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List factors that put pt at risk for candida
Broad spectrum antibiotics, neutropenia, immunosuppression, prolonged antibiotic use, implantable prosthetic device, prolonged ICU stay > 7-14 days, High APACHEE II score, central venous catheter, TPN, > 2 days mechanical
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When would you use an echinocandin over azol
Severe infection or recent azol exposure
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2 pros and 2 cons of using echinocandin vs fluconazole in candidiasis
- Pro: broader spectrum cover C. galbrata and C. krusei, no adjustment for renal, fewer D/D interactions
- Con: only IV, Cost, no clear evidence of superiority, resistance in the future
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Duration of therapy for Candida infection
Treat for 2 weeks past documented clearance from blood stream
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What are risk factors for infection with C. glabrata
Elderly, cancer, DM
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What are sepsis, severe sepsis, and shock
- Sepsis: 2 SIRS + infection
- Severe sepsis: sepsis + organ dysfunction
- septic shock: severe sepsis + hypotension
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Name 2 pros and 2 cons of using Echinocandin vs fluconazole in candidiasis
- Pro: broader spectrum cover C. galbrata and C. krusei, no adjustment for renal, fewer D/D interactions
- Con: only IV, Cost, no clear evidence of superiority, resistance in the future
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What are the SIRS criteria?
RR > 20, HR > 90, WBC < 4000, >12000, 10% bands, Tem < 36 or > 38
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How much do you want to lower BG and why
Lower by 10 % 1st hr then 50-75 mg/dl/hr to prevent cerebral edema and electrolyte abnormalities
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Ketones in DKA and how to measure them
Acetone, acetoacetate, beta hydroxybutyrate Measure in blood and urine, dos a nitroprusside reaction which estimates the acetoacetate and acetone levels. Measure the serum B-hydroxybutyrate if possible
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When can you transition to SQ insulin
When ketones have cleared, anion gap normalized and pt able to eat
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When do you stop the infusion after you have given SQ insulin
1-2 hrs
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What electrolytes are important to monitor in DKA
Mg+, Phos, Na+, K+
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Difference btwn HHS and DKA
- HHS: mostly in type 2 DM, slower onset, normal pH, Glucose > 600
- DKA: fast onset, mostly in type 1 DM, low pH acidosis, glucose > 250
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What is the pathophysiology of DKA
1. Insulin deficiency 2. ↑ counter regulatory hormones (cortisol, glucagon, catecholamines)lead to insulin resistance
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What are the components of a diabetic foot exam
Dermatologic, Musculoskeletal, Neurological assessment, vascular assessment
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What does LOPS stand for
Loss of protective sensation
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What is the triad of causes that interact and ultimately result in ulceration
Neuropathy, deformity, and trauma
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Risk factors for DFI
- Poor glycemic control,
- peripheral neuropathy
- duration of DM > 10 yrs
- high plantar pressure
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3 differences btwn AACE and ADA guidelines
- ADA: A1C < 7, pre-prandial 70-130, post prandial < 180
- AACE: A1C < 6.5, pre-prandial < 110, post prandial < 140
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Sitagliptin and Byetta give one pro and one con of each
- Sitagliptin-
- Pro: weight neutral, oral, well tolerated 1% ↓ A1V
- Con: expensive, may ↑ digoxin levelsb.
