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Pharm Final review > ALL > Flashcards

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1
Q

What does the glomerulus do

A

filtration

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2
Q

What does the proximal tubule do

A

reabsorption (mostly NaCL)
- also secretes hydrogen, foreign substances, organic anions and cations
- isotonic

Carbonic Anhydrase Inhibitors and osmotic diuretics work here

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3
Q

What does the loop of Henle do

A

concentrates urine
-isotonic, hypertonic, hypotonic

Descending Loop: NaCl diffuses in, water reabsorbed
Ascending Loop: NaCl actively reabsorbed, water stays in

Loop diuretics work here

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4
Q

What does the distal tubule do

A

Reabsorption of Nacl, water (ADH required), bicarb

  • isotonic or hypotonic

Thiazides work here

This is where blood pressure changes are made - thiazides work here and they work on decreasing pressure…WHERE THE RAAS system begins

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5
Q

What does the collecting duct do

A

final concentration
- reabsorbs water (ADH required), NaCL

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6
Q

What is the GFR for CKD diagnosis

A

less than 60 for over 3 months with/without kidney damage

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7
Q

Are longer intervals between HD and surgery associated with a higher risk of post-op mortality?

A

YES

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8
Q

What BUN/SCR is dehydration?

A

BUN/SCR > 20

1.5 SCR or GFR drop 25%. risk
2. 50. injury
3 75. failure

urine .5. 6 hrs
.5. 12 hrs
under .3. for 24 or no urine for 12

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9
Q

Where does each group of diuretic work?

A

Proximal tubule - Carbonic anhydrase inhibitors AND osmotic diuretics
Loop of Henle - Loop diuretics
Distal Tubule - Thiazides
Distal tubule / collecting duct - potassium sparing

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10
Q

Are carbonic anhydrase inhibitors used as diuretics these days?

A

Not really - Acetazolamide (Diamox) is used off label for metabolic alkalosis (commonly happens when “over-diuresing” CHF patients)

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11
Q

What is an interesting use for Acetazolamide?

A

Altitude sickness

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12
Q

What do carbonic anhydrase inhibitors do?

A

Inhibit CA which inhibits H+ secretion in the proximal tubule. Bicarb and sodium are blocked from reabsorption

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13
Q

Do carbonic anhydrase inhibitors cross the BBB?

A

YES

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14
Q

What do osmotic diuretics do (mannitol and urea)

A

Uncouples Na and H2O reabsorption by increasing the osmotic gradient in the proximal tubule. Na reabsorption initially, but H2O is not, leading to decreased Na reabsorption distally.

They “pull water” and increase intravascular volume.

Osmotic diuretics primarily inhibit water reabsorption in the proximal convoluted tubule and the thin descending loop of Henle and collecting duct, regions of the kidney that are highly permeable to water.

Osmotic diuretics also extract water from intracellular compartments, increasing extracellular fluid volume. Overall, urine flow increases with a relatively small loss of Na+. In fact, urine osmolarity actually decreases.

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15
Q

What are Mannitol’s different uses?

A

Prophylaxis against acute renal failure (ARF)…loop diuretics are too

Differential diagnosis of acute oliguria (if the patient responds to mannitol, they are just dehydrated…if not, they have actual renal damage)

Treatment of increased intracranial pressure (ICP)

Decreasing intraocular pressure (IOP)

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16
Q

Is mannitol REALLY nephroprotective? What does current research say about it?

A

NOPE.

No better than plain saline pre-radiocontrast dye
EXCEPT: renal transplant surgery

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17
Q

Do you need an intact BBB when using mannitol?

A

YES

If not, it will pull water into the brain and increase ICP, which is the opposite of what we want

Urinary ph NOT altered by mannitol

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18
Q

What are dangerous side effects of mannitol?

A

Pulmonary edema, hypovolemia, hypernatremia

electrolyte disturbances, plasma hyperosmolarity d/t water and NaCl secretion (hypernatremia)

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19
Q

What electrolyte abnormality can mannitol create?

A

Hypernatremia from excess water loss

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20
Q

What negative side-effect is urea associated with?

A

Venous thrombosis and tissue necrosis after extravasation (not seen with mannitol)

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21
Q

What is loop diuretics MOA?

A

Inhibits Na and Cl reabsorption in the ascending loop and to a lesser extent in the proximal tubule

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22
Q

Which two diuretics are nephroprotective?

A

mannitol (osmotic) and loop diuretics (furosemide)

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23
Q

What are loop diuretics clinical uses?

A

Mobilization of edema fluid due to renal, hepatic, or cardiac dysfunction

Treatment of increased ICP

Treatment of hypercalcemia

Differential diagnosis of acute oliguria

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24
Q

What happens when you take NSAIDS while on a loop diuretic?

A

Furosemide-induced increases in renal blood flow are inhibited by NSAIDs resulting in an attenuated diuretic effect

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25
Q

What is braking phenomenom?

A

Acute Tolerance (Braking Phenomenon) – ceiling effect with diuretic where giving more doesn’t increase outcome but can increase side effects.

Associated with loop diuretics

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26
Q

Loop diuretics electrolyte side-effects

A

All low basically

Hypokalemia
Hypochloremia
Hyponatremia
Hypomagnesemia

Hypokalemic Metabolic alkalosis (thiazides also cause this)

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27
Q

Which diuretic can cause deafness?

A

Loop diuretics

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28
Q

Which type of medication are loop diuretics cross-sensitive to?

A

Sulfa antibiotics, sulfonylureas, thiazide diuretics

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29
Q

Do antibiotics increase the chance of nephrotoxicity when using loop diuretics?

