October - November 2020 Flashcards

1
Q

What is the concern in regards to the use of ACEi to COVID 19?

A

COVID 19 enters the cells via the ACE 2 receptors, which is located in many cells, not only the pneumatocytes

Pathophysiology:

  • COVID 19’s viral spike protein will bind to the ACE 2 receptor of a cell
  • Certain cells will also have a concomitant protease called TMPRSS2 - Type 2 Transmembrane Serine Protease - that cleaves ACE2 and activates the viral spike protein
  • Activated viral spike protein is endocytosed
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2
Q

Postoperative atrial fibrillation following CABG is common. Does it lead to longterm risk of CVA?

A

OCT 2020

Yes
Retrospective study

Population: 3023 patients, of whom 734 (24.3%) developed pAF with the remaining 2289 maintaining sinus rhythm

Results: At 10 years, the cumulative incidence of CVA was 6.3% (4.6%-8.1%) versus 3.7% (2.9%-4.5%) in patients with pAF and sinus rhythm, respectively.

pAF was an independent predictor of CVA at 10 years (hazard ratio, 1.53 [95% CI, 1.06-2.23]; P=0.025) even when CVAs that occurred during the index admission were excluded from the analysis (hazard ratio, 1.47 [95% 1.02-2.11]; P=0.04).

Benedetto U, Gaudino MF, Dimagli A, et al. Postoperative Atrial Fibrillation and Long-Term Risk of Stroke After Isolated Coronary Artery Bypass Graft Surgery. Circulation. 2020 Oct 6;142(14):1320-1329. doi: 10.1161/CIRCULATIONAHA.120.046940. Epub 2020 Oct 5.

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3
Q

Does empiric antibiotic treatment of acute cholecystitis include anaerobic coverage?

A

No

IDSA 2010

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4
Q

What scenario would empiric antibiotic treatment of acute cholecystitis include anaerobic coverage?

A

Biliary-enteric anastomosis

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5
Q

What is the EKG criteria for LVH?

A

Criteria must be met in BOTH precordial AND limb leads

Precordial leads: “25, 35, 45” rule

  • R wave in V4, V5 or V6 > 26 mm
  • R wave in V5 or V6 plus S wave in V1 > 35 mm
  • Largest R wave plus largest S wave in precordial leads > 45 mm

Limb leads: “10, 15, 20, 25” rule
- TIP: LRF - cross my heart like catholic

  • R wave in aVL > 11 mm
  • S wave in aVR > 14 mm
  • R wave in aVF > 20 mm
  • R wave in lead I + S wave in lead III > 25 mm
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6
Q

Metabolic causes of bradycardia?

A

TIP: all of the causes are LOW electrolytes EXCEPT Hyperkalemia

Hyperkalemia (> 8 mmol/L) can cause sinus bradycardia, sinus arrest, and intraventricular (IV) conduction blocks, especially in patients with renal failure

Hypoxemia

Hypothyroidism (uncommon, usually causes sinus bradycardia with first-degree atrioventricular [AV] block)

Hypothermia due to environmental exposure can cause sinus bradycardia

Hypogonadotropic hypogonadism

Hypoglycemia
Hypokalemia
Hypocalcemia

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7
Q

What ACS can lead to bradycardia?

A

Acute ischemic and infarction, especially inferior ischemia due to right coronary artery occlusion

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8
Q

How to decide what empiric antibiotics to initiate for a patient who presents with acute cholecystitis?

A

Mild and moderate:

  • Cefazolin
  • Cefuroxime
  • Ceftriaxone

If patients with “severe physiologic disturbance, advanced age, immunocompromised OR bilioenteric anastomosis” or APACHE II >15, treat with

Monotherapy (mostly the penems)

  • Mero
  • Imipenem-Cilastatin
  • Doripenem
  • Pip-Tazo

OR dual therapy
Metronidazole

PLUS

Ceftazidime
Cefepime
Ciprofloxacin
Levoflox

IDSA 2010

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9
Q

Diagnosis of Posterior MI in the EKG?

A

V1-V3

TIP: posterior part of heart is at the opposite side of anterior part of heart. Since EKG only reads the anterior part, the V1-V3 findings should be reciprocal

Horizontal ST depression
Tall, broad R waves (>30ms)
Upright T waves
Dominant R wave (R/S ratio > 1) in V2

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10
Q

What is the role of surgery in SCLC?

A

In general, surgical resection is not routinely recommended for patients because even patients with LD-SCLC still have occult micrometastases.

TIP: “Small cell” really means small cell - its everywhere

TIP: if patient had pneumonectomy or lobectomy, then cancer must be one of the NSCLC

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11
Q

What is the staging of SCLC? What is the basis of the staging criteria?

A

Based on tolerable radiation window

Limited disease vs extensive disease; limited means it can be encompassed by radiation window

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12
Q

Patient with SCLC diagnosed by pleural effusion. Limited or extensive disease?

