is it affected?

A

Normal

98
Q

In restrictive lung disorders, what volumes are increased/decreased?

A

Pretty much everything decreases except FEV1/FVC

99
Q

What disease states should and shouldn’t have normal DLCO (diffusing capacity of CO)?

A

Normal levels that affect airways only (like asthma and bronchitis)

Abnormal that cause parenchymal disease (like interstitial lung disease or emphysema)

100
Q

Risk factors of asthma?

A

Genetics; ATOPY is the biggest factor, others include, obesity and male

Endogenous factors; low exposure to childhood infections, Th2 overproduction

Environmental (typical stuff, but also APAP :o)

101
Q

What are triggers? what are some triggers for asthma?

A

Something that makes an ESTABLISHED disease worse

URTI, exercise, cold air, irritant gases, rx such as non-selective BB, NSAIDs

102
Q

How does an allergen cause early phase reaction of acute asthma?

A

Allergen activates IgE, activates mast cells and macrophages, airway contraction/mucus secretion/vasodilation

103
Q

How does late phase acute asthma work?

A

6-8hrs after early phase

Recruits eosinophils, CD4 T cells, neutrophils, and macrophages, releases cytokines and recruits inflammatory cell recruitment

104
Q

How does chronic asthma work?

A

Pretty much late phase acute asthma + fibroblasts and bronchial smooth mucles

Releases cytokines and growth factors

Remodeling of lungs, causes greater decline in lung function in non-asthma pt

105
Q

Main symptoms of asthma?

A

Episodic dyspnea which can go and stop anytime

Chest tightness

**unless its acute severe asthma, then they can only say a few words, unresponsive to quick relief meds

106
Q

Spirometry findings of Asthma?

A

Reduced FEV1/FVC with REVERSIBILITY followed by B2 agonist

107
Q

Exercise induced bronchospasm info?

A

Likely caused by heat loss/water loss from central airways

Drop in FEV1 of 15%+ from pre-exercise value

108
Q

Nocturnal Asthma info?

A

Worsening of asthma during sleep

Its a sign of inadequately treated persistent asthma

109
Q

Peak flow meter zones?

A

Green = 80% of best

Yellow 50-79% of best

Red = <50% of best

Best = Achieved by getting a reading over a 2 wk period

Take readings twice daily for 2-3wks and 15-20 min after SABA use

**used every 1-2yrs to demonstrate reversibility in severe cases

110
Q

Level of asthma symptom control and their levels?

A

Well controlled = 0 points

Partially controlled = 1-2 points

Uncontrolled = 3-4 points

  1. Daytime Sx more than 2x a week?
  2. Any night waking due to asthma?
  3. Reliever needed more than 2x a week?
  4. Any activity limitations due to asthma?

Check every 1-2 yrs

Other risk factors include being intubated, in ICU or having 1+ exacerbation in the last 12 months

111
Q

Mild, Moderate, Severe asthma, what step treatment do they need? general

A

Mild = asthma controlled w/ step 1 or 2

Moderate = 3 or 4

Severe = 5

112
Q

What is Step 1 Tx for asthma?

A

PRN low dose ICS-formoterol or w/ SABA is taken

113
Q

What is Step 2 Tx for asthma?

A

Daily low dose ICS or PRN ICS-formoterol

Can take Leukotriene RA

114
Q

What is Step 3 Tx for asthma?

A

Low dose ICS-LABA

Can take medium dose ICS or low dose ICS+LTRA

115
Q

What is Step 4 Tx for asthma?

A

Medium dose ICS-LABA

Can take high dose ICS, addon tiotropum or LTRA

116
Q

What is Step 5 Tx for asthma?

A

High dose ICS-LABA

Refer to phenotypic assessment

Can add tioproium, anti-IgE,IL5,IL4

Can also add OCS (watch for AE)

117
Q

What are risk factors for obstructive disease?

A

External factors

Smoking

Endogenous factors (AAT deficiency - emphysema)

118
Q

If obstructive is neutrophil driven, what is it in asthma?

A

Eosinophils and mast cells

119
Q

If asthma is eosinophils and mast cell driven, what is in obstructive disease?

A

Neutrophils

120
Q

What are the main physiological changes in obstructive disease?

