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Internal Medicine > September 2020 > Flashcards

September 2020 Flashcards

1
Q

What are the categories of testicular cancer?

A

3 Categories:

  • 1) Seminomatous - TIP: Semen
  • 2) Nonseminomatous - TIP: Baby cells
  • 3) Stromal Cell tumors - TIP: Cells surrounding the semen

1) Seminoma - from germ epithelial of the seminiferous tubules
2) Nonseminomatous - TIP: all baby parts
- Choriocarcinoma - the placenta
- Yolk sac tumor - the amniotic sac
- Embryonal tumor - the embryo
- Teratoma - mature embryo
- mixed germ cell tumor - mixture of all the cell types
3) Stromal Cell Tumors - TIP: Cells surrounding the semen
- Sertoli cell tumor
- Leydig cell tumor
- Granulosa cell tumor

TIP: “Sir” cells, “Lady” cells and the “Granny” cells are needed to care for babies

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2
Q

What is a germ cell?

A

A germ cell is ANY cell that has HALF the number of chromosomes a somatic cell has.

Ex: egg, sperm

ALL testicular cancers are GERM cell tumors, regardless of seminoma vs nonseminoma vs stroll cell tumors

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3
Q

What is the rate at which you should lower patient’s BP in hypertensive emergency?

A

Reduce systolic blood pressure by ≤ 25% in first hour, then (if stable) to goal of 160/100-110 mm Hg by 2-6 hours, with cautious return to normal blood pressure over next 24-48 hours in cases other than aortic dissection, severe preeclampsia/eclampsia, or pheochromocytoma crisis (ACC/AHA Class I, Level C-EO)

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4
Q

What is the rate at which to lower BP in the setting of Hypertensive Emergency AND

1) Ischemic Stroke?
2) ICH?

A

Plain ‘ol HTN crisis:

  • First hour: Reduce SBP by ≤ 25%
  • 2-6 hours: (if stable) to goal of 160/100-110 mm Hg
  • 24-48 hours: return to normal BP in cases other than aortic dissection, severe preeclampsia/eclampsia, or pheochromocytoma crisis (ACC/AHA Class I, Level C-EO)

Ischemic stroke:

  • TPA eligible: treat to < 180 sbp /105 DBP to be eligible for TPA
  • IF NOT TPA eligible: only treat IF > 220/120 and lower BP by 15% in the first 24 hours

KEY: in ischemic stroke, since you are ischemic, you are more lenient with high BP

ICH:

  • IF BP 150 to 220 AND No contraindications to BP meds AND no concern for increased ICP: lower to 140 mmHg
  • IF BP > 220: lower aggressively with IV - no goal provided

KEY: In hemorrhagic stroke, since high BP means more bleeding, you are NOT as lenient

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5
Q

What is the connection between IBD and multiple sclerosis?

A

Those with MS have an increase risk by 50% of developing IBD

The opposite is the same as well

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6
Q

Differences between Crohns and UC?

A

Crohns

TIP:

  • Crypt abscesses
  • Transmural (since crypts are deep in the ground)
  • non caseating granulomas (grannies are old and in crypts)
  • skip lesions

UC

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7
Q

Patient with pancreatitis, when should enteral to be initiated?

A

Within 24 hours

AGA 2018

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8
Q

In patients with gallstone pancreatitis, when is the best timing for cholecystectomy?

A

During same admission

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9
Q

What is the reversal agent for Rivaroxaban? What is its mechanism of action?

What alternative agent for reversal exists?

A

1) Andexanet Alfa
AndeXa

2) Acts as a decoy by which the Anti-Xa inhibitor will bind to it instead
3) 4PCC (TIP: makes sense since it has Factor X)

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10
Q

Does correction of INR prior to invasive procedure in patients with liver coagulopathy prevent bleeding?

A

No; PT/INR is corrected, but evidence hasn’t shown that that correction of INR in due to liver coagulopathy reduces bleeding

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11
Q

How to reverse Pradaxa?

A

Idarucizumab

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12
Q

What are the medications of choice to reverse warfarin toxicity?

A

Vitamin K

PCC (TIP: P stands for PT, PT goes with INR, INR is measured for patients on Warfarin)

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13
Q

What blood product is given in cases of fibrinoginemia?

A

CRYOprecipetate (Fibrinogen/Factor 13, vWF/Factor8)

TIP: CRYO for FIBRO

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14
Q

In patients with cirrhotic liver disease who are actively bleeding (including esophageal varices), what is the suggestion in regards to transfusion with plasma products?

A
  • Neither FFP, PCC nor rFVIIa reduces bleeding though they will correct PT/INR
  • IF a product is chosen, PCC is preferred given low volume
  • Kujovich JL. Coagulopathy in liver disease: a balancing act. Hematology Am Soc Hematol Educ Program. 2015;2015:243-9
  • AASLD 2017
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15
Q

There is only ONE case in which Vit K is used in patient who is bleeding - what case is that?

A

In patients bleeding while on VKA (Vitamin K Antagonist)

TIP: This means DO NOT give Vit K for cirrhotic with INR > 2 and bleeding. It is NOT produced Vit K dependent coagulation factors in the setting of liver disease.

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16
Q

What are the general reasons to use FFP vs 4PCC vs CRYO?

A
  • FFP - Major bleeding since all factors are used up
  • 4PCC - WARfarin bleeding since PCC is Prothrombin (PT/INR) Concentrate Complex
  • CRYO for FIBRO (fibrinoginemia)
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17
Q

How to generally bridge a patient on DOAC in preparation for an elective procedure?

A

TRICK!

Unlike VKA like Warfarin, DOAC’s rarely require bridging because the half life is so short. Meaning they wear off quickly and they restart quickly. Patients can stop DOAC’s day prior to surgery for the most part and undergo the procedure soon after. Hence, the window NOT being anti-coagulated is short and there is NO need for bridging.

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18
Q

Patient is anticipating a procedure, but is currently on a DOAC for Atrial Fibrillation. What 2 parameters determines the most appropriate timing when DOAC should be held?

A

CrCl and bleeding risk since a high bleeding risk and a lower CrCl means earlier time to discontinue AC to ensure the majority has cleared the system by the time of procedure

CrCl: DOAC’s are renally dosed. Hence, CrCl is a marker for “amount” of DOAC, really, the time till DOAC leaves the system entirely

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19
Q

What equation is used to calculate CrCl for patients on DOAC’s?

A

Cock Croft Gault using patient’s ACTUAL weight

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20
Q

What specific procedure is it recommended that DOAC’s be stopped up to 5 days prior to the procedure?

A
  • Neuroaxial procedures such as epidural for pain management
  • Given concern for catastrophic nature of spinal hematoma or epidural hematoma

TIP: Stands out because it is the only scenario in which DOAC’s are treated like VKA, that is, stop 5 days prior to procedure

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21
Q

What agents are available for anticoagulation bridging?

A

UFH and LMWH

TIP: LMWH is less cumbersome and therapeutic in most cases unlike UFH which is a hassle; LMWH is likely best used if AC is for a chronic condition like history of VTE and patient is not expected to have multiple procedures or bleeding risk

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22
Q

Patient is on UFH for bridging. Planned procedure is tomorrow. When to stop the Heparin drip?

A

4 hours prior to procedure

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23
Q

Patient is on LMWH for bridging. Planned procedure is tomorrow. When to stop the LMWH?

A

24 hours prior to the procedure, so last dose should be 24 hours prior to expected procedure

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24
Q

INR is to Warfarin as _________ is to DOAC

A

CrCl: tells you the “amount” of DOAC in patient’s system. Really, how long it will take to clear the DOAC

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25
Q

What factor determines timing of reinitiating VKA after a procedure?

A

Post procedural bleeding risk (which includes complications/bleeding during procedure, type of procedure, and patient’s own bleeding risk)

TIP: Post procedural bleeding risk is the same risk as procedural bleeding risk

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26
Q

When can most VKA be restarted following a procedure?

A

Within 24 hours

TIP: Since INR won’t be therapeutic until 5 days, it is VERY safe to restart VKA within 24 hours after procedure

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27
Q

Patient has returned from procedure. When is it appropriate to restart LMWH or UFH for VTE prophylaxis?

A

6 - 8 hours after procedure

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28
Q

What is the preferred blood product to reverse bleeding in the setting of Xa inhibitor? (Assuming specific reversal agent is NOT available)

A

4 PCC

Tip: Since 4PCC has factor X and all the Xa inhibitors, Apixaban, Rivaroxaban and Edoxaban block factor X.

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29
Q

What is preferred for induction of remission of mild to moderate UC: 5-ASA vs sulfasalazine?

A
  • 5-ASA given better tolerability
  • Efficacy between the two are the same

Murray A, Nguyen TM, Parker CE, et al. Oral 5-aminosalicylic acid for induction of remission in ulcerative colitis. Cochrane Database Syst Rev. 2020 Aug 12;8:CD000543. doi: 10.1002/14651858.CD000543.pub5.

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30
Q

What is considered normal pulmonary artery pressure?

A

25/10

TIP: 25 matches the systolic pressure of the RV, 10 is the diastolic pressure of the pulmonary artery

Hence any PAP > 25 mmHg is elevated

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31
Q

What is the CT findings consistent with Talc Granulomatosis?

A

Centrilobular micronodules

TIP: talc invades the arterial walls into the interstitial space and is eaten up by macrophages. Imagine macrophages eating opioids.

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32
Q

Framework Question:

How does a stem cell transplant affect immunity to vaccinations?

A

Regardless of vaccination status pre-transplant, immunity will wane post-transplant. Soon after transplant, patient’s immune system hasn’t reached full recovery (physiologically and because of immunosuppressives). Given that, patient will need to be revaccinated 1 year after transplant and at least 6 months after cessation of immunosuppression

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33
Q

What anatomically is involved when referring to peripheral vertigo?

A

Inner ear

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34
Q

What anatomically can be involved in central vertigo?

A

CN 8, brainstem and central areas

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35
Q

What part of the brain circulation is involved if vertigo is central?

A

Posterior circulation, so think brainstem and cerebellum

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36
Q

What are common causes of peripheral vertigo?

A
  • BPPV
  • vestibular neuronitis (which includes labyrinthitis)
  • Meniere disease
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37
Q

What are common causes of central vertigo?

A
  • Stroke (vertebrobasilar)
  • TIA
  • Vestibular migraine
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38
Q

What is the utility of the HINTs exam?

A
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39
Q

Early and intense glycemic control in diabetics leads to what known outcomes?

A

Protection against microvascular complications. This is called the legacy effect.

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40
Q

What are the possible interventional options in evaluating a patient with a LGIB?

A

Colonoscopy/EGD -> CT Angiogram (w/ or w/o embolization) -> exploratory laparotomy

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41
Q

What are the possible options in finding the source of LGIB? (without intervention)

A
  • EGD/Colonoscopy
  • Capsule Endoscopy
  • Tagged RBC
  • Angiogram
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42
Q

In what patients is it recommended to treat with a PCSK9 inhibitor?

A

1) Patients with familial hypercholesteremia with LDL >100 in the setting of maximally tolerated statin/ezetimibe
2) Patients with hypercholesteremia with baseline LDL >220 in the setting of maximally tolerated statin/ezetimibe, but still have LDL > 130
3) Secondary prevention for patients with ASCVD who are maxed out on statin/ezetimibe and considered “very high risk”

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43
Q

What is the expected EKG changes associated with Digitalis toxicity?

A

Combination of Atrial Tachycardia and AV block

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44
Q

What is the reference range for Digoxin level?

A

0.8 to 2.0, though really it is 0.5 to 0.9.

TRICK: depends on the indication. For atrial fibrillation, there is no therapeutic level. For HF, it is 0.5 to 0.9

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45
Q

What are the electrolyte abnormalities predispose patients to digoxin toxicity and the associated arrhythmias?

A

Hypomagnesemia and Hypokalemia

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46
Q

How to diagnose CF related diabetes?

A

Oral glucose tolerance test since A1c is not reliable on high turn over state

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47
Q

What are the steps to treating acute, unstable bradycardia (i.e. first line meds, second, etc)?

A

Atropine 0.5 mg every 5 minutes (max: 3 mg, hence 6 times)

Then, either of the following:

IV dopamine 2-10 mcg/kg/min
IV Epinephrine 2-10 mcg/kg/min
IV Isoproterenol 2-10 mcg/kg/min

Then, if not working:

Temporary pacing: transcutaneous or IV

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48
Q

Definition of bradycardia?

A

< 60 bpm

BUT, according to ACC/AHA, < 50 bpm

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49
Q

2 broad categories of bradyarrhythmias?

A

1) Sinus node dysfunction (aka sick sinus syndrome)
- failure to generate and propagate appropriate cardiac pulse from the sinoatrial node e.g. sinus brady

2) AV nodal block
- delay or failure of atrial impulse to conduct to the ventricles via the atrioventricular node

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50
Q

What type of MI can lead to bradyarrhythmia?

A

Inferior MI involving the RCA

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51
Q

What is the acronym to help form a differential diagnosis when approaching difficult case?