A

YES, for aminoglycosides and cephalosporins
- penicillins and furosemide together are associated with allergic interstitial nephritis

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30
Q

What is thiazides (chlorothiazide, hydrochlorothiazide) MOA?

A

Compete for the Na-Cl cotransporter in the distal tubule to inhibit reabsorption. Inhibit only urinary diluting capacity, not concentrating capacity.

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31
Q

Which electrolyte do thiazide diuretics INCREASE?

A

calcium (increased calcium reabsorption)

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32
Q

What are thiazides clinical uses?

A

hypertension and mobilization of edema

Thiazides also can cause arrhythmias along with loop diuretics because of the hypokalemia

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33
Q

Thiazides electrolyte side-effects

A

Hyperglycemia
Hyperuricemia
Hypercalcemia

Decreased renal or hepatic function
Decreased intravascular volume
metabolic alkalosis with chronic administration

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34
Q

Are thiazides associated with hyper or hypo blood sugar and uric acid?

A

HYPERglycemia and HYPERuricemia

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35
Q

Do potassium-sparing diuretics cause hyperglycemia and hyperuricemia like thiazides?

A

NOPE

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36
Q

What are the MOA of potassium-sparing diuretics?

A

Amiloride and Triamterene: inhibit Na reabsoprtion induced by aldosterone. Inhibit active counter transport of Na and K in the collecting duct. MESS UP THE the Na-K-ATPase pump

Spironolactone and Eplerenone: competes for aldosterone receptor sites in the distal tubule to block Na reabsorption and K secretion. Competitive inhibitors of aldosterone

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37
Q

What is the main side-effect of potassium-sparing diuretics and what makes this issue worse?

A

HYPERKALEMIA

Made worse when also taking NSAIDs, Ace inhibitors (i.e. lisinopril), Beta-blockers

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38
Q

Which two diuretics cause hypokalemic, hyperchloremic metabolic alkolosis?

A

Thiazides and loop diuretics

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39
Q

EKG changes with hyperkalemia

A

Tall peaked T wave
Loss of P wave
Widened QRS with tall T wave

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40
Q

Why do we give calcium when correcting hyperkalemia?

A

Stabilizes the heart and lowers the threshold potential of the myocardium.

Caution in patients who are on digoxin – calcium has been reported to worsen the myocardial effects of digoxin toxicity..could use Mg as an alternative to stabilize the myocardium

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41
Q

Treatment for hyperkalemia

A

C = Calcium (cardiac stabilizer)
B = inhaled beta2 agonists (intracellular shift)
I = Insulin (followed by..)
G = Glucose (given with insulin)
K = Kayexalate (mainly chronic RF)
D = Diuretics (renal elimination)
ROP = Renal unit for dialysis Of Patient

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42
Q

What are some causes of hyponatremia?

A

Loss of body fluid, thiazides, loops, CHF, SSRIs, Carbamazepine, Lithium, Liver disease

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43
Q

Hyponatremia correction rates

A

Severe symptomatic hyponatremia: 6-12 mEq/L in the first 24 hrs and 18 mEq/L or less in 48 hrs

Chronic hyponatremia: 0.5 mEq/L/hr with max change of 8-10 mEq/L in a 24 hr period

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44
Q

What is calcium dependent on?

A

Albumin

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45
Q

What are some causes of hypercalcemia?

A

Hyperparathyroidism

Chronic renal failure or vitamin D deficiency

Vitamin D intoxication

Malignancy

Diuretics (usually mild)

Lithium

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46
Q

What antibiotics can cause nephrotoxicity when using with loop diuretics?

A

Aminoglycosides and cephalosporins

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47
Q

Which antiepileptic is the treatment of choice for status epilepticus according to most recent treatment guidelines?

A

lorazepam (Ativan)

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48
Q

Order of meds to give for seizure

A
  1. Benzodiazepine

If benzo not available try: phenobarbital IV, diazepam rectal, nasal or buccal midazolam

  1. Second phase: fosphenytoin IV, valproic acid IV, levetiracetam IV
  2. Repeat of any second line therapy
    Anesthetic doses of thiopental, midazolam, pentobarbital, or propofol
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49
Q

Which sodium channel blocker has the most side-effects, drug interactions, and causes hyponatremia?

A

Carbamazepine

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50
Q

Which sodium channel blocker induces its own metabolism (reduces its own levels)?

A

Carbamazepine

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51
Q

Which sodium channel blocker has unpredictable pharmacokinetics and has similar antiarrhythmic properties as lidocaine?

A

Phenytoin (fosphenytoin is the oral prodrug)

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52
Q

Which sodium channel blocker causes gingival hyperplasia, arrythmias due to class 1B antiarrythmic association, and can cause cleft palate/congenital heart disease/slowed growth rate/mental deficiency if given during pregnancy?

A

Phenytoin

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53
Q

Which sodium channel blocker, when given with depakote, can cause TERRIBLE rash that is life-threatening and basically Steven-Johnson X 1,000?

A

Lamotrigine (lamictal)

Lam”oh my god”trigine

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54
Q

Which sodium channel blocker has the highest rates of kidney stones?

A

Zonisamide

Kidney ZONES…zonisamide!

KIDNEYZONISAMIDE

STONEISAMIDE

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55
Q

Which sodium-channel blocker has the best safety profile?

A

Lacosamide

La”coast”amide

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56
Q

Which benzodiazepine has the highest rates of withdrawal?

A

Clobazam (Onfi)

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57
Q

Which benzo is the most and least lipophilic?

