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PHM 604 Final > Final > Flashcards

Final Flashcards

1
Q

Cirrhosis patho

A
  1. Cells become fibrotic adn dead -> enlarge
  2. Vessel becomes narrow
  3. Pressure increase, fluid abck up
  4. Distension, varice formation
  5. Third-spacing
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2
Q

Causes of cirrhosis

A

EtOH abuse

HCV

Fatty liver disease

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3
Q

Child Pugh Scoring

A

Grade A <7
Grade B 7-9
Grade C 10-15

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4
Q

Clinical manifestations of cirrhosis

A

Jaundice
LFTs (only acutely)
Low albumin
High PT and INR (d/t low clotting factors)
Decrase in platelets

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5
Q

Cirrhosis complications

A

Ascites
Portal HTN
Variceal bleeding
Spontaneous bacterial peritonitis
Hepatic encephalopathy
Hepatorenal syndrome

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6
Q

Ascites presentation

A

Full tense bulging abdomen

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7
Q

Ascites dx

A

Abdomen ultrasound then paracentesis

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8
Q

Ascites treatment

A

MRA (aldosteorne antag; spironolactone)

Add Loops to avoid hyperkalemia (40:100 ratio for optimal diuresis

Midodrine to raise bp if needed

LVP if above no longer works (remove 4-8L QOW; give with 8g IV albumin)

TIPS if above no longer works

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9
Q

Portal HTN dx

A

SAAG (serum albumin - paracentesis albumin) > 1.1

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10
Q

Portal HTN treatment

A

If varices present on endoscopy: non-selective beta blocker (start low and then titrate until HR ~60; HOLD if SBP <90, DBP <60 or HR <50

Agents: propranolol, nadolol carvedilol (strongest bp lowering effect)

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11
Q

Acute variceal bleeding treatment

A

Supportive care (isotonic fluids, O2 PRN, PRBC PRN for goal Hgb 8g/dL)

Octreotide
EVL - choke off bleeding

Ceftriaxone (or other 3rd gen cephalosporin) 7D F SBP PPX

Non-selective beta blocker once bleed stabilizes

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12
Q

Spontaneous bacterial perotonitis (SBP) pathogens

A

Enteric gram (-): E. coli, K. pneumoniae

Gram (+): S. pneumoniae

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13
Q

SBP dx

A

Paracentesis: calculate absolute PMN count and take culture

PMN count: WBC in ascitic fluid * %PMN
Have SBP if PMN >250

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14
Q

SBP treatment

A

3rd gen cephalosporiin (ceftriaxone, cefotaxime) 5D
can do cipro if anaylactic reaction to beta-lactams

Take a repeat paracentesis 48H after ABX start, PMN didn’t drop 25% -> escalate to carbapenems

IV albumin 1.5g once then 1g/kg on day 3

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15
Q

Which pts should receive SBP PPX indefinetly and what agents are used

A

PMHx of SBP
Low ascitic protein + other risk factors

Cipro or bactrim DS

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16
Q

Hepatic encephalopathy presentation

A

Altered mental status (d/t high ammonia levels, levels do NOT correspond with severity)
Slow to respond
Eventual coma

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17
Q

Hepatic encephalopathy treatment

A

Remove precipitating factors

Dairy and vegetable protein (even though they make ammonia, these specific proteins are less likely to cross BBB than animal)

Lactulose - traps ammonia in bowel to be eliminated in stool

Rifaximin - decreases the amount of ammonia-producing bacteria in colon

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18
Q

Hepatorenal syndrome dx

A

No improvement in SCr 2D after diuretic cessation and 2D of IV alumn

Cirrhosis with ascites with a SCr increase >0.3 from baseline or 50% increase from baseline in last 7D

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19
Q

Hepatorenal syndrome treatment

A

IV NE
IV albumin 1g/kg/day

Success if in 2 weeks SCr decreases to 1.5 or returns to <0.3 above baseline

D/C therapy if in 4 days SCr remains the same or rises above treatment values

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20
Q

Cirrhosis PKPD changes

A

Decreased blood flow -> higher systemic [ ] of high first pass drugs -> decrease dose

Loss of hepatocyte function -> affects phase I metabolism (CYP) -> try to use drugs with phase II metabolism

Decreased albumin production -> more unbound drug -> more therapeutic effect -> dose decrease