A

VINDICATE:

V - Vascular
I - Iatrogenic/Ingestion (Toxins/Meds)/Physiologic
N - Neoplastic
D - Degenerative/Neuro
I - Infectious/Infiltrative
C - Congenital
A - Autoimmune/Collagen vascular disease/Allergy
T - Trauma
E - Endocinologic/Electrolytes/Metabolic/Vitamins/IEM

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52
Q

What Albumin concentration is preferred for fluid resuscitation?

A

Albumin 5% is preferred for conditions associated with a volume deficit and albumin 25% is preferred when an osmotic or oncotic effect is necessary. If oncotic pressure is lower than 20 mmHg (total serum protein 5.2 g/100 mL or lower), administer albumin 25% with diuretics

For example: for shock

Initial, 12.5 to 25 g IV (250 to 500 mL of 5% solution, 50 to 100 mL of 25% solution), may repeat in 15 to 30 minutes; further doses based on clinical response, blood pressure, and anemia assessment ; MAX 2 g albumin/kg/day; do not exceed infusion rate of 1 mL/min for patients with normal blood volume

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53
Q

How to diagnose a diabetic foot infection?

A

SAME as you would any other infection - the presence of 2 cardinal signs or solely the presence of pus

  • Redness (rubor)
  • Swelling (tumor)
  • Pain (dolor)
  • Warmth
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54
Q

How to classify the severity of DFI?

TIP: severity determines setting (inpatient vs outpatient) and route of antibiotics (IV vs PO).

A

Mild: at least 2 signs of inflammation + <2cm of redness around ulcer

Moderate: at least 2 signs of inflammation + > 2 cm of redness

Severe: at least 2 signs of inflammation + > 2 cm of redness + 2 sirs

TIP: “Rule of 2, 2, 2” for Diabetic foot infections

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55
Q

What parts of the clinical exam may suggest underlying osteomyelitis in patients presenting with DFI?

A 
Probe to bone (exposed bone) 
Non-healing ulcer after 6 weeks of care 
Large ulcer area
Peripheral vascular disease 
CRP/ESR
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56
Q

What are metabolic causes of bradyarrhythmias?

A
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57
Q

Diff/diag exercise: Using VINDICATE, what is your differential diagnosis of bradyarrhythmias?

A

VINDICATE:

V - Vascular 
I - Iatrogenic/Toxins/Meds/Physiologic
N - Neoplastic 
D - Degenerative/Neuro 
I - Infectious/Infiltrative 
C - Congenital
A - Autoimmune/Collagen vascular disease/Allergy
T - Trauma
E - Endocinologic/Metabolic
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58
Q

Lesson from mistakes:

A

MI can occur in the setting of seizures

Lessons: MI can occur in ANY stressful event. Argument against Ockham’s razor (kinda)

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59
Q

What organs can be involved in disseminated blastomycosis?

A

PICMONIC

“BLASTO IS BROAD, BASED BUDDING YEAST THAT BLASTS BALLS, BONES, BRAIN, AND CAUSES BOILS”

Don’t forget lungs!

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60
Q

Why is it important to treat a patient with sustained ventricular tachycardia eventhough they are stable?

A

VT can degenerate to Ventricular fibrillation

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61
Q

In patient with hemodynamically stable Vtach, what medications are recommended to terminate Vtach?

A

1) Procainamide (level A evidence)
2) Amiodarone (Level BR evidence)

TIP: interesting that we ALWAYS use Amiodarone

AHA Guidelines 2017

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62
Q

A patient has recurrent HDS VTach while on Amiodarone drip. Next step?

A

Amiodarone 150mg bolus PRN

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63
Q

A patient has recurrent HDS VTach. You want to terminate the rhythm. When ordering Amiodarone, what do you order?

A
  • Amiodarone 150mg IV bolus over 10 minutes
  • Followed by 1mg/min infusion 6 hours, then 0.5mg/min infusion 18 hours
  • Amiodarone 150mg IV boluses PRN for recurrence
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64
Q

A patient has recurrent HDS VTach while on Amiodarone drip. Amio boluses PRN are ineffective. Next step?

A

Electro Cardioversion

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65
Q

How to transition a patient to Amiodarone PO after having started IV therapy?

A

PO: 400 mg 12 h for 1–2 wk, then 300–400 mg daily; reduce dose to 200 mg daily if possible

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66
Q

Can beta blockers be used to prevent Vtach?

A

Yes! (along with PVC’s. Think of Vtach as a string of PVC’s)

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67
Q

Should patients presenting with life-threatening ventricular arrhythmias undergo coronary angiography as part of their evaluation?

A

Coronary angiography should be considered to establish or exclude significant obstructive CAD in patients
with life-threatening VAs or in survivors of SCD, who have an intermediate or greater probability of having CAD by age and symptoms.

ESC 2017 Guidelines

Interesting: AHA notes angiography for those following sudden cardiac arrest with suspicion of ventricular arrhythmia. No mention of angiography for hemodynamically stable patients who present with VA.

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68
Q

What is the Sgarbossa criteria and purpose?

A

Patients with underlying LBBB will have ST changes at baseline that make diagnosis of STEMI difficult.

Sgarbossa is a criteria that aids in identifying ST changes that are drastic enough and may indicate STEMI:

Concordant ST elevation > 1mm
Concordant ST depression > 1 in V1-V3
Excessively discordant ST elevation > 5mm

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69
Q

What are 2 clues on EKG that can help distinguish Vtach from SVT with aberrancy?

A

1) Fusion beats

2) AV dissociation (inferior leads can show P and QRS that are not correlating)

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70
Q

Vtach, sustained, not responsive to Amio. Electrocardioversion pursued. What settings?

A

Biphasic
Synchronized
200J

If not working, increase by 100J

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71
Q

What dose of steroids is used to treat Crohns and UC flares?

A

40-60 mg daily of IV Methylpred

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72
Q

What are the 2 major risk factors for emphysematous UTI? (Pyelo, pyel, cystitis)

A

Diabetes and obstruction

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73
Q

What are the 2 major organisms for emphysematous UTI? (Pyelo, pyel, cystitis)

A

1) E. Coli - just like all of the UTI
2) Klebsiella Pneumoniae

Hence empiric treatment for pyelonephritis would adequately cover patient

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74
Q

What is the differential diagnosis of presence of air in or around the renal parenchyma?

A

The differential diagnosis for the presence of air either in or adjacent to the renal parenchyma includes the following conditions: reflux of air from the bladder, air in a renal abscess, entero-renal or cutaneo-renal fistula formation, retroperitoneal perforation of abdominal viscus, psoas abscess with gas-forming organisms, or recent urologic or radiologic intervention such as nephrostomy insertion

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75
Q

What is the preferred regimen or means to treat hyperglycemia in the inpatient setting?

A

Basal Bolus insulin + correctional sliding scale insulin

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76
Q

If a patient is NPO, should patient continue basal insulin?

A

Two options:

1) Continue basal insulin as is
2) Decrease basal insulin by 20%

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77
Q

If a patient is NPO, how should inpatient insulin regimen be adjusted?

A

Basal: 1) Continue basal insulin as is or 2) Decrease basal insulin by 20%

Meal time: bolus insulin must be held until nutrition is resumed

Correctional insulin:doses of correction insulin can be continued to treat BG above the desired range

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78
Q

In regards to maintenance of remission of ulcerative colitis, what is more efficacious, sulfasalazine or 5-ASA?

A

Sulfasalazine is more efficacious
Both drugs had similar adverse affects
Cochrane review

Murray A, Nguyen TM, Parker CE, et al. Oral 5-aminosalicylic acid for maintenance of remission in ulcerative colitis. Cochrane Database Syst Rev. 2020 Aug 28;8:CD000544. doi: 10.1002/14651858.CD000544.pub5.

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79
Q

Does revascularization for stable ischemic heart disease lead to improve outcomes?

A

In patients with stable ischemic heart disease, routine revascularization was not associated with improved survival but was associated with a lower risk of nonprocedural MI and unstable angina with greater freedom from angina at the expense of higher rates of procedural MI.

  • Excluded main disease

Bangalore S, Maron DJ, Stone GW, et al. Routine Revascularization Versus Initial Medical Therapy for Stable Ischemic Heart Disease: A Systematic Review and Meta-Analysis of Randomized Trials. Circulation. 2020

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80
Q

Framework Question:

Explain the difference between the following tests in evaluating a patient for a plasma cell dyscrasia:

  • SPEP
  • Serum Immunfixation
  • Serum Free Light Chain (FLC)
A
  • SPEP, or serum protein electrophoresis, answers the question, is there a monoclonal protein, hence M spike. It DOES NOT identify what protein, whether light chain or heavy chain or which kind
    • TIP: SPEP: is there an M Protein?
  • Serum immunofixation answers the question of what the IDENTITY of the M protein is, that is, both the heavy chain and light chain identity e.g. IgG kappa
    • TIP: Serum immunofixation: what is the M protein
  • Serum Free Light Chain answers the question of if the M protein is a free light chain (“free” in that it is NOT attached to a heavy chain)
    • TIP: Free light chain: is the M protein a free light chain
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81
Q

When to perform the UPEP and Urine Immunofixation when evaluating a patient with concern for plasma cel dyscrasia?

A

Depends on the diagnosis:

  • MM
  • MGUS
  • Amyloidosis

In the case of MM, they NCCN recommends UPEP and Urinary immunfixation in the cases of MM

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82
Q

What is the difference in the sensitivity among the following tests:

  • SPEP
  • Serum immunofixation electrophoresis
  • Serum FLC
A

Overall, going from SPEP -> Serum Immunfixation Electrophoresis -> Serum free light chains, the sensitivity increases. Free light chains detects serum levels of free light chains that serum immunofixation can’t detect, and serum immunfixation detects levels heavy/light chains that SPEP can’t detect.

Hence, SPEP can be negative, but SIFE can detect M protein. Or, SIFE can be negative, but serum FLC can detect M protein.

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83
Q

What is the most common organ affected by Cryptococcus?

A

Cryptococcal meningitis

Headache is the #1 presentation

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84
Q

Diagnosis of STEMI?

A

STEMI is diagnosed by ECG in the absence of left ventricular hypertrophy or left bundle branch block (LBBB) in the presence of new ST elevation (at J point) and either of:

≥ 2 mm (0.2 millivolts [mV]) in men or ≥ 1.5 mm (0.15 mV) in women in leads V2-V3

OR

≥ 1 mm (0.1 mV) in 2 other contiguous chest leads or limb leads

TIP: >2 in 1 lead (V2-V3) or > 1 in 2 contiguous leads

“2112”

“2 in V2”

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85
Q

Reasons for immediate cath for revascularization in patients with NSTEMI due to ACS?

A

Refractory angina, hemodynamic instability, or electrical instability

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86
Q

What is the presentation consistent with erythoderma?

A

Generalized sustained erythema with or without scaling > 90% of the skin surface area

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87
Q

What are the 5 broad categories of causes of erythroderma?

A

Dermatoses (exacerbation of underlying known dermatoses)

Drug reactions

Malignancies

Infections

Idiopathic disorders

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88
Q

What is the most common causes of erythroderma?

A

1) 50% underlying dermatoses exacerbation

2) Drug reaction

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89
Q

What is the difference between the presentation of mycosis fungoides vs Sezary syndrome?

A
  • mycosis fungoides - well defined and pruritic erythematous
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90
Q

Differential diagnosis for anterior mediastinal mass?

A

4 Ts:

Teratoma
Thymic mass
Terrible lymphoma
Thyroid tissue

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91
Q

Does early rhythm control for atrial fibrillation lead to reduced cardiovascular events?

A

YES

  • NEJM 2020
  • Type: In this international, investigator-initiated, parallel-group, open, blinded-outcome-assessment trial
  • Primary end point: Composite of death from cardiovascular causes, stroke, or hospitalization with worsening of heart failure or acute coronary syndrome
  • 5 year follow up
  • 135 centers, 2789 patients

Kirchhof P, Camm AJ, Goette A, et al. Early Rhythm-Control Therapy in Patients with Atrial Fibrillation. N Engl J Med. 2020 Aug 29. doi: 10.1056/NEJMoa2019422

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92
Q

What are EKG findings that imply with ischemia (NOT including the obvious ST elevation)?

A

T wave changes

ST depression

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93
Q

What are STEMI equivalents?

A

Posterior MI

New LBBB (caveat: it is very difficult to know if a LBBB is new at most presentations)

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94
Q

How does “unstable angina” differ in presentation to stable angina?

A
  • Pain at rest
  • Pain with less exertion than before
  • Pain that is prolonged
  • Pain that is more severe
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95
Q

Which coronary artery, if affected from ACS, can be electrically silent on EKG?

A

Left circumflex and right coronary artery

Clinical tip: you don’t have to have a STEMI to have an ACS.

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96
Q

What EKG changes, not including ST elevation, are clinically significant for CAD?

A
  • symmetrical TWI > 2mm in precordial leads
  • transient ST elevations >0.5 mm WITH symptoms
  • Horizontal or downsloping ST depression
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97
Q

What are non ACS causes of elevated troponin?