A

Extensive since it CAN’T be encompassed by a radiation window

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13
Q

Patient with known history of hives recently had a cardiac arrest when skinny dipping. The cause?

A

Cold urticaria

Though cold urticaria is a localized disease, vascular collapse may occur if an individual is submerged in cold water.

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14
Q

Treatment for cold urticaria

A

H1 blocker

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15
Q

Framework Question:

What is the cause of Sarcoidosis?

A

An infectious or non-infectious environmental agent that triggers an inflammatory response in genetically susceptible patients

Infectious: mycobacterium proteins found in histology; Propionibacterium acnes has been found in LN tissue

Non-infectious: linked to exposure to molds, insecticides; health care workers with higher risk

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16
Q

What are the different domains of speech to evaluate when evaluating for aphasia?

A

When evaluating someone who reports difficulty with language, it is important to assess speech in several different domains:

spontaneous speech
comprehension
repetition
naming
reading
writing
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17
Q

What domain is most commonly affected in aphasic patients?

A

Anomia refers to the inability to name common objects and is the most common finding in aphasic patients

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18
Q

How does the FSH/LH levels vary from birth to puberty to menopause

A

After birth and the loss of placenta-derived steroids, gonadotropin levels rise. FSH levels are much higher in girls than in boys. This rise in FSH results in ovarian activation

By 12–20 months of age, the reproductive axis is again suppressed, and a period of relative quiescence persists until puberty. At the onset of puberty, pulsatile GnRH secretion induces pituitary gonadotropin production.

Gonadotropin levels are cyclic during the reproductive years and increase dramatically with the loss of negative feedback that accompanies menopause

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19
Q

Diagnosis of peritonitis in patient with PD catheter?

A

This can be diagnosed by the presence of >100/μL leukocytes with >50% polymorphonuclear cells on microscop

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20
Q

Most common organism implicated in PD catheter related peritonitis?

A

Staph epi

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21
Q

Peritonitis from PD cath: IV vs PD antibiotics?

A

A Cochrane review (Wiggins KJ et al: Cochrane Database Syst Rev 1:CD005284, 2008) concluded that intraperitoneal administration of antibiotics was more effective than intravenous administration

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22
Q

What is the cause of the massive diuresis from post obstructive diuresis?

A

This is likely due to postobstructive diuresis, which results from release of obstruction, increase in GFR over the course of days, decreased tubule pressure, and increased solute load per nephron, resulting in increased urine output. Decreased medullary osmolarity is a feature of chronic obstruction and persistent obstruction

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23
Q

Characteristic odor of sulfur mustard?

A

Burnt garlic or horseradish

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24
Q

What is the presentation of sulfur mustard exposure?

A

Predominantly mucocutaneous

Eye: Red eyes = most sensitive part, almost always present
Skin: Sunburn, vesicular rash in moist areas - axilla, groin, neck
Airway: Laryngospasm, necrosis

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25
Q

Ascites in cirrhosis: Na restriction vs fluid restriction?

A

Na restriction 2 gm/day

Tip: Common misconception is fluid restriction

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26
Q

First line treatment for cryptogenic organizing pneumonia?

A

Steroids

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27
Q

Biospy for a patient with subacute symptoms of shortness of breath. Concern for cryptogenic organizing pneumonia - expected histology?

A

Pathology shows the presence of granulation tissue plugging airways, alveolar ducts, and alveoli.

EWWW

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28
Q

What is the gram stain findings consistent with Actinomyces?

A

Sulfur granules are an in vivo concretion of Actinomyces bacteria, calcium phosphate, and host material. Gram stain of Actinomyces infection shows intensely positive staining at the center with branching rods at the periphery

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29
Q

Most common physical exam finding in HCC?

A

Hepatomegaly is the most common physical sign in patients with HCC, occurring in 50%–90% of the patients.

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30
Q

Difference between the following:

  • Gilbert Syndrome
  • Dubin Johnson
  • Criggler Najjar Type I/Type 2
A

Gilbert: UDP glucuronosyltransferase deficiency - inability to conjugate unconjugated bili to conjugated
- TIP: hence autoimmune hemolytic anemia is on the diff diagnosis

  • Criggler Najjar Type I/Type 2: same enzyme defect but more severe
  • Type I: U. Bili > 20 - present since birth and stays as compared to Gilbert
  • Type II: U. Bili < 20

Dubin Johnson: elevated CONjugated bili
- TIP: hence obstructive jaundice is on the diff diag

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31
Q

Common initial presentation of pemphigus vulgaris?

A

Clinically, most patients with pemphigus vulgaris present after age 40, and the initial lesions are on mucosal surfaces, predominantly the oral mucosa. These lesions erode quickly to ulcers and are typically quite painful.

They may be the only manifestation or precede the development of blistering skin lesions by several months

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32
Q

Biopsy findings consistent with pemphigus vulgaris

A

Acantholytic blister formation in the suprabasal layer of the epidermis with intradermal vesicle formation. Means junctions between the keratinocytes are lost.

