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Hospital Medicine > Hospital Med > Flashcards

Hospital Med Flashcards

1
Q

What are the 4 different types of hospital admissions?

A
  1. In patient
  2. Observation
  3. Outpatient in bed
  4. General inpatient (hospice)
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2
Q

What are the components of a hospital admission? (6)

A
  1. Ambulance record
  2. Prior-hospitalizations
  3. Outpatient records, notes, labs
  4. Meds
  5. Examine patient
  6. Admit the pt (med rec, orders, documentation)
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3
Q

What are things to consider when discharging a patient?

A
  1. Where will they go?
  2. family dynamics
  3. Environmental factors (weather)
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4
Q

What are some manifestations of AKI? (4)

A
  • frequently astmptomatic
  • edema
  • HTN
  • decreased UO
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5
Q

What are some lab manifestations of AKI?

A
  • albumineria
  • increased BUN
  • hyperK
  • hypoK
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6
Q

What are 2 ways to prevent AKI?

A
  • Sustain renal perfusion

- don’t clog the pipes (preparation for contrast due, aggresive IVF in presence of hemolysis/rhabdo)

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7
Q

What is the most important step in managing AKI?

A

identify the cause!

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8
Q

What are 3 other ways to manage AKI?

A
  1. meticuous management of intake (water- UO and 500mL, phosporus monitoring (calcinosis- aluminum containting p-binders)
  2. renal consult
  3. dialysis
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9
Q

What are 3 criteria used to stage AKI?

A
  1. RIFLE (risk, injury, failure)
  2. AKIN (AKI network)
  3. KDIGO:
    - rise in cr more than 0.3
    - decrease in UO (less than 3 over 6 hours)
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10
Q

What is the most often cause of prerenal azotomia?

A

inadequate perfusion

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11
Q

What are 3 ways of inadequate perfusion?

A
  1. Hypovolemia
  2. Oliguric
  3. prolonged renal ischemia
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12
Q

What are 4 manifestations of renal azotemia?

A
  1. glomerulonephritis
  2. nephrotoxins
  3. Nephritis (immune modulated)
  4. minimal change disease (nephrotic syndrome)
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13
Q

What are some nephrotixic conditions? (6)

A
  • ischemia
  • radiocontrast
  • toxins
  • DIC
  • intrinsic obstruction
  • intrarenal precipitation (Ca, etc)
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14
Q

Which kidney disease is immune-modulated?

A

Nephritis

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15
Q

What is the usual culprit of post-renal azotemia?

A

urinary obstruction

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16
Q

What are 4 ways of getting urinary obstruction?

A
  • prostatism
  • tumors
  • calculi
  • urethral obstruction
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17
Q

What are 4 comorbidities that can lead to CKD?

A
  • AKI
  • HTN
  • DM
  • Vascular disease
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18
Q

What is microalbumineria defined as?

A

30-300 mg/day albumin

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19
Q

What are spot urine albumin/cr ratios?

A
  • 17-250 men

- 25-355 women

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20
Q

What GFR qualifies as stage 1 CKD?

A

GFR over 90

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21
Q

What qualifies as stage 2 GFR?

A

GFR 60-89

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22
Q

What qualifies as stage 3A?

A

GFR 45-59

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23
Q

What is 3B CKD?

A

30-44

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24
Q

What is stage 4 CKD?

A

15-29

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25
Q

What is stage 5 CKD?

A

Under 15

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26
Q

How to manage somone with CKD inpatient to avoid AKI?

A
  1. Diet (low Na, protein, K, P)
  2. Avoid nephrotoxins (NSAIDS, radiocontrast)
  3. water management (THINK about IVF)
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27
Q

What are some causes of HYPERkalemia? (8)

A
  1. AKI/CKD
  2. adrenal insufficiency
  3. dietary intake (potatoes, bana)
  4. hemolysis (blood draw, clottin
  5. Metabolic acidosis
  6. BB
  7. insulin deficiency
  8. aldosterone antagonists
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28
Q

What clinical manifestations of HYPERk?

A
  • weakness
  • paralysis
  • cardiac arrythmias (peaked T)
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29
Q

How do you treat HYPERk?

A
  • Treat the cause
  • IVF
  • kayexalate (if not hypovolemic)
  • limit K intake
  • insulin + dextrose (dextrose so they don’t get hypoglycemic)
  • Beta-adrenergics
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30
Q

what does HYPOmagnesia cause?

