Final Review Flashcards

1
Q

Which generation of Cephalosporins will cross the BBB?

A

Cephalosporins 3rd Generation

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2
Q

What generation of Cephalosporins will treat Meningitis?

A

Cephalosporins 3rd Generation

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3
Q

What is an example of a 3rd generation cephalosporin?

A

Ceftrixone/Rocephin

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4
Q

How are the 2nd generation cephalosporins eliminated?

A

All by the kidneys

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5
Q

What is an example of the 2nd generation cephalosporin?

A

Cefoxitin/Mifoxin

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6
Q

Which generation of cephalosprorins are inexpensive and exhibit low toxicity?

A

1st generation cephalosprorins

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7
Q

Cephalosproins - About 95% of patients allergic to penicillin form what conjugate? (hint: this is the major antigenic determinant)

A

Penicilloyl-protein conjugate

The remaining allergic patients form 6-aminopenicillic acid and benzylpenamaldic acid (minor antigenic determinants)

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8
Q

Cross-Reactivity cephalosporins and PCN are rare, although they share a common (BLANK) ring

A

B-Lactam Ring

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9
Q

How long before the surgical incision should the prophylactic antimicrobial be administered? According to SCIP-1

A

SCIP-1 recommends that prophylactic antimicrobials should be administered IV 1 hour before surgical incision

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10
Q

According to SCIP-2, the ABX chosen should be appropriate for what two things?

A

Type of surgery and patient characteristics

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11
Q

SCIP-7 states that anesthesia contributes to what?

A

SCIP-7 Anesthesia contributes to “normothermia”

Hypothermia will result in peripheral vasoconstriction, decreased wound oxygen tension and recruitment of leukocytes, favoring infection and impaired healing.

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12
Q

PCN interferes with the synthesis of (BLANK), which is an essential component of the cell wall

A

Interfere with synthesis of PEPTIDOGLYCON which is an essential component of cell wall

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13
Q

PCN decrease s the availability of an inhibitor of (BLANK) such that the uninhibited enzyme can then destroy (lyse) the structural integrity of bacterial cell walls

A

Decrease the availability of an inhibitor of MUREIN HYDROLASE such that the uninhibited enzyme can then destroy (lyse) the structural integrity of bacterial cell walls

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14
Q

Cell membranes of resistant gram-negative bacteria are in general resistant to penicillin’s because (what)?

A

Cell membranes of resistant gram-negative bacteria are in general resistant to penicillin’s because they prevent access to sites where synthesis of peptidoglycan is taking place

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15
Q

Large doses of Clindamycin can cause what?

A

Large doses can inducce NMB in the absence of a non-depolarizer

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16
Q

What are the SE of clindamycin?

A

Pseudomembranous colitis, diarrhea, skin rash

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17
Q

You need an echo before someone takes Doxorubin, why?

A

CausesCardiomyopathy- dose related increased plasma concentrations of troponin T (late), CHF, LV dysfunction***(

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18
Q

Why are we considered with someone taking Bleomycin?

A

Pulmonary toxicity- dose related 4% patients*****

SE include Cough, dyspnea, rales, fibrosis, infiltrates

Mgt: FIO2 <30%, SpO2 >90%, decrease fluids

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19
Q

What are the clinical signs of Red Man Syndrome?

A

Clinical signs: flushing, erythema, and pruritus. Affects upper body, neck and face > lower body. Myalgia, dyspnea and hypotension.

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20
Q

What is Red Man Syndrome?

A

Not a true allergy. Dose dependent infusion reaction. Vancomycin can act on mast cells and releases histamine.

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21
Q

What is the management of Red Man Syndrome?

A

Management: stop infusion administer an antihistamine and restart at a lower rate when symptoms subsides.

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22
Q

SE of vanco are what?

A
  • Hypotension
  • Cardiac arrest
  • Histamine release
  • Red Man Syndrome
  • Erythema
  • Bronchospasm
  • Arterial hypoxemia/ low SPO2
  • Ototoxocity & nephrotoxicity with given with aminoglycoside*
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23
Q

What happens when you give Vanco and succs?

A

can result in NMB (will act like a Phase II neuromuscular blockade)

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24
Q

What are the SE of Gentamicin?