Basal keratinocytes remain attached to the epidermal basement membrane - hence a blister made from keratinocytes, hence easily broken blisters

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33
Q

First line for pemphigus vulgaris?

A

Prednisone at a dose of 1 mg/kg daily

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34
Q

Framework question:

Cause of pemphigus vulgaris?

A

Autoimmune mediated blistering skin disorder in which IgG antibodies target desmoglein, the junction proteins between keratinocytes, causing blistering lesions that easily burst.

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35
Q

Diagnosis of pulmonary alveolar proteinosis?

A

BAL - shows macrophages with PAF stain demonstrating a lot of protein and amorphous proteinacious material

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36
Q

CT findings consistent with pulmonary alveolar proteinosis?

A

Classically, the CT appearance is described as “crazy pavement” with ground-glass alveolar infiltrates in a perihilar distribution and intervening areas of normal lung

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37
Q

Do IVC filters yield a clinical benefit for prevention of PE and death?

A

OCT 2020

Cochrane Systematic Review and Meta-analysis

Studies: randomised controlled trials (RCTs) and controlled clinical trials (CCTs)
- 6 studies, but only 2 could be evaluated

Conclusion:

Two of the six identified studies were relevant for current clinical settings. One showed no evidence of a benefit of retrievable filters in acute PE for the outcomes of PE, death, DVT and bleeding during the initial three months in people who can receive anticoagulation (moderate-certainty evidence). The other study did not show any benefit for prophylactic filter insertion in people who sustained multiple traumatic injuries, with respect to symptomatic PE, mortality, or lower extremity venous thrombosis (moderate-certainty evidence). We can draw no firm conclusions regarding filter efficacy in the prevention of PE from the remaining four RCTs identified in this review. Further trials are needed to assess vena caval filter effectiveness and safety, and clinical differences between various filter types

Young T, Sriram KB Vena caval filters for the prevention of pulmonary embolism. Cochrane Database Syst Rev. 2020 Oct 8;10:CD006212. doi: 10.1002/14651858.CD006212.pub5.

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38
Q

What is the difference between the following trials:

  • RCT
  • Controlled Non-randomized Study of Investigation (NRSI)
  • Non-controlled non-randomized study of investigation
A

“Controlled” refers to control group, hence in controlled studies, researchers are able to determine which subjects receive the intervention and which do not. Uncontrolled may mean there is NO control group.

“Randomized” refers to randomization of the intervention

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39
Q

Convalescent plasma in COVID 19?

A

Studies: 19 studies (2 RCTs, 8 controlled NRSIs, 9 non-controlled NRSIs) with 38,160 participants, of whom 36,081 received convalescent plasma

LOE: The overall certainty of evidence was low to very low, due to study limitations and results including both potential benefits and harms

Conclusion:
- We are uncertain whether convalescent plasma is beneficial for people admitted to hospital with COVID-19

  • here was limited information regarding grade 3 and 4 AEs to determine the effect of convalescent plasma therapy on clinically relevant SAEs.
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40
Q

What are the neurologic symptoms of COVID? How common are they?

A

Neurologic manifestation at any time during disease course in 82.3%

  • 42.2% at symptom onset
  • 62.7% at hospital admission

Neurologic manifestations included

myalgia in 44.8%
headache in 37.7%
encephalopathy in 31.8%
dizziness in 29.7%
dysgeusia in 15.9%
anosmia in 11.4%
syncope in 4.3%
rhabdomyolysis in 3.5%
orthostatic hypotension in 3.1%
ischemic stroke in 1.4%
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41
Q

Efficacy of mRNA COVID 19 Vaccine?

A

NEJM Sept 2020

messenger RNA vaccine encoding stabilized prefusion SARS-CoV-2 spike protein (mRNA-1273) reported to illicit neutralizing antibody response in all adults, but with high rate of mild-to-moderate adverse events

Non controlled randomized trial

45 adults aged 18-55 years received mRNA-1273, 2 intramuscular injections given 28 days apart

Conclusion:

  • High adverse rate:
  • > 30 % after first vaccination, dose dependent, that is, high the vaccine dose, more likely to get symptom
  • > 50% after second - chills, HA, myalgias
  • ALL had seroconversion at 15 days with virus-neutralizing activity capable of reducing infectivity by ≥ 80% by day 43
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42
Q

What may ST elevation in aVR be indicative of?

A
  • Occlusion in the LMCA
  • Proximal left anterior descending artery (LAD) occlusion
  • Severe triple-vessel disease (3VD)

TIP: Almost all the indications for CABG

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43
Q

MOA of Tranexamic acid? Relation to aminocaproic acid?