A
  • tachyarrhythmia
  • hypotension or hypertension,
  • cardiac trauma
  • acute HF
  • myocarditis and pericarditis
  • acute pulmonary thromboembolic disease
  • severe noncardiac conditions such as sepsis, burns, respiratory failure, acute neurological diseases, and drug toxicity (including cancer chemotherapy).
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98
Q

What are cases in which trop can be chronically elevated?

A

Chronic elevations can result from structural cardiac abnormalities such as LV hypertrophy or ventricular dilatation and are also common in patients with renal insufficiency including ESRD

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99
Q

Patient presents with NSTE-ACS - what are the options in regards to treatment? (categorized by timing of invasive therapy)

A

1) immediate invasive
2) Early invasive
3) Delayed invasive
4) Ischemia guided medical therapy

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100
Q

What tools can help determine whether a patient who presents with NSTE-ACS receives immediate vs early invasive vs delayed invasive vs medical therapy?

A
  • Risk stratification: TIMI and GRACE
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101
Q

How does TIMI score aid in determining the best treatment for patients with NSTE-ACS?

A

TIMI 3 patients benefit from early invasive therapy

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102
Q

What makes up the TIMI score? What is considered a high score?

A
  • ST changes >0.5 mm
  • Trops
  • Age > 65
  • 3 CAD risk factors: DM, renal disease, Smoking, FMH of CAD
  • Known CAD > 50%
  • ASA use
  • 2 episodes in 24 hours
  • TIP: “TIMI and 3 rhyme” TIMI 3
  • TIP: note that there are 3 objective measures, and the rest are historical details about the patient
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103
Q

What meds should be started on for ALL NSTE-ACS patients?

A

ASA, Plavix, BB (extended release), Statin, heparin drip

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104
Q

What is the basic reasoning about why it may be good to do early invasive? delayed? ischemia guided?

A
  • early invasive leads to definitive eval/treat
  • delayed invasive allows plaque to stabilize via antithrombotic/coagulant therapy before invasive strategy
  • ischemia guided does work for some patients and leads to less invasive procedures

TIP: think of coronary angiography similar to a procedure or surgery. Immediate surgery may not be the best option if the patient is not in the optimized state.

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105
Q

Framework Question:

What is an easy way to know who gets the following treatment when presenting w/ NSTE-ACS?

1) immediate invasive
2) Early invasive
3) Delayed invasive
4) Ischemia guided medical therapy

A
  • STEMI- like complications: Immediate (think the worse MI possible): Hemodynamic instability, HF, VT/VF, new regurg, refractory, recurrent or angina at rest
  • NSTEMI- like: Early invasive: ST depression OR Tn changes
  • UA + co-morbidities: Delayed invasive: NO ST depression, NO Tn changes
  • TIMI 0-1 : Ischemia-guided therapy
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106
Q

Is early invasive better than ischemia guided therapy?

A
  • Overall: early invasive is better than ischemia guided therapy for mortality/recurrent MI, buuuuuut, when you look at groups, it benefits (actual clinical significance) the highest risk groups most and doesn’t affect mortality in low/intermediate (clinically insignificant)

2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes

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107
Q

Is early invasive better than delayed invasive therapy?

A

Studies show no difference

2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes

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108
Q

What type of beta blocker should be initiated on patients with NSTE-ACS?

A

SUSTAINED RELEASE Metoprolol
Carvedilol
Bisoprolol

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109
Q

What are the antianginal options in NSTE-ACS?

A

NTG (PO)

  • > NTG IV
  • > Beta blocker (if not started already)
  • > NDP CCB (as long as NO heart failure present)
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110
Q

What is the contraindications to starting BB on patient presenting with NSTE-ACS?

A
  • Shock, low output state, risk for shock
    • TIP: Risk factors for shock include patients >70 years of age, heart rate >110 beats per minute, systolic BP <120 mm Hg, and late presentation
  • AV block
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111
Q

What medications provide mortality benefit in the setting of NSTE ACS (or MI)?

A
  • ASA
  • ACEi (if you can find a reason, such as HFrEF, HTN, Type II DM, CKD)
  • Eplerenone (LV dysfunction present)
  • Beta Blockers
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112
Q

What are P2Y inhibitor options?

A

Clopidogrel
Prasugrel
Ticagrelor

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113
Q

Framework Question:

Explain the MOA of the following anti platelet therapies in reference to the steps for platelet aggregation:

  • ASA
  • P2Y 12 inhibitor
  • GP IIb/IIIa inhibitor
A

ASA: like an NSAID, is a COX inhibitor, but irreversible COX inhibitor that leads to the inhibition of TXA2. TXA2 encouraged platelet aggregation and vasoconstriction

P2Y 12 inhibitor: When platelets are bound to damaged vasculature (via GP1B receptor + vWF + collagen), dense granules are released from the platelets. ADP from the granules will bind to the P2Y 12 receptor, leading to the expression of GP IIb/IIIa

GP IIb/IIIa inhibitor: prevents the binding of fibrinogen to the receptor.

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114
Q

When is Clopidogrel stopped prior to surgery?

A

5 days

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115
Q

What are the FDA approved P2Y inhibitors for NSTE-ACS (and ischemic heart disease in general)

A

Clopidogrel
Prasugrel
Ticagrelor

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116
Q

What are the options for bowel clean out in preparation for colonoscopy?

A
  • PEG low-volume same-day (15 mg bisacodyl the day before, 2 L the morning of the procedure)
  • Low-volume split-dose (15 mg bisacodyl the day before and 1 L, 1 L the next day)
  • High-volume split-dose (2 L day prior + 2 L day after)
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117
Q

What antihypertensive may have the added benefit of improving neurocognitive function in patients with MCI?

A

Candesartan

  • JAMA 2020
  • RCT Double Blinded
  • Candesartan vs Lisinopril
  • Total: 176 patients
  • The primary outcome was executive function (measured using the Trail Making Test, Executive Abilities: Measures and Instruments for Neurobehavioral Evaluation and Research tool)
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118
Q

Framework Question:

Explain the steps involved in platelet aggregation.

TIP: think of the anti platelet drugs such as ASA, Clopidogrel, Eptifibatide and their targets

A
  • Endothelium damaged, reflexive neural stimulation causes transient vasoconstriction
  • Additionally, the damaged cells release endothelin, further promoting vessel constriction (limit blood loss)
  • Subendothelial collagen exposed.
  • The plasma glycoprotein von Willebrand factor (vWF), released from the Weibel-Palade bodies of endothelial cells, binds to the exposed collagen and serves as the site of platelet adhesion to the disrupted vessel surface.
  • Platelets bind to vWF using their GPIb receptor.
  • Collagen + vWF + GP1b receptor >-platelet
  • This binding results in a conformational change and activation of the platelet via degranulation and release of vWF (further aggregation) and ADP
  • Adenosine diphosphate (ADP) released from dense granules bind to P2Y1 and P2Y12 receptors located on the platelet’s membrane, inducing the expression of the GPIIb/IIIa receptor.
  • This newly inserted platelet receptor, along with thromboxane A2 (TXA2) produced by platelet enzyme cyclooxygenase, allows for platelet aggregation.
  • Fibrinogen from alpha granules acts as a link between GPIIb/IIIa receptors on different platelets.
  • Platelet (GPIIb/IIIa) -< fibrin >-(GPIIb/IIIa)platelet
  • Once platelets have linked together, a temporary platelet plug has formed, which is later fortified by the coagulation cascade of secondary hemostasis.
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119
Q

What is the correction for Na in the setting of severe hyperglycemia?

A

Corrected sodium = measured sodium + [1.6 (glucose – 100) / 100]

Add 1.6 for every BG 100 over 100

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120
Q

Gold standard for achalasia?

A

Manometry

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121
Q

What is the first diagnostic test of choice for esophageal dysphasia?

A

EGD

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122
Q

What organs can be involved in DRESS? What are the most common organs involved in DRESS apart from skin?

A

ALL ORGANS: kidneys, lungs, heart - nephritis, pneumonitis, myocarditis

Liver: 95% of the time elevated

Heme: leukopenia (lymphopenia), atypical lymphocytes, leukocytosis, eosinophilia, thrombocytopenia, anemia

Lymphatic: lymphadenopathy

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123
Q

What is the dermatologic manifestation of DRESS?

A

Classic: Diffuse morbilliform rash

Significant facial and/or hand and foot edema and cervical, axillary, and/or inguinal lymphadenopathy is also frequently seen.

Mucosal involvement, such as cheilitis, erosions, erythematous pharynx, and enlarged tonsils is also common

TIP: ALMOST KAWASAKI’s like, but no RED eyes

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124
Q

What are the indications for CABG in patient who presents with ACS?

A

TIP: “1, 2, 3 vessel rule” for Class 1, Level A evidence for CABG

1 vessel: > 50% Left Main Coronary Artery Disease
2 vessel: >70% Proximal LAD + any other vessel with significant disease
3 vessel: significant disease in 3 vessels e.g. LAD, RCA and LCx

TIP: the indications for CABG differ depending on the scenario: STEMI vs ACS vs Stable IHD

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125
Q

What is considered “significant” disease in a atherosclerotic coronary artery?

A

> 70% stenosis (except for LEFT MAIN, which is > 50%)

TIP: just like carotid stenosis! >70%-99% is significant

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126
Q

In STEMI, what is the 1 indication for CABG? (Class 1, Level A)

A

Cardiogenic shock in the setting of STEMI in patients < 75 years old

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127
Q

What are the indications for CABG in patients with Stable IHD?

A

TIP: “1, 2, 3 vessel rule” for Class 1, Level B evidence for CABG. Same rule used for ACS. The difference, the Level is B for stable IHD instead of A in ACS.

1 vessel: > 50% Left Main Coronary Artery Disease
2 vessel: >70% Proximal LAD + any other vessel with significant disease
3 vessel: significant disease in 3 vessels e.g. LAD, RCA and LCx

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128
Q

Patient is going for CABG - what to do about patient’s Aspirin? Clopidogrel?

A

Continue Aspirin

Stop Clopidogrel 7 to 10 days prior to CABG

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129
Q

What medication known to provide mortality benefit to patients with CAD should be held prior to planned CABG?

A

ACEi

preoperative ACE inhibitor use associated with increased risk of mortality and postoperative complications

130
Q

What does it mean to have a “right dominant” coronary anatomy?

A

It means that the RCA will give rise to the posterior descending artery to give supply to the left posterior ventricular wall.

TIP: the PDA is the artery that is the mirror image of the LAD and attempts to connect with it at the apex

This is present in 85% of the population

131
Q

How to calculate the amount of breakthrough pain medication to give?

A

Rule of thumb: Total amount of break through dosage available in 24 hours = total amount of basal drug given in 24 hours.

If a patient is receiving 60mg of Morphine per day via infusion, that is, 2.5mg/hour

60 mg / 24 = 2.4 mg

In this case, patient’s available breakthrough should be 60mg/ 24 hours.

2.5 mg / hr = 0.625 mg / 15 minutes

Hence 0.625 mg IV morphine Q15 prn

132
Q

What is the relationship between milligram and microgram?

A

1 miligram = 1000 microgram

Ex: Fentanyl is measured in micrograms

133
Q

A patient receives a 50 mcg fentanyl patch - what is the hourly dose that he is receiving?

A

He is receiving 50mcg of Fentanyl/hour!

That means, yes, he is receiving 1200 mpg Fentanyl/day!

134
Q

What is the difference between Type 1 and Type 2 error?

A

Type 1 error is a false positive. This occurs when the researcher incorrectly rejects a null hypothesis (remember: null hypothesis argues that there is no difference between the 2 interventions)

Type 2 error is a false negative. This occurs when the researcher fails to reject the null hypothesis which is REALLY false.

135
Q

Patient just had an MI (or PAD or stroke). What is better for secondary prevention - ASA or Clopidogrel indefinitely?

A

2020
Systematic review/Meta-analysis
Primary end point: myocardial infarction and stroke
Result:
- Slight decrease in MI, but NNT 244
- No difference in stroke
- No difference in death by vascular cause

“The benefit of P2Y12 inhibitor monotherapy is of debatable clinical relevance, in view of the high number needed to treat to prevent a myocardial infarction and the absence of any effect on all-cause and vascular mortality”

Chiarito M, Sanz-Sanchez J, Cannata F, et al. Monotherapy with a P2Y12 inhibitor or aspirin for secondary prevention in patients with established atherosclerosis: a systematic review and meta-analysis. Lancet. 2020 May 9;395(10235):1487-1495. doi: 10.1016/S0140-6736(20)30315-9.

136
Q

Does treatment of H. Pylori reduce the risk of gastric cancer? What patient population is this clearest in?