A

Mucus secretion via goblet cell hypertrophy

Air trapping

Diaphragm is flattened, impaired inspiration

121
Q

What are the subtypes of COPD?

A

Emphysema

Chronic bronchitis

122
Q

What is emphysema?

A

Destruction of airways distal to terminal bronchioles

Cant oxygenate blood well

Compensates by hyperventilating

123
Q

What is chronic bronchitis?

A

Excessive mucus production

No damage to pulmonary capillary beds

Compensates by decreasing ventilation and increasing cardiac output

124
Q

Asthma vs COPD, which one requires spirometry for diagnosis?

A

Only COPD

125
Q

What is the GOLD classification of COPD?

A

FEV1/FVC <70 for all pt

Based on FEV1 values:

Mild ≥80%
Moderate 50-79%
Severe 30-49%
Very severe <30%

126
Q

What is the MMRC scale?

A

For COPD

0 = not trouble unless on strenuous exercise

1 = SOB when hurrying on level or walking up hill

2 = walks slower for same aged ppl due to breathlessness or has to stop when walking with pace

  1. Stops after 100m or a few min on level
  2. Too breathless to leave house or breathless when dressing up/down

Theres also a CAT scale (>10 or <10)

127
Q

What is the COPD assessment and classification step?

A

Assessment of severity with C….D then A….B

D = most severe

A = least severe

Exacerbation history = 1 w/ hospital or ≥2 = C or D line

= 0 or 1 not leading to hospital = A or B line

MMRC and CAT score of 0-1 or <10 = A C line

≥2 or ≥10 = B D line

128
Q

Besides B2 receptor agonists and inhaled corticosteroids, what antagonist can help with bronchodilation and is effective in COPD?

A

Muscarinic receptor antagonists

129
Q

B2 receptor agonist MOA?

A

B2 adrenergic receptors couples to Gs protein and stimulates adenylyl cyclase which increases cAMP

cAMP stimulates phosphorylation of an enzyme that NEGATIVELY regulates excitation-contraction, which leads to smooth muscle relaxation

Also decreases release of inflammatory mediators and bronchoconstrictors from mast cells

130
Q

Albuterol, Salmeterol, Formoterol

Which one is given PRN?

A

All of them, but with ICS

131
Q

How often is salmeterol and formoterol given in prophylaxis of asthma?

A

q12hrs daily

Can be used PRN w/ ICS

132
Q

What is the GINA 2019 recommendation Tx on SABAs?

A

Use ICS + SABA

or

ICS/LABA

133
Q

B2 receptor agonist AE?

A

Tremors, Tachycardia

Hypokalemia

Hyperglycemia

Restlessness

134
Q

B2 receptor agonist DDI?

A

Salmeterol w/ azoles

Formoterol with mesoridazine

^^Both have increased % of QT prolongation^^

Albuterol with atomoxetine, increases BP/HR

135
Q

What are the inhaled muscarinic receptor antagonists?

A

Ipratropium and tiotropium

136
Q

Ipratropium and tiotropium MOA?

A

Muscarinic Receptor Antagonists

ACh stimulates and constricts smooth muscle in lung. These drugs block that

Limited role by itself and in asthmatics

137
Q

Corticosteroid MOA?

A

Positively/negatively regulates gene transcription takes time

Inhibit production/release of cytokines, lipolytic/proteolytic enzymes. Decrease mobilization of leukocytes to area of injury + fibrosis

138
Q

Can ICSs be used for acute exacerbation?

A

Nope

139
Q

What is the first line anti-inflammatory therapy for asthma?

A

ICS, must pair it with B2 agonist per GINA

140
Q

ICS, regardless of asthma severity, reduces asthma exacerbation and what else?

A

Reduces hospitalizations, death, and improves overall lung function

141
Q

ICS is used for their glucocorticoid/mineralocorticoid effects

A

Glucocorticoid effects only

142
Q

Examples of ICS?

A

Beclomethasone, budesonide, mometasone, fluticasone

143
Q

Can ICS reach systemic circulation?

A

Yes, a significant fraction is swallowed and can reach GI tract

144
Q

If ICS dose is high, which one is preferred?

A

Any except beclomethasone

145
Q

Which ICS is a pro-drug?

A

Beclomethasone

146
Q

How do you reduce the amount of ICS being swallowed?