A

HYPOk

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31
Q

What are other causes of HYPOk? (8)

A
  1. decreased intake
  2. diuretics
  3. diarrhea
  4. laxatives
  5. insulin
  6. beta-agonists
  7. stress hypothermia
  8. alkalosis
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32
Q

What are clinical manifestations of HYPOk?

A
  • weakness/rhabdo
  • glucose intolerance
  • cardiac arrhythmias
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33
Q

How do you treat HYPOk?

A
  • potassium replacement
  • PO vs IV
  • Mg replacement (ALWAYS CHECK MAGNESIUM!)
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34
Q

How do you dx HYPERna?

A

urine osmolality

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35
Q

What do you think if urine osmolality is low (under 150?)

A

diabetes insipidus

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36
Q

What do you think if urine osmolality is high? (over 300)

A

osmotic diuresis

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37
Q

How do you treat hyperNA?

A
  1. NS initially if volume depleted
  2. transition to 1/2 NS and 1/2 D5
  3. Avoid correction faster than 0.5/L/hr to avoid cerebral edema
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38
Q

What is diabetes insipidus?

A

low ADH

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39
Q

What is an iatrogenic way of giving someone hyperna?

A

1 amp bicarb

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40
Q

What is generally associated with elevated ADH?

A

hyponatermia

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41
Q

What is hyperosmolar hyponatremia?

A

Elevated levels of another osmolyte (glucose, proteins, lipids)

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42
Q

What type of hypoNA does SIADH generally cause?

A

euvolemic hypoNA

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43
Q

What does CHF/cirrhosis typically cause?

A

hypervolemic hypoNA

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44
Q

What can cause hypovolemic hypoNA?

A
  1. Extra-renal losses(vomiting, diarrhea, dehydration)

2. Renal losses (thiazides, adrenal insufficiency)

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45
Q

What is the risk of correcting hypnatremia too quickly?

A

osmotic demyelination syndrome

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46
Q

What are common causes of ADH elevation in hospitalized patients (7)?

A
  1. Pain
  2. Volume depletion
  3. Trauma
  4. Medications (SSRIs, thiazides)
  5. neoplasm
  6. severe nausea
  7. neuropsychiatic meds
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47
Q

Who can present atypically with MIs?

A
  • women
  • elderly
  • diabetics (NAUSEA)
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48
Q

How long does it take for troponins to show up?

A

6 hours

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49
Q

How soon do you want to get an EKG someone with a suspected ACS?

A

w/n 10 minutes

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50
Q

Who is at risk for ACS? (6)

A
  1. ST elevation/new LBBB
  2. ST depression/T-wave inversion
  3. Chest pain w/hemodynic instability
  4. dynamic EKG changes
  5. known CAD w/reminiscent pain
  6. high risk hx pos/neg troponins
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51
Q

Who is at moderate risk for ACS? (4)

A
  1. atypical CP w/CAD and normal/unchanged EKG
  2. CP with nonspecific ST depression (dominant R leads)
  3. Low risk hx w/normal EKG and positive troponins
  4. Angina patient with rest angina w/spontaneous resolution or promptly after NTG
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52
Q

Who is at low risk?

A

atypical chest pain with atypical

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53
Q

What is the tx plan for someone with an uncertain CP dx?

A
  1. Admission
  2. MONA (morphine, oxygen, nitro, ASA)
  3. ACLS prn
  4. CBC, electrolytes (K and Mg– arrhythmias!)
  5. Troponin (serial check)
  6. telemetry
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54
Q

How do you tx someone with a known STEMI/UAP?

A
  1. MONA
  2. ASA/antiplatelet agents
  3. P2Y12-R blocker
  4. BB (long-term CHF)
  5. heparin
  6. statin
  7. If CHF- diuretics, NTG IV
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55
Q

What are the criteria used to determine patients TIMI score? (7)

A
  1. over 65
  2. over 3 risk factors for CHD
  3. Prior coronary stenosis (over 50 percent)
  4. ST deviation on admit EKG
  5. Over 2 anginal episodes in 24grs
  6. elevated cardiac biomarkers
  7. Use of ASA in prior 7 days
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56
Q

What does the TIMI tell you?