A

clobazam and temazepam

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58
Q

______ is only available through a very specific program with REMS monitoring because of risk of permanent vision loss,

A

Vigabatrin

Vi”sual”gabatrin

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59
Q

What is gabapentin mostly used for?

A

Neuropathic pain or anxiety. Helps reduce pain post-operatively

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60
Q

Which combination of medications greatly increases the risk of hyponatremia?

A

SSRIs and Carbamazepine (Tegretol)

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61
Q

What is a fairly common yet weird side-effect of pregabalin?

A

Difficulty walking, gait abnormalities

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62
Q

This seizure medication may raise ammonia levels leading to possible confusion, agitation, and delirium

A

Valproic Acid

Valproic A”mmonia”cid

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63
Q

With in utero exposure, ______ can lower IQ in children compared to other anti-epileptics (category D-X)

Hint: it also raises ammonia levels

A

Valproic Acid

“Valprammonia”

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64
Q

Which anticonvulsant can make you feel like your mind and body are disconected?

A

Topiramate

Top”off”iramate

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65
Q

This seizure med can cause SEVERE cognitive impairment? Example of professors friend who would forget everything

A

Levetiracetam (keppra)

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66
Q

What the fuck does dantrolene do

A

Blocks ryanodine channel, reduces Ca ++ release from SR

Med of choice for malignant hyperthermia

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67
Q

Which class of antidepressant has significant anticholinergic properties?

A

TCAs- tricyclic antidepressants

Tricyclic anticholinergic antidepressants..

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68
Q

What do you give for a tricyclic antidepressant overdose?

A

NaHCO3 d/t metabolic acidosis, supportive therapy

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69
Q

What do all anti-depressants have BLACK BOX WARNING FOR?

A

Suicidal ideations

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70
Q

Which SSRI has a black box for QT prolongation

A

Citalopram (Celexa)

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71
Q

______ are the most highly sedating anti-depressants

A

5HT2A antagonist (trazadone is an example)

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72
Q

_______ is used for Pseudobulbar affect (laughing inappropriately)

A

Nuedexta

“Nuts”dexta

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73
Q

Which generation of antipsychotics are supposed to be safer, but aren’t really?

A

2nd

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74
Q

_______ have a black box warning for dementia related death, agranulocytosis

A

Antipsychotics

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75
Q

Levodopa is a ______, and carbidopa is _______

A

Levodopa = dopamine precursor
Carbidopa = false dopamine

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76
Q

What are the two classes of Alzheimer’s Medications

A

Acetylcholinesterase Inhibitors

NMDA receptor antagonists

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77
Q

What is the most common side effect of AChEi

A

Rest/digest side effects

Bradycardia
Loose stools
OAB

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78
Q

What do alzheimers meds do to succinylcholine and other NMB?

A

POTENTIATE succinylcholine

REDUCE blockade of other NMB

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79
Q

Antipsychotics - too much dopamine
Parikinsons - not enough dopamine

A

Yep

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80
Q

Carbidopa/Levodopa (Sinemet) improves Parkinson’s symptoms via which mechanism of action?

A

Dopamine receptor agonist

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81
Q

One way to predictably reduce the incidence of post-operative delirium is to use lighter sedation.

A

FALSE

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82
Q

Aricept (Donepezil), a medication used for Alzheimer’s disease, may antagonize the effects of succinylcholine.

A

FALSE

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83
Q

Which seizure medication has similar antiarrhythmic properties as Lidocaine?

A

Phenytoin (Dilantin)

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84
Q

An FDA safety communication from 12/2019 stated that gabapentinoids (like Gabapentin) increase the risk of which side effect when combined with opiates?

A

Respiratory depression

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85
Q

Is bactericidal better than bacteriostatic?

A

Nope! Equal

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86
Q

Do greater concentrations kill bacteria faster or in greater numbers?

A

NOPE

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87
Q

Does vancomycin work on gram-positive or gram-negative bacteria?

A

gram-positive

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88
Q

What are the 3 main nosocomial infections?

A

Urinary
Respiratory
Blood

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89
Q

What devices are associated with nosocomial infections?

A

Ventilator
Vascular access catheter
Urethral catheter

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90
Q

Which central lines cause the most infections?

A

Femoral> I.J. >Subclavian

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91
Q

Primary cause of c-diff?

A

clindamycin

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92
Q

What is the treatment for c-diff?

A

Oral vancomycin

Dificid (fidaxomicin)- similar cure rates as vanco, reduced recurrence for moderate to severe infection

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93
Q

What are the risk factors for c-diff?

A

Antimicrobial use
Acid suppressant therapy
Inappropriate handwashing and cleaning techniques

94
Q

Do you always need surgical antibiotic prophylaxis?

A

NO.

Also, usually not necessary to continue past the 1st Post-op day

Usually use 1st generation cephalosporin (cefazolin)

95
Q

Wound classification

A

Class I: Clean (1.3-2.9%)
Atraumatic
No break in sterile technique
Respiratory, G.I., and G.U. tracts not entered

Class II: Clean-Contaminated (2.4-7.7%)
Surgery in areas known to harbor bacteria
no spillage of contents

Class III: Contaminated (6.4-15.2%)
Major break in sterile technique
Surgery on traumatic wounds
Gross G.I. spillage
Entrance into an infected biliary or G.U. tract

Class IV: Dirty-Infected (7.1-40%)
Infection existed before the surgery
Old wound with devitalized tissue
Perforated viscera

96
Q

Is prophylaxis for fungal infections proven to always work?

A

Efficacy of prophylaxis is difficult to prove

97
Q

When do you give ancef, and when do you give vanco for prophylaxis?

