Final Flashcards
Cirrhosis patho
- Cells become fibrotic adn dead -> enlarge
- Vessel becomes narrow
- Pressure increase, fluid abck up
- Distension, varice formation
- Third-spacing
Causes of cirrhosis
EtOH abuse
HCV
Fatty liver disease
Child Pugh Scoring
Grade A <7
Grade B 7-9
Grade C 10-15
Clinical manifestations of cirrhosis
Jaundice
LFTs (only acutely)
Low albumin
High PT and INR (d/t low clotting factors)
Decrase in platelets
Cirrhosis complications
Ascites
Portal HTN
Variceal bleeding
Spontaneous bacterial peritonitis
Hepatic encephalopathy
Hepatorenal syndrome
Ascites presentation
Full tense bulging abdomen
Ascites dx
Abdomen ultrasound then paracentesis
Ascites treatment
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
Portal HTN dx
SAAG (serum albumin - paracentesis albumin) > 1.1
Portal HTN treatment
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)
Acute variceal bleeding treatment
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
Spontaneous bacterial perotonitis (SBP) pathogens
Enteric gram (-): E. coli, K. pneumoniae
Gram (+): S. pneumoniae
SBP dx
Paracentesis: calculate absolute PMN count and take culture
PMN count: WBC in ascitic fluid * %PMN
Have SBP if PMN >250
SBP treatment
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
Which pts should receive SBP PPX indefinetly and what agents are used
PMHx of SBP
Low ascitic protein + other risk factors
Cipro or bactrim DS
Hepatic encephalopathy presentation
Altered mental status (d/t high ammonia levels, levels do NOT correspond with severity)
Slow to respond
Eventual coma
Hepatic encephalopathy treatment
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
Hepatorenal syndrome dx
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
Hepatorenal syndrome treatment
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
Cirrhosis PKPD changes
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
Fat soluble vitmains
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
Water soluble vitamins
B, C
Not retained well in body (except B12, stored in liver)
Readily excreted
Vitamin A function
Vision
Immunity
Cell differentiation
Vitamin A sources
Carrots
Leafy greens
Oranges
Dairy; animal products
Vitamin A signs of deficiency
Dermatitis
Night blindness
Bitot’s spots
Poor wound healing
Vitamin A signs of toxicity
Headache
N/V
Rash
Skin peeling
Vitamin D function
Ca and phosphate homeostasis
Bone metabolism
Vitamin D sources
Fish
Dairy products
Cereal
Sunlight
Vitamin D signs of deficiency
Osteomalacia, osteoporosis
Rickets
Muscle weakness
Poor growth
Vitamin D signs of toxicity
Hypercalcemia
Hypercalciuria
Soft tissue calcification -> kidney and CV damage
Vitamin E function
Antioxidant (protect from free radicals)
Prevent clotting
Enhance immune system
Vitamin E sources
Nuts/seeds
Fruits
Veggies
Vitamin E signs of deficiency
Hemolysis
Peripheral neuropathy
Skeletal muscle atrophy
Vitamin E signs of toxicity
Bleeding
Vitamin K function
Regulate clotting factors II, VII, IX, X
Vitamin K sources
Leafy greens
Meat
Vitmain K signs of deficiency
Bleeding
Elevated PTT
Vitamin B1 function
(Thiamine)
ATP generation
Peripheral nerve conduction
Vitamin B1 signs of deficiency
Anorexia
Fatigue
Depression
Impaired memory
Paresthesia
Wernicke’s encephalopathy
Vitamin B6 function
(Pyridoxine)
AMino acid metabolism
Neurotransmitter synthesis
Metabolism of lipids/steroids
Vitamin B6 signs of deficiency
Pellagra
Limb numbness/paresthesia
Convulsions
Microcytic anemia
Vitamin B 9 function
(Folic acid)
Neural tube formation