A
  • Ototoxicity**
  • Vestibular and auditory
  • Nephrotoxicity
  • Skeletal muscle weakness
  • Contraindicated in Myasthenia Gravis patients
  • Potentiation of non-depolarizing neuromuscular blocking drugs*
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25
Q

What are the SE of Aminiglycoside?

A
  • Ototoxicity**
  • Vestibular and auditory
  • Nephrotoxicity
  • Skeletal muscle weakness
  • Contraindicated in Myasthenia Gravis patients
  • Potentiation of non-depolarizing neuromuscular blocking drugs*
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26
Q

Calvulanic Acid MOA?

A

Bind irreversibly to the β-lactamase enzymes, which are produced by many bacteria, thus inactivating these enzymes and rendering the organisms sensitive to β-lactamase–susceptible penicillins

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27
Q

Why are cephalorsporins used? (not asking what they treat)

A

The are cost effective

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28
Q

Patient on Bleomycin, what should the intraop FiO2 be?

A

FIO2 <30%, SpO2 >90%, decrease fluids

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29
Q

Patient on Mitomycin, what should the intraop FiO2 be?

A

Low FiO2 perhaps < 40%

Induces pulmonary fibrosis w/ hyperoxia and thoracic radiation. Limit the inspiratory pressure to not more than 30 mmHg, limit the tidal volume to not more than 8 ml/kg to avoid barotrauma and volutrauma.

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30
Q

What is Serotonin syndrome?

A

Cluster of autonomic, motor and mental status changes resulting from excess 5-HT

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31
Q

What happens when you give Meperidine with someone taking an MAOi?

A

Administration of meperidine to a patient treated with MAO inhibitors may result in an excitatory (type I) response (agitation, headache, skeletal muscle rigidity, hyperpyrexia) or a depressive (type II) response characterized by hypotension, depression of ventilation, and coma*****

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32
Q

How is Mannitol eliminated?

A

Its only means of clearance from the plasma is by glomerular filtration**

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33
Q

HCTZ SE?

A

a. Hypo K, Cl, and metabolic alkalosis with chronic HTN usage
b. Increase risk of digitalis Toxixity
c. Cardiac Dysrhythmia due to Hypo K and Hypo Mag
d. Hyper Ca
e. Potentiate NMB
f. Increase Lithium levels
g. Glucose intolerance
h. Increase lipedema
i. Poss cross reactivity with sulfa allergy due to structure

34
Q

What is the clinical use of Spironolactone?

A

HTN with Thiazide diuretics in pt with low renin state or metabolic syndrome

Refractory HTN

iPromotes diuresis in liver cirrhosis, nephrotic syndrome, and heart failure

Decreases cardiac morbidity and mortality

35
Q

What is the SE of Spironolactone?

A

Hyper K esp with impaired renal function esp with spironolactone

Nonspecific mineralocorticoid receptor antagonist

Spironolactone and ACE inhibitor can exacerbate K

Block androgen and progesterone receptor leading to gynecomastia and breast tenderness

36
Q

MOA of Thiazide?

A

i. Inhibit the Na+-Cl− cotransporter in the cortical portion of the ascending loop of Henle and the distal convoluted tubule, inhibiting reabsorption of 5% to 10% of the filtered sodium
ii. Enhanced distal delivery of Na+ results in increased excretion of potassium into the renal tubules, resulting in an increase in the urinary excretion of Na, Cl, and K ions.
iii. In addition, thiazide diuretics stimulate the reabsorption of Ca in the distal convoluted tube

37
Q

Acetazolaminde is used to Tx what?

A

Reduces intraocular pressure/ Glaucoma**

Altitude sickness**

38
Q

Lithium SE

A

i. Polydipsia and Polyuria most common SE
ii. Hypothyroid- Women
iii. SA Node dysfunction (Pt with SSS contraindicated)
iv. Hand tremor w/ Beta antagonist
v. EPS Effects Rare
vi. T wave inversion- rare
vii. Acne & Psoriasis
viii. Cognitive dysfunction

39
Q

What happens with anesthesia and someone who is taking Lithium?

A

i. Decreased anesthesia requirements
ii. High levels of Lithium may delay recovery from CNS depressant effects of barbiturates
iii. Depolarizing and non-depolarizing blocking drugs may be prolonged

40
Q

What kind of diet does a patient need to be on if they are taking an MAOi

A

Tyramine free diet due to SE HTN*

41
Q

What is Anticholinergic Syndrome?