A

Tranexamic acid, a synthetic amino acid, is a competitive inhibitor of plasminogen activation, and at much higher concentrations, a noncompetitive inhibitor of plasmin (ie, actions similar to aminocaproic acid). Tranexamic acid is about 10 times more potent in vitro than aminocaproic acid

TIP: Think of plasma (or lava) melting away clots

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44
Q

Patient presents with a severe GIB. Utility of Tranexamic acid?

A

LANCET JUNE 2020

NO

Study design: international, multicentre, randomised, placebo-controlled trial

Participants: >16 yo, significant (defined as at risk of bleeding to death) upper or lower gastrointestinal bleeding
- 5956 patients in the tranexamic acid group and 5981 patients

Intervention: loading dose of 1 g tranexamic acid, which was added to 100 mL infusion bag of 0·9% sodium chloride and infused by slow intravenous injection over 10 min, followed by a maintenance dose of 3 g tranexamic acid added to 1 L of any isotonic intravenous solution and infused at 125 mg/h for 24 h, or placebo (sodium chloride 0·9%

Results: Death due to bleeding within 5 days of randomisation occurred in 222 (4%) of 5956 patients in the tranexamic acid group and in 226 (4%) of 5981 patients in the placebo group (risk ratio [RR] 0·99, 95% CI 0·82-1·18)

Effects of a high-dose 24-h infusion of tranexamic acid on death and thromboembolic events in patients with acute gastrointestinal bleeding (HALT-IT): an international randomised, double-blind, placebo-controlled trial. Lancet. 2020 Jun 20;395(10241):1927-1936. doi: 10.1016/S0140-6736(20)30848-5.

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45
Q

What cells do cyclosporine/tacrolimus target?

A

Primarily on T helper cells, although some inhibition of T suppressor

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46
Q

Cyclosporine and tacrolimus are primarily used in the treatment of what type of transplant?

A

Solid organ transplant

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47
Q

What is the MOA of tacrolimus and cyclosporine?

A

End goal: T lymphocyte proliferation is reduced

Both drugs bind with high affinity to a family of cytoplasmic proteins present in most cells: cyclophilins for cyclosporine and FK-binding proteins for tacrolimus. The drug-receptor complex specifically and competitively binds to and inhibits calcineurin, a calcium- and calmodulin-dependent phosphatase [1-4]. This process inhibits the translocation of a family of transcription factors (NF-AT), leading to reduced transcriptional activation of cytokine genes for interleukin (IL)-2, tumor necrosis factor (TNF)-alpha

TIP: “Cyclo”philin bound by “cyclo”sporine; “FK Tacro”

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48
Q

What part of the conduction system is affected in 2nd degree AV block, Mobitz Type I vs II?

A

Mobitz Type I: at the AV node (hence progressive prolongation of the PR interval)

Mobitz Type II: His purkinje system

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49
Q

What is the relationship between the presence of 2nd degree AV block, Mobitz Type I vs II with structural heart disease?

A

Mobitz Type II is more likely to be related to underlying structural heart abnormalities (e.g. infarction, fibrosis or necrosis)

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50
Q

What other EKG abnormality accompany 2nd degree AV block, Mobitz Type II?

A

Patients typically have an underlying LBBB OR bifascicular block, hence the 2nd degree AV block is produced by the intermittent failure of the remaining fascicle

TIP: “Bilateral bundle branch block”

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51
Q

What EKG finding can further localize where the block is in the conduction system in patients with 2nd degree AV block, Mobitz Type I vs II?

A

In around 75% of cases, the conduction block is located distal to the Bundle of His, producing broad QRS complexes.

In the remaining 25% of cases, the conduction block is located within the His Bundle itself, producing narrow QRS complexes.

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52
Q

What are key characteristics to distinguish a Mobitz Type I compared to both Type II and complete heart block?

A

Intermittent non-conducted P waves WITHOUT progressive prolongation of the PR interval (compare this to Mobitz I).

The PR interval in the conducted beats remains CONSTANT.

The P waves ‘march through’ at a CONSTANT rate.

The RR interval surrounding the dropped beat(s) is an exact multiple of the preceding RR interval (e.g. double the preceding RR interval for a single dropped beat, treble for two dropped beats, etc).

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53
Q

Role of Tocilizumab in COVID?

A

NEJM OCT 2020

No

  • Type: Randomized, Double Blind, Controlled Trial
  • Patients: COVID patients on supplemental O2; 243 patients; 141 (58%) were men, and 102 (42%) were women. Median age 59.8 years (range, 21.7 to 85.4), and 45% of the patients were Hispanic or Latino
  • Design: 2:1, single dose, 8mg/kg of Tocilizumab (IL 6 blocker)
  • Outcome: death + preventing intubation
  • Results: The hazard ratio for intubation or death in the tocilizumab group as compared with the placebo group was 0.83 (95% confidence interval [CI], 0.38 to 1.81; P = 0.64)
  • Conclusion: Tocilizumab was not effective for preventing intubation or death in moderately ill hospitalized patients with Covid-19.