Increased SCr -> decreased renal function

Increased BBB permeability -> increased therapeutic response -> decrease dose

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21
Q

Fat soluble vitmains

A

A, D, E, K

Well retained in body and stored in fatty tissue (adipose, muscles, liver)

Takes a while to reach deficiency state but more likely to cause toxicity

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22
Q

Water soluble vitamins

A

B, C

Not retained well in body (except B12, stored in liver)

Readily excreted

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23
Q

Vitamin A function

A

Vision
Immunity
Cell differentiation

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24
Q

Vitamin A sources

A

Carrots
Leafy greens
Oranges
Dairy; animal products

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25
Q

Vitamin A signs of deficiency

A

Dermatitis
Night blindness
Bitot’s spots
Poor wound healing

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26
Q

Vitamin A signs of toxicity

A

Headache
N/V
Rash
Skin peeling

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27
Q

Vitamin D function

A

Ca and phosphate homeostasis
Bone metabolism

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28
Q

Vitamin D sources

A

Fish
Dairy products
Cereal
Sunlight

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29
Q

Vitamin D signs of deficiency

A

Osteomalacia, osteoporosis
Rickets
Muscle weakness
Poor growth

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30
Q

Vitamin D signs of toxicity

A

Hypercalcemia
Hypercalciuria
Soft tissue calcification -> kidney and CV damage

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31
Q

Vitamin E function

A

Antioxidant (protect from free radicals)
Prevent clotting
Enhance immune system

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32
Q

Vitamin E sources

A

Nuts/seeds
Fruits
Veggies

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33
Q

Vitamin E signs of deficiency

A

Hemolysis
Peripheral neuropathy
Skeletal muscle atrophy

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34
Q

Vitamin E signs of toxicity

A

Bleeding

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35
Q

Vitamin K function

A

Regulate clotting factors II, VII, IX, X

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36
Q

Vitamin K sources

A

Leafy greens
Meat

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37
Q

Vitmain K signs of deficiency

A

Bleeding
Elevated PTT

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38
Q

Vitamin B1 function

A

(Thiamine)
ATP generation
Peripheral nerve conduction

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39
Q

Vitamin B1 signs of deficiency

A

Anorexia
Fatigue
Depression
Impaired memory
Paresthesia
Wernicke’s encephalopathy

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40
Q

Vitamin B6 function

A

(Pyridoxine)
AMino acid metabolism
Neurotransmitter synthesis
Metabolism of lipids/steroids

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41
Q

Vitamin B6 signs of deficiency

A

Pellagra
Limb numbness/paresthesia
Convulsions
Microcytic anemia

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42
Q

Vitamin B 9 function

A

(Folic acid)
Neural tube formation
RBC production
Cell growth/function

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43
Q

Vitamin B9 signs of deficiency

A

Macrocytic anemia
Neural tube defects

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44
Q

Vitamin B12 function

A

(Cobalamin)
Syntehsis of DNA/RNA cell division

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45
Q

Vitamin B12 signs of deficiency

A

Spinal cord degeneration
Peripheral neuropathy
Paresthesia
Macrocytic anemia

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46
Q

Vitamin C function

A

Antioxidant acitivity
Immune function
Fe absorption
Connective tissue metabolism
Wound healing

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47
Q

Vitamin C sources

A

Citrus fruits
Leafy veggies

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48
Q

Vitamin C signs of deficiency

A

Scurvy
Petechiae
Bleeding gums
Poor wound healing

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49
Q

Vitamin C signs of toxicity

A

Abdominal pain
Diarrhea
N/V

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50
Q

Major minerals

A

Ca, Mg, Phos, K, Na
Need >100mg/day

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51
Q

Minor minerals

A

Need <100mg/day

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52
Q

Hypocalcemia

A

< 8.5 mg/dL

Tachycardia, seizures

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53
Q

Hypercalcemia

A

> 10.5 mg/dL

Confusion, kidney stones

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54
Q

Ca corrected equation

A

Ca corrected = Ca serum + [0.8 (4 - albumin)]