A
AMS
Mydriasis
Flushed Skin
Dry skin
Dry mucous membranes
42
Q

What is the black box warning for the SSRI?

A

SUICIDAL TENDENCIES IN CHILDREN and ADOLESCENTS

43
Q

What is Neuroleptic Malignant Syndrome?

A

Normal pupils, drooling, pallor, lead-pipe rigidity, hyporeflexia, alert mutism, coma

44
Q

What is the MOA of MAOi?

A

Block the enzyme that metabolizes biogenic amines, increasing the availability of these neurotransmitters in the CNS and peripheral autonomic nervous system**

45
Q

What is the MOA of Spirionolactone?

A

Prevent the synthesis and the activation of the aldosterone-dependent basal cell Na+-K+-ATPase pump.

Both mechanisms result in decreased Na+ reabsorption without the increased K+ secretion that would otherwise occur

46
Q

What will Spironolactone and ACEi do, if given together?

A

Spironolactone and ACE inhibitor can exacerbate K

47
Q

Amitriptyline SE

A

causes ANTICHOLINERGIC- esp at high doses

Amitriptyline causes highest risk of

  • Dry mouth, blurred vision, Tachy, urinary retention, delayed gastric emptying
  • Elderly more sensitive to anticholinergic effects and anticholinergic delirium at normal doses
  • Anticholinergic toxicity if given w/ other anticholinergic meds ( diarrhea and insomnia meds OTC)
48
Q

Baclofen SE

A

Sedation, confusion, skeletal muscle weakness

49
Q

How much will lipid lowering drugs lower LDL?

A

Lowers LDL 20-60%**

50
Q

Most studies suggest (which drugs?) should be continued during the perioperative period, the risk of myopathies is small and the benefits outweigh the risks**

A

Statins

51
Q

SE of Statins

A

i. Liver toxicity (elevation of transaminases) in a dose related fashion
ii. Rhabdomyolysis increases in proportion to dose and plasma concentration
iii. Factors that inhibit statin catabolism, age, hepatic or renal dysfunction, perioperative periods & untreated hypothyroidism
iv. CYP3A inhibitors can increase statin levels in blood causing harmful side effects
v. Drugs likely to be administered during anesthesia, including succinylcholine, have NOT been shown to increase the incidence of statin-induced myopathy.

52
Q

Clinical uses for Caffeine?

A

i. Neonates apnea of prematurity
ii. Post-dural headache
iii. Common cold

53
Q

MOA of caffeine in infants?

A

Primary apnea of prematurity by stimulating medullary respiratory centers by increasing the sensitivity of these centers to carbon dioxide*

54
Q

What are the adverse SE of Phenytoin?

A

Adverse side effects of phenytoin such as nystagmus, diplopia, vertigo and ataxia are likely when the plasma concentration of drug is >20 µg/mL

55
Q

Phenytoin induces what drugs?

A

Induces lipid soluble drugs carbamazepine, valproic acid, ethosuximide, anticoagulants, and corticosteroids

Neurotoxic effects

56
Q

If someone is on Phenytoin, what should you be concerned with someone taking an oral contraceptive?

A

Oral contraceptive ineffective.

57
Q

If someone is on Phenytoin, what should you keep in mind when you use a paralytic?

A

Need higher doses of non-depolarizing muscle relaxants

58
Q

What does Dozapram do to Minute ventilation?

A

Centrally acting analeptic that selectively “increases minute ventilation” by activating the carotid bodies***

59
Q

What is the dose for Datrolene?

A

2.5MG/KG IV,UNTIL SYMPTOMS SUBSIDE OR A CUMULATIVE DOSE OF 10MG/KGIV IS REACHED.

60
Q

What is the SE of Datrolene?

A

Review labs for liver dysfunction

Poss Hepatotoxicity***

61
Q

MOA for Dantrolene?

A

Binds to the ryanodine calcium channel and reduces Ca efflux from the sarcoplasmic reticulum counteracting the abnormal intracellular Ca levels accompanying MH

62
Q

What receptor does cocaine inhibit?