Stone JH, Frigault MJ, Serling-Boyd NJ, et al. Efficacy of Tocilizumab in Patients Hospitalized with Covid-19. N Engl J Med. 2020 Oct 21. doi: 10.1056/NEJMoa2028836.

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54
Q

Vericiguat - What is it? What disease has it been tested for? Efficacy?

A

Oral soluble guanylate cyclase stimulator

HFpEF

Not effective in regards to improvement of physical limitation scores

Armstrong PW, Lam CSP, Anstrom KJ, et al. Effect of Vericiguat vs Placebo on Quality of Life in Patients With Heart Failure and Preserved Ejection Fraction: The VITALITY-HFpEF Randomized Clinical Trial. JAMA. 2020 Oct 20;324(15):1512-1521. doi: 10.1001/jama.2020.15922.

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55
Q

What is the mutation associated with Hereditary Hemochromatosis?

A

Type 1 HFE-related is a mutation in the HFE gene where patients are homozygous for the C282Y mutation

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56
Q

What ethic population is at the highest risk for Hereditary hemochromatoiss?

A

Caucasians have 6x higher risk compared to blacks

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57
Q

What organ can hereditary hemochromatosis affect?

A

Virtually any organ

Clinical tip: on differential diagnosis of “infiltrative” diseases affecting multiple organs

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58
Q

What iron tests are indicative and can be diagnostic of hereditary hemochromatosis?

A

Transferrin saturation > 45% is diagnostic

Ferritin > 300, but extremely high like > 4000 is highly suggestive

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59
Q

Patients with Hereditary Hemachromatosis are at particular risk for which bacterial organisms?

A

Yersinia Enterolitica

Vibrio vulnificus

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60
Q

Conventional treatment of Hereditary Hemachromatosis? Goal Ferritin/iron saturation?

A

Tip: simply iron overload, RBC’s are the source, hence remove the RBCs

Phlebotomy weekly initially

Goal: Iron sat < 50%, Ferritin 50-100

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61
Q

What is the relationship between liver and spleen with mesenteric ischemia?

A

Splenic infarcts or hepatic infarcts can be indicative of mesenteric ischemia.

TIP: Makes sense since the celiac artery and possibly the SMA feeds spleen/liver

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62
Q

What is Weil’s Disease?

A

A severe form of Leptospirosis that is characterized by

  • Pulmonary hemorrhage
  • Renal failure
  • Jaundice

Hence, liver, renal and respiratory failure

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63
Q

Leptospirosis PICMONIC about transmission

A
  • Gram negative aeriobic spirochete
    - Arab mouse with drills for hands
  • Penetrates non-intact skin
    - drills for hands penetrate skin
    -
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64
Q

What is conjunctival suffusion?

A

Conjunctival erythema WITHOUT presence of an inflammatory exudate

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65
Q

Treatment of Leptospirosis?

A

Doxycycline

TIP: Just like syphilis’s second line treatment

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66
Q

What is the definition of “Typical Atrial Flutter”?

A

Typical atrial flutter (90% of the cases), also called counterclockwise atrial flutter, is characterized by

1) POSITIVE waves in lead V1
2) NEGATIVE flutter waves in leads II, III, and aVF

Tip: counter intuitive, because one would think “typical” is “clockwise”, but its the reverse

Clinical tip: the “teeth” or the “pointed” ends of the flutter waves indicate if they are positive or negative waves

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67
Q

What is the definition of “Atypical Atrial Flutter”? (AKA reverse typical atrial flutter)

A

Atypical atrial flutter, also called clockwise atrial flutter, is characterized by

1) NEGATIVE waves in inferior leads V1
2) POSITIVE flutter waves in leads II, III, and aVF

Tip: counter intuitive, because one would think “typical” is “clockwise”, but its the reverse

Clinical tip: the “teeth” or the “pointed” ends of the flutter waves indicate if they are positive or negative waves

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68
Q

What is the pathway or the reentrant tract that atrial flutter takes?

A

In typical atrial flutter, the reentrant wavefront travels up the interatrial septum and down the right atrial free wall anterior to the crista terminalis and traverses the cavotricuspid isthmus to complete the circuit in a counterclockwise direction in the right atrium

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69
Q

Apart from typical atrial flutter and atypical, what are other uncommon ones that exist?

A

Simply different in the pathway of the circuit

Left atrial flutter, double wave reentry atrial flutter (two reentrant wave fronts simultaneously circulating in the same reentrant circuit), lower loop and upper loop reentry right atrial flutter, and atrial flutter caused by reentry around a surgical incision160 have also been described

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70
Q

What is the relationship between Atrial fibrillation and Atrial Flutter?

A

Atrial flutter often is initiated by AF. Atrial flutter occurs commonly in association with AF

And hence, ANY disease state that is commonly associated with Afib, can easily cause Atrial Flutter such as chronic obstructive pulmonary disease, mitral or tricuspid valve disease, thyrotoxicosis, and postsurgical repair of certain congenital cardiac lesions (eg, atrial septal defect, the Mustard procedure, the Senning procedure, or the Fontan procedure), as well as enlargement of the atria for any reason, especially the right atrium.