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55
Q

Hypomagnesmia

A

<1.4 mEq/L

Tremors, hypokalemia, nystagmus, seizures, ventricular arrhytmias, torsades

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56
Q

Hypermagnesemia

A

> 2mEq/L

Confusion, bradycardia, muscle weakness, heart block, delirium

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57
Q

Hypophosphatemia

A

<3.5 mEq/L

Muscle cramps, abdominal distension, dysrrhythmias

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58
Q

Hyperphosphatemia

A

> 5 mEq/L

Heart palpitaions, vfib

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59
Q

Vitamin and mineral goal in pts with eating disorders

A

Nutritional rehab
Restore weight gradually
Prevent refeeding syndrome

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60
Q

Vitamin and mineral goal in pts with EtOH abuse

A

Supportive therapy; replace fluids
Electrolytes
Ca
Phos
Mg
Fat soluble vitamins
Thiamine
Folic acid

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61
Q

Vitamin and mineral goal in pts who are pregnant

A

Prenatal vitamins
- folic acid
- Fe
- Ca
- VitD
- Iodine

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62
Q

Vitamin and mineral goal in pediatric pts

A

Supplement breastmilk with VitD and iron (formula already supplemented)

No whole milk until 1yr

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63
Q

Vitamin and mineral goal in geriatric pts

A

Focus on K, Ca, VitD, dietary fiber, B12

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64
Q

Vitamin and mineral goal in pts with macular degeneration

A

Give VitA, C, E

ARED (beta-carotene) or AREDS@ (lutein and zeaxanthin)

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65
Q

Interactions with vitamins and minerals

A

ABX
H2RA
Isoniazid
Methotrexate
PPI
Diuretics

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66
Q

When to consider (enteral) nutritional support

A

Inpt after 7 days of no eating (though ICU may need to start sooner)

Outpt pt with malnutrition or at risk for it

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67
Q

Why do we try to use enteral nutrition whenever we can?

A

Gut is biggest immune system organ

Using gut maintains gut integrity

Maintains bile flow (prevent bacteria from moving up and prevent stones)

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68
Q

Which medications require that feeds be held for 1-2 hrs before and after

A

Phenytoin
Quinnolones
Levothyroxine
Warfarin

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69
Q

Enteric nutrition: calorie requirement

A

20-30 kcal/kg/day

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70
Q

Special nutrition requirement for renal pts

A

Less volume
Less K and phosphate

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71
Q

Special nutrition requirement for pts with HF

A

Less volume

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72
Q

Special nutrition requirement for diabetic pts

A

More cal from fat and less from carbs
Fiber to slow absorption of carbs

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73
Q

Special nutrition requirement for burn/trauma pts

A

High protein
High cal

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74
Q

Special nutrition requirement for pts with pancreatitis

A

Low fat

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75
Q

Special nutrition requirement for pts with COPD/pulmonary disease

A

Lower carbs
Higher fat

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76
Q

How to determine amount of free water an enteral nutrition pt needs

A

1ml/kcal/day or 30-40 ml/kg/day

Check enteral formula and determine how much free water is coming from that, then subtract from total daily requirement. Split this remainder over 4-6 admins a day as free water

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77
Q

Which methods of enteral nutrition can use the crush and flush method for meds?

A

Gastric (NG and G tubes; mimic actual meals)
Duodenum

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78
Q

Which method of enteral nutrition canNOT use the crush and flush method and what do you do instead?

A

Jejunum (NJ and tubes) - meds have to be given as liquid

Crush med between 2 spoons and mix into 10mL of sterile water

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79
Q

Above which osmolality can liquid preps for enteral nutrition cause diarrhea?

A

> 600 Osm

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80
Q

What needs to be monitored in pts on enteral nutrition

A

Diarrhea (>3 liquid stool/day)

Bloating, abdominal distention (treat with pro-kinetic, switch to continuous infusion)

Electrolytes (Na, K, phos, Mg)

Exit site infection, leaking, bleeding if GI wall

Sinusitis if nasal tube

Asipiration (keep head of bed elevated at 30-45 degrees)

Maintain tube patency (flushing)`

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81
Q

At what point is peripheral admin of TPN no longer appropriate and TPN needs to be adminned centrally

A

mOsm/L >900 or dextrose > 10-12.5%

82
Q

What are the macro nutrients and micro nutrients in TPN

A

Macro: protein (amino acids), carbs (dextrose), fats (lipids)

Micro: electrolytes, vitamins, trace elements

83
Q

When to use TPN in adults

A

ONLY IF PT UNABLE OR UNLIKELY TO RECEIVE ADEQUATE NUTRITION FROM ENTERAL ROUTE

After 7 days in nutritionally stable pts

Within 3-5 days in nutritional at-risk pts (increased metabolic requirements, BMI <18.5, involuntary weight loss)