A

2 week risk of death, new/recurrent MI or severe recurrent ischemia requiring revascularization

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57
Q

Do you get TTE or TEE for afib?

A

TTE

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58
Q

When would you get TEE for afib?

A

indicated for presence of LA thrombus

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59
Q

What are benefits of rhythm control for afib tx?

A
  • optimal CO

- improve LV function

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60
Q

What are adverse effects of rhythm control

A
  • high chance of recurrence of afib
  • pro-arrhytmia
  • lots of SE
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61
Q

Who are good candidates for rhythm control?

A
  1. younger, more active patients
  2. pts with contraindication for anticoag
  3. patient who rate is uncontrollable and or can’t tolerate AF
  4. patients who REQUEST IT
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62
Q

What are different options for rhythm control?

A
  1. DC cardioversion (if afib for over 48 hours, 3-4 weeks full anticoag first)
  2. pharm (amiodarone, flecainide)
  3. non-pharm (MAZE procedure, radiofrequecy, catheter ablation)
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63
Q

What are meds you can give for rate control?

A

diltiazem. verapamil, digoxin

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64
Q

Why do you have to watch out for with CCBs?

A

hypotension!

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65
Q

How does digoxin work?

A

slows HR and INCREASES CO

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66
Q

What are high risk factors that increase a patients stroke risk with chronic AF?

A
  • Over 65yo
  • hx stroke
  • DM
  • HTN
  • CHF (LV dysfunction)
  • Increased LA size
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67
Q

What are some low risk factors for stroke risk in patients with chronic AF?

A
  • Under 60

- heart disease with preserved LV function, normal LA size

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68
Q

What is the CHAD score used for?

A

to determine if a patient should be anticoagulated

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69
Q

What are the components of CHAD score? (8)

A
  1. CHF (1 point)
  2. HTN (1 point)
  3. Over 75yo (2 points)
  4. DM (1 point)
  5. Stroke/TIA/TE (2 points)
  6. Vascular disease (prior MI/PAD) (1 point)
  7. Age 65-74 (1 point)
  8. Female (1)
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70
Q

What should you do with someone with a CHAD score of 1?

A

consider anticoag

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71
Q

What should you do with someone with a CHAD score od 2 or higher?

A

anticoag

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72
Q

what is a benefit of novel anticoag agents?

A

no bridging needed!

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73
Q

What are precipitating causes of acute CHF?

A
  1. IVF (main culprit)
  2. medication adjustments/erros
  3. Transfusion
  4. post-op
  5. afib
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74
Q

What classifies systolic heart failure?

A

EF under 40 percent

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75
Q

What classifies diastolic HF?

A

impaired relaxation

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76
Q

What is acute management of CHF?

A
  1. IV diuretic
  2. O2
  3. NTG SL
  4. Morphine
  5. Na restriction
  6. Fluid restriction
  7. AVOID NSAIDS
  8. Avoid empiric use of antiarrhythmics
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77
Q

When should you get a consult for CHF?

A

Presenting with TRIAD of hypotension, oliguria and low CO (low pulse, cool/pale extremities)

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78
Q

When do you need to admit someone with CHF?

A

moderate to severe

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79
Q

What is considered hypoglycemia?

A

glucose under 70

80
Q

What are complications associated with hypoglycemia?

A
  1. arrhythmias
  2. delerium
  3. aspiration events
  4. falls
81
Q

What are the most common culprits of hypoglycemia?

A
  1. sulfonylureas
  2. sliding scales
  3. intensive insulin therapy
82
Q

What are the glucose goals for non-critically ill hospitalized patients?

A

Pre-meal: under 140
Fasting no lower than 90
Average random glucose under 180

83
Q

What do you want to do when prescribing sulfonylureas?

A
  1. hold for any chance of poor PO intake
  2. Write SPECIFIC nursing orders
  3. don’t forget about other oral agents
84
Q

What so you want to do when prescribing sliding scale?

A
  1. safer with short-acting insulin

2. don’t “set it and forget it”

85
Q

How do you treat someone is asymptomatic or midly symptomatic hypoglycemia?

A
  • 20g oral glucose (glucose tabs/gels, juice/milk, snack , full meal)
  • one amp of D50
86
Q

What are the adverse effects of hyperglycemia? (3)

A
  1. increased risk infection (decreased immune system/neutrophil function)
  2. Volume depletion/dehydration (renal failure, severe electrolyte disturbances)
  3. calorie and protein loss (poor healing, edema)
87
Q

What is the glucose goal when treating hyperglycemia?