A

YES, East Asians

2020
Systematic review/Meta-analysis
8323 patients
Results:
-Healthy individuals, eradication therapy reduced incidence of gastric cancer (RR=0.54; 95% CI 0.40 to 0.72, NNT=72), and reduced mortality from gastric cancer (RR=0.61; 95% CI 0.40 to 0.92, NNT=135), but did not affect all-cause mortality
- Gastric neoplasia: eradication therapy also reduced incidence of future gastric cancer (RR=0.49; 95% CI 0.34 to 0.70, NNT=21)

Ford AC, Yuan Y, Moayyedi P Helicobacter pylori eradication therapy to prevent gastric cancer: systematic review and meta-analysis. Gut. 2020 Mar 23. pii: gutjnl-2020-320839. doi: 10.1136/gutjnl-2020-320839.

137
Q

What is an “interim analysis”?

A

In clinical trials and other scientific studies, an interim analysis is an analysis of data that is conducted before data collection has been completed. Clinical trials are unusual in that enrollment of subjects is a continual process staggered in time. If a treatment can be proven to be clearly beneficial or harmful compared to the concurrent control, or to be obviously futile, based on a pre-defined analysis of an incomplete data set while the study is on-going, the investigators may stop the study early.

138
Q

What drugs increase the risk of priapism?

A
  • PDE 5 inhibitor
  • Alpha blockers
  • Sympathomimetics
  • Antidepressants
  • Trazadone (has alpha blocking properties)
139
Q

What is the window of time that priapism requires treatment prior to development of irreversible damage?

A

4 hours

That is the definition of priapism! Unwanted erection > 4 hours.

140
Q

How well does serum iron concentration correlate with iron deficiency?

A

There is poor correlation between serum iron concentration and iron deficiency

TIP: in case of iron toxicity in children, it is recommended that iron levels be checked at 4-6 hours. This example shows how serum iron levels can change even with ingestion of iron.

Serum iron is less effective than ferritin and transferrin saturation in the detection of iron depletion, but more sensitive than traditional red blood cell indices

141
Q

How to use the serum iron level in evaluating a patient for iron deficiency?

A

Low serum iron in the presence of elevated total iron-binding capacity and low serum ferritin is considered diagnostic for iron deficiency.

Because of the wide variety of factors that affect serum iron levels, serum iron ALONE is of limited clinical utility.

There is poor correlation between serum iron concentration and iron deficiency

142
Q

Framework Question:

How does morphine PO compare to other opioid types/formulations?

A 
Morphine PO: 1 
Hydrocodone: 1.5x ( ~2 )
Oxycodone 1.5x ( ~2 )
Morphine IV 3x
Hydromorphone PO 4-7x
Hydromorphone IV 20x
Fentanyl 100x

TIP: 1:2:3:4-7;20;100

143
Q

In an attempt to reduce the amount medication burden that a new onset diabetic may accrue as time passes, what may be an appropriate medication to start?

A

Canaglafozin

Study compared the rates of initiation of insulin and other anti hyperglycemic agents in 2 groups: Canaglafozin group vs placebo group

Canaglafozin group: After 1 year, fewer participants treated with canagliflozin versus placebo initiated any AHA (7% vs. 16%), insulin (3% vs. 9%) or any non-insulin AHA (5% vs. 12%) (P < .001 for all); overall AHA initiation rates increased over time but were consistently lower with canagliflozin compared with placebo

Matthews DR, Wysham C, Davies M, et al. Effects of canagliflozin on initiation of insulin and other antihyperglycaemic agents in the CANVAS Program. Diabetes Obes Metab. 2020 Jul 20. doi: 10.1111/dom.14143.

144
Q

What are the subtypes of Primary Cutaneous B Cell Lymphomas?

A

From most common to least:

  • Follicule center lymphoma
  • Marginal zone lymphoma
  • Diffuse Large B Cell lymphoma
145
Q

How to diagnose Primary Cutaneous B Cell Lymphomas?

A

Punch biopsy, followed by staging

TIP: ALL forms of lymphomas can have dermatologic manifestations. So staging is key to determine if cutaneous lesions represent a primary cutaneous B cell lymphoma OR cutaneous disease from distant primary.

146
Q

Presentation of Primary Cutaneous B Cell Lymphomas, subtype PC-DLBCL, Leg type?

A

Distal leg

Solitary or localized red to brown ulcerated papule or nodules

147
Q

Does reducing uric acid levels lead to improved blood pressure control?

A

NO

Cochrane Review 2020

Background: Epidemiological and experimental studies suggest a link between hyperuricaemia and hypertension

Conclusion: e current RCT data are insufficient to know whether UA-lowering therapy lowers BP. More studies are needed.

Gois PHF, Souza ERM Pharmacotherapy for hyperuricaemia in hypertensive patients. Cochrane Database Syst Rev. 2020 Sep 2;9:CD008652. doi: 10.1002/14651858.CD008652.pub4.

148
Q

Can primary care based weight loss and lifestyle programs lead to weight loss?

A

Yes

  • NEJM 2020
  • Cluster-randomized trial
  • 452 intensive-lifestyle group vs 351 usual care
  • Primary outcome: percent weight loss
  • The % weight loss at 24 months was significantly greater in the intensive-lifestyle group (change in body weight, -4.99%; 95% confidence interval [CI], -6.02 to -3.96) than in the usual-care group (-0.48%; 95% CI, -1.57 to 0.61), with a mean between-group difference of -4.51 percentage points (95% CI, -5.93 to -3.10) (P<0.001).

Katzmarzyk PT, Martin CK, Newton RL Jr, et al. Weight Loss in Underserved Patients - A Cluster-Randomized Trial. N Engl J Med. 2020 Sep 3;383(10):909-918. doi: 10.1056/NEJMoa2007448.

149
Q

What does “individual patient data” Meta analysis mean?

A

IPD meta-analysis is a specific type of systematic review. Rather than extracting summary (aggregate) data from study publications or from investigators, the original research data are sought directly from the researchers responsible for each study. These data can then be re-analysed centrally and combined, if appropriate, in meta-analyses.

150
Q

What are organisms to consider and evaluate for in culture negative endocarditis?

A

HACEK

Tip: modern culture capabilities allow for easy growth of the HACEK organisms so they are not technically considered culture negative

TIP: Think of the “Ellas”

  • Coxiella Burnetti
  • Legionella
  • Brucella
  • Bartonella
  • Mycoplasma
  • Tropheryma whipplei
151
Q

What does the term “open-label” mean?

A

A term used to describe the situation when both the researcher and the participant in a research study know the treatment the participant is receiving.

152
Q

What is the benefit of IV Dexamethasone in treatment of COVID 19 patients

A

Ventilator free days in COVID patients with ARDS as defined by Berlin Criteria

  • RCT
  • Intervention: 5 days of 10mg IV Dex, 5 days of 10 mg PO Dex vs usual care
  • Results: Dexamethasone group had a mean 6.6 ventilator-free days (95% CI, 5.0-8.2) during the first 28 days vs 4.0 ventilator-free days (95% CI, 2.9-5.4) in the standard care group (difference, 2.26; 95% CI, 0.2-4.38; P = .04).
  • Conclusion: Among patients with COVID-19 and moderate or severe ARDS, use of intravenous dexamethasone plus standard care compared with standard care alone resulted in a statistically significant increase in the number of ventilator-free days (days alive and free of mechanical ventilation) over 28 days.

Tomazini BM, Maia IS, Cavalcanti AB, et al. Effect of Dexamethasone on Days Alive and Ventilator-Free in Patients With Moderate or Severe Acute Respiratory Distress Syndrome and COVID-19: The CoDEX Randomized Clinical Trial. JAMA. 2020 Sep 2. pii: 2770277. doi: 10.1001/jama.2020.17021.

153
Q

Do SGLT 2 inhibitors lead to increased risk for limb amputations?

A

No

  • Trial level meta analysis
  • 6 studies: empagliflozin (EMPA-REG OUTCOME study), canagliflozin (CANVAS Program and CREDENCE study), dapagliflozin (DECLARE-TIMI 58 and DAPA-HF trials) and ertugliflozin (VERTIS CV study)
  • 51000 patients
  • Results: Event rate of amputation 2.0% (535/26 778) and 1.3% (323/24 927) in the SGLT-2 inhibitor and control groups, respectively

Huang CY, Lee JK Sodium-glucose co-transporter-2 inhibitors and major adverse limb events: A trial-level meta-analysis including 51 713 individuals. Diabetes Obes Metab. 2020 Aug 3. doi: 10.1111/dom.14159.

154
Q

Can Metformin be used safely in pregnant women with Type II DM? (regards to both mother and fetus)

A
  • RCT, randomized, double blind
  • 502 women, 253 (50%) to metformin and 249 (50%) to placebo
  • Primary outcome: composite of fetal and neonatal outcomes, for which we calculated the relative risk and 95% CI between groups
  • Results: no significant difference in the primary composite neonatal outcome between the two groups
  • Secondary results
    • Metformin group: less insulin use, less weight gain in mothers, less LGA in infants, improved glycemic control
    • Con: higher risk for SGA

Feig DS, Donovan LE, Zinman B, et al. Metformin in women with type 2 diabetes in pregnancy (MiTy): a multicentre, international, randomised, placebo-controlled trial. Lancet Diabetes Endocrinol. 2020 Oct;8(10):834-844. doi: 10.1016/S2213-8587(20)30310-7

155
Q

What are the anti phospholipid antibodies to evaluate in a patient suspected for APS?

A

Anti cardiolipin antibodies

Anti Beta 2 Glycoprotein Ab

Lupus Anticoagulant

156
Q

What are considered high intensity statins?

A

Atorvastatin 40-80 mg daily

Rosuvastatin 20-40 mg daily

TIP: 20-40, 40-80

157
Q

What are considered high intensity statins?

A

Atorvastatin 40-80 mg daily

Rosuvastatin 20-40 mg daily

TIP: 20-40, 40-80

158
Q

Patient has AKI and unable to have CT Angiogam to evaluate for colonic ischemia? What supplementary work up can be made to help suggest diagnosis of colonic ischemia?

A

Blood tests: LDH, Lactate, CK, Amylase, Metabolic acidosis

KUB: looking for pneumoperitoneum, pneumatosis intestinalis, thumbprinting

159
Q

What are considered high intensity statins?

A

Atorvastatin 40-80 mg daily

Rosuvastatin 20-40 mg daily

TIP: 20-40, 40-80

160
Q

Framework Question:

What part of the bowel is supplied by the celiac artery? Superior mesenteric artery? Inferior mesenteric artery?

A

Celiac artery:
- TIP: Foregut + extraintestinal but related to GI tract

esophagus/Duodenum + many extra intestinal organs such as spleen/liver/pancreas

SMA: “midgut” – which spans from the major duodenal papilla (of the duodenum) to the proximal 2/3 of the transverse colon.

IMA: inferior mesenteric artery supply the structures of the embryonic “hindgut”. These include the distal 1/3 of the transverse colon, splenic flexure, descending colon, sigmoid colon and rectum

161
Q

In patients with cancer related VTE, what is the preferred anticoagulation? Can DOAC’s be used instead of LMWH?

(What does the evidence demonstrate?)

A
  • 2020
  • Type: Systematic review and meta-analysis
  • Compared DOACs and (LMWHs)
  • Primary end point: recurrent VTE and major bleeding
  • 2607 patients, the risk of recurrent VTE was nonsignificantly lower with DOACs than with LMWHs (RR, 0.68; 95% CI, 0.39-1.17). Conversely, the risks of major bleeding (RR, 1.36; 95% CI, 0.55-3.35) and CRNMB (RR, 1.63; 95% CI, 0.73-3.64) were nonsignificantly higher.
  • Conclusion: DOACs are an effective treatment option for patients with cancer and acute VTE, although caution is needed in patients at high risk of bleeding.

Review: In cancer-associated venous thromboembolism, direct oral anticoagulants reduce the risk of recurrent venous thromboembolism more than low-molecular-weight heparins

162
Q

Framework Question:

What is the difference between a “host”, “reservoir” and a “vector”?

A
  • Host: The host is the living being that the bacteria, virus, protozoan, or other disease-causing microorganism normally resides in
  • Reservoir: Or also known has reservoir host, is a living being that a disease causing organism resides and multiples
  • Vector: is a living thing that transmits the disease causing organism

EX:

  • West Nile Virus resides in some bird species, hence birds are the hosts and reservoirs for WNV
  • Mosquitos that feed on these birds will obtain the WNV and are vectors since they transmit the disease to humans through bite
163
Q

What is the difference between an “intermediate” host and a “primary” host?

A

Intermediate host: hosts in which the disease causing organism doesn’t obtain full maturity

Primary host: full mature form of the disease causing organism is achieved

164
Q

What cancers are associated with the BRCA1/2 mutations?

A
  • Breast cancer
  • Ovarian cancer
  • Prostate cancer
  • Melanoma
  • Pancreatic cancer
165
Q

What are the CNS findings on brain imaging in patients with infection by Taenia Solium?

A

Brain cysts

166
Q

What are the most common symptoms of Adult Onset Still’s Disease?

A
  • Fever
  • Polyarthritis
  • Skin rash (evanescent, salmon color)
  • Sore throat
167
Q

What is the inheritance pattern of Brugada’s syndrome?

A

Autosomal Dominant

PICMONIC: monster truck on a tsunami wave

168
Q

What is the skin manifestation of Mucormycosis?