RBC production
Cell growth/function
Vitamin B9 signs of deficiency
Macrocytic anemia
Neural tube defects
Vitamin B12 function
(Cobalamin)
Syntehsis of DNA/RNA cell division
Vitamin B12 signs of deficiency
Spinal cord degeneration
Peripheral neuropathy
Paresthesia
Macrocytic anemia
Vitamin C function
Antioxidant acitivity
Immune function
Fe absorption
Connective tissue metabolism
Wound healing
Vitamin C sources
Citrus fruits
Leafy veggies
Vitamin C signs of deficiency
Scurvy
Petechiae
Bleeding gums
Poor wound healing
Vitamin C signs of toxicity
Abdominal pain
Diarrhea
N/V
Major minerals
Ca, Mg, Phos, K, Na
Need >100mg/day
Minor minerals
Need <100mg/day
Hypocalcemia
< 8.5 mg/dL
Tachycardia, seizures
Hypercalcemia
> 10.5 mg/dL
Confusion, kidney stones
Ca corrected equation
Ca corrected = Ca serum + [0.8 (4 - albumin)]
Hypomagnesmia
<1.4 mEq/L
Tremors, hypokalemia, nystagmus, seizures, ventricular arrhytmias, torsades
Hypermagnesemia
> 2mEq/L
Confusion, bradycardia, muscle weakness, heart block, delirium
Hypophosphatemia
<3.5 mEq/L
Muscle cramps, abdominal distension, dysrrhythmias
Hyperphosphatemia
> 5 mEq/L
Heart palpitaions, vfib
Vitamin and mineral goal in pts with eating disorders
Nutritional rehab
Restore weight gradually
Prevent refeeding syndrome
Vitamin and mineral goal in pts with EtOH abuse
Supportive therapy; replace fluids
Electrolytes
Ca
Phos
Mg
Fat soluble vitamins
Thiamine
Folic acid
Vitamin and mineral goal in pts who are pregnant
Prenatal vitamins
- folic acid
- Fe
- Ca
- VitD
- Iodine
Vitamin and mineral goal in pediatric pts
Supplement breastmilk with VitD and iron (formula already supplemented)
No whole milk until 1yr
Vitamin and mineral goal in geriatric pts
Focus on K, Ca, VitD, dietary fiber, B12
Vitamin and mineral goal in pts with macular degeneration
Give VitA, C, E
ARED (beta-carotene) or AREDS@ (lutein and zeaxanthin)
Interactions with vitamins and minerals
ABX
H2RA
Isoniazid
Methotrexate
PPI
Diuretics
When to consider (enteral) nutritional support
Inpt after 7 days of no eating (though ICU may need to start sooner)
Outpt pt with malnutrition or at risk for it
Why do we try to use enteral nutrition whenever we can?
Gut is biggest immune system organ
Using gut maintains gut integrity
Maintains bile flow (prevent bacteria from moving up and prevent stones)
Which medications require that feeds be held for 1-2 hrs before and after
Phenytoin
Quinnolones
Levothyroxine
Warfarin
Enteric nutrition: calorie requirement
20-30 kcal/kg/day
Special nutrition requirement for renal pts
Less volume
Less K and phosphate
Special nutrition requirement for pts with HF
Less volume
Special nutrition requirement for diabetic pts
More cal from fat and less from carbs
Fiber to slow absorption of carbs
Special nutrition requirement for burn/trauma pts
High protein
High cal
Special nutrition requirement for pts with pancreatitis
Low fat
Special nutrition requirement for pts with COPD/pulmonary disease
Lower carbs
Higher fat
How to determine amount of free water an enteral nutrition pt needs
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
Which methods of enteral nutrition can use the crush and flush method for meds?
Gastric (NG and G tubes; mimic actual meals)
Duodenum
Which method of enteral nutrition canNOT use the crush and flush method and what do you do instead?
Jejunum (NJ and tubes) - meds have to be given as liquid
Crush med between 2 spoons and mix into 10mL of sterile water
Above which osmolality can liquid preps for enteral nutrition cause diarrhea?