ASAP in pts with moderate-severe malnutrition

84
Q

When to use TPN in peds

A

If unable to tolerate enteral nutrition for extended period of time
- 1-3 days for infants (1mo-1yr)
- 4-5 days for children (1-10 yrs)

Very low birth weight (<1.5 kg): ASAP
Pre term and critically ill neonate: ASAP

85
Q

3 in 1 TPN

A

TNA

Contains all 3 maco nutrients in 1 bag, potential destabiliziation when lipids added (creaming safe to use after massaging, cracking, not safe)

Minimum of 4% amino acid, 10% dextrose, 2% lipids

86
Q

2 in 1 TPN

A

Contains only dextrose and amino acids

Primary method for peds

87
Q

Neonates have a (higher/lower) mL and kcal to kg ratio than adults

A

higher

88
Q

kcal and mOsm of amino acids

A

4 kcal/gm

10 (mOsm * L)/g

89
Q

Nitrogen balance

A

Energy in should be greater than energy out

Nitrogen in = g protein / 6.25
Nitrogen out = urine urea nitrogen + 4

90
Q

kcal and mOsm of dextrose

A

3.4 kcal/gm

5 (mOsm * L)/g

91
Q

kcal of lipid

A

~9 kcal/gm

92
Q

Lipid infusion requirements

A

1.2 micron filter (anything smaller will filter out the fat)

0.15 g/kg/hr max infusion rate in peds
0.11 g/kg/hr max infusion rate in adults

Hang time only 12 hrs

93
Q

How to reduce Ca-phos precipitation risk

A

Put phos in first and Ca in last
Lower pH
Low temp
Quick hang time
Use Ca gluconate

94
Q

How to handle metabolic acidosis and alkalosis in TPN pts

A

Acid: increase acetate, decrease Cl
Base: decrease acetate, increase Cl

95
Q

How to evaluate appropriateness of TPN

A
  1. Evaluate fluid goal and energy requirement
  2. Calcualte kcal/day, g/day and mL for each macronutrient
  3. Determine final [ ] of dextrose, protein, lipids
  4. Calculate electrolyte dose
  5. Select appropriate anion balance
  6. Performs safety checks
    1. Lipid infusion rate
    2. Glucose infusion rate
    3. Estimate Osm for proteins and dextrose
    4. Check line/access
    5. If 3-in-1 ensure stablity
96
Q

Types of general N/V and treatment options

A

Gastroenteritis; pancreatitis

Treatment
- 5-HT3 antags (ondestron)
- Metoclopramide
- Phenothiazines

97
Q

Opioid induced constipation treatment options

A

Lubiprostone (Amitiza)

Mu peripheral antags
- Methylnaltrexone
- Naloxegol
- Naldemidine

98
Q

Corticosteroid AE

A
  • Hyperglycemia (increase in blood glucose)
  • Increased bp
  • Insomnia
  • Agitation/manic-type feelings
  • Do NOT give with NSAIDs → increased risk of GI ulceration
99
Q

Preggers N/V treatment options

A

Doxylamine + VitB6 combo

Second line:
- 5-HT3 antags
- metoclopramide

100
Q

Types of disorders of balance N/V and treatment options

A

Motion sickenss, vertigo, dizziness

Treatment: antihistamines

101
Q

JAKi BBW

A
  • Infection
  • MACE (cardiac)
  • Thrombosis
  • Cancer
  • Death

because so many BBW, ony used int pts who have failed therapy with 1 or more anti-TNF alpha

102
Q

Anti-TNF alpha BBW

A
  • Infection - prior to starting, need:
    - PPD
    - Chest x-ray
    - Ciral hepatitis screening
    - HIV screening
    • If pt gets active infection, stop biologic (even though the maintenance dose is typically QOW)
  • Malignancy - particularly lymphoma particularly when taken with azathioprine
103
Q

When should you prophylactically use PPIs against NSAID PUD

A

If pt is starting ASA + P2Y12 and has 2 of the following
- Older age (65+)
- Hx of PUD
- Conmitttant drug use (anticoag, antiplatelets, steroids)
- Non-COX selective NSAIDs
- High dose
- Multiple NSAIDs (e.g. asa + ibuprofen)