A

Cutaneous mucormycosis begins as erythema and induration at the site of inoculation. Tissue infarction may ensue rapidly, which is manifested typically as a BLACK ESCHAR with central ulceration

Necrotizing fasciitis is a severe complication of cutaneous mucormycosis, and can present as rapid expansion of tissue erythema, induration, pain, and eschar formation.

169
Q

What 3 organs are the most commonly affected in Wilson Disease?

A
  • Hepatic
  • Neuropsychiatric
  • Ocular
170
Q

What is the MOA of Fingolimod?

A

Fingolimod stands for “Sphingo” + “Mod” and hence is a sphingosine receptor modulator

Sequestration of lymphocytes in LN, supposed protecting them from the brain where they would mediate damage from Multiple Sclerosis

171
Q

MOA of PSCK9 inhibitors?

A

Inhibits PSCK9

  • LDL receptors are on the liver
  • The amount of LDL receptors is proportional to the ability of the liver to get rid of cholesterol
    • TIP: LDL receptors are trash bins for cholesterol
  • PSCK9 BREAKS down LDL receptors, hence keeping high levels of cholesterol in the blood

The PCSK9 protein breaks down low-density lipoprotein receptors before they reach the cell surface, so more cholesterol can remain in the bloodstream.

172
Q

What is motor aphasia? Difference with Broca’s aphasia?

A

Transcortical Motor Aphasia (TMA or TMoA) is a type of aphasia that is similar to Broca’s aphasia. TMA is due to stroke or brain injury that impacts, but does not directly affect, Broca’s area

Halting speech (which is a type of “non-fluent” aphasia”), word finding difficulty, difficulty initiating speech

DIFFERENCE: Broca CANNOT repeat phrases

TIP: Transcortical motor apasia CAN repeat phrases like a “motor”

173
Q

What is global aphasia?

A

Global aphasia is the most severe form of aphasia. In global aphasia, all language modalities are affected – speaking, comprehension, reading, and writing.

TIP: the comprehension and the production of both verbal and written language is affected, hence, no language at all

174
Q

What is conductive aphasia?

A

A person with conduction aphasia can usually read, write, speak, and understand spoken messages

They just can’t repeat words or phrases

175
Q

What is anomic aphasia?

A

This term is applied to persons who are left with a persistent inability to supply the words for the very things they want to talk about-particularly the significant nouns and verbs. As a result their speech, while fluent in grammatical form and output is full of vague circumlocutions and expressions of frustration.

TIP: “TABOO” aphasia because just like the game taboo, patients can’t use the main word, but describe it instead

176
Q

What does it mean for the hemisphere to be dominant?

A

The hemisphere with language is dominant

TIP: the one who talks is the most dominant one in the room

For 90% of people, the left hemisphere is dominant for language

177
Q

Framework Questions:

What explains partial syndromes in strokes?

(That is, we don’t see the wide and full range of deficits expected for a stroke in a specific distribution of brain experiencing ischemia)

A
  • Collateral arterial blood supply
  • Large emboli may not be totally occlusive, and instead travel distally

Clinical tip: partial syndromes can be indicative of the location the emboli has traveled to

178
Q

What is the possible motor responses when evaluating GCS of a patient?

A

From best to worst:

  • Obeys commands for movement 6 points
  • Purposeful movement to painful stimulus 5 points
  • Withdraws in response to pain 4 points
  • Flexion in response to pain (decorticate posturing) 3 points
  • Extension response in response to pain (decerebrate posturing) 2 points
  • No response 1 point
179
Q

What part of the brain, if affected by stroke, will present with aphasia?

A

“LEFT” for “LANGUAGE”

Technically, which ever hemisphere is dominant, which in 90% of the cases is the left brain

180
Q

What side of the brain is the dominant side?

A

The one who speaks up is dominant

Hence, the side of the brain with language

90% if the case, it is the LEFT

181
Q

What are clinical scenarios other than PE/DVT that can lead to elevated levels of D-Dimer?

A

o Multisystem affected diseases such as burns, sepsis, trauma, infection, DIC

o Specific chronically damaged organs such as CKD, liver disease

o Vascular diseases such as CVA, PVD, Aortic dissection and ACS

o Normal states: pregnancy and older age

182
Q

What does POLST stand for?

A

Physician Order for Life Sustaining Treatment

However, no longer known as that. And now simply known as Portable Medical Order

TIP: “Portable” because it goes with the patient everywhere. “Medical order” because like a physician script, it acts like an order and needs to be signed by physician. Think of it as a script for “end of life”

183
Q

What is the difference between Advanced Directives vs POLST? Their relationship with each other?

A

Both are types of “Advanced Care Plans”

Simply, Advanced Directives specify WHO will be the POA (or Surrograte) in case the patient can no longer make decisions for themselves

POLST specifies WHAT to do in specific medical situations. Most simply, if cardiac arrest then what, if critical illness then what, if malnourished then what.

POLST complements the AD

184
Q

What is the difference between what population of people should have an advanced directive vs those who should have POLST?

A

ALL patients should have advanced directives

Advanced Frailty/Severely Ill patients should have POLST forms

185
Q

Who is required to sign the POLST form for it to be valid?

A

Physician

AND either patient OR the decision maker

186
Q

Demented patient presents the hospital. As the hospitalist, you contact the sister who is the POA. After discussion, she agrees that it would be best for the patient to be DNR and DNI in case that she were to decompensate. However, the POA lives out of state. How to fill out the POLST form?

A

Verbal orders are acceptable with follow-up signature by physician/NP/PA in accordance with facility/community policy

187
Q

Under what conditions is a UTI considered “complicated”?

A

TIP: all these conditions have the commonality that treatment failure is higher or higher risk of adverse outcomes

Stages in life: Pregnancy, postmenopausal, men

Kidney related: obstruction, indwelling catheter, stone and neurogenic bladder

Disease: immunocompromised, Type II DM

TIP: Type II DM and postmenopausal women are PREVALENT! But clinically, many will NOT treat these as complicated

188
Q

What work up is required for all patients presenting with a TIA?

A

Head imaging: CT first, but MRI preferred

Vascular imaging: Carotid US or MRI Angio head/neck OR CT Angio Head/neck

TTE

Holter monitor

TIP: going backwards from brain to heart as the source of emboli

189
Q

At what Blood Alcohol Level is considered intoxication?

A

> 80 mg/dl (legally)

190
Q

At what Blood Alcohol Level is a patient at risk for respiratory depression and arrest?

A

> 300 mg/dL

Clinical tip: A patient who is alert at this level of BAC is likely tolerant, hence alcohol use disorder is on the differential

191
Q

What lab is the earliest marker for iron deficiency?

A

Ferritin (then TIBC)

192
Q

What is the difference between ferritin, TSAT and TIBC in regards to the specific information it reveals?

A

Ferritin - the gold standard for iron storage (in the absence of inflammation)

TSAT - indicator of iron deficient erythropoiesis - NOT iron depletion

  • AKA iron supplies for the bone marrow
  • represented as a percent, it indicates the percent of transferrin occupied by iron; normal is 33%; if <16%, indicates that iron supply inadequate for erythropoiesis

TIBC
- related to TSAT in that, TSAT = iron/TIBC

Special note: Ferritin/TSAT/TIBC are ALL affected in inflammation/infection

193
Q

What SLGT2 can be used to slow the progression CKD (without the patient even having DM)?

A
  • NEJM Sept 2020
  • DAPA- CKD Trial
  • Dapaglaflozin
  • RCT, 4000 patients, CKD (GFR 20-75) with AND without DM
  • Dapaglaflozin 10mg vs placebo
  • Primary outcome: The primary outcome was a composite of a sustained decline in the estimated GFR of at least 50%, end-stage kidney disease, or death from renal or cardiovascular causes
    Results: 197 of 2152 participants (9.2%) in the dapagliflozin group and 312 of 2152 participants (14.5%) in the placebo group (hazard ratio, 0.61; 95% confidence interval [CI], 0.51 to 0.72; P<0.001; number needed to treat to prevent one primary outcome event, 19 [95% CI, 15 to 27])

Conclusion: NNT 19! Dapa for CKD (without Type II DM)

Heerspink HJL, Stefansson BV, Correa-Rotter R, et al. Dapagliflozin in Patients with Chronic Kidney Disease. N Engl J Med. 2020 Sep 24. doi: 10.1056/NEJMoa2024816.

194
Q

What drug, normally indicated for HFrEF, demonstrates improved renal outcomes, that is, slow progression of CKD in patients with HFpEF?

A
  • Sept 2020, Double Blind RCT
  • PARAGON HF Trial
  • Angiotensin-Neprolysin Inhibitors (Valsartan-Sacubitril)
  • 2000 Val-Sacub vs 2000 Valsartan
  • Primary Outcome: prespecified renal composite outcome (time to first occurrence of either: =50% reduction in estimated glomerular filtration rate (eGFR), end-stage renal disease, or death from renal causes), the individual components of this composite, and the influence of therapy on eGFR slope.

Result: composite renal outcome occurred in 33 patients (1.4%) assigned to sacubitril/valsartan and 64 patients (2.7%) assigned to valsartan (hazard ratio, 0.50 [95% CI, 0.33-0.77]; P=0.001)

Mc Causland FR, Lefkowitz MP, Claggett B, et al. Angiotensin-Neprilysin Inhibition and Renal Outcomes in Heart Failure With Preserved Ejection Fraction. Circulation. 2020 Sep 29;142(13):1236-1245. doi: 10.1161/CIRCULATIONAHA.120.047643. Epub 2020 Aug 17

195
Q

Does breast cancer screening starting at age 40 (normally age 50) lead to reduced mortality due to breast cancer screening?

A

LANCET Oncology September 2020

YES!

  • RCT, 22 year follow up
  • 53 883 women (33·5%) vs 106 953 (66·5%) to the control group
  • Primary outcome: mortality from breast cancers (with breast cancer coded as the underlying cause of death) diagnosed during the intervention period, before the participant’s first 50 yo screen.
  • Results: at 10 years of follow-up, 83 breast cancer deaths in the intervention group versus 219 in the control group (relative rate [RR] 0·75 [95% CI 0·58-0·97]; p=0·029).

Conclusion: Yearly mammography before age 50 years, commencing at age 40 or 41 years, was associated with a relative reduction in breast cancer mortality, which was attenuated after 10 years, although the absolute reduction remained constant. Reducing the lower age limit for screening from 50 to 40 years could potentially reduce breast cancer mortality.

Duffy SW, Vulkan D, Cuckle H, et al. Effect of mammographic screening from age 40 years on breast cancer mortality (UK Age trial): final results of a randomised, controlled trial. Lancet Oncol. 2020 Sep;21(9):1165-1172. doi: 10.1016/S1470-2045(20)30398-3. Epub 2020 Aug 12.

196
Q

What is the technical definition of CSF pleocytosis?

What is the general difference in regards to the range of pleocytosis between asceptic meningitis vs bacterial?

A

Pleocytosis (white blood cell count > 5 cells/mm3) - SINCE CSF should be sterile

Asceptic: 10-1000 cells/mm3

Bacterial: >500 at least

197
Q

Contraindications to fentanyl patch

A

Fever
Topical heat application
Exertion

Increased absorption can cause overdose

198
Q

How to convert IV Fentanyl to transdermal Fentanyl?

A

1:1 ratio

What ever hourly rate a patient is receiving, that is the hourly rate used for the patch form

199
Q

How long do fentanyl patches last?

A

72 hours

TIP: but end of dose failure could occur earlier

200
Q

Can break through opioids be used when patient is on Methadone? Fentanyl patch?

A

YES and YES

201
Q

Best time to initiate Fentanyl patch?

A

Opioid tolerant patient who is well controlled on current regimen

DO NOT start when patient is having unstable pain

202
Q

What is the oral morphine conversion to Fentanyl?

A

100mg of PO Morphine = 1 mg of Fentanyl

Tip: 1 mg = 1000mcg

The MME conversion factor for fentanyl patches is based on the assumption that one milligram of parenteral fentanyl is equivalent to 100 milligrams of oral morphine and that one patch delivers the dispensed micrograms per hour over a 24 hour day. Example: 25 ug/hr fentanyl patch X 24 hrs = 600 ug/day fentanyl = 60 mg/day oral morphine milligram equivalent.
In other words, the conversion factor not accounting for days of use would be 60/25 or 2.4.
However, since the fentanyl patch remains in place for 3 days, we have multiplied the conversion factor by 3 (2.4 X 3 = 7.2). In this example, MME/day for ten 25 μg/hr fentanyl patches dispensed for use over 30 days would work out as follows:
Example: 25 ug/hr fentanyl patch X (10 patches/30 days) X 7.2 = 60 MME/day. Please note that because this allowance has been made based on the typical dosage of one fentanyl patch per 3 days, you should first change all Days Supply in your prescription data to follow this standard, i.e., Days Supply for fentanyl patches= # of patches X 3

203
Q

What is “cross tolerance” and how does that affect how opioids are converted from one formlation to the next?