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71
Q

What is clinical tip to diagnose Atrial flutter if they EKG shows a rhythm that is too fast to accurately identify saw tooth waves?

A

Adenosine or vagal maneuvers to slow the AV node so that there will be longer time between every QRS and hence P or saw tooths can be seen more easily

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72
Q

What is the difference between Atrial fibrillation and A flutter in regards to the choice between rate control and rhythm?

A

Although the choice between rate and rhythm control is similar to that in AFib, there is bias toward rhythm control in atrial flutter as a result of the relative ease and HIGH success rate of catheter ablation, but also to the difficulty in many patients to achieve good rate control.

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73
Q

What is considered “valvular atrial fibrillation”?

A

Valvular AF is defined as moderate-to-severe mitral stenosis or mechanical heart valves

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74
Q

What is the CHADS VASC score that most guidelines will recommend anticoagulation?

A

There is agreement among guideline recommendations that women with a CHA2DS2-VASc score of ≥ 3 and men with a score of ≥ 2 are at an increased risk of stroke and should be given anticoagulant therapy based on the benefits greatly outweighing the bleeding risk.

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75
Q

Patient has new onset afib, but CHADSVASC score of 1. Anticoag?

A

Most will say consider AC

American College of Chest Physicians (ACCP) - offer stroke prevention to patients with atrial fibrillation and ≥ 1 non-sex CHA2DS2-VASc stroke risk factor, such as males with CHA2DS2-VASc score ≥ 1

Strong recc, moderate evidence

TIP: Almost ALL patients with Afib should be treated with AC

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76
Q

ASA for Afib?

A

No

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77
Q

Definitive treatment of atrial flutter?

A

Catheter ablation is highly successful, typically 90% or greater, to eliminate the typical atrial flutter

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78
Q

How accurate is Chest CT for the diagnosis of COVID 19?

A

Cochrane Review Sept 2020

TLDR: Sensitive, but no specific

Our findings indicate that chest CT is sensitive but not specific for the diagnosis of COVID-19 in suspected patients, meaning that CT may not be capable of differentiating SARS-CoV-2 infection from other causes of respiratory illness. This low specificity could also be the result of the poor sensitivity of the reference standard (RT-PCR), as CT could potentially be more sensitive than RT-PCR in some cases.

Salameh JP, Leeflang MM, Hooft L, et al. Thoracic imaging tests for the diagnosis of COVID-19. Cochrane Database Syst Rev. 2020 Sep 30;9:CD013639. doi: 10.1002/14651858.CD013639.pub2.

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79
Q

In patients with candiduria, who gets treatment?

A

Treatment is not recommended for asymptomatic patients except for high-risk patients such as neonates and those with neutropenia or having urologic procedures

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80
Q

What is the treatment from candida UTI

A

Fluconazole 200 mg orally daily for 14 days

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81
Q

What population of patients are at risk of candiduria and fungal UTI?

A

Most commonly arises in catheterized, instrumented, or obstructed patients

In inpatient settings:

diabetes
indwelling catheter
urinary tract obstruction
recent surgery
ICU patients 

Patients receiving immunosuppressive therapy

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82
Q

What is relationship between the presence of candiduria and disseminated candidal infection?

A

Rarely, the presence of yeast in the urine is a sign of disseminated infection.

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83
Q

What is the expected axis of the R wave in aVR?

A

Expected R wave is NEGATIVE

Why: aVR is positive, located in the right arm, and since the overall vector goes in a down and left direction, AWAY from aVR, then aVR shows a NEGATIVE R wave.

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84
Q

Differential diagnosis of a dominant R wave in AVR?

A

Poisoning with sodium-channel blocking drugs (e.g. TCAs)
Dextrocardia
Incorrect lead placement (left/right arm leads reversed)
Commonly elevated in ventricular tachycardia (VT)

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85
Q

What is the first line imaging modality for concern for ovarian malignancy?

A

US

Yes, EVEN if CT already obtained. It is because US characteristics are taken into account to determine risk of malignancy

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86
Q

What patient requires a Ca 125 upon diagnosis of ovarian cyst?

A

ALL postmenopausal women with ovarian cyst regardless of the characteristics

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87
Q

Does CA 125 rule out ovarian cancer in patients with ovarian cysts?

A

NO

It can be low in limited disease, and tends to be high in extensive disease. So it could rule out extensive disease, but not the presence of disease

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88
Q

What anticoagulant has shown some evidence of reduced incidences of post thrombotic syndrome?