104
Q

Alarm symptoms in pts complaining of GERD

A
  • Substernal pain → can be cardiac instead
  • Blood → could be GI bleed
  • Unexplained weight loss → could be cancer
  • Dysphagia (difficulty swallowing)
  • Anorexia
105
Q

mu peripheral antags agents

A
  • Methylnaltrexone: SQ
  • Naloxegol: PO
  • Naldemidine: PO
106
Q

Diarrhea treatment options

A

Peripheral mu agonist
- loperamide (imodium)
- Diphenoxylate (lomotil): treats IBS-UC

Octreotide

107
Q

5-Amiosalicylates (5-ASA) MOA and agents

A

works on COX enzymes (ASA is in the name) in gut → knockout prostaglandins/inflammation and pain

Agents
- Mesalamine
- Sulfasalazine
- Olsalazine
- Balsalazide

108
Q

PPI AE

A

AE a have to do with decreased acid
- Bone fracture
- C. diff/gastroenteritis
- B12 deficiency
- CKD (thought to be d/t acute interstitial nephritis)
- Dementia

109
Q

GERD therapy treatment options

A

PPI QD 8 weeks ACB
- If recurring, lowest dose possible to relieve s/x’s
- Can also add a PRN H2RA

  • If s/s not improved with daily therapy → consider BID (can consider GHT BID first before G1T BID)
    • Can also add H2RA QHS
110
Q

Which pts might be a candidate for longterm GERD therapy

A

Barrett’s esophageal

Pts with copmlications from GERD (severe erosive esophgitis; strictures)

111
Q

Guanylate cyclase receptor agonists AE

A

Diarrhea (around 20% of pts)

112
Q

Chronic idiopathic constipation treatment options

A

Lubiprostone (Amitiza)

Guanylate cyclase receptor agonists (secretagogues)
- Linachlotide (Linzess)
- Plecanamide

113
Q

Osmotics MOA, agents, and usage

A

Constipatoin

pulls water into colon → expand and soften stool → trigger contraction and make it easier to puh

PEG3500 (Miralax)
Lactulose

114
Q

How to approach a pt when considering initation of a QTc prolongation agent

A

Avoid agents with QTc side effect if >450 msec

Decrease dose or d/c if there is a 60 msec increase from baseline
- If QTc becomes >500 msec, d/c

Keep K>4 and Mg >2 ← stabilize cardiac membrane

115
Q

Corticosteroid agents for N/V

A

Dexamethasone

116
Q

Corticosteroid MOA against N/V

A

decrease prostaglandin formation

release 5-HT3 in the gut

117
Q

Erythromycin MOA

A

agonist of motlin receptors → increase peristalsis in stomach and duodenum

118
Q

Octreotide MOA

A

Somatistatin analog→
- inhibit serotonin
- inhibit secretion of
- gastrin
- secretin
- motilin
- insulin
- glucagon

→ reduces intestinal motility and secretion

119
Q

Erythromycin AE

A
  • N/V
  • Diarrhea
  • QTc prolongation
120
Q

metoclopromide (Reglan) AE

A
  • diarrhea
  • EPS: higher risk with IV admin
  • Dystonia: higher risk with IV admin
  • QTc prolongation
121
Q

metoclopromide (Reglan) MOA

A
  • block dopamine and serotonin
  • enhance acetocholine response

→ increase gastric emptying and increase lower esophageal tone

122
Q

5-HT3 AE

A
  • Constipation
  • Headache
  • QTc prolongation: more of a concern at higher doses (like 16mg BID) and with IV admin
123
Q

5-HT3 agents

A

Ondasetron

124
Q

Phenothiazines AE

A
  • Tissue damage
  • Hypotension: avoid by if giving as IV, give as slow push (30 min infusion); pt should lay down during inufion and 30 min after
  • QTc prolongation
  • Dystonia: pt frozen/locked
  • Extrapyramidal symptoms (EPS): purposeless movements that a pt can’t control
125
Q

Phenothiazine MOA and agents

A

inhibit dopamine, H1, and muscarinic receptors

  • Promethazine
  • Prochlorperazine - also rectal (Compazine)
  • Chlorpromazine
126
Q

Antihistamine AE

A
  • Drowsiness; impaired congition/confusion in older pts → increased fall risk
  • Dry mouth
  • Constipation
127
Q

Antihistamine agents

A

Meclinzine: safest in older pts due to lower CNS penetration

Dimenhydrinate

Doxylamine (VitB6 combo)