A
  • Cross tolerance is the tolerance that crosses from one opioid to the other

Since tolerance doesn’t cross completely from one opioid to the next, every time an opioid conversion occurs, the new dose should be adjusted

  • Ex: If patient is effectively experiencing pain control with current meds, then decrease the new form/dose by 25-50%
  • Ex: if patient is NOT effectively experiencing pain relief from meds, then start new dose/form by 100 to 125%
204
Q

What is the rule of thumb for the dose of break through opioid?

A

10-20% of the 24 hour total dose

OR

total break through dose = total continuous dose

Divide by the frequency patient should receive

EX: 60 mg PO Morphine daily for background pain control

Breakthrough = 60 mg as well

Each dose: 60/6 = 15mg
Hence, 10 mg Q4H PRN

205
Q

MOA of Tramadol?

A

Weak mu opioid agonist

NE and Serotonin receptor reuptake inhibitor

206
Q

What patient would benefit from Tramadol for pain control?

A
  • Mild to moderate pain
  • Healthy: NO renal/liver dysfunction
  • No concomitant antidepressants
  • No seizure risk
  • < 75 yo

TIP: VERY VERY healthy patient.

207
Q

Risk factors for drug resistant and Pseudomonal infection in patients with CAP?

A
  • Risk factors for nosocomial infections
  • structural lung disease, such as bronchiectasis
  • COPD
  • smoking
  • immunosuppression
  • recent steroid exposure
  • HEMIPLEGIA
  • history of antibiotic treatment against gram-positive organisms
  • recent hospitalization - SAME AS MRSA

TIP: aside from recent hospitalization, the risk factors for Pseudomonal involvement in CAP is totally different

208
Q

What are risk factors for MRSA in patients with CAP?

A
  • age > 74 years
  • prior hospitalization
  • history of MRSA infection
  • residence in nursing or long term care facility
  • long-term dialysis
  • lung abscess
209
Q

What is empiric coverage for Pseudomonas in CAP?

A 
piperacillin/tazobactam 4.5 g IV every 6 hours
cefepime 2 g IV every 8 hours
ceftazidime 2 g IV every 8 hours
aztreonam 2 g IV every 8 hours
meropenem 1 g IV every 8 hours
imipenem 500 mg IV every 6 hours
210
Q

What are empiric choices of antibiotics for CAP in patients with risk factors for MRSA?

A

Linezolid

Vancomycin

211
Q

First line treatment for autoimmune hemolytic anemia? Second line?

A

Steroids 1 mg/kg + pRBC transfusions

Plasmaphersis if severe

212
Q

One blood test required for diagnosis of AIHA?

A

Positive DAT

213
Q

Why should autoimmune encephalitis be in the differential diagnosis for new onset schizophrenia?

A

Age of Anti NMDAR encephalitis is 25-35, near the age of expected new onset schizophenia

214
Q

How to diagnose Anti NMDA Receptor Encephalitis?

A

Antibody in CSF, which is HIGHLY specific and sensitive

215
Q

What are CSF findings (outside of the antibodies) that are consistent with Anti NMDA receptor encephalitis?

A

Lymphocytic pleocytosis

Oligoclonal bands

216
Q

First line therapy for Anti NMDA Receptor Encephalitis?

A

IV Methylprednisolone (1 gm/day) and IVIG

217
Q

Associated malignancies that need to be screened for in patients with Anti NMDA Receptor Encephalitis?

A

Women: Ovarian teratomas

Men: Germ cell tumor like testicular cancer; And Mediastinal teratomas

218
Q

What is the difference between a conventional meta-analysis and a network meta-analysis?

A

Conventional meta-analysis can only compare two interventions at a time

Network meta-analysis (NMA) is a relatively recent development, which extends principles of meta-analysis to the evaluation of multiple treatments in a single analysis. This is achieved by combining the direct and indirect evidence. Direct evidence refers to evidence obtained from randomized control trials (RCTs); for example, in a trial comparing treatments A and B, direct evidence is the estimate of relative effects between A and B. Indirect evidence refers to the evidence obtained through one or more common comparators [7]. For example, in the absence of RCTs that directly evaluate A and B, interventions A and B can be compared indirectly if both have been compared to C in studies (forming an A-B-C “loop” of evidence). The combination of direct and indirect evidence is called mixed evidence

219
Q

What is detection bias?

A

Detection bias refers to systematic differences between groups due to HOW outcomes are determined. Blinding (or masking) of outcome assessors may reduce the risk that knowledge of which intervention was received, rather than the intervention itself, affects outcome measurement

AKA Bias in “detecting” a primary outcome

220
Q

What is performance bias?

A

Systematic differences between groups in the CARE that is provided, or in exposure to factors other than the interventions of interest

If the clinician knows that a HF patient is receiving a specific therapy, he may be more apt to monitor the patient more frequently, which in itself could change the outcomes as the patient is receiving better care

Solution: Blind both the participants and the personnel

221
Q

Do patients with HTN and established cardiovascular disease (CVA, CAD or PAD) benefit from more strict blood pressure control?

A

Cochrane Meta-analysis Sept 2020
NO

This Cochrane meta- analysis of 6 blinded controlled trials with 9484 participants showed that targeting a BP of 135/85 versus 140-160/90-100 did not lead to fewer deaths, fewer cardiovascular deaths, or fewer vascular events in patients with underlying vascular disease. There was no difference in side effects but perhaps more withdrawals in the low BP group.

Moderate level quality evidence

Saiz LC, Gorricho J, Garjon J, et al. Blood pressure targets for the treatment of people with hypertension and cardiovascular disease. Cochrane Database Syst Rev. 2020 Sep 9;9:CD010315. doi: 10.1002/14651858.CD010315.pub4.

222
Q

Tocilizumab - Viable treatment for COVID 19?

A

Lancet Rheumatology Aug 2020

  • Conclusion: Tocilizumab associated with reduced all-cause mortality in patients with severe COVID-19 pneumonia
  • Retrospective study
  • 544 patients: 178 received treatment
  • Caveat: overall, patients receiving tocilizumab were significantly lower median age and had lower median baseline PaO2/FiO2, higher median baseline SOFA score, longer median duration of symptoms
223
Q

What is the inheritance pattern of ARVC (Arrhythmogenic Right Ventricular Cardiomyopathy)?

A

Autosomal dominant!

TIP: there are a few other heart conditions that are AD that place patients at risk for sudden death such as HOCM, Brugada, Romano Ward Syndrome (type of Long QT Syndrome, and the most common)

224
Q

Framework Question:

What is the cause ARVC (Arrhythmogenic Right Ventricular Cardiomyopathy)?

A

It is a genetic disorder cause by mutation in the desmosomal genes

It leads to fatty fibrous replacement of tissue in the RV (or even LV) leading to both cardiomyopathy as well as a nidus for ventricular arrhythmias.

225
Q

Patient presents with STEMI, undergoes cardiac catheterization and found to have significant CAD apart from the culprit lesion - What leads to reduced MACE - culprit only PCI or complete vascularization

A

Complete vascularization

Systematic Review/Meta-analysis Aug 2020

Conclusion: Compared with culprit-only PCI, complete revascularization was associated with a substantial reduction in major adverse cardiovascular events (13.1% vs 22.1%; RR: 0.54; 95%CI: 0.43 to 0.66), repeat myocardial infarction (4.9% vs 6.8%; RR: 0.64; 95%CI: 0.48 to 0.84), and repeat revascularization (3.7% vs 12.3%; RR: 0.33; 95%CI: 0.25 to 0.44)

  • 6 RCT’s
  • 6700 patients
  • Complete revascularization versus culprit-only PCI

Levett JY, Windle SB, Filion KB, et al. Meta-Analysis of Complete Versus Culprit-Only Revascularization in Patients with ST-Segment Elevation Myocardial Infarction and Multivessel Coronary Disease. Am J Cardiol. 2020 Aug 29. pii: S0002-9149(20)30887-0. doi: 10.1016/j.amjcard.2020.08.030.

226
Q

What is the utility of the 4C score in evaluating COVID patients?

A

BMJ Sept 2020 Clinical Prediction Rule

Dynamed Level 1 Evidence

Study: Derivation/Validation
Patients: 35k in the derivation group/22k in the validation group

8 factors

  • male sex at birth
  • increasing age
  • number of comorbidities
  • respiratory rate
  • urea levels
  • reactive protein levels
  • decreasing peripheral oxygen saturation on room air (SpO2)
  • Glasgow Coma Scale score

TIP: Age/Gender/Co-morbidities can be obtained by hx alone. If >60, Male, and > 2 co-morbidities, already 11 points and considered high risk at the lower end

low-risk: 0-3 points - > 1.2% mortality
intermediate-risk: 4-8 points -> 9.9% mortality
high-risk: 9-14 points -> 31.4% mortality
very high-risk: ≥ 15 points -> 61.5% mortality

Risk stratification of patients admitted to hospital with covid-19 using the ISARIC WHO Clinical Characterisation Protocol: development and validation of the 4C Mortality Score

227
Q

What do reciprocal ST depressions in other leads generally indicate in STEMI?

A

Larger area of infarct

228
Q

TIP:

LAD occlusion leading to STEMI may show inferior infarct on the EKG - why?

A

Occlusion can embolize to the distal LAD which supplies the inferior part of the heart

229
Q

Are any RCT’s available in regards to anticoagulation in COVID patients?

A

No

230
Q

What is the difference in mild, moderate, severe and critically ill COVID per the NHC

A
  • TIP: Different from the WHO, as WHO defines “severe” as < 90% on RA
    • Mild: upper respiratory sx
    • Mod: upper and lower tract (i.e. pneumonia)
    • Severe: upper/lower tract sx and RR > 30, Sat < 94% on RA, PaO2/FiO2 ratio < 300
    • Critically ill: MV, Shock other organ failure requiring ICU
231
Q

What are the choices/dosing of chemical VTE ppx for acutely ill medical/surgical patients?

A
  • TIP: going from best renal function to worse
    • CrCl> 30: Enox 40mg daily
    • CrCl 15-29: Enox 30mg daily
    • CrCl < 15: Heparin 5000U Q12H
232
Q

What are choices of chemical VTE ppx in patients with history of HIT?

A
  • Argatroban
  • Bivalirudin
  • Fondaparinux
  • Rivaroxaban
233
Q

How is Argatroban similar to Heparin in the use of it?

A

Drip, nor renally dosed (as its ok with CrCl >5), aPTT 45-90

234
Q

What is dosing for acute VTE if enoxaparin is to be used?

A

If CrCl >30 ml/min, Enoxaparin 1 mg/kg BID SC

235
Q

What to do if patient has acute VTE in the setting of PLT < 50k (Kaiser)?

A
  • Transfuse with PLT and start therapeutic AC

- OR can reduce AC to 50% if PLT 25-50K

236
Q

What the recommendation for post discharge extended VTE prophylaxis in COVID patients?

A
  • CHEST: Reccomends AGAINST extended VTE ppx post-discharge

- KAISER: Consider if persistent risk factors, d/c to facility or low risk of bleeding

237
Q

What objective prediction score can predict a patient’s risk of developing a VTE? (Helpful in deciding extended VTE ppx post-discharge)

A
  • Padua

- IMPROVE score

238
Q

What platelet count is it a contraindication to Heparin/LMWH VTE prophylaxis?

A
  • “severe thrombocytopenia” per Dynamed which is < 20k

- KAISER: 25 K

239
Q

What COVID patients should receive systemic thrombolysis with confirmed PE?

A
  • CHEST: just like every other population, hemodynamically unstable patients from massive PE (BP < 90) OR in patients with deterioration despite SBP > 90 (.e.g. sinus tachy, worse gas exchange, signs of shock, increase JVP)
240
Q

Next step in management in COVID patient with recurrent VTE while on anticoagulation?

A

CHEST: increase LMWH to 25% to 50%

241
Q

In COVID patients with confirmed VTE treated with Heparin, what is the preferred lab to monitor therapeutic levels?

A
  • ISH Forum: Anti Xa levels as some COIVD patients will have baseline prolonged aPTT and Heparin resistance, requiring much higher doses of Heparin compared to others
242
Q

Which AC’s are breastfeeding friendly?

A

UFH, LMWH and Warfarin

243
Q

What is the recommendation in regards to extended chemical VTE prophylaxis in COVID pregnant patients?

A

Ten days of LMWH post-discharge 40mg daily

244
Q

Recommendations of the COMBINATION of both mechanical VTE ppx and chemical VTE ppx?

A

CHEST/ASH: recommend one or the other and NOT both

245
Q

What is the chemical VTE prophylaxis of choice in patients with COVID?

A
  • CHEST: LMWH or Fondaparinux > UFH since it decreases exposure for healthcare workers
  • KAISER:
    - Acutely ill patients: LMWH/Fonda > UFH
    - Critically ill patients: LMWH > UFH; and LMWH/UFH > Fonda
246
Q

What is the recommended dosing of chemical VTE prophylaxis for critically ill COVID patients?

A
  • CHEST/NIH: standard dosing
  • ISTH: intermediate dosing (e.g. LMWH 0.5mg/kg BID)
  • KAISER: intermediate dosing
247
Q

Does chemical VTE prophylaxis need to be held prior to procedures/surgeries?