A

Gargle and rinse. Use spacer if aerosolized

147
Q

ICS AE?

A

Local - candidiasis (use spacer and rinse), dysphonia, cough.

Systemic - growth retardation (beclomethasone), skin thinning and capillary fragility. Osteoporosis if used with oral and ICS steroids

148
Q

Oral corticosteroid AE?

A

Only in burst doses (high doses in short time ie 5-14 days) = insomnia, PUD, pancreatitis

149
Q

For asthma, what should be used prophylactically vs episodic use vs exacerbation?

A

Prophylactic (daily) ICS or ICS w/ LABA.

Episodic use = ICS w/ SABA/LABA (prn).

Exacerbation = ORAL corticosteroid for 5-14 days or inj corticosteroids

150
Q

What are the leukotriene inhibitors?

A

Montelukast

151
Q

Montelukast should be used in (asthma/COPD)

A

Asthma only, leukotrienes don’t exist in COPD

152
Q

Montelukast MOA?

A

LTD4 antagonist. Not as effective as ICS, just an add-on. Good for kids

153
Q

Montelukast AE?

A

Hepatic issues and Churg-Strauss syndrome

154
Q

Pharmacophore for B2 agonists?

A

Substituted phenethylamine (NH-R group at the end with an R-N)

155
Q

B2-agonist general structure?

A

Benzene ring with 2 -OHs and 2 carbons to the right with another -OH group and NH-R

156
Q

Purpose of -OH groups in B2 agonists?

A

Direct action to B2 receptors

157
Q

Purpose of R groups in B2 agonists?

A

Gives it B selectivity. Larger = greater and longer

158
Q

What is the key structure in ACh?

A

CCOORN

159
Q

Which compound for asthma/COPD contains quaternary ammonium group?

A

Anticholinergics; cant cross BBB because of it unlike atropine

160
Q

What is the goal of Asthma Tx per GINA?

A

Achieve and maintain CONTROL and REDUCE risk

161
Q

What is the asthma management cycle parts?

A

Review/Response. Assess. Adjust

162
Q

What is the preferred reliever for asthma?

A

Regardless of what step they’re in, use ICS-formoterol

163
Q

Which Rx are used for quick-relief of bronchoconstriction, cough, chest tightness, and/or wheezing?

A

SABAs, anticholinergics, systemic corticosteroids

164
Q

What is the typical dosing regimen for SABAs?

A

Albuterol and levalbuterol = 90mcg/actuation = 1-2 inhalations q4-6hrs PRN

165
Q

Brand name of levalbuterol?

A

Xopenex

166
Q

Brand name of albuterol?

A

AccuNeb, Proventil, Ventolin, ProAir

167
Q

Pearls of SABAs?

A

AE are predictable and dose-dependent, desensitization due to frequent use

168
Q

What is the preferred “reliever medication” and what is the max dose/day?

A

Budesonide + Formoterol. 72mcg formoterol (12 inhalations) is the max

169
Q

In which case can you use SABAs by itself for asthma?

A

Never! Increases risk of severe exacerbations

170
Q

What is the onset of action and duration for albuterol/levalbuterol and formoterol (w/ ICS)?

A

Onset of action for albuterol/levalbuterol = 5 min. Duration of action for those two = <4hrs.

Onset of action of formoterol + ICS is about 5 min (peaks at 15), however the duration is 12 hrs

171
Q

Brand name of Ipratropium?

A

Atrovent

172
Q

Brand name of Ipratropium w/ albuterol?

A

Combivent, DuoNeb

173
Q

A B2 agonist has a big R group due to what other characteristics?

A

High lipophilicity + resistance to MAO/COMT metabolism

174
Q

For systemic corticosteroids, what functional group increased anti-inflammatory effects?

A

6-methyl, but decreases mineralocorticoid effects

175
Q

For the ICS, what functional groups increased anti-inflammatory effects?

A

9-Cl,F, but increases mineralocorticoid effects

16,17 ester/cyclic ester groups decrease mineralocorticoid effects, but increase binding affinity

176
Q

Which Rx are alpha-1-antitrypsin?

A

Prolastin

Aralast

Zemaira

**COPD only, targets protease

177
Q

Which Rx are methylxanthines?

A

Theophylline

Targets PDE

178
Q

Which Rx are mast cell stabilizers?