A

Ancef 60 minutes
Vanco 120 minutes

98
Q

Is increasing duration of antimicrobial prophylaxis associated with higher odds of AKI and C difficile infection in a duration-dependent fashion?

A

YES. Increasing prophylaxis is bad.

99
Q

What is the half life of cefazolin, clindamycin, and vanomycin?

A

Cefazolin: 2 hrs, so dose at 4hrs
Clindamycin: 3 hrs, so dose at 6 hrs
Vancomycin: 12 hours..so..unecessary

100
Q

Do beta-lactamase Inhibitors have any antimicrobial effect on their own?

A

NO

101
Q

Which group of antibiotics causes Jarisch-Herxheimer rxn – looks like a tick infection (high fevers and rash)?

A

Penicillins

102
Q

Do patients with a penicillin allergy have an increased risk of SSI?

A

YES, about 50% higher

103
Q

Which antibiotic can you give if someone has a penicillin allergy?

A

Cefazolin
Vancomycin

104
Q

Which infections are higher in patients with a penicillin allergy?

A

MRSA and C.difficile

105
Q

What are the two strongest cephalosporins that cover basically everything?

A

Ceftaroline (Teflaro) and Cefiderocol (Fetroja)

106
Q

What is the drug of choice for MRSA?

A

Vanco

107
Q

Side effects of vanco?

A

Red-Man, nephrotoxicity, ototoxicity, TTP (thrombocytopenia)

108
Q

Which antibiotic can cause serotonin syndrome because of an interaction with MAO, and also causes myelosuppression (anemia, leukopenia)?

A

Linezolid (Zyvox)

109
Q

Which antibiotic can cause QT prolongation?

A

Azithromycin (Zithromax)

Macrolides (azithromycin, clarithromycin, erythromycin)

110
Q

Which antibiotic is a potent inhibitor of cyp3a4?

Which antibiotic can prolong QT?

A

Cypa3a4 - Clarithromycin (Biaxin)

Prolong QT - azithromycin

Macrolide family

111
Q

Which antibiotic has increases the risk for tendonitis – rupture of achilles tendon, neurologic – seizures, confusion, and severe hypoglycemia and increased Morbidity/mortality

A

Fluoroquinolones

112
Q

Which antibiotic should be last line because of the multiple FDA warnings?

A

Fluoroquinolones

113
Q

Which fluroquinolone is the first fluoroquinolone antibiotic with activity against methicillin-resistantStaphylococcus aureus(MRSA) and, unlike the other fluoroquinolones, is not associated with QT prolongation or photosensitivity.

A

Delafloxacin (Baxdela)

Dela”firstfluroquinolone”oxacin

114
Q

Which antibiotic causes inhibition of bone growth (2nd/3rd trimester through the age of 8), hepatotoxicity, tooth discoloration and enamel hypoplasia

A

Tetracyclines

(doxycycline)

115
Q

Which antibiotic works on acne but has a host of negative side effects?

A

Doxycycline (Vibramycin)

Tetracycline family

116
Q

Which antibiotic interferes with DNA synthesis….Not enough folic acid

A

Trimethoprim/Sulfamethoxazole (Bactrim, Septra)

Aminoglycoside

117
Q

Which med is used for patients with implanted device that is growing biofilms over it

A

Rifampin and Rifabutin

Also a potent inducer of the CYP 450 system with significant interactions
Rare hepatotoxicity, **orange-red body fluids
*Mostly for TB and prosthetics

118
Q

Which antibiotics are safest for use in pregnancy?

A

Penicillins, Cephalosporins, Erythromycin

119
Q

Which antibiotic in pregnant women is associated with acute fatty necrosis of the liver, pancreatitis, and possible renal injury?

A

Tetracycline

120
Q

Which antibiotics should you avoid in pregnancy?

A

Metronidazole, ticarcillin, rifampin, trimethoprim, fluoroquinolones, and tetracyclines

121
Q

What should you think when you hear antifungals?

A

anti-fungal – think drug interactions

122
Q

What are some characteristics of type 1 DM?

A

Before Age 30 (Child)
Abrupt Onset
Requires exogenous insulin to treat
Ketoacidosis prone
Wide fluctuations in BG concentration
Thin body habitus

Altered Human Lymphocyte Antigen on the short arm of chromosome 6
Defect causes “insulinitis”
Autoantibodies may be detected at the time of diagnosis but maybe absent years later.

The pathologic hallmark of T1D has long been considered the inflammatory lesion of the pancreatic islets, which is termed insulitis and is characterized by the presence of immune and inflammatory cells within and around the pancreatic islets 6. Insulitis is the manifestation of the autoimmune attack against beta cells.

123
Q

What are some characteristics of type 2 diabetes?

A

Adult onset: historically
May require exogenous insulin
Not ketoacidosis prone
Relatively stable BG concentration
Obese body habitus

124
Q

How do you diagnose DM?

A

Fasting BS 126mg/dl or greater (usually x 2)

Random BS >200mg/dl

125
Q

What is HgA1C?

A

Measure of the percent of Hgb that has been non-enzymatically glycosylated by glucose on the Beta chain

Normal: 4-6%

ADA recommends <7-8.5% depending on the age of the diabetic patient.

Gives an idea of the degree of control of BG levels over the past 3 months.

Assesses the long-range effectiveness of glucose control.

126
Q

Urinary ketones

A

Monitor patients at risk of going into diabetic ketoacidosis (Type I DM)

Used by patients if they develop symptoms of cold, flu, vomiting, abdominal pain, polyuria, or on finding an unexpectedly high glucose lev

127
Q

What does insulin do to electrolytes?