A

Under 180!

88
Q

What DM med can cause lactic acidosis when used with contast dye?

A

metformin

89
Q

What DM meds can cause ventricular dysfunction?

A

TZDs

90
Q

What are some barriers to consider when discharging a DM patient?

A
  1. insurances
  2. pharmacy
  3. equipment
  4. can patient work equipment
  5. sustainability
91
Q

What are some common causes of upper GI bleeds?

A
  • Ulcers (NSAIDs, Stress)
  • esophageal varices (cirrhosis)
  • esophagitis/gastritis (candida, ETOH)
  • portal HTN (cirrhosis)
  • Angiodysplasia
  • mass lesions
  • mallory-weiss syndrome
  • no lesion identified (10-15 percent)
92
Q

what does orthostatic hypotension mean?

A

15 percent total volume loss

93
Q

What does supine hypotension mean?

A

40 percent total volume loss

94
Q

What tests does everyone with a GI bleed get?

A
  1. CBC (H/H)
  2. CMP
  3. coag panel
  4. type and cross
95
Q

What indicates an emergency GI bleed?

A

hypotension (of any kind) and frank blood witnessed

96
Q

What is initial management of an anticoag patient with a GI bleed?

A
  1. stop medication
  2. rank severity of bleed
  3. call PharmD
  4. reverse effects (INR over 1.5, Vit K IV/po, Kcentra)
97
Q

What are some clinical features of a COPD exacerbation?

A
  • increased cough
  • increased sputum
  • worsening dyspnea
  • wheezing
  • tachynea
  • increased respiratory effort (SOB, accessory muscle use, tripoding)
  • hypoxia
98
Q

Does a normal spirometry r/o COPD/asthma risk of exacerbation?

A

NOPE

99
Q

What is GOLD staging?

A

Stage 1: mild COPD (over 60 percent)
Stage 2: Moderate COPD (under 60 percent)
Stage 3: Severe COPD (under 30 percent)

100
Q

How much oxygen can a nasal cannula supply?

A

Up to 6L

101
Q

What is a vapotherm?

A

high flow nasal O2 and positive pressure

102
Q

Should steroids be given for COPD exaberbation?

A

YES (IV first 24 hrs and then PO)

103
Q

When should someone with COPD get abx?

A

Mod/severe exacerbation

104
Q

What qualifies as a mod/severe COPD exacerbation?

A

At least 2 or 3 cardinal sxs (dyspnea, increased sputum, increased sputum purulence)

105
Q

What abx should you give someone with uncomplicated COPD with no risk factors?

A

Macrolide

106
Q

What abx do you give someone with complicated COPD and at least 1 risk factor?

A

flouroquinolones or augmentin

107
Q

What are risk fartors for COPD?

A
  1. Over 65
  2. FEV1 under 50 percent
  3. Over 3 exacerbations/year
  4. Cardiac disease
108
Q

What is the average length of stay for someone with a COPD exacerbation?

A

5 days

109
Q

What do you do initially on admission with COPD patient?

A

maximize therapy (albuterol, oxygen, solu-medrol)

110
Q

What do you do mid-way (day 2-3) of COPD patient?

A
  1. change to PO steroid
  2. continue inhalants
  3. start to wean O2
  4. encourage patient to ambulate
111
Q

What do you do just before d/c of COPD patient?

A
  1. all meds converted to PO
  2. ambulate patient, check ambulatory O2
  3. Be sure patient has good f/u
112
Q

What are high risk populations for VTEs?

A
  • critical illness
  • cancer
  • stroke
  • PG
  • heart failure
  • MI
  • Over 75yo
  • hx VTE
  • prolonged immobility
  • renal failure
  • inherited hypercoagable state
113
Q

What do you need to be careful of with someone on heparin?

A

HIT

114
Q

What is a red flag for HIT?

A

50 percent reduction in platelets

115
Q

What are the components of Wells score for DVT?

A
  1. Active cancer (w/n 6 months) (1 point)
  2. paralysis/recent plaster immobilization of LE (1 point)
  3. recently bedridden for 3 days or major surgery w/n 4 weeks (1 point)
  4. entire leg swollen (1 point)
  5. calf swelling by more than 3cm when compared to asx leg (1 point)
  6. pitting edema (1 point)
  7. collateral superficial veins (1 point)
  8. alternative dx less likely than that of DVT (2 points)
116
Q

When does the well score qualify as likely DVT?