Scopolamine

Hydroxyzine

128
Q

PONV treatment

A

Apfels score of 4:
1. Scopolamine 2 hrs porior to anesthsia
2. IV dexamethsone after anesthesia induction
3. 5-HT3 antag at end of surgery (also do for Apfels score 2-3)

129
Q

Apfels score

A

identifies pt at high risk for PONV; get +1 for each of the following factors:

  • female
  • non-smoker
  • hx of motion sickness or PONV
  • planned use of post op opioids
130
Q

Lubiprostone (amitiza) MOA

A

works directly on Cl channels → increase Cl (and water) secretion into stool

131
Q

Lubiprostone (amitiza) AE

A

Diarrhea (like 20% of pts) ← reduce by taking with food

Nausea ← reduce by taking with food

132
Q

IBS-D treatment options

A

Rifaximin (Xifaxin):, used if small intestine bacteria overgrowth (SIBO)

eluxadoline/Vibrezi

alosetron: in women with severe IBS-D

Tricyclic antidepressant (specifically amitriptyline)

Soluble fibers

133
Q

List the soluble fibers

A
  • Pysllium (metamucil)
  • Oatbraun
  • Barley
  • Beans
134
Q

IBS-C treatment options

A

linachlotide/Linzess:

Lubiprostone (amitiza): only for women

tegaserod/Zelnorm: only for women < 65 w/o a pmh of CV events
- D/C med if no effect in 4 weeks

tenapanor/Ibsrela

Tricyclic antidepressants (specifically nortriptyline)

Soluble fibers

135
Q

AE for biologics in general and how to treat

A

IV formulations: infusion related reacton
- acute onset: apap and diphenhydramine
- chronic onset: apap and short course steorids

SQ formualtions: inj site reactions

136
Q

Selective adhesion molecule (integrin) inhibitors BBW

A

For natalizumab (Tysabri) NOT vedolizumab (Entyvio)

PML (progressive multi-focal leukoenphalopathy - CNS infection; can lead to death → has a REMS program)

137
Q

Available corticosteroid agents for IBD

A

Prednisone: PO

Methylprednisolone: IV

Hydrocortisone: IV

Budesonide: PO
- Entocort for Crohn’s: site of action is in terminal ileum
- Uceris for UC: colon

138
Q

Azathioprine monitoring parameters and BBW

A

Monitoring
- CBC: d/t ability to cause bone marrow suppression
- LFTs and pancreatic enzymes: d/t hepatoxicity and potential for pancreatitis

BBW
- lymphoma: particularly when used in combo with biologics

139
Q

Available immunomodulator agents for IBD

A

Azathioprine
6-mercaptopurine
methotrexate
cyclosporine

140
Q

Why is azathioprine frequently used with biologics or steroids for ABD

A
  • Due to azathioprine’s long onset (3 mo.)
  • Can help taper a pt off of steroids
  • Can improve efficacy of biologics and decrease ADA formation
141
Q

Treatment options for mild UC

A

Mesalamine
If that fails, budesonide

(use both mesalamine and budesonide of extensive)

142
Q

Treatment options for moderate-severe UC

A

Budesonide -or- systemic steroids -or- biologic

+/- azathioprine

143
Q

Treatment options for fulminant UC

A

IV steroid -or- IV infliximab -or- IV cyclosproine -or- colonectomy

Blood transfusion if Hgb <8

144
Q

What is the maintenance agent for someone who with mild UC

A

mesalamine

145
Q

What is the maintenance agent for someone who achieved IBD remission with a steroid?

A

Azathioprine

146
Q

What is the maintenance agent for soemone who achieved IBD remission with a biologic

A

That same biologic +/- azathioprine

147
Q

What is the maintenance agent for someone who achieved UC remission with cyclosporine

A

Azathioprine -or- vedolizumab (entyvio)

148
Q

Treatment options for perianal involement in Crohn’s

A

ABX (flagyl, cipro)
Surgery
Inflxiimab

149
Q

Treatent options for mild-moderate Crohn’s

A

Budesonide

150
Q

Treatment options for moderate-severe Crohn’s

A

PO systemic steroids -or- biologic

+/- azathioprine

151
Q

Treatment options for fevere-fulminant Crohn’s

A

Surgery -or- IV steroid -or- infliximab

152
Q

Upper GI bleed treatment

A
  • inj epinephrine
  • targeted contact therapy (cauterize or free it off)
  • PPI 80mg IV bolus 3D then 40mg IV BID then PO PPI BID 2W
  • Isotonic fluids
  • O2
  • Reverse anticoag
  • PRBC if Hgb <7
153
Q