A

Potassium in
Magnesium in
Phosphorus in
Sodium out

128
Q

Does insulin facilitate glycogenesis, gluconeogenesis, or glycogenolysis?

A

Shift intracellular glucose metabolism toward storage (Glycogenesis)

glycogenolysis - the breakdown of glycogen into glucose. gluconeogenesis - the manufacture of glucose from non carbohydrate sources, mostly protein.

129
Q

When does insulin resistance occur?

A

Occurs when there is an impaired intracellular insulin signal that results in decreased recruitment of glucose transport proteins to the plasma membrane and subsequent decrease glucose uptake.

Compensatory hyperinsulinemia occurs to overcome this resistance

130
Q

When does insulin receptor saturation occur?

Insulin receptors are ______ related to plasma concentrations of insulin

A

Occurs with low circulating concentrations of insulin

Body increases insulin receptors in response to insulin resistance. INVERSELY related to the plasma concentration of insulin.

131
Q

How much insulin does the body secrete per day?

A

Normally release about 1 unit of insulin an/hr… per day about 40-50 units

132
Q

What types of insulin can you give via IV pump?

A

Any short acting

133
Q

What are symptoms of hypoglycemia?

A

Symptoms reflect the compensatory effects of increased epinephrine (body kicks out epi in response to hypoglycemia)(beta blockers hide this and mask hypoglycemia symptoms):
Diaphoresis
Tachycardia
Hypertension

Basically epinephrine’s effects

134
Q

What is re-feeding syndrome?

A

When the body up-regulates insulin receptors in response to not eating in a LONG time and then that person smashes several double quarter pounders and a few kit-kat bars and all those new insulin receptors move in ALL the electrolytes and kicks out sodium and that person dies

135
Q

What defines insulin resistance?

A

Patients requiring > 100 units/day

136
Q

Has immunoresistance been eliminated with the switch from animal insulin to human insulin?

A

YES

137
Q

Method of insulin injection

A

Administer 70% of total dose as intermediate or long acting at bedtime (basal insulin)

Type I DM may require intermediate or long acting insulin in the AM as well

Additional doses (30%) based on meals size

Administer a rapid acting prep before each meal or snack (4 doses)

138
Q

What is inhaled insulin (afreeza) used for?

A

People VERY frightened of injections

139
Q

Can you ever use sliding scale alone?

A

NEVER NEVER use sliding scales alone

140
Q

What are some risks of hyperglycemia?

A

Microangiopathy
Impaired leukocyte function
Cerebral edema
Impaired wound healing
Postoperative sepsis
Hyponatremia

141
Q

Wha are perioperative goals for blood sugar?

A

Optimal BG levels 110-180mg/dl
<150mg/dl for total joints
Glucose infusion if BG decreases to <80mg/dl

Loose control: ¼ to ½ the dose of intermediate or long acting insulin – the last dose prior to procedure
If the procedure is short, may give regular daily dose

Tight control: infusion

142
Q

How do you treat someone with an insulin pump?

A

Prior to surgery clear liquids with or without sugar

Maintain basal infusion rate

Turn off preprandial boluses

Measure BG every hour

Know the typical bolus for the patient to decrease BG 50mg/dl

143
Q

Which class of oral hypoglycemics has the highest risk of hypoglycemia?

A

Sulfonylureas (Ex: Glipizide)

144
Q

What class of oral hypoglycemics have a high rate of failure?

A

Sulfonylureas

sul”fail”ureas

145
Q

Is there any cross-sensitivity with sulfonylureas and sulfa drugs?

A

YES. Not necessarily sulfa antibiotics

146
Q

True/False The risk of hypoglycemia is worse with sulfonylureas in kidney patients because this class is excreted by the kidneys?

A

TRUE

147
Q

Which sulfonylurea is the worst for kidney patients?

A

Glyburide longest acting and most touchY with kidneys GFR LESS THAN 50 CONTRAINDICATED.

148
Q

Which sulfonylurea is the least safe?

A

Glyburide (DiaBeta®, Micronase®):

Gly”bad”uride

149
Q

Which sulfonylurea is the longest lasting and can cause severe hyponatremia?

A

Chlorpropamide (Diabinese®)

Ch”longlasting”rpropamide

150
Q

Which med reduces Absorption of carbs by inhibiting the breakdown of carbs?

A

Alpha- Glucosidase Inhibitors

Acarbose (Precose®)
Miglitol (Glyset®)

151
Q

Which med should you NEVER give while fasting because it secretes insulin?

A

Meglitinides

megliti”nevergivewhilefasting”idines

Repaglinide (Prandin ®)
Nateglinide (Starlix®)

152
Q

Metformin has a black box warning for which of the following side effects?

A

Lactic acidosis

153
Q

What is the #1 med for DM II

A

Metformin

154
Q

Why is metformin great?

A

Decrease BG concentrations with only a very low risk of hypoglycemia.

Have a positive effect on lipid concentrations.

Lead to mild weight reduction in obese pts.

NO weight gain

Risk of hypoglycemia FAR lower

Dec hepatic glucose production
Reduces glucose absorption from the intestine
Increases insulin sensitivity

155
Q

Discontinue metformin _____ days before elective surgery and ____ before contrast dye.

A

48 hours before both…also hold 48 hours post-dye

156
Q

What are the parameters for metformin contraindication?