A

2

117
Q

What Wells Score qualifies as high probability?

A

3 or higher

118
Q

How do you treat DVT?

A
  1. admit to hospital
  2. start IV heparin or lovenox AND po coumadin (AT THE SAME TIME!)
  3. continue for 5 days
  4. once INR at goal (2-3) stop IV (after 5 days) and rely just on PO coumadin
119
Q

What is the clinical presentation of a submassive PE?

A
  • dyspnea and tachypnea at rest/with exertion
  • pleuritic pain
  • cough
  • orthopnea
  • calf/thigh pain and/or swelling
  • wheezing and coarse breath sounds
  • hemoptysis
120
Q

What are sxs of a massive PE?

A

All submassive sxs PLUS HYPOTENSION

121
Q

When should you order a hypercoagable panel for a patient with PE?

A

AFTER initial tx period is over (3 months out) and anticoag has been stopped

122
Q

What are indications for an IVF filter?

A
  • can’t use pharm anticoag
  • developed complication/recurrence
  • retrievable filter designs preferred
123
Q

What are general variables associated with SIRS?

A
  • Temp over 100, under 96.8
  • HR over 90
  • RR over 20
  • altered mental status
  • significant edema (over 20mL/kg over 24hrs)
  • HYPERGLYCEMIA (glucose over 140)
124
Q

What are inflammatory variables of SIRS?

A
  1. leukocytosis or leukopenia
  2. Normal WBC with over 10 percent immature forms
  3. plasma CRP elevated
  4. plasma procalcitonin
125
Q

How do you treat someone with SIRS?

A
  • start gentle fluid resuscitation and admit patient

- obtain blood cultures

126
Q

What is sepsis?

A

SIRS plus infection

127
Q

What classifies severe sepsis?

A

2 SIRS criteria AND infection AND end organ damage

128
Q

What qualifies as end organ damage? (6)

A
  1. Hypotension
  2. Renal failure
  3. Shock liver (bilirubin over 2)
  4. coagulopathy (platelets under 100, INR over 2.5, PTT over 60)
  5. Respiratory failure
  6. elecated lactic acid

***Does NOT count organ dysfunction that is from chronic conditions/medications

129
Q

What qualifies as septic shock?

A

Severe hypotension persistent in the first few hours AFTER aggressive fluid resuscitation

130
Q

How do you manage severe sepsis?

A

broad spectrum abx

131
Q

What are the major Duke criteria?

A
  1. postive blood culture x2 with common offenders and NO CLEAR PRIMARY FOCUS
  2. persistenly positive blood cultures after or during treatment
  3. TTE evidence of vegetation or NEW regurg mumur
  4. Other imaging starting question of intracardiac abnormality
132
Q

What are Duke minor criteria?

A
  1. Presence of valvular heart disease NOS
  2. IVDU
  3. fever
  4. unexplained vascular phenomenon (conjunctival hemorrahge, cutaneous petechiae, embolism, hemorrhage)
133
Q

What are common pathogens of endocarditis?

A
  • Strep viridians
  • Staph aureus
  • Enterococcus
134
Q

What is the imaging test of choice for endocarditis?

A

TEE

135
Q

What is hematogenous osteomyelitis?

A
  1. bacteremia (from whatever source) leads to seeding of bacteria w/n bone
  2. monomicrobial
  3. blood and bone cultures should match
136
Q

What is contiguous osteomyelitis?

A
  1. bacteria seeds the bone from adjacent tissue
  2. polymicrobial
  3. blood cultures may or may not be positive
137
Q

What type of osteomylelitis is associated with DM?

A

contiguous

138
Q

What is the presentation of someone with DM and contigurous oestomyelitis?

A

slow, insidious onset with skin disruptions that slow to heal

139
Q

How do you dx osteomyelitis?

A
  • inflammatory markers may or MAY NOT be positive

- Imaging (MRI PREFERRED)

140
Q

How do you treat osteomyelitis?

A
  1. ID and surgery (podiatrist)
  2. broad spectrum IV abx (metronidazole, cefepime and vanco)
  3. follow bone cultures DAILY and laser in on tx once organism/sensitivity identified
141
Q

How long is the treatment for osteomyelitis?