A

YES! Just like therapeutic anti-coagulation

248
Q

Recommended treatment for VTE (PE/DVT) in acutely ill COVID patients?

A
  • CHEST: UFH or LMWH (but even suggest DOAC if patient doesn’t have any drug-drug interactions)
  • KAISER: UFH and LMWH only since clinical deterioration can occur quickly
249
Q

Recommended treatment for VTE (PE/DVT) in critically ill COVID patients?

A
  • CHEST: Parenteral AC, LMWH/Fondaparinux > UFH

- KAISER: UFH may be better than LMWH/Fonda given high risk of bleeding in certain individuals

250
Q

Framework Question:

What is the difference between “odds” and “risks”? What are they used for in medical research?

A
  • “Risk” refers to the probability of occurrence of an event or outcome in a “specific group”
  • Ex:
    • 1% risk of MI in patients treated with ASA
    • 1 heart attack in patient with ASA/100 patients treated with aspirin
    • Risk of lung cancer in smokers amongst all smokers: smoker w/ lung cancer/All smokers
    • Risk of lung cancer in the general population: anyone with lung cancer/entire population
    • number of new cases/population
  • Relationship with incidence: Incidence and risk are the same, and incidence is commonly referred to as incidence risk

“Relative risk” is the ratio of risks between 2 groups

  • Ex: Relative risk = Incidence among exposed/ incidence among non- exposed
  • Compared to simply “risk”, relative risk tells you how much MORE at risk you are compared to another group (exposed or not exposed to a certain factor)
  • The term “odds” is often used instead of risk.
    Statistically: “Odds” refers to the probability of occurrence of an event/probability of the event NOT occurring.
    • Ex: Odds of rolling a 6 with a dice = 1:5

Both are used to describe the strength of an association between an exposure (being a risk factor or a medical intervention) and an outcome

  • Ex: OR of lung cancer in smokers
  • Ex: RR of ARDs in COVID patients treated with convalescent plasma
251
Q

What is the recommended formulation of Vit D for treatment of Vitamin D deficiency?

A

CholeCalCiferol - Vitamin D3

252
Q

Framework Question:

What is the difference between the different formulations of Vitamin D?

A

Storage form: 25 OH Vit D, AKA CalciDIol
- Exact drug formulation: CalcefiDIol

Active form: 1, 25 OH Vit D, AKA CalciTRIol

  • Exact drug formulation: CalciTRIol (Calcijex)
  • Drugs formulations (BOTH are ACTIVE forms of Vit D though not exactly 1,25 OH Vit D):
    • Vit D2, AKA ErgoCalCiferol
    • Vit D3, AKA CholeCalCiferol - PREFERRED form for Vit D Deficiency
253
Q

What is the Urinary findings consistent with Adrenal Insufficiency induced hyponatremia?

A
  • Urine Na > 40
  • UOsm > 100

Overall, shows inappropriate labs in the setting of hyponatremia

254
Q

What finding on the WBC differential may be indicative of Adrenal Insufficiency?

A

Peripheral Eosinophilia

Why: Endogenous glucocorticoids are responsible for apoptosis of eosinophils. Hence, the absence of glucocorticoids leads to the increase in eosinophils in the periphery

255
Q

Framework Question:

Explain how to use and interpret the Urine Anion Gap

A

Urine anion gap is used mainly to evaluate a patient with NAGMA

UAG: Urine ([Na] + [K]) - [Cl-]

UAG basically answers the question of how much Ammonium there is. Ammonium, being positive, is bound to Cl-. Hence, the UAG will tell you how much Cl there is, which tells you how much Ammonium there is, which tells you how much ACID there is since acid exists in the form of ammonium in the urine.

EX:

  • UAG positive means low Cl, low Ammonium, low acid. Low urinary acid in the setting of metabolic acidosis means inability to appropriately secrete H+.
    • TLDR: Type I RTA or Type 4 RTA
  • UAG negative means high Cl, high Ammonium, high acid. High urinary acid in the setting of metabolic acidosis is appropriate.
    • TLDR: Type 2 RTA or GI loss of bicarb.
256
Q

In paracoccidioides infection, what determines how patients present?

A

The chronicity

Acute/subacute paracoccidioides infections present differently than chronic paracoccidioides infections

257
Q

What population is at risk of paracoccidioides infection?

A

Latin American, rural

Usually those who work in agriculture

258
Q

Most common organs involved upon presentation in patients who present with chronic paracoccidioides infection?

A
  • Lungs (90%):
    - Cough, shortness of breath, chest pains
  • Mucosal lesions (50%):
    - oropharynx, larynx and nasal cavity
    - Oral ulcers (STANDS OUT! Not many infections with oral ulcers)
  • Adrenal gland (50%)
    - Adrenal insufficiency only in 10%
  • Skin (46%):
    - Papules, pustules, ulcers and verroucous lesions
259
Q

What is the toxidrome of anticholinergic toxicity?

A

“Red as a beet” - cutaneous vasodilation

“Dry as a bone” - anhidrosis

“Hot as a hare” - fever

“Blind as a bat” - Dilated pupils, nonreactive

“Mad as a hatter” - delirium, hallucinations and disorientation

260
Q

According to the NIH COVID Guidelines in Oct 2020, what treatments should a COVID patient receive?

A

Not hospitalized: no treatments

Hospitalized, on O2, but NOT High Flow: Remdesivir
- TIP: RCT, Grade A1 (that is strong recc, level 1 evidence AKA RCT)

Hospitalized, on High flow ( or NIV): Remdesivir + Dexamethasone (Grade AIII, expert opinion)

Hospitalized, on Invasive MV (or ECMO): Dexamethasone alone (Grade A1)

CAVEAT: In ALL of the cases of hospitalized patients, guideline does approve the use of Remdesivir + Dexamethasone, BUT makes it a point to mention that there have been NO RCTs of this combination

261
Q

Does pre-exposure prophylaxis with HCQ prevent health care workers from acquiring COVID 19?

A

JAMA SEPT 2020
RCT, double blinded, placebo controlled

NO
132 Health care workers
HCQ 600mg daily for 8 weeks
Outcome: COVID via nasopharyngeal swab at 8 weeks

Results: There was no significant difference in infection rates in participants randomized to receive hydroxychloroquine compared with placebo (4 of 64 [6.3%] vs 4 of 61 [6.6%]; P > .99).

Abella BS, Jolkovsky EL, Biney BT, et al. Efficacy and Safety of Hydroxychloroquine vs Placebo for Pre-exposure SARS-CoV-2 Prophylaxis Among Health Care Workers: A Randomized Clinical Trial. JAMA Intern Med. 2020 Sep 30. pii: 2771265. doi: 10.1001/jamainternmed.2020.6319.

262
Q

What measures can reduced or prevent the development of cows milk protein allergy?

A

J Allergy Immunology Sept 2020

Early Introduction of Cows Milk Formula
RCT

There were 2 CMA cases (0.8%) among the 242 members of the ingestion group and 17 CMA cases (6.8%) among the 249 participants in the avoidance group (risk ratio = 0.12; 95% CI = 0.01-0.50; P < .001). The risk difference was 6.0% (95% CI = 2.7-9.3).

Conclusion: Daily ingestion of CMF between 1 and 2 months of age prevents CMA development. This strategy does not compete with breast-feeding

TIP: Exclusively breastfed infants until 6 months of age has shown decreased incidence of milk protein allergy

Sakihara T, Otsuji K, Arakaki Y, et al. Randomized trial of early infant formula introduction to prevent cow`s milk allergy. J Allergy Clin Immunol. 2020 Sep 2. pii: S0091-6749(20)31225-2. doi: 10.1016/j.jaci.2020.08.021.

263
Q

What is the relationship between AL Amyloidosis and Plasma cell dyscrasias?

A

“Not all plasma cell dyscrasias lead to AL Amyloidosis, but all AL Amyloidosis is due to plasma cell dyscrasias”

AL Amyloidosis = Amyloid Light chain Amyloidosis which means that the source of the amyloid is light chains. Light chains come from plasma cells. Hence the underlying cause is a plasma cell dyscrasia, e.g. Multiple Myeloma or Waldenstrom Macroglobinemia

Hence, you can have Multiple myeloma complicated by AL Amyloidosis. Or you can simply have multiple myeloma without any signs of AL amyloidosis. It all depends on which immunoglobulin component is being created.

264
Q

What transplants place a patient at risk for Post Transplant Lymphoproliferative Disorder?

A

Solid organ transplant AND Allogeneic hematopoietic cell transplantation as a result of immunosuppression

265
Q

What is the cause of most cases of PTLD?

A

EBV infection (55-65%)

266
Q

When does PTLD tend to occur?

A

Depends on the transplant:

  • Solid organ transplant: within 12 months of transplant
  • HSCT: within 6 months

NOTE: wonder if it has to do with high immunosuppression in the setting of HSCT

267
Q

How may timing of PTLD in solid organ transplant patients suggest the specific cause of PTLD?

A

If “early-onset PTLD” (that is, < 12 months), likely EBV related

If “late onset PTLD” (that is, > 12 mos), likely NOT related to EBV

268
Q

How does stroke differ between the US and world in regards to death?

A

US: 5th cause of death

World: 2nd cause of death

269
Q

Framework:

What is the definition of stroke?

A

Abrupt onset of neurologic deficit that is attributable to a focal vascular cause

TIP: the definition of a stroke is CLINICAL, and the lab and imaging studies are used to SUPPORT the diagnosis

270
Q

Framework Question:

Why does cerebral ischemia lead to acute neurologic symptoms?

A

Neurons lack glycogen so ischemia leads to acute energy failure and symptoms

271
Q

What does FAST stand for in regards to stroke evaluation?

A

F – Facial weakness
A – Arm weakness
S – Speech abnormality (slurring)
T – TIME

272
Q

What are some clinical findings that may suggest migraine as the cause of acute neurologic deficit compared to cerebrovascular accident?

A

Migraine:
- Sensory > motor sx and the progression of symptoms occurs over minutes – NOT seconds
- Visual disturbance characterized by scintillating scotomas
Cortical disturbances cross vascular boundaries

273
Q

Looking at the brain from the outside, that is, the cortical surface, what parts are supplied by the MCA vs PCA vs ACA?

A
274
Q

Describe the MCA and its branching pattern and course

A

Imagine the circle of willis as a mythical animal crucified onto the brainstem

The ACA are large horns that curve backwards like slick back hair

The MCA are horns that jut out laterally from where ears would be, travels between what is the thumb of the boxing glove and the glove (the temporal lobe/frontal lobe), heading toward the surface of the brain. Travelling laterally (M1) it gives off deep penetrating branches (feeding a lot of the basal ganglia – putamen, globus pallidum, caudate nucleus; and posterior limb of the int capsule/corona radiata)

When reaching the surface, that is, the sylvian fissure, there is a superior and an inferior division (M2). There the arteries wrap around the brain, almost cradle the brain.

275
Q

What is the presentation of a stroke involving the MCA?

A

Contralateral hemiplegia

Contralateral hemianesthesia

Homonymous Hemianopia (Homymous: same visual field, that is both left or both right; Hemianopia: visual field is cut in half as opposed to quarters e.g. quadrantopia)

Ipsilateral gaze preference (looks at the side of stroke)

Dyarthria (2/2 facial weakness)

Global aphasia (dominant sphere)

Neglect/Anosognosia (lack of awareness of disease)/constructional apraxia (non-dominant sphere)

276
Q

What is anosognosia?

A

Anosognosia is a self-awareness disorder which prevents brain-damaged patients from recognizing the presence or appreciate the severity of deficits in sensory, perceptual, motor, behavioural or cognitive functioning, which are evident to clinicians and caregiver

Patients can’t appreciate their illness for what it is, in totality, in severity, in it’s implication on their lives, etc.

277
Q

What physical exam maneuver can evaluate a patient for neglect?

A

Demonstrate extinction on double simultaneous stimulation. Thus, patients may detect a stimulus on the affected side when presented alone, but when stimuli are presented simultaneously on both sides, only the stimulus on the unaffected side may be detected – Sensory neglect

In motor neglect, normal strength may be present, however, the patient often does not move the affected limb unless attention is strongly directed toward it – motor neglect

TIP: neglect is in some ways a poor man’s version of anosognosia. The latter is a total disregard for something, and neglect isn’t

278
Q

What are stroke syndromes that are indicative of a lacunar stroke of the M1 division? (That is occlusion of the lenticulostriate vessels of M1)

A

Pure motor stroke of the contralateral side

Sensory motor stroke of the contralateral side

Clumsy hand clumsy speech syndrome

Easily forget: Pure facial weakness (genu of internal capsule) followed by progressive arm, trunk, then leg weakness (as ischemia travels posteriorly)

279
Q

What cerebral artery is vulnerable to iatrogenic stroke caused by aneurysmal clipping?

A

Anterior choroidal artery given its location ot the anterior communicating artery

280
Q

What is the presentation of a stroke involving the ACA?