A

Cromolyn

Targets calcium channel

179
Q

Which Rx are anti-IgE?

A

Omalizumab

180
Q

Which Rx are anti-IL5?

A

Mepolizumab

181
Q

Which Rx are PDE4 inhibitors?

A

Roflumilast

182
Q

What are the other leukotriene modifiers besides Montelukast?

A

Zafirlukast

Zileuton

183
Q

What is the onset of action and duration of ipratropium?

A

Onset = 15 min

Duration 3-5 hrs

184
Q

When is ipratropium utilized in asthma?

A

Quick relief of ACUTE bronchospasm in combo w/ albuterol in ED

185
Q

What is the typical dosing of ipratopium?

A

Neb = 0.5mg q20min for 3 doses

MDI = 8 inhalations q20min PRN up to 3 hrs

186
Q

Corticosteroid onset and duration of action?

A

Onset = 1-2hrs (IV) and 2hrs (PO)

Duration = 18-36hrs

187
Q

Albuterol AE?

A

Tachycardia, tremors, hypokalemia

188
Q

Levalbuterol vs albuterol, what is the benefit of taking levalbuterol?

A

Possibly less tachycardic issues, but not by much

189
Q

Formoterol + ICS AE?

A

Tachycardia, tremors, hypokalemia, anxiety, dizziness

190
Q

Ipratropium AE?

A

Dry mouth

191
Q

Corticosteroid AE?

A

Hyperglycemia, fluid retention, wt gain, GI issues

192
Q

Response of ICS on body and time?

A

Just know that symptomatic improvements dont go into effect until 1-2weeks and baseline FEV1 and PEF improvements in 3-6wks

193
Q

At what age can you take zafirlukast, zileuton, and montelukast?

A

≥5 - zafirlukast

≥12 - zileuton

≥1 - montelukast

194
Q

AE of zafirlukast, zileuton, and montelukast?

A

Eosinophilia and vasculitis - zafirlukast + montelukast (+ neuropsychiatric events)

Hepatotoxicity (monitor ALT x3months) - zileuton

195
Q

DDI of zafirlukast, zileuton, and montelukast?

A

May increase theophylline concentration + 1A2 inhibitors - zafirlukast and zileuton

May increase gemfibrozil + 2C8, 2C9 inhibitor

196
Q

Dosing consideration for zafirlukast, zileuton, and montelukast?

A

Empty stomach, 1hr before or 2 hrs after meals - zafirlukast

1 hr after AM and PM meals - zileuton

evenings, may dissolve in certain things - montelukast

197
Q

Which LABA has the quickest onset?

A

Formoterol (5min, peak in 15min)

Others are salmeterol (30min) and vilanterol (15-30min)

198
Q

What are the durations for LABAs?

A

Salmeterol and formoterol = 12hrs

Vilanterol = 24hrs

199
Q

Which LABA is a combo product?

A

Vilanterol; comes with fluticasone

200
Q

What is the approved age for LABAs?

A

> 4 = salmeterol

> 5 = formoterol

> 18 = vilanterol

201
Q

When can you use LABAs by itself?

A

Never, should always be used w/ ICS

202
Q

What is an example of a long-acting anticholinergic?

A

Tiotropium

203
Q

What are the anti-IL5 agents for asthma?

A

MRB

Mepolizumab
Reslizumab
Benralizumab

204
Q

Which immomodulators for asthma are anti-IL4R alpha?

A

Dupilumab

205
Q

Dupilumab MOA?

A

anti-IL4R alpha

206
Q

Benralizumab MOA?

A

anti-IL5

207
Q

Reslizumab MOA?

A

anti-IL5

208
Q

Mepolizumab MOA?

A

anti-IL5

209
Q

Omalizumab MOA?

A

anti-IgE

210
Q

Which immunomodulator for asthma is IV only?

A

Reslizumab (Cinquair), the rest are SQ

211
Q

When is omalizumab approved for use?

A

≥6 yrs old w/ step 4/5 ALLERGIC asthma

positive skin test

inadequate controlled w/ ICS and LABA

IgE level before treatment and body weight required for dosing

212
Q

Omalizumab AE?

A

Anaphylaxis and delayed anaphylaxis, required that pt wait 2 hours after SQ inj

213
Q

When is Mepolizumab approved for use?