A

6 weeks

142
Q

What is the most common pathogen of CAP?

A

strep pneumonia

143
Q

How do you determine whether to treat someone with CAP inpatient or outpatient?

A

CRB-65 scoring

144
Q

What is CRB-65 scoring?

A
  1. confusion (1 point)
  2. RR over 30bpm (1 point)
  3. hypotension (1 point)
145
Q

What CRB-65 qualifies for inpatient management?

A

OVER 1

146
Q

What qualifies for an automatic admission for someone with CAP?

A

hypoxia

147
Q

What type of abx treatment is used in pneumonia treatment?

A

EMPIRIC

148
Q

What is abx of choice for CAP?

A

fluroqunolone (moxiflocain, levofloxacine, gemifloxacin)

149
Q

Are steroids usually used for treatment of CAP?

A

not commonly used but supported in critical illness cases where the pathogen is NOT influenza/aspergillus

150
Q

Is repeat imaging needed for CAP?

A

not needed it clinical improvement (consider CT chest)

151
Q

What are factors associated with HCAP? (5)

A
  1. IV therapy, wound care, or IV chemotherapy w/n 30 days
  2. LTC living
  3. hospitalization in acute care hosp. for at least 2 days w/n 90 days
  4. Pna that occurs 48hrs or more after admission and did not appear to be incubating at time of admission (nosocomial pna)
  5. Pna that develops more than 48-72hrs after endotracheal intubation (ventilator associated pna)
152
Q

How do you manage HCAP?

A
  1. ALL need hospitalizations

2. almost ALL need EMPIRIC abx

153
Q

Why is HCAP harder to treat than CAP?

A

longer list of offending agents– MULTI-DRUG RESISTANCE (MDR)

154
Q

What antibiotics do you use to treat someone with HCAP WITHOUT risk facors for MDR?

A
  1. Ceftriaxone

2. Levaquin or Avelox

155
Q

How do you treat someone with HCAP WITH MDR risks? (worry about pseudomonas, MRSA, etc)

A

“Triple antibiotic therapy”

  1. Zosyn
  2. Fluoroquinolone (cipro/levaquin)
  3. vancomycin

ALL GIVEN IV (PICC line)

156
Q

What is the length of treatment for someone with HCAP

A

7 days minimum

157
Q

When can you change abx to PO equivalents for HCAP?

A

48-72hrs after start of treatment ONLY if excellent clinical response to IV therapy

158
Q

What are risk factors for MDR? (5)

A
  1. receipt abx w/n preceding 90 days
  2. current hospitalization longer than 5 days
  3. High frequency of abx resistance in the community or in the specific hospital unit
  4. Immunosuppresion
  5. severe septic shock
159
Q

What is aspiration pneumonia?

A

Compromise in usual defenses that protect lower airways (glottic closure, cough reflex, other clearing mechanisms)

160
Q

What is management of someone with aspiration pna?

A
  1. STRICT NPO until speech therapy eval and can recommend safe swallowing strategies
  2. modified barium swallow to better define dysphagia
  3. Repeat MBS may be needed to re-eval and determine if patient can graduate to more liberal diet modification plan
161
Q

What is abx of choice for aspiration pneumonia?

A
  1. Clindamycin IV if hospitaliztion needed
  2. PO augmentin if oral therapy preferred/needed
  3. If MDR risk: Zosyn in “triple abx therapy” takes place of clindamycin
162
Q

What qualifies as a complicated UTI?

A
  1. DM
  2. PG
  3. Sx more than 7 days
  4. hospital-acquired infection
  5. renal failure
  6. urinary obstruction
  7. PRESENCE INDWELLING CATHETER, stent, nephrostomy tube
  8. recent urinary tract intstrumentation
  9. functional/anatomic abnormality in urinary tract
  10. Hx childhood UTIs
  11. renal transplantation
  12. Immunosuppression
163
Q

What are atypical signs of UTI?

A
  1. fatigue/malaise
  2. “moms not herself”- forgetful, confusion, disorientation
  3. unsteady on feet
  4. foul-smelling urine
  5. elevated cr/actual renal failure
164
Q

How do you dx UTI?

A

UA (clean catch or straight cath sample)

165
Q

What are you looking for on UA?