> 600 Osm
What needs to be monitored in pts on enteral nutrition
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)`
At what point is peripheral admin of TPN no longer appropriate and TPN needs to be adminned centrally
mOsm/L >900 or dextrose > 10-12.5%
What are the macro nutrients and micro nutrients in TPN
Macro: protein (amino acids), carbs (dextrose), fats (lipids)
Micro: electrolytes, vitamins, trace elements
When to use TPN in adults
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
When to use TPN in peds
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
3 in 1 TPN
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
2 in 1 TPN
Contains only dextrose and amino acids
Primary method for peds
Neonates have a (higher/lower) mL and kcal to kg ratio than adults
higher
kcal and mOsm of amino acids
4 kcal/gm
10 (mOsm * L)/g
Nitrogen balance
Energy in should be greater than energy out
Nitrogen in = g protein / 6.25
Nitrogen out = urine urea nitrogen + 4
kcal and mOsm of dextrose
3.4 kcal/gm
5 (mOsm * L)/g
kcal of lipid
~9 kcal/gm
Lipid infusion requirements
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
How to reduce Ca-phos precipitation risk
Put phos in first and Ca in last
Lower pH
Low temp
Quick hang time
Use Ca gluconate
How to handle metabolic acidosis and alkalosis in TPN pts
Acid: increase acetate, decrease Cl
Base: decrease acetate, increase Cl
How to evaluate appropriateness of TPN
- Evaluate fluid goal and energy requirement
- Calcualte kcal/day, g/day and mL for each macronutrient
- Determine final [ ] of dextrose, protein, lipids
- Calculate electrolyte dose
- Select appropriate anion balance
- Performs safety checks
- Lipid infusion rate
- Glucose infusion rate
- Estimate Osm for proteins and dextrose
- Check line/access
- If 3-in-1 ensure stablity
Types of general N/V and treatment options
Gastroenteritis; pancreatitis
Treatment
- 5-HT3 antags (ondestron)
- Metoclopramide
- Phenothiazines
Opioid induced constipation treatment options
Lubiprostone (Amitiza)
Mu peripheral antags
- Methylnaltrexone
- Naloxegol
- Naldemidine
Corticosteroid AE
- Hyperglycemia (increase in blood glucose)
- Increased bp
- Insomnia
- Agitation/manic-type feelings
- Do NOT give with NSAIDs → increased risk of GI ulceration
Preggers N/V treatment options
Doxylamine + VitB6 combo
Second line:
- 5-HT3 antags
- metoclopramide
Types of disorders of balance N/V and treatment options
Motion sickenss, vertigo, dizziness
Treatment: antihistamines
JAKi BBW
- 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
Anti-TNF alpha BBW
- 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
When should you prophylactically use PPIs against NSAID PUD
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)
Alarm symptoms in pts complaining of GERD
- Substernal pain → can be cardiac instead
- Blood → could be GI bleed
- Unexplained weight loss → could be cancer
- Dysphagia (difficulty swallowing)
- Anorexia
mu peripheral antags agents
- Methylnaltrexone: SQ
- Naloxegol: PO
- Naldemidine: PO
Diarrhea treatment options
Peripheral mu agonist
- loperamide (imodium)
- Diphenoxylate (lomotil): treats IBS-UC
Octreotide
5-Amiosalicylates (5-ASA) MOA and agents
works on COX enzymes (ASA is in the name) in gut → knockout prostaglandins/inflammation and pain
Agents
- Mesalamine
- Sulfasalazine
- Olsalazine
- Balsalazide
PPI AE
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
GERD therapy treatment options
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
Which pts might be a candidate for longterm GERD therapy
Barrett’s esophageal
Pts with copmlications from GERD (severe erosive esophgitis; strictures)
Guanylate cyclase receptor agonists AE
Diarrhea (around 20% of pts)
Chronic idiopathic constipation treatment options
Lubiprostone (Amitiza)
Guanylate cyclase receptor agonists (secretagogues)
- Linachlotide (Linzess)
- Plecanamide
Osmotics MOA, agents, and usage
Constipatoin
pulls water into colon → expand and soften stool → trigger contraction and make it easier to puh
PEG3500 (Miralax)
Lactulose
How to approach a pt when considering initation of a QTc prolongation agent
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
Corticosteroid agents for N/V
Dexamethasone
Corticosteroid MOA against N/V
decrease prostaglandin formation
release 5-HT3 in the gut
Erythromycin MOA
agonist of motlin receptors → increase peristalsis in stomach and duodenum
Octreotide MOA
Somatistatin analog→
- inhibit serotonin
- inhibit secretion of
- gastrin
- secretin
- motilin
- insulin
- glucagon
→ reduces intestinal motility and secretion
Erythromycin AE
- N/V
- Diarrhea
- QTc prolongation
metoclopromide (Reglan) AE
- diarrhea
- EPS: higher risk with IV admin
- Dystonia: higher risk with IV admin
- QTc prolongation
metoclopromide (Reglan) MOA
- block dopamine and serotonin
- enhance acetocholine response
→ increase gastric emptying and increase lower esophageal tone