- Byetta-
- Pro: weight loss, A1C ↓ by 0.5-1%
- Con: injection bid, expensive, GI SE
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What is insulin and what is its major role in the body
Anabolic/anti-catabolic hormone Plays major role in protein, CHO, and fat metabolism
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What peptide can be used as and endogenous marker of insulin production
Peptide C, cleaved when insulin is made
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What does the DOSE trial tell us about bolus vs. continuous infusion of furosemide in ADHF
There is no difference in outcomes, start with bolus easier to use, continuous if resistant
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2 pros and 2 cons of using nitroglycerin in ADH
- Pro: improves PCWP, slight ↓ in MAP
- Con: tolerance so have to continually titrate, pro-arrhythmic
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How much K + do you give a pt in a central line vs. peripheral
Central 20 mEq, Peripheral 10 mEq
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How much Mg+ do you give a pt in a central line vs. peripheral
Central 2 gram/hr, peripheral 1 gram/hr
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What is the mechanism by which a thiazide added to a loop produces more diuresis
Loop work on the ascending loop of Henle, leading to more Na+ reaching the distal convoluted tubule which atrophies and therefore takes up more Na+, Thiazides block this
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What are the causes of hyperglycemia in the hospital setting
Acute metabolic and hormonal changes due to injury and stress, counter regulatory hormones (glucagon, cortisol) lead to alteration in CHO metabolism, insulin resistance, gluconeogenesis, lipolysis
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What is the risk of hyperglycemia in the hospital
↑ Mortality, prolonged length of hospital stay, poor long term outcomes, high health costs
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When would you leave a patient on their home regimen
Clinically stable, and have normal nutritional intake, normal BK and stable renal and cardiac function
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which echinocandind do you not need to dose adjust for hepatic impairment
Anidulafungin
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Name two pros and two cons to S/S insulin
Pro: convenient, easy to implement, doesn’t depend on physician for dosing Con: reactive not proactive, hyper or hypoglycemia, can lead to DKA
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2 pros and 2 cons of Milrinone in ADHF
- Pro: can use with BB and it is ver effective at increasing cardiac output and cardiac index
- Con: has long half-life so SE will last longer, and can cause arrhythmias so must monitor EKG
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Name a inotropic agent and what you need to monitor while using them
Dobutamine, Milrinone, Dopamine
Monitor: BP
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When is it appropriate/ or not appropriate to use Nesiritide
Only in the absence of symptomatic hypotension, in addition to diuretic therapy for rapid improvement of congestive symptoms or if persistent ADHF despite aggressive treatment w/ diuretics and standard oral therapy
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When would you use migraine prophylaxis
> 2 HA a month, pt expresses desire to not experience HA and wants therapy
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Name 3 diffrences btwn migraine and tension HA
- migraine can be accompained by N/V and photophobia
- Migraine typically last 24 + hrs, tension HA are shorter duration
- Tension HA are bilateral, migraines are unilateral (but can go bilateral)
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What are the diffrences btwn Sumatriptan, Eletriptan and Frovatriptan
- Sumatriptan: fast onset, short duration of action
- Eletriptan: fast onset, long duration of action
- Frovatriptan: slower onset, longer duration
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What two triptans come in ODT
Rizatriptan and Zolmitriptan
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What are the 4 potent vasodilators released in migraine HA
NO, CGRP, Neurokinin A, Substance P
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What is the risk of using triptan w/i 24 hrs of using a ergotamine
they both cause vasoconstriction so it will produce extreme basoconstriction, which leads to hypertensive crisis, MI
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Why would you not use and SSRI and a triptan together
Risk of serotonin syndrome
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What is the mechanism of action for triptans
agonist of the 5HT receptor leading to vasoconstriction
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list 3 AED medications that are renally eliminated
Levtiracetam, Gabapentin, Pregabalin, Lacosamide, Zonisamide
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List 3 AED that are enzyme inducers
Phenytoin, Phenobarbital, Primidone, Carbamazepine,
at high doses: Oxcarbazepine, Topiramate, Gelbamate
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Describe the diffrence btwn saccades and nystagmus
Saccades: break up of smooth pursuit- choppy eye movement when following finger (marker that pt is taking med)
Nystagmus: eye darts back and forth (or up and down) very rapidly when following finger (indication of toxcity)
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What 2 AED have FDA indication for migrain prophylaxis
Topiramate, Valproic acid
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What are the hematology class effects of all AED
decrease WBC, PLT and RBC
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What is an auto inducer and name one AED example
- auto inducer is a drug that induces the metabolism of itself
- Carbamazepine
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What two seizure medications should not be give in hyponatremia
- Carbamazepine
- Oxcarbazepine
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What do you need to screen pt for before starting Levetiracetam
History of psychosis, can unmask
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What is a mojor adveres effect of Ezogabine