A

Sept 2020

Meta-analysis and Systematic Review

RIVAROXABAN

  • Seven comparative studies, comprising 2364 participants
  • VKA vs Rivaroxaban
  • Results:
  • [pooled unadjusted odds ratio (OR): 0.53, 95%CI: 0.43-0.65, P < 0.00001]
  • reduced risk of mild PTS (OR: 0.64, 95%CI: 0.50-0.82, P = 0.0005)
  • moderate PTS (OR: 0.64, 95%CI: 0.45-0.91, P = 0.01),
  • severe PTS (OR: 0.52, 95%CI: 0.33-0.82, P = 0.005).

CONCLUSION: In comparison to VKAs, the use of rivaroxaban for DVT treatment has the potential to reduce PTS events. However, well-designed studies with larger sample sizes are needed to corroborate these findings.

Li R, Yuan M, Cheng J, et al. Risk of post-thrombotic syndrome after deep vein thrombosis treated with rivaroxaban versus vitamin-K antagonists: A systematic review and meta-analysis. Thromb Res. 2020 Sep 17;196:340-348. doi: 10.1016/j.thromres.2020.09.014.

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89
Q

What is the efficacy of Tocilizumab for moderate to severe COVID 19?

A

OCT 2020
JAMA

  • NO
  • Cohort-embedded, investigator-initiated, multicenter, open-label, bayesian randomized clinical trial
  • Intervention Tocilizumab at 1 and 3 days
  • 64 pts vs 63 pts, admitted on at leas 3 L NC, BUT not intubated OR in the ICU
  • Outcomes: progression score, death at 14 days, and need for MV

Conclusion: TCZ did NOT reduce WHO-CPS scores lower than 5 at day 4 but MIGHT have reduced the risk of NIV, MV, or death by day 14. NO difference on day 28 mortality was found

Hermine O, Mariette X, Tharaux PL, et al. Effect of Tocilizumab vs Usual Care in Adults Hospitalized With COVID-19 and Moderate or Severe Pneumonia: A Randomized Clinical Trial. JAMA Intern Med. 2020 Oct 20. pii: 2772187. doi: 10.1001/jamainternmed.2020.6820.

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90
Q

How much of Ca is bound to Albumin?

A

About 50% of total calcium is ionized, and the rest is bound principally to albumin.

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91
Q

What is the correction of Ca for a low albumin level?

A

Every 1.0 g/dL of albumin below 4, add 0.8mg/dL to the Calcium

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92
Q

What is the difference in the characteristics of the ST elevation in acute pericarditis vs acute myocardial infarction?

A

In acute myocardial infarction, ST elevations are CONVEX (big hill), and reciprocal depression is usually more prominent

TIP: counter intuitive to what I would think. Con CAVE, makes me think of cave, that is, hill shaped. ConVEX, makes be think of the big V between the T wave and the QRS.

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93
Q

What EKG characteristics of pericarditis that are helpful in distinguishing from acute myocardial infarction?

A
  • Q waves
  • Concave (pericarditis) vs convex ST elevation (tombstone)
  • PR depression (compared to TP segment) - interesting: caused by atrial involvement
  • T wave inversion AFTER ST changes return to baseline is characteristic of pericarditis (TWI can occur in acute setting of AMI)
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94
Q

Most common cardiac abnormality in newborns of mothers with SLE?

A

AV block

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95
Q

Patient with brain tumor diagnosed. What are the chances that it is primary vs metastatic?

A

3 times more likely that a new diagnosis of brain tumor is metastatic

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96
Q

Differential diagnosis of brain tumor?

A

3x more likely metastatic

If primary:

  • 30% glioma
  • 35% meningiomas
  • 10% vestibular schwannoma
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97
Q

What type of glioma is more likely to present with acute seizures?

A

Low grade glioma

NOTE: Interesting!

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98
Q

Best imaging choice for suspected brain tumor?

A

Malignant brain tumors—whether primary or metastatic—typically enhance with gadolinium and may have central areas of necrosis; they are characteristically surrounded by edema of the neighboring white matter.

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99
Q

FDA treatment for IPF - idiopathic pulmonary fibrosis?

A

Nintedanib is an intracellular tyrosine kinase inhibitor that inhibits several growth factors including vascular endothelial growth factor, fibroblast growth factor, and platelet-derived growth factor. A recent trial demonstrated that use of this medication slowed the rate of decline in FVC and could potentially decrease mortality.

Pirfenidone is an oral antifibrotic medication that has been demonstrated to decrease fibroblast proliferation and collagen synthesis.

NOTE: both have antifibrotic qualities

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100
Q

Expected PFT for IPF?

TLC
VC
RV
DLCO

A

Pulmonary function tests demonstrate restrictive ventilatory defect (low TLC, low RV, low VC) with a low DLCO.

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101
Q

CT findings that are clue that diagnosis of subacute shortness of breath is likely NOT IPF?

A

Atypical findings that should cause one to consider an alternative diagnosis include the presence of ground-glass infiltrates, nodular opacities, an upper lobe predominance of disease, and prominent hilar or mediastinal lymphadenopathy

Clinical: acute exacerbations of IPF will have GOO on imaging

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102
Q

What is the difference between phototoxic and photoallergic reaction when exposed to glyburide?