A

Contraindicated SCr >1.5 (males), 1.4 (females) (old recommendations)

STOP IF Contraindicated eGFR <30 ml/min,

do not initiate for new patients or re-evaluate patients with eGFR <45 ml/min (new recommendations)

Age > 80 years old
Hepatic impairment
CHF

157
Q

What the heck do DPP (Dipeptidyl peptidase)-4 Inhibitors do?

A

Dipeptidyl peptidase-4 (DPP-4) inhibitors block the breakdown of GLP-1 and GIP to increase levels of the active hormones. In clinical trials, DPP-4 inhibitors have a modest impact on glycemic control. They are generally well-tolerated, weight neutral and do not increase the risk of hypoglycemia

158
Q

Which class delays gastric emptying and is made from guila monsters?

A

Amylin analog (GLP-1?)

Amylin analoguila-monster

159
Q

Although sulfonylureas are the worst for hypoglycemia, which other class has a black-box warning for hypoglycemia and causes severe gastroparesis?

A

Amylin analog (GLP-1)?

160
Q

Which class increases urinary excretion of glucose and sodium?

A

SGLT2 Inhibitor

SG”Let it go” T2 inhibitors

Canagliflozin (Invokana)
Dapagliflozin (Farxiga)
Empagliflozin (Jardiance)

161
Q

Which class of med increases the risk of increased risk of perioperative euglycemic ketoacidosis as well as
amputations (primarily toe) AND can cause hypotension??

A

SGLT2 Inhibitor

SGLow ph, low pressure, low toe” T2 inhibitors

Canagliflozin (Invokana)
Dapagliflozin (Farxiga)
Empagliflozin (Jardiance)

162
Q

Which two meds are contraindicated with a GFR under 30?

A

metformin and SGLT2 inhibitors

163
Q

Because of increased risk of ketoacidosis, how long should SGLT2 inhibitors be held prior to surgery?

A

Canagliflozin, dapagliflozin, and empagliflozin should be discontinued 3 days before scheduled surgery.

“C,D,Empa, THREE”

Ertugliflozin should be stopped at least 4 days before scheduled surgery.

“Ertu for EFFORT”

164
Q

What two meds can delay the onset of type 1 diabetes?

A

Teplizumab-mzwv (Tzield) and verapamil

165
Q

Which thyroid med is a combo of T3 AND T4?

A

Armour Thyroid (combo T3&T4)

166
Q

Which thyroid med is just T4, and is the most commonly prescribed med for hypothyroidism?

A

Levothyroxine (T4) (Synthroid®)

167
Q

Which thyroid med is just T3 and has increased cardiovascular side-effects?

A

Liothyronine (T3) (Cytomel®)

168
Q

Here’s a laundry list of anesthetic considerations for patients with hypothyroidism

A

Basically, your body and metabolism are SLOW so meds effect you more…

Increased sensitivity to depressant drugs
Including inhaled anesthetics.

Hypodynamic cardiovascular system.
Decreased CO due to decreased HR and SV.

Slowed metabolism of drugs, particularly opioids.

Unresponsive baroreceptor reflexes.

Decreased intravascular fluid volume.

Impaired ventilatory response to low PaO2 and/or increased PaCO2…

Delayed gastric emptying.

Hyponatremic.

Hypothermic.

Anemic.

Hypoglycemic.

Primary adrenal insufficiency.

169
Q

Which antithyroid meds are useful in treating hyperthyroidism (including thyroid storm) before elective thyroidectomy?

A

Propylthiouracil (PTU)
Methimazole (Tapazole®)

170
Q

What is the oldest effective treatment for hyperthyoid?

A

Iodines:

Lugol’s Solution
Saturated KI solution

171
Q

Here’s the treatment for thyroid storm

A

I.V. infusion of cold crystalloid solns.

Sodium iodide I.V.:
Reduce the release of active hormones from the thyroid gland.

Cortisol I.V.:
Treat acute primary adrenal insufficiency from increased metabolism and use of corticosteroids.

Propranolol I.V.:
Alleviate the cardiovascular effects of thyroid hormones.

Propylthiouracil P.O.:
Reduce the synthesis of new thyroid hormone.

Avoid ASA/NASID for elevated temperature because it may displace thyroxine from carrier proteins.

172
Q

Which oral hypoglycemic may exacerbate hypotension?

A

Canagliflozin (Invokana)

173
Q

Insulin produces all of the following effects except…

A

Stimulate glycogenolysis

174
Q

Which of the following is not significantly shifted intracellularly when insulin binds to its cellular receptors?

A

Sodium

175
Q

SGLT2 inhibitors may increase the risk of perioperative euglycemic ketoacidosis. The FDA recommends stopping this class of medications how many days prior to a procedure to reduce this risk?

A

3 days

176
Q

Which insulin is the most rapid acting?

A

Humalog (Lispro)

177
Q

A patient uses 20 units of Lantus (Glargine) at bedtime and has surgery scheduled in the morning. How much Lantus should be administered the night before the procedure?

A

10 units

178
Q

Reduces absorption of carbs by inhibiting the breakdown of carbs?

Which med should you NEVER give while fasting because it secretes insulin?

A

Alpha- Glucosidase Inhibitors (Acarbose (Precose®)
Miglitol (Glyset®)

Meglitinides (megliti”nevergivewhilefasting”idines)

Amylin analog (GLP-1?) (Amylin analoguila-monster)

179
Q

What percent of inhaled meds actually get to the lungs?

A

12%

180
Q

What order do you give inhaled meds?

A

Give bronchodilators, then anything with a steroid second. Open up lung field to increase surface area

181
Q

What muscarinic receptors act where?