S/S of an upper GI bleed

A

Black stool, blood vomit

Low bp; light headedness
Low hr, low H&H; chest pain

154
Q

H. pylori treatment

A

Quad: PPI, bismuth subsalicylate, tetracycline, flagyl

Triple: PPI, clarithromycin, amoxicillin (flagyl if allergy)
- confirm eradication

155
Q

S/S of PUD

A
  • Dyspepsia (indigestion)
  • Epigastric pain
  • Gnawing/burning pain
  • Early satiety
  • Pain that wakes them from sleep
  • GI bleed (main complication from PUD)
156
Q

eluxadoline (Vibrezi) MOA

A

mu agonist/delta/kappa agonist: inhibit bowel construction

157
Q

eluxadoline (Vibrezi) AE

A
  • Sphincter of Oddi dysfuntion/spasm → CI pts with pmh of pancreatitis, alcoholism (3+ drinks a day)
158
Q

tenapanor (Ibsrela) AE

A

diarrhea

159
Q

tegaserod (Zelnorm) MOA

A

5-HT4 agonist

increase GI secretion and motility; decrease visceral pain

160
Q

tegaserod (Zelnorm) AE

A
  • Increased risk of CV events
  • Headache
  • Diarrhea
161
Q

mu peripheral agonist agents

A
  • Loperamide (Imodium): PO
  • Diphenoxylate (Lomotil): PO
162
Q

mu peripheral antags AE

A
  • Caution in IBD, diverticulitis, GI malignancies
  • Severe abdominal pain → d/c agent
  • Diarrhea → d/c agent
163
Q

Guanylate cyclase receptor agonists MOA and agents

A

Secretagogues: pull Cl and bicarb into stool; can derease abdominal pain in IBS-C

  • Linachlotide (Linzess)
  • Plecanamide (Trulance)
164
Q

NSAID induced PUD treatment

A
  • D/c NSAID + PPI QD 4-8 weeks
    • If can’t d/c NSAID → long term therapy
  • Switch to APAP when possible or use COX2 selective NSAIDs
  • Add misoprostol
165
Q

What differentiates a mild from a severe drug-induced dermatology disorders?

A

FEver

166
Q

Penicillin allergy cross reactivity

A

cross reactivity between penicillins and cephalosporins is 1-2%, dependent on R1 sidechain

167
Q

Sulfa ABX allergy cross reactivity

A

a sulfa ABX allergy has almost no cross reactivity with non-ABX sulfa drugs (unless it was a life threatening allergy, then better safe than sorry)

168
Q

Nasolacrimal occlusion

A

method to reduce systemic AE by pressing on lacrimal tear duct a min after applying

169
Q

FTU method

A

1 FTU = 0.5g

170
Q

Oral isotretinoin dosing

A

0.5-1 mg/kg/day

OR

15-20 weeks of cumulative total dose of 120-150 mg/kg

171
Q

How often do you need to take pregancy tests while on isotretinoin

A

2 (negative) before starting

monthly after starting

172
Q

Fixed drug eruption treatment

A

Resolves within a few days upon discontinuation (though the hyperpigmentation may last for months)

173
Q

Simple maculopapular eruption treatment

A

Resolves 7-14 days after stopping drug

174
Q

Simple maculopapular eruption presentation

A

Rash

175
Q

What is the pH of healthy skin

A

4.7-5.7

176
Q

What is considered an elevated IOP?

A

> 21 mmHg

177
Q

DEET

A
  • Topical bug repellant
  • don’t use more often than q4h
  • children should use [ ] < 30%
  • 20% or higher to repel ticks
  • need to be older than 2 months old
178
Q

Urticaria/angioedema treatment

A

Self-moitoring, symptoms will resolve in 1-2 weeks

179
Q

Primary angle CLOSURE glaucoma treatment

A

Surgery

Meds
- IV or PO carbonic anyhdrase inhibtior (acetazolamide) + topical beta blocker + topical alapha agonist + pilocarpine

Check OIP Q15-30 min, if not working switch pilocarpine to a hyperosmotic; redose at 1hr mark

180
Q

Rho kinase inhibitor examples and AE

A

Netarsudil

  • Hyerpemia (high rate): eye turns red due to inflammaton of blood vessels
  • Conjunctival hemorhage
181
Q