A

Inhibits NE reuptake

High abuse potential due to euphoric effects caused by inhibition of catecholamine uptake specially dopamine

63
Q

What is the MOA of Phenobarbital? (effects which two things)

A

Partly through potentiation of the postsynaptic actions of the inhibitory neurotransmitter GABA and inhibition of the excitatory postsynaptic actions of glutamate

Prolong Cl channel opening limits the spread of seizure activity and increase seizure threshold

64
Q

What is the drug of choice for Status Epilepticus?

A

Diazepam

First line drug for status epilepticus and LA induced seizures

can be given IV or rectal

65
Q

MOA for Sulfonylurea

A

i. Sulfonylurea receptors are found on pancreatic and cardiac cells.
ii. These drugs inhibit adenosine triphosphate–sensitive potassium ion channels (now known as the sulfonylurea receptor-1) on pancreatic β cells.
iii. As a result, there is an influx of calcium and stimulation of exocytosis (release) of insulin storage granules.
iv. Although sulfonylureas decrease insulin resistance, this effect is minor, if at all, in decreasing blood glucose concentrations.

66
Q

SE of Dantrolene

A

Review labs for liver dysfunction

Poss Hepatotoxicity***

67
Q

What is the Tx for DI?

A

i. DDAVP or Vasopressin V2
ii. Chlorpropamide (sulfonylurea hypoglycemic agent)
iii. Carbmazepine (anticonvulsant)
iv. Thiazide diuretics

68
Q

DoA for Levothyroxine?

A

Long ½ life 7- 10 days

69
Q

MOA for Mineralocorticoid (aldosterone), where does it work in the renal tubular system?

A

Evokes distal renal tubular reabsorption of Na in exchange for K ions

Receptors present in distal renal tubules, colon salivary glands and hippocampus

Protects volume status via the Renin-angiotensin-aldosterone system

70
Q

What happens in Cushing Syndrome? (Glucocorticoid Excess)

A

i. Excess glucocorticoid hormones (Cortisol) from overproduction of adrenal cortex or exogenously administered
ii. ACTH dependent causes pituitary adenoma and ectopic secretion of ACTH non pituitary tumor
iii. ACTH independent causes adrenal tumor, adrenal carcinoma
iv. Iatrogenic causes supraphysiologic doses of glucocorticoids for arthritis, allergies and asthma- most common cause

71
Q

DoA of T3

A

Rapid onset and short duration

Used for long term replacement

72
Q

Aldosterone is a Mineralcorticoid that has no glucocorticoid action***.

It is released by the kidneys in response to what?

A

Released by the kidney in response to hypovolemia, SNS, hypotension and hyponatremia.

Aldosterone is a Mineralcorticoid no glucocorticoid action.***

73
Q

SE of Cushings

A

Red cheeks, moon face, Buffalo hump, thin skin, high B.P., pendulous abdomen, red striation, poor wound healing

74
Q

Patients taking greater than (what dose of prednisone) or its equivalent for more than 3 weeks have a suppressed HPA axis.* (will prob get stress dose)

A

20 mg per day of prednisone

75
Q

Patients taking less than (what dose of prednisone) or its equivalent can be considered not to have suppression of their HPA axis.* (prob not get a stress dose)

A

5 mg per day of prednisone

76
Q

What is the Tx for SIADH

A

Treatment**
Fluid restriction 0.9% normal saline 800-1000 ml per day

If patient symptomatic of Na 115-120 mEq/L consider hypertonic saline

77
Q

What are the two Posterior pituitary hormones?

A

a. Arginine Vasopressin (AVP)/ADH

b. Oxytocin

78
Q

What is the Acromegaly hormone?

A

a. Hypersecretion of GH usually caused by GH secreting pituitary adenoma 99% of the time
b. Somatotropin

79
Q

What is the Tx for Conn Syndrome?

A

Treatment

  • Surgical removal of adenoma
  • Medical Management
  • K supplement
  • HTN drugs
80
Q

What are the manifestations for Conn Syndrome?

A

HYPERsecretion of aldosterone from an adrenal adenoma independent of stimulus*

Manifestations
iSystemic HTN with coexisting HYPOkalemia

81
Q

What is the pre op considerations for Metformin?

A

Serious SE Lactic acidosis***

For this reason, some have recommended discontinuing metformin 48 hours or longer before elective operations