A
  • leuko esterase

- NITRITES (most predictive of UTI)

166
Q

What signifies the urine specimen has been contaminated?

A

epithelial cells

167
Q

What should you always make sure to get when someone has a UTI?

A

culture and sensitivity

168
Q

How long until the culture results?

A

12-24 hrs

169
Q

How long until the sensitivity results?

A

48-72 hrs

170
Q

What are some commonly uncommon pathogens of UTIs?

A
  1. Vancomycin resistant enterococcus (VRE)
  2. Extended spectrum beta-lactamase E. coli or Klebsiella (ESBL)
  3. Methicillin-resistant staph aureus (MRSA)
171
Q

What are BAD abx choices for complicated UTIs?

A
  1. Macrobid
  2. Bactrim

Due to resistance and renal toxicity in elderly

172
Q

What are recommened abx for complicated UTIs?

A

Flouroquinolone (CIPRO)

173
Q

What are S/S of acute alcohol withdrawal?

A
  • insomnia
  • tremulousness
  • mild anxiety
  • GI upset
  • anorexia
  • HA
  • diaphoresis
  • palpitations
174
Q

How do you treat acute alcohol withdrawal?

A
  1. Banana baf (IVF, dextrose, minerals, THIAMINE)
  2. Electrolytes (
  3. BENZOS
  4. CIWA
175
Q

What are S/S of delirium tremens? (5)

A
  1. delirium (encephalopathy)
  2. hallucinations
  3. tachycardia
  4. HTN
  5. Hyperthermia
176
Q

When does delirium tremens begin?

A

onset 48-96hrs after last drink (can persist as long as 5 days)

177
Q

What are risk factors for developing DT?

A
  1. Sustained drinking
  2. hx DT
  3. Older than 30yo
  4. concurrent illness
  5. significant withdrawal sxs in presence of elevated BAL
178
Q

How do you treat DT?

A
  • NOT behavioral health unit!!

- aggressive IV BENZOS

179
Q

What is wenicke encephalopathy?

A

ACUTE brain disorder causing petechial hemorrhaging and necrosis in midbrain structures

180
Q

What is the classic triad of wernickes?

A
  1. encephalopathy/delirium
  2. gait ataxia
  3. oculomotor dysfunction (EOM not intact)
181
Q

Does a normal thiamine exclude WE?

A

Nope!

182
Q

How do you treat WE?

A

IV thiamine

183
Q

What do you have to be careful of when treating WE?

A

glucose admin can precipitate WE!

184
Q

What is Korsakoff’s?

A

consequence of untreated/repeated episodes of WE

Chronic, late neuropsychiatric d/o

185
Q

What are 3 characteristics of Korsokoffs?

A
  1. cognitive impairment
  2. retrograde and anterograde amnesia
  3. brain imaging positive for atrophy
186
Q

What causes cerebellar degeneration?

A

nutritional deficiency and neurotoxic effects of chronic alcohol use

187
Q

What are S/S of cerebellar degeneration?

A
  1. gait ataxia
  2. poor gross motor coordination
  3. inability to handwrite
  4. dysarthria (speech difficulty)

Cognitive capability still INTACT

188
Q

What is prognosis for someone with cerebellar atrophy?

A

may improve slightly with abstinence and good nutrition but is LARGELY IRREVERSIBLE

189
Q

What is alcohol hallucinosis?

A

visual hallucinations in absence of other autonomic/neuro complications

190
Q

What is the course of alcohol hallucinosis?

A

presnet in 24hrs after last drink and are self-limited by 3rd day

**May be mistaken for DT/WE

191
Q

What are neuromuscular complications from drinking?

A
  1. peripheral neuropathy

2. myopathy

192
Q

What is treatment for peripheral neuropathy?

A
  1. abstinence
  2. ongoing thiamine PO
  3. maximize nutrition
193
Q

What are sxs of myopathy?

A

Weakness, pain, swelling, of affected muscles

194
Q

What can myopathy be associated with?

A
  • rhabdo
  • dysphagia
  • heart failure
195
Q

What is management of myopathy?

A
  1. Check CK and cr

2. careful with IVF and monitor for arrhythmias (check phosphate)

196
Q

What are people with myopathy at risk for?

A

dysphagia (get speech therapy eval before feeding)

Hospital Medicine (1 decks)

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