A

Contralateral hemiparesis leg/foot

Contralateral hemianesthesia leg/foot

Urinary incontenince

Abulia (akinetic mutism), slowness, delay intermittent interruption, lack of spontaneity, whispering, reflex distraction to sights/sounds

Gait apraxia

281
Q

What vascular territory, even with a stroke, will often have little to no presentation or presentations that result in substantial recovery?

A

Anterior cerebral artery given the many collaterals it has with MCA and PCA

282
Q

What vascular territory is most affected by a stroke involving the internal carotid artery?

A

MCA

283
Q

What is the description of monocular blindness that patients with ICA stenosis may describe (amarosis fugax)?

A

Horizontal shade that sweeps up or down across the field of vision

284
Q

What does the “posterior circulation” of the brain consist of?

A

Vertebral arteries

Basilar artery

Paired PCA

285
Q

PCA strokes are often caused by what underlying mechanism?

A

Emboli lodging into the basilar artery

Dissection of vertebral artery or fibromuscular dysplasia

286
Q

The presence of CN III palsy in the right setting is indicative of what specific stroke?

A

Posterior Cerebral Artery Stroke (since that artery wraps around the midbrain – 3,4 nerves)

287
Q

Describe how the course of posterior cerebral artery?

A

The posterior cerebral artery arises from the proximal bifurcation of the basilar artery

Since it is high, it is located at the level of the midbrain. There are 2 parts P1, then P2. P1 is the first branch and mainly hugs the midbrain (hence its syndrome involves midbrain structures). P2 heads toward the temporal and occipital lobes as if holding them up

288
Q

Why may PCA and MCA strokes present similarly? Difference?

A

PCA/MCA both can present with contralateral weakness and contralateral hemianopia

PCA stroke: DOES NOT spare the macula
MCA strokes: spares the macula

289
Q

What are the components of a pacemaker?

A
  • Easy way is also to think of the PM as just another pacemaker cell of the heart, such as SA or AV, with its own intrinsic rhythm and rate. So, if the original SA node doesn’t fire, the PM, just like the natural AV node or myocardium would, will take over. Just like the conducting cells of the heart, if a cell fires first, it sets the pace, and the others follow. Think of this as sensing and triggering.
    • Pulse generator: the heart is made up of myocardial contractile cells and the myocardial conducting cells, both which can act as pulse generators, BUT the conducting cells, including the SA and AV node are the main pulse generators
    • Pacing Lead: The lead connects the pulse generator to the myocardium, hence it acts as the highway for the impulse to reach the myocardium. In the case of the heart, this would be the conduction system, including the bundle of his, perkinjes, etc.
290
Q

What is the difference between “asynchronous” and “synchronous” pacemakers? What mode are most pace makers?

A
  • Asynchronous means that the pacemaker paces without any synchronization with the heart’s rhythm. Also known as “fixed rate mode”, this means the PM paces at a set mode regardless of the heart’s rhythm which leads to competition
  • Synchonous means synchronized with the heart. Hence, it implies sensing with subsequent triggering or inhibiting. This is called “demand” mode as it fired “on demand” only, that is, when the heart is not discharging its own natural impulses
291
Q

What is the difference between “single chamber” vs “dual chamber” pacemakers?

A
  • Chamber can refer to atria OR ventricle
  • Hence, single pacemaker can be atrial or ventricular
  • Dual chamber involves 2 leads, one in the RA and the other in the RV
292
Q

In regards to temporary pacemakers, what is more common - single vs dual chamber? Permanent pacemakers?

A
  • Temporary - single in the RV

- Permanent - dual, in the RA and RV

293
Q

What is the fiver letter pacemaker identification code?

A
  • TIP: think beer: Pilsner, Stout, IPA
  • P: Paced chamber
  • S: Sensed chamber
  • I: inhibit, trigger or Both
  • P: programmable function
  • A: Anti tachycardia pacing
294
Q

What is “automatic mode switching” in permanent pacemakers? What is the main purpose of “automatic mode switch”?

A
  • Mode switch means the pacemaker, at certain instances, will actually switch to another 5 digit mode
  • This is most often used to prevent tachyarrhythmias that may be induced by paroxysmal atrial tachycardias (like Afib/flutter/SVT) and perpetuated by the triggered ventricular impulse.
  • How can a PM perpetuate a tachyarrhythmia: The main purpose of a dual chamber pacemaker is to achieve atrioventricular synchrony. This is achieved by the atrial lead sensing atrial depolarization and triggering the ventricular lead to depolarize the ventricle AFTER some atrioventricular delay. In patients with no native atrioventricular conduction as in complete heart block, if the native atrial rate increases, the ventricular lead follows suit and discharges at the corresponding rate to maintain atrioventricular synchrony - which can lead to tachyarrhythmia in instances of paroxysmal atrial tachycardias such as Afib/flutter, SVT. However, the maximum rate at which the ventricular lead can respond is usually programmed at 120–130 beats/min to prevent very rapid ventricular rate
295
Q

What is the finding on EKG that indicates PM has fired?

A
  • Spike or vertical line
296
Q

What does “sensing” mean and how is that demonstrated on an EKG?

A
  • The purpose of sensing is to sense or recognize intrinsic electrical impulse of the heart and to inhibit and trigger appropriately. PM that sense intrinsic impulse should inhibit. PM that senses a lack of intrinsic impulse should fire
  • Hence, EKG should show spike when no intrinsic electrical activity is sensed. And EKG should not show spike when intrinsic electrical activity is sensed.
297
Q

What does “capture” mean and how is that represented in EKG?

A
  • Capture is the successful stimulation of the myocardium by a PM stimulus
  • Represented by actual PM spike followed by P or QRS complex - depending on the chamber stimulated
298
Q

Why are some PM spikes long and very prominent and others tiny and hard to see?

A

How long the spikes are depends on how far the impulse has to travel from one pole to the next.

Unipolar systems: electrode is the negative pole, pulse generator is the positive pole. Since impulse travels long distance, EKG spike is long

Bipolar systems: Negative and positive electrodes are close to each other, shorter distance, small - even difficult to see- spike on EKG

299
Q

What is the difference between the QRS produced from a paced stimulus vs a normal QRS from the native heart?

A

Native QRS: narrow (depolarization occurs down the His Purkinje system, and both LV/RV are simultaneously stimulated)

Paced QRS: wide since depolarization occurs from RV to LV (lead stimulates RV first)

300
Q

What is the “pacing interval” of a pacemaker? How to figure out the pacing interval from EKG?

A
  • It is the HR at which the PM is set. Measure from pacer spike to pacer spike to find out
301
Q

What is the cause of fusion beats in patients with PM?

A

PM fires a stimulus but at the same time the patient fires his own electrical stimulus, resulting in the ventricular depolarization being caused by both

302
Q

What are EKG findings of a fusion beat occurring in a patient with a PM?

A

Following a ventricular pacer spike that occurs at the programmed rate, the QRS is different in morphology from BOTH the paced beats AND the intrinsic beats

303
Q

What are “pseudofusion” beats? And how do they look like in the EKG?

A

Pacer spike followed by QRS that looks exactly like the patient’s NATIVE QRS

304
Q

How to describe a pacemaker rhythm in which the majority of the beats start with a pacer spike followed by p wave and natural QRS?

A
  • Atrial paced rhythm
305
Q

How to describe a pacemaker rhythm in which the majority of the beats start with a pacer spike followed by p wave, pacer spike, then wide QRS?

A
  • AV paced rhythm
306
Q

How to describe a pacemaker rhythm in which the majority of the beats start with a pacer spike wide QRS?

A
  • Ventricular paced rhythm
307
Q

What is “undersensing” and what should EKG show?

A
  • PM doesn’t sense or “see” the native electrical activity

- Undersensing is recognized on the ECG by a pacing spike that occurs earlier than expected.

308
Q

What is “oversensing” and what are the corresponding EKG findings?

A
  • The PM is too sensitive and “sees” too much, interpreting artifacts as P waves. EKG shows paced beat LATER than expected
309
Q

What is the best way to evaluate paced rhythms?

A
  • 1) Determine the automatic interval or the set HR of the PM via a note card (between 2 spikes)
  • 2) Going from left to right, evaluate all pacer spikes: place left marker on the pacer spike PRIOR to the spike being evaluated
  • 3) Categorize: on time, too early or too late which will tell you the problem
  • 4) Then evaluate the complex that follows the pacer spike: none, P, QRS, fusion beat, pseudofusion beat
310
Q

What is the cause of Lymphogranuloma Venereum?

A

Chlamydia Trachomatis - Serovar L1-L3

“L” for Lymphogranuloma Venereum

TIP: Chlamydia has 15 different serovars

311
Q

Treatment for Lymphogranuloma Venereum?

A

Doxycycline 100mg BID

312
Q

Relationship between Lymphogranuloma Venereum (LGV) and HIV?

A

86% of patients with LGV have HIV!

Lesson: The presence of and history of other STD’s influences the risk of HIV. Remember, STDs cause inflammation, inflammation leads to CD4 cells, CD4 cells that interact with HIV become infected.

313
Q

Most common presentation of LGV?

A

Developed countries: proctitis and proctocolitis

Undeveloped: genital ulcer and tender inguinal/femoral LN

314
Q

Differential diagnosis of PAINLESS genital ulcer?

A

Syphilis

Granuloma inguinale - Klebsiella

Lymphogranuloma Venereum - Chlamydia

315
Q

Framework Question:

Draw the Circle of Willis Diagram

A
316
Q

Is Hydroxychloroquine effective for the treatment of COVID 19?

A

OCT 2020 - NEJM

  • RCT, open label platform
  • 1561 HCQ vs 3155 Usual care
  • Primary outcome: Death at 28 days

Death within 28 days occurred in 421 patients (27.0%) in the hydroxychloroquine group and in 790 (25.0%) in the usual-care group (rate ratio, 1.09; 95% confidence interval [CI], 0.97 to 1.23; P = 0.15)

Conclusion: Among patients hospitalized with Covid-19, those who received hydroxychloroquine did not have a lower incidence of death at 28 days than those who received usual care

Horby P, Mafham M, Linsell L, et al. Effect of Hydroxychloroquine in Hospitalized Patients with Covid-19. N Engl J Med. 2020 Oct 8. doi: 10.1056/NEJMoa2022926.

317
Q

Is Lopinavir-Ritonavir effective in the treatment of COVID?

A

OCT 2020 - LANCET

  • Randomised, controlled, open-label, platform trial
  • Primary outcome: Death at 28 days
  • Results: 374 (23%) patients allocated to lopinavir-ritonavir and 767 (22%) patients allocated to usual care died within 28 days (rate ratio 1·03, 95% CI 0·91-1·17; p=0·60).

Conclusion: n patients admitted to hospital with COVID-19, lopinavir-ritonavir was not associated with reductions in 28-day mortality, duration of hospital stay, or risk of progressing to invasive mechanical ventilation or death.

Lopinavir-ritonavir in patients admitted to hospital with COVID-19 (RECOVERY): a randomised, controlled, open-label, platform trial. Lancet. 2020 Oct 5. pii: S0140-6736(20)32013-4. doi: 10.1016/S0140-6736(20)32013-4.

318
Q

Most common types of hypersensitivity pneumonitis?

A

Farmer’s lung and bird fancier’s lung

319
Q

Framework Question:

What is hypersensitivity pneumonitis?

A

It is an interstitial lung disease resulting from an immune reaction to an inhaled antigen that is often time aersolized and dispersed in the lung parenchyma

320
Q

Patient presents with acute respiratory symptoms and CT shows ground glass opacities. You entertain the idea of a hypersensitivity pneumonitis. Does the chronicity fit with the clinical presentation?

A

Hypersensitivity pneumonitis, or HSPs, can present in an acute, subacute or chronic picture

321
Q

What are suggestive findings of hypersensitivity pneumonitis for the following work ups

  • Clinical history:
  • CXR:
  • CT Chest:
  • PFT:
  • BAL:
A
  • Clinical history: evidence of plausible offending antigen
  • CXR: can be normal
  • CT Chest: ground-glass opacities, poorly defined centrilobular nodules, mosaic attenuation, and air trapping on HRCT; mid to UPPER zone preference
  • PFT: restrictive pattern, hypoxemia, and reduced diffusing capacity for carbon monoxide (DLCO)
  • BAL: >40% of lymphocytes in BAL
322
Q

What is the presentation of gait apraxia?

A

Frontal (apraxic) gait — Bilateral frontal lobe dysfunction can result in a higher-level gait disorder, in which basic motor and sensory functions are intact but there is a failure of motor programming, or an apraxia.

Patients with a frontal (apraxic) gait may have some or all of the following features [13]:

●Cautious, slow gait.

  • The stride length is shortened
  • on a normal or slightly wide base
  • hesitation, freezing, and en bloc turns
  • “magnetic,” as if the feet are stuck to the floor.

● Gait ignition failure

  • characterized by difficulty initiating
  • three or four steps in place before a normal stride ensues.

● Postural instability: The patient may be easily displaced backwards, precipitating falls.

● wide-based and lurching gait that resembles cerebellar ataxia

Internal Medicine (6 decks)

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