5-HT3 AE
- Constipation
- Headache
- QTc prolongation: more of a concern at higher doses (like 16mg BID) and with IV admin
5-HT3 agents
Ondasetron
Phenothiazines AE
- 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
Phenothiazine MOA and agents
inhibit dopamine, H1, and muscarinic receptors
- Promethazine
- Prochlorperazine - also rectal (Compazine)
- Chlorpromazine
Antihistamine AE
- Drowsiness; impaired congition/confusion in older pts → increased fall risk
- Dry mouth
- Constipation
Antihistamine agents
Meclinzine: safest in older pts due to lower CNS penetration
Dimenhydrinate
Doxylamine (VitB6 combo)
Scopolamine
Hydroxyzine
PONV treatment
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)
Apfels score
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
Lubiprostone (amitiza) MOA
works directly on Cl channels → increase Cl (and water) secretion into stool
Lubiprostone (amitiza) AE
Diarrhea (like 20% of pts) ← reduce by taking with food
Nausea ← reduce by taking with food
IBS-D treatment options
Rifaximin (Xifaxin):, used if small intestine bacteria overgrowth (SIBO)
eluxadoline/Vibrezi
alosetron: in women with severe IBS-D
Tricyclic antidepressant (specifically amitriptyline)
Soluble fibers
List the soluble fibers
- Pysllium (metamucil)
- Oatbraun
- Barley
- Beans
IBS-C treatment options
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
AE for biologics in general and how to treat
IV formulations: infusion related reacton
- acute onset: apap and diphenhydramine
- chronic onset: apap and short course steorids
SQ formualtions: inj site reactions
Selective adhesion molecule (integrin) inhibitors BBW
For natalizumab (Tysabri) NOT vedolizumab (Entyvio)
PML (progressive multi-focal leukoenphalopathy - CNS infection; can lead to death → has a REMS program)
Available corticosteroid agents for IBD
Prednisone: PO
Methylprednisolone: IV
Hydrocortisone: IV
Budesonide: PO
- Entocort for Crohn’s: site of action is in terminal ileum
- Uceris for UC: colon
Azathioprine monitoring parameters and BBW
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
Available immunomodulator agents for IBD
Azathioprine
6-mercaptopurine
methotrexate
cyclosporine
Why is azathioprine frequently used with biologics or steroids for ABD
- 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
Treatment options for mild UC
Mesalamine
If that fails, budesonide
(use both mesalamine and budesonide of extensive)
Treatment options for moderate-severe UC
Budesonide -or- systemic steroids -or- biologic
+/- azathioprine
Treatment options for fulminant UC
IV steroid -or- IV infliximab -or- IV cyclosproine -or- colonectomy
Blood transfusion if Hgb <8
What is the maintenance agent for someone who with mild UC
mesalamine
What is the maintenance agent for someone who achieved IBD remission with a steroid?
Azathioprine
What is the maintenance agent for soemone who achieved IBD remission with a biologic
That same biologic +/- azathioprine
What is the maintenance agent for someone who achieved UC remission with cyclosporine
Azathioprine -or- vedolizumab (entyvio)
Treatment options for perianal involement in Crohn’s
ABX (flagyl, cipro)
Surgery
Inflxiimab
Treatent options for mild-moderate Crohn’s
Budesonide
Treatment options for moderate-severe Crohn’s
PO systemic steroids -or- biologic
+/- azathioprine
Treatment options for fevere-fulminant Crohn’s
Surgery -or- IV steroid -or- infliximab
Upper GI bleed treatment
- 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
S/S of an upper GI bleed
Black stool, blood vomit
Low bp; light headedness
Low hr, low H&H; chest pain
H. pylori treatment
Quad: PPI, bismuth subsalicylate, tetracycline, flagyl
Triple: PPI, clarithromycin, amoxicillin (flagyl if allergy)
- confirm eradication
S/S of PUD
- Dyspepsia (indigestion)
- Epigastric pain
- Gnawing/burning pain
- Early satiety
- Pain that wakes them from sleep
- GI bleed (main complication from PUD)
eluxadoline (Vibrezi) MOA
mu agonist/delta/kappa agonist: inhibit bowel construction
eluxadoline (Vibrezi) AE
- Sphincter of Oddi dysfuntion/spasm → CI pts with pmh of pancreatitis, alcoholism (3+ drinks a day)
tenapanor (Ibsrela) AE
diarrhea
tegaserod (Zelnorm) MOA
5-HT4 agonist
increase GI secretion and motility; decrease visceral pain
tegaserod (Zelnorm) AE
- Increased risk of CV events
- Headache
- Diarrhea
mu peripheral agonist agents
- Loperamide (Imodium): PO
- Diphenoxylate (Lomotil): PO
mu peripheral antags AE
- Caution in IBD, diverticulitis, GI malignancies
- Severe abdominal pain → d/c agent
- Diarrhea → d/c agent
Guanylate cyclase receptor agonists MOA and agents
Secretagogues: pull Cl and bicarb into stool; can derease abdominal pain in IBS-C
- Linachlotide (Linzess)
- Plecanamide (Trulance)
NSAID induced PUD treatment
- 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
What differentiates a mild from a severe drug-induced dermatology disorders?