A

≥12 yrs old w/ severe eosinophilic phenotype asthma

214
Q

Mepolizumab AE?

A

Hypersensitivity/anaphylaxis

Herpes zoster infection

215
Q

When is Reslizumab approved for use?

A

≥18 yrs old as an add-on Tx with eosinophilic phenotype

216
Q

Reslizumab AE?

A

Hypersensitivity/anaphylaxis

Malignancy

217
Q

When is Benralizumab approved for use?

A

≥12 yrs old with severe eosinophilic asthma at steps 4-5

218
Q

Benralizumab AE?

A

Hypersensitivity/anaphylaxis

Headache

219
Q

When is Dupilumab approved for use?

A

≥12 yrs old w/ severe eosinophilic type 2 asthma OR requiring maintenance OCS

220
Q

Dupilumab AE

A

Hypersensitivity/anaphylaxis

Oral HSV

Conjunctivitis

Inj site rxn

221
Q

Methylxanthines have okay bronchodilation or anti-inflammatory properties?

A

Just okay bronchodilation

222
Q

Theophylline dosing and monitoring?

A

ER 300mg daily (600 max)

100mg q8h oral solution

Therapeutic range 5-15 (adults) or 5-10 (kids)

223
Q

Theophylline AE?

A

Therapeutic AE = insomnia, GI issues, hyperactivity

Toxic effects = heart issues, N/V, seizures, hypokalemia

224
Q

Theophylline or aminophylline (IV) can be used for (exercise-induced asthma/nocturnal symptoms)

A

Theophylline - nocturnal

225
Q

Cromolyn can be used for (exercise-induced asthma/nocturnal symptoms)

A

Exercise induced asthma

226
Q

Cromolyn vs theophylline, which one has less toxicity issues?

A

Cromolyn

227
Q

MDI education points?

A

If you havent used it for 3 days - 4 wks, spray 2-4 times in the air

Shake for 5 sec

Breath in for 5-7 sec as you push the canister and hold for 10 seconds or as long as you can

Wait 1 min between puffs

228
Q

Dry powder inhaler education points?

A

Never exhale into inhaler

If inhaler uses capsules, make sure its empty (may take 2 inhalations)

229
Q

Nebulizer education points?

A

Every 4-5 breaths, take a deep breath and hold for a few seconds, then exhale completely

230
Q

Initially, when is someone placed in step 1 treatment?

A

Sx less than twice a month

231
Q

Initially, when is someone placed in step 2 treatment?

A

Sx twice a month but less than daily

232
Q

Initially, when is someone placed in step 3 treatment?

A

Sx most days or waking with asthma once a week or more

233
Q

Initially, when is someone placed in step 4 treatment?

A

Sx most days or waking with asthma once a week or more AND low lung function

234
Q

After starting treatment for asthma, when should they be reevaluated?

A

q1-3 months

235
Q

Once stable on their asthma treatment, how often should they be reevaluated?

A

q3-12 months

236
Q

If pregnant, how often should they be reevaluated for asthma?

A

q4-6 weeks

237
Q

After an exacerbation, how often should they be reevaluated for asthma?

A

Within 1 week

238
Q

When should you step up therapy for asthma?

A

If Sx not controlled using those 4 questions

239
Q

When should you refer to a specialist for asthma?

A

Step 4 or 5

Not meeting goals after 3-6 months of Tx

> 2 oral corticosteroid bursts in a year

Life-threatening exacerbation

Immunotherapy consideration

240
Q

What should you do if you’re in the green, yellow, and red zone?

A

Green - continue maintenance meds

Yellow - use SABA +/- prednisone and contact physician

Red - use SABA + seek medical attention

241
Q

Asthma and ED, how is it treated?

A

Oxygen at 93-95%

SABA +/- ipratropium (3 Tx every 20-30 min)

Systemic corticosteroids can be used (IV or PO), continue for 5-7 days after d/c

If they have impending respiratory failure, use IV magnesium and high dose ICS

242
Q

What are some risk factors for death from asthma?

A

≥1 hospitalization due to asthma in the past year

> 1 canisters of SABA use/month

Not on ICS

Illicit rx use

Comorbid conditions

Previous severe exacerbation (intubation, ICU admission)

IPT: GI/Resp (4 decks)

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