Caronic anhydrase inhibitor examples

A
  • Acetazolamide PO

Combos:
- dorzalamide/timolol
- brinzolamide/brimonidine

182
Q

Alpha agonist (eyedrops) examples and AE

A

Brimonidine

AE
- Conjunctival hyperemia
- Irritation
- Allergic reaction
- Drowsiness
- Xerostomia (dry mouth)
- Tachyphylaxis

183
Q

Beta blocker (eyedrops) examples and AE

A

timolol and other “-olols”

AE
- local ocular irritation
- Cardiac effects (conduction, contracitliy, pressure)
- Pulmonary
- CNS
- Tachyphylaxis

184
Q

Prostaglandin F2alpha analog AE

A

bimatoprost
travoprost
latonoprost

AE
- local ocular irritation
- conjunctival hyperemia (red eye)
- hypertrichosis (eyelashes)
- periocular/iris pigmentation changes (turn darker)
- infection
- headache

185
Q

Primary OPEN angle glaucoma treatment goals

A

Preserve the nerve/stabilize visual fields; prevent progression

Lower IOP (aim for >25% below pretreatment IOP); readjust/reassess based on clincal progression
- If not at goal and poor efficacy despite adherence: switch
- If not at goal, but still close to goal: add on something else

186
Q

Priary OPEN angle glaucoma risk factor

A
  • Elevated IOP
  • Age (>60, >40 for black)
  • Family hx
  • Race
  • Central corneal thickness (thinner = higher risk)
  • Ocular perfusion pressure
  • T2DM
  • Myopia (near sighted); acuity: anything greater than 20/20 (e.g. 20/50) is nearsightedness
187
Q

Moderate-severe plaque psoriasis treatment optios

A

Methotrexate
Cyclosporine
Phosphidesterase inhibitor
Biologics (Il inhibitors and TNF alpha)

188
Q

Atopic dermatitis (eczema) treatment options

A

TCS
Topical CI (tacrolimus)
JAKi
Cyclosporine
Methotrexate
Azathioprien

189
Q

SJS/TEN treatment

A

Supportive care: pain, fluids, nutrition

  • Systemic corticosteroid: possible harm
  • IVIG: possible benefit
  • cyclossporine: posssible benefit
190
Q

DRESS treatment

A

FLuids, electrolytes, nutrition management

No organ involvment: topical steroid
Organ involvement: 0.5-3mg/kg/day prednisone then taper off

191
Q

Causes of simple maculopapular eruption

A

Penicillins/cephalosporins

Sulfonamides

Anticonvulsants

192
Q

Causes of DRESS

A

Allopurinol

Sulfonamides

Anticonvulsants

Dapsone

193
Q

Causes of urticaria/angioedema

A

Penicillins and related ABX

Sulfonamides

ASA

Opiates

Latex

194
Q

Ccauses of serum-sisckness-like

A

Penicillins/cephalosporins

Sulfonamides

195
Q

Causes of fixed drug eruption

A

Offending drugs aren’t the usual culprits

196
Q

Causes of SJS/TEN

A

Drugs
- Sulfonamides
- Penicillins
- Anticonvulsants
- NSAIDs: particularly “-oxicams”
- Allopurinol

Other
- HIV infection
- Lupus (SLE)
- Malignancy
- UV light or radiation therapy
- Genes: HLA-B*15:02

197
Q

Fixed drug eruption presentation

A

Simple eruptions with pruitic, erythematous, raised lesions that can blister

same exact rash in same exact spot if drug is given again

198
Q

Serum-sickness-like presentation

A

Urticaria

Fever

Arthralgias

199
Q

Urticaria/angioedema presentation

A

Hives

Pruitic (itcchy)

Red raised wheals that blanch

May have angioedema and swelling of mucous membranes

Type I sensitivity reaction, can lead to anaphylaxis reaction

200
Q

Drugs that can cause photosensitivity

A
  • Sulfonamides
  • Tetracyclines
  • Amiodarone
  • Coal tar
201
Q

Drugs taht can cause hyperpigmentation

A

Increased melanin:
- Phenytoin

Direct deposition
- Tetracyclines
- Silver, mercury
- Antimalarials
- Amiodaronne

Dermal lipofuscinosis
- Amiodarone

PHM 604 Final (1 decks)

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