FEver
Penicillin allergy cross reactivity
cross reactivity between penicillins and cephalosporins is 1-2%, dependent on R1 sidechain
Sulfa ABX allergy cross reactivity
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)
Nasolacrimal occlusion
method to reduce systemic AE by pressing on lacrimal tear duct a min after applying
FTU method
1 FTU = 0.5g
Oral isotretinoin dosing
0.5-1 mg/kg/day
OR
15-20 weeks of cumulative total dose of 120-150 mg/kg
How often do you need to take pregancy tests while on isotretinoin
2 (negative) before starting
monthly after starting
Fixed drug eruption treatment
Resolves within a few days upon discontinuation (though the hyperpigmentation may last for months)
Simple maculopapular eruption treatment
Resolves 7-14 days after stopping drug
Simple maculopapular eruption presentation
Rash
What is the pH of healthy skin
4.7-5.7
What is considered an elevated IOP?
> 21 mmHg
DEET
- 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
Urticaria/angioedema treatment
Self-moitoring, symptoms will resolve in 1-2 weeks
Primary angle CLOSURE glaucoma treatment
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
Rho kinase inhibitor examples and AE
Netarsudil
- Hyerpemia (high rate): eye turns red due to inflammaton of blood vessels
- Conjunctival hemorhage
Caronic anhydrase inhibitor examples
- Acetazolamide PO
Combos:
- dorzalamide/timolol
- brinzolamide/brimonidine
Alpha agonist (eyedrops) examples and AE
Brimonidine
AE
- Conjunctival hyperemia
- Irritation
- Allergic reaction
- Drowsiness
- Xerostomia (dry mouth)
- Tachyphylaxis
Beta blocker (eyedrops) examples and AE
timolol and other “-olols”
AE
- local ocular irritation
- Cardiac effects (conduction, contracitliy, pressure)
- Pulmonary
- CNS
- Tachyphylaxis
Prostaglandin F2alpha analog AE
bimatoprost
travoprost
latonoprost
AE
- local ocular irritation
- conjunctival hyperemia (red eye)
- hypertrichosis (eyelashes)
- periocular/iris pigmentation changes (turn darker)
- infection
- headache
Primary OPEN angle glaucoma treatment goals
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
Priary OPEN angle glaucoma risk factor
- 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
Moderate-severe plaque psoriasis treatment optios
Methotrexate
Cyclosporine
Phosphidesterase inhibitor
Biologics (Il inhibitors and TNF alpha)
Atopic dermatitis (eczema) treatment options
TCS
Topical CI (tacrolimus)
JAKi
Cyclosporine
Methotrexate
Azathioprien
SJS/TEN treatment
Supportive care: pain, fluids, nutrition
- Systemic corticosteroid: possible harm
- IVIG: possible benefit
- cyclossporine: posssible benefit
DRESS treatment
FLuids, electrolytes, nutrition management
No organ involvment: topical steroid
Organ involvement: 0.5-3mg/kg/day prednisone then taper off
Causes of simple maculopapular eruption
Penicillins/cephalosporins
Sulfonamides
Anticonvulsants
Causes of DRESS
Allopurinol
Sulfonamides
Anticonvulsants
Dapsone
Causes of urticaria/angioedema
Penicillins and related ABX
Sulfonamides
ASA
Opiates
Latex
Ccauses of serum-sisckness-like
Penicillins/cephalosporins
Sulfonamides
Causes of fixed drug eruption
Offending drugs aren’t the usual culprits
Causes of SJS/TEN
Drugs
- Sulfonamides
- Penicillins
- Anticonvulsants
- NSAIDs: particularly “-oxicams”
- Allopurinol
Other
- HIV infection
- Lupus (SLE)
- Malignancy
- UV light or radiation therapy
- Genes: HLA-B*15:02
Fixed drug eruption presentation
Simple eruptions with pruitic, erythematous, raised lesions that can blister
same exact rash in same exact spot if drug is given again
Serum-sickness-like presentation
Urticaria
Fever
Arthralgias
Urticaria/angioedema presentation
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
Drugs that can cause photosensitivity
- Sulfonamides
- Tetracyclines
- Amiodarone
- Coal tar
Drugs taht can cause hyperpigmentation
Increased melanin:
- Phenytoin
Direct deposition
- Tetracyclines
- Silver, mercury
- Antimalarials
- Amiodaronne
Dermal lipofuscinosis
- Amiodarone