A

M3 – primary in lungs.
M2 in heart.
M4 CNS

182
Q

Is glycopyrrolate used for acute management?

A

NO

Probably for long-term COPD

183
Q

Which agent is most effective in treating bronchospasm due to beta antagonists?

A

Ipratropium (atrovent)

More effective than beta-agonists in chronic bronchitis or emphysema

Duoneb/Combivent ®- in combo with albuterol

184
Q

What are the two main side-effects of inhaled anticholinergics?

A

Narrow angle glaucoma
Urinary retention

185
Q

Are beta-2 agonists metabolized by COMT and MAO?

A

Non-catecholamine structure makes them resistant to COMT. MAO only

186
Q

What are the uses for inhaled beta 2 agonists?

A

Preferred treatment for acute episodes of asthma.

Prevention of exercise-induced asthma.

Improve airflow and exercise tolerance in patients with COPD.

Tocolytic to stop premature uterine contractions.

Treatment of hyperkalemia

187
Q

What is the preferred treatment for acute episodes of asthma?

A

Inhaled beta 2 agonists

188
Q

Which med is inhaled epinephrine?

A

Primatene Mist

189
Q

Isoproterenol

A

Non-selective sympathomimetic
Act at Beta1 and Beta2 receptors.

Highly pro-arrhythmic.

190
Q

What is the preferred Beta2 agonist for acute bronchospasm?

A

Albuterol

191
Q

Why were short acting beta agonists made? Meds like levoalbuterol and metaproterenol?

A

Made because of “less cardiostimulatory effects”…for people with a-fib, etc…

192
Q

What is terbutaline and ritodrine?

A

Tocolytic- reduces contractions to postpone labor for hours to days – used in O.B

193
Q

What are beta-2 agonists also used for?

A

Treating hyperkalemia….they cause hypokalemia

They also CAUSE hyperglycemia

194
Q

Which class of medication is unsafe to use as monotherapy due to an increased risk of asthma related death?

A

Long acting beta agonist (LABA)

195
Q

Which class of med is used in prophylactic treatment of bronchial asthma and has
no role in the treatment of established (acute) bronchoconstriction?

A

Membrane Stabilizers like cromolyn sodium

196
Q

What are methylxanthines?

A

Theophylline/Aminophylline
Caffeine
Theobromine

They are non-selective Phosphodiesterase Inhibitors and inhibit all fractions of PDE isoenzymes

Stimulate the CNS.

Inc BP

Increase myocardial contractility and heart rate
PDE3

Relax smooth muscle (airways). PDE4

197
Q

Which methylxhanthine is used for treatment of bronchospasm due to acute exacerbation of asthma and has various toxicity levels associated with v-tach and seizures?

A

Theophylline

15-25 mcg/ml: GI upset, N/V, tremor
25-35: Tachycardia, PVCs
> 35: VTach, seizures

198
Q

Caffeine

A

Adenosine releases Gaba leading to drowsiness. Caffeine blocks adenosine leading to less GABA.

Vasoconstriction from adenosine A1 effects…helps headaches by constricting..

199
Q

Histamine receptors

A

4 types, but drugs typically target H1 and H2

Benadryl plus Pepcid to combat the H1 AND H2 receptors..have to give both

200
Q

H-1 Receptors

A

Evoke smooth muscle contraction in the respiratory and G.I. tracts.

Cause pruritus and sneezing by sensory nerve stimulation.

Causes nitric oxide mediated vasodilitation.

Slow the heart rate by decreasing A-V nodal conduction.

Mediate epicardial coronary vasoconstriction.

201
Q

H-2 Receptors

A

Activates adenyl cyclase and increases intracellular cAMP.
Activates proton pump of gastric parietal cells to secrete hydrogen ion.

Increase myocardial contractility and heart rate.
Vasodilating effects on coronary vasculature opposes the vasoconstricting effects of H1 receptors.

With H1 receptors increase capillary permeability and vasodilitation.

202
Q

H-2 Receptors

A

Activates adenyl cyclase and increases intracellular cAMP.
Activates proton pump of gastric parietal cells to secrete hydrogen ion.

Increase myocardial contractility and heart rate.
Vasodilating effects on coronary vasculature opposes the vasoconstricting effects of H1 receptors.

With H1 receptors increase capillary permeability and vasodilitation.

203
Q

Which histamine receptors do you need to completely block to block the vasodilatory effects?

A

Need H1 and H2 blockers

204
Q

What is the triple response (wheel and flare)?

A

Edema due to increased permeability.

Dilated arteries around the edema (Flare).
Due to histamine stimulating nerve endings.

Pruritus due to histamine in the superficial layers of the skin.

205
Q

H1 vs H2 on airway

A

H1 constricts, H2 relaxes

206
Q

What is the difference between the two generations of H1 receptor antagonists?

A

The first generation is more sedating and have anticholinergic effects and have more QT prolongation

207
Q

What are H1 clinical uses?

A

prevent allergic rhinitis, antipruritic, sedative, antiemetic, some protection against bronchospasm

208
Q

What are H1 clinical uses?

A

prevent allergic rhinitis, antipruritic, sedative, antiemetic, some protection against bronchospasm

209
Q

Does having Benadryl on board make for a difficult reversal with naloxone?

A

YEP

210
Q

What is Dimenhydrinate (Dramamine®) used for?

A

Used to treat motion sickness and PONV.

211
Q

What are some 2nd generation antihistamines?

A

Zyrtec/Xyzal = Cetirizine/Levocetirizine

Claritin= Loratidine

Allegra: Fexofenadine

212
Q

What is the closest thing we have to cortisol?