Need to do bladder scan, pt can't feel bladder/if it is empty
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What are the two newest AED
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2 pro and 2 cons of using bivalirudin in HIT
- Pro: no hepatic/renal adjustment, short half-life
- Con: not FDA approved, fewer studies compared to other agents
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2 pros and 2 cons of Argatroban in HIT
Pro: FDA approved, no renal adjustment, reversible
Con: metabolized by the liver, difficult to transition to warfarin
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What is the difference btwn HIT assay and SRA
- ASSAY: more sensitive ( many ppl will have antiboidies), faster, doesnt tell if diesease is present
- SRA: more specific, expensive, takes long time, tells that disease is present
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4 T's of HIT
Thrombosis, thrombocytopenia, time and other causes
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What is the role of fondaparinux in HIT
For pt with history of HIT but not active HIT
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If pt has gonorrhea what partners need to be treated
all partners w/i 60 days
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What does of acyclovir would you give for initial treatment of herpes
Acyclovir 400 mg TID x 7 days
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What are contraindications to metformin
SCr > 1.5 men > 1.4 women
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How would you initiate rapid insulin in pt uncontrolled on basal insulin
start with highest meal of the day and have pt take 4 units or aspart, lispro, apidar and titrate by 2 units q 3 days until BG is w/i goal of < 180 2 hrs post
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Sitagliptin vs Exenatide 1 pro and 1 con of each
- Sitagliptin: pro: available PO and no hypoglycemia
- Con: expensive, long term safety not established
- Exenatide: Pro: weith loss and improved satiety
- Con: renal adjustment and injection
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What did the ACCORD trail teach us about BP, Lipids and glucose in DM
- BP: compared lower BP 120 to 140 w/no diffence in outcomes
- Lipids: statin+ fibrate vs. statin alone: no diff in outcomes
- Glucose: A1C < 6 showed a increase in mortality with no CV venefits
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Diffrence btwn pioglitazone and rosiglitazone
rosiglitazone has a BB warning for HF and increase risk of MI
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Metfromin and SU MOA and how it relates to hypoglycemia
- Metromin is an insulin sensitizer and does not cause hypo alone
- SU stimulate insulin release form the pancreatic beta cell and can cause hypoglycemia
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Pt in ED w/ asthma exacerbation and has had several doses of SABA and oxygen with no relief what can you give him and why
Ipratropium can be added bc it is short acting anticholinergic that will work quickely to decrease the exacerbation. Studies have shown that in combo with SABA in ED it helps to decrease the severity of exacerbation and length of hospital stay
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what is the diffrence btwn allergic rhinitis and asthma
- Asthma: chronic inflammatory condiciton of the lower airways characterized by reversible airflow obstruction, hyper responsiveness and episodic respiratory symptoms
- Allergic rhinitis: disorder of upper airway, resulting for IgE mediated inflammation of the nose upon contace with allergen
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what is the diffrence btwn albuterol and levalbuterol
Levalbuterol is R isomer of albuterol so it has less SE of tachycardia and tremor compared to albuterol which is a racemic mixture
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when to use IV vs. PO steroids in acute exacerbations of asthma
IV is for life threatening only, PO for mild-moderate and severe
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Role of IV Mag sulfate in asthma exacerbation
used when incomplete response to initial treatment w/i 1-2 hrs, used to avoid the need for intubation
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what is the role of omalizumab in asthma
treatment step 5 and 6 with allergic component
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what is an asthma action plan and why is it used
to help assist the pt in understanding their disease and teach how to self manage it. Focuses on 2 things: daily managment and how to recognize worsening symptoms
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3 counseling pts for oral inhalers
store at room temp, wash mouth piece w/ soap and water, prime before use, inhaler technique
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when would you use spironolactone for resistant HTN
Refractory HTN, advanced HF or CKD
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50 yr old perimenopausal female give 2 reasone venlafaxine is a good option
treats the vasomotero symptoms and is non-hormonal so no increased risk of CV event
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Name two drug that are used to treat hot flashes
Venlafaxine, prempro, OC, gabapentin
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What does ACHES stand for
abdominal pain, chest pain, headache, eye pain, sever leg pain
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What does PAINS stand for, and when would you use it
Period late, Abdominal pain, Infection exposure, Not feeling well, String missing (what to look for with the use of IUD)
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when and why would you add on progesterone to estrogen hormone therapy in perimenopause
add when pt still has uterus to decrease the risk of endometrial cancer and endometrial hyperplasia
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What is the role of glucosamine in OA
Guidelines say not to use it but it does prevent cartilage loss
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what is the mechanism of orlistat and the SE
- reversible inhibitor of intestinal lipases, prevents TG absorption
- SE: fatty stool, decreased absorption of fat soluble vitamins
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