A

Hydrocortisone

213
Q

Tell me about aldosterone..

A

Secreted secondary to inc K, dec Na, dec BP/fluid volume

Renin -> AG1 -> AG2 -> Aldosterone

Effects:
K excretion
Na retention
Increase water retention, increase blood volume

renin released from the kidney, angiotensinogen released from the liver…renin acts on angiotensinogen to make angiotensin 1…ACE acts on angiotensin 1 to make angiotensin 2…angiotensin 2 acts on the adrenal gland to make aldosterone..aldosterone acts on the kidney to absorb NA and water! yay! go fuck yaself!

214
Q

What is another name for primary adrenal insufficiency, and what is happening with it?

A

Addison’s Disease

Adrenals do not secrete cortisol or aldosterone

Replacement therapy must include glucocorticoid and mineralocorticoid (must include both)

215
Q

What is secondary adrenal insufficiency?

A

Due to chronic steroid use and suppression of the H-P-A axis.

Aldosterone secretion maintained

Replacement usually requires only glucocorticoid (anti-inflammatory)

216
Q

Glucocorticoids have a _____ effect while mineralocorticoids have a _____ effect

A

glucocorticoids are anti-inflammatory

mineralocorticoids reabsorb NA for K excretion

217
Q

Which steroids are naturally occurring?

A

Cortisol (hydrocortisone)
Cortisone
Corticosterone
Desoxycorticosterone
Aldosterone

218
Q

Which steroids are synthetic?

A

Glucocorticoids:
Prednisolone
Prednisone
Methylprednisolone
Betamethasone
Dexamethasone
Triamcinolone

Mineralocorticoids:
fludrocortisone

219
Q

What is the antiinflammatory:NA absorbent (glucocorticoid:mineralcorticoid) relationship for cortisol?

A

Cortisol (hydrocortisone) has 1:1 effect

220
Q

Anti-inflammatory alone AND mixed

A

anti-inflammatory only:
dexamethasone, betamethasone, triamcinolone

Both:
cortisol, cortisone, prednisolone, prednisone, methylprednisolone

fludrocortisone does both but WAY more sodium retaining

221
Q

Which of the following has both anti-inflammatory and mineralocorticoid effects?

A

Methylprednisolone

Also, cortisol, hydrocortisone, prednisone, prednisolone, methylprednisone

222
Q

Which corticosteroid has WAYYYYY more NA retaining (mineralocorticoid) properties than anti-inflammatory (glucocorticoid)?

A

FLUDRACORTISONE

10:125

223
Q

Do we need to taper steroids?

A

YES we need to stop steroids SLOWLY or they will go into an adrenal crisis

224
Q

Which is an absolute contraindication for corticosteroid use?

A

None of the above!!

Answers:
A.
Hyperglycemia

B.
Edema

C.
Infection

CorrectD.
None of the above

225
Q

What are the electrolyte changes with corticosteroids?

Hint: this also happens with thiazides and loop diuretics

A

Hypokalemic Metabolic Alkalosis:
Mineralocorticoid effect of cortisol on distal renal tubules leading to enhanced absorption of Na+ and loss of K+

226
Q

What do corticosteroids do regarding blood sugar?

A

Promote hepatic gluconeogenesis

Resultant hyperglycemia may require diet, insulin, or both to manage

227
Q

What does taking too may steroids do to the body?

A

CUSHINGS DISEASE YUCK

Redistribution of body fat:
Deposition on back (buffalo hump), supraclavicular, and face (moon facies)
Loss of fat from the extremities

228
Q

What can happen if you give even small doses of glucocorticoids to children?

A

Arrest of growth can result from the administration of relatively small doses of glucocorticoids to children

229
Q

Why do surgeons care about giving steroids intraoperatively?

A

Masking infection or further complicating surgery intended to treat infection

Altering glucose control in diabetics

Aseptic necrosis of the femoral head

Failure of bone fusion

230
Q

HPA suppression

A

Therapies unlikely to suppress H-P-A Axis:

Prednisone 5mg/day or less or 10 mg QOD
Long term every other day dosing associated with less suppression
Glucocorticoids, any dose < 3 weeks does not clinically suppress the H-P-A Axis

Prednisone or Dexamethasone (even physiologic doses) given as a single daily dose at bedtime is associated more commonly with H-P-A Axis suppression
Bedtime dosing more commonly associated

Therapies assumed to suppress H-P-A Axis (absolutely yes it will):

Prednisone 20mg/day (or equivalent) for > 3 weeks within the previous year

Patient with clinical signs of Cushing Syndrome from any steroid dose

No need to test the H-P-A Axis in these patients, just supplement with stress dose steroids

Therapies that may or may not suppress H-P-A Axis:
> 5mg/day but < 20mg/day of prednisone (or equivalent) for > 3 weeks the previous year
May have suppression of the H-P-A function depending on:
Dose
Duration
Individual patient
*After cessation of steroid therapy, recovery of the H-P-A function can take 12 months or longer
H-P function returns to normal before adrenal function
Options:
Test for responsiveness of the adrenals if time permits
Cosyntropin (ACTH) stimulation test
Give stress doses of glucocorticoids prophylactically (assume suppressed)

231
Q

Do burns or sepsis increase the need for steroids?

A

YES they surely do

232
Q

Signs and Symptoms of Acute Adrenal Crisis

A

Hypotension unresponsive to vasopressors
Hypoglycemia
Hyponatremia
Hypovolemia

Hyperdynamic circulation
Hyperkalemia

Metabolic acidosis
Decreased level of consciousness

Pharm Final review (24 decks)

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