A

The sulfonylureas are sulfa drugs!

Phototoxicity: nonimmunologic reaction that can occur without a latency period after taking a drug. The response resembles a sunburn and occurs in sun-exposed areas. Like a sunburn, a phototoxic reaction can blister and desquamate

Photoallergy: UV rays transform the drug into an unstable hapten capable of stimulating an immune response. This delayed hypersensitivity response is intensely pruritic. Sun-exposed skin appears lichenified and leathery. In rare cases (5%–10%), persistent hypersensitivity to light will persist even after the offending drug is discontinued, a condition known as persistent light reaction

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103
Q

At what lung volume does the outward recoil of the chest wall equal the inward elastic recoil of the lung?

A

The functional residual capacity of the lung refers to the volume of air that remains in the lung following a normal tidal respiration

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104
Q

What is head and neck cancer staging?

A

Stage I and II (NO nodal involvement at all)

  • Stage I: Tumor < 2 cm WITHOUT extraparenchymal involvement
  • Stage II: Tumor > 2 cm WITHOUT extraparenchymal involvement

Stage III - automatically once 1 LN has metastatic disease

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105
Q

What is stage I or II head and neck cancer? Treatment of choice?

A

Stage I and II (NO nodal involvement at all)

  • Stage I: Tumor < 2 cm WITHOUT extraparenchymal involvement
  • Stage II: Tumor > 2 cm WITHOUT extraparenchymal involvement

Radiation therapy to preserve voice - NOT surgery

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106
Q

What BMI is lethal for men vs women?

A

Normal BMI ranges between 20 and 25 kg/m2, and a patient is considered underweight with likely moderate malnutrition at a BMI of 18.5 kg/m2.

Severe malnutrition is expected with a BMI of <16 kg/m2.

In men, a BMI of <13 kg/m2 is lethal
In women, the lethal BMI is <11 kg/m2

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107
Q

How many homeless are there in Ca?

A

134,000 on any given night (2017)

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108
Q

Most common composition of renal stones?

A

Calcium (75 to 85%) > Uric acid > Cysteine > Struvite

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109
Q

What are non-acs causes of elevated troponins?

A

ESRD

Heart specific: PE, myo/pericarditis, hypotension, hypertension

Lesson: It is important to remember that although cardiac troponin biomarkers (troponin I or T) are quite sensitive for myocardial infarction due to coronary occlusion, they lack somewhat in specificity.

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110
Q

What are the components that contribute to oxygen delivery to tissue? Least important part?

A

QO2 = CO × [1.39 × hemoglobin × SaO2 + (0.003 × PaO2)]

Delivery of O2 is dependent on the CO and the Oxygen content.

Note that the PaO2 is negligible in regards to the content of O2

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111
Q

Most common extra-articular complication of ankylosing spondylitis?

A

Anterior uveitis is the most common, occurring in 40% of patients with ankylosing spondylitis.

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112
Q

What criteria is the gold standard for diagnosis VAP?

A

There is NO gold standard, not even endotraheal cultures (as this can be due to colonization)

Usually, its the presence of a constellation of symptoms that point toward VAP:

  • New O2 requirement
  • Fever
  • Increased secretions
  • Leukopenia or leukocytosis
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113
Q

What are the suggested regimens for H. Pylori treatment?

A

“Bismuth Quadruple therapy” - notice the QID for 14 days

  • Bismuth QID
  • PPI BID
  • Metronidazole QID
  • Tetracycline QID

“Concomitant therapy” - not sure the meaning, but the tip is that each med is BID for 14 days

  • PPI BID
  • Clarithro BID
  • Amox 1gm BID
  • Metro 500 mg BID

Tip: PPI and Metronidazole is the same for both regimens

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114
Q

How do opioids provide relief of dyspnea for patients in hospice care?

A

Opioids reduce the sensitivity of the central respiratory drive center and often reduce the sensation of dyspnea.

Clinical tip: Opioids are first line for dyspnea in end of life care

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115
Q

Monitor AST/ALT during initiation of statin therapy?

A

Because clinically meaningful aminotransferase elevations are so rare after statin use and do not differ in meta-analyses from the frequency of such laboratory abnormalities in placebo recipients, the National Lipid Association’s Safety Task Force concluded that liver test monitoring was not necessary in patients treated with statins and that statin therapy need not be discontinued in patients found to have asymptomatic isolated aminotransferase elevations during therapy

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116
Q

Most common organs involved in cryoglobulinemic vasculitis?

A

The most common manifestations of cryoglobulinemic vasculitis are cutaneous vasculitis, arthritis, peripheral neuropathy, and glomerulonephritis

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117
Q

Which RTA is associated with Srogrens?

A

RTA Type I

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118
Q

Expected Urine pH in RTA Type I?

A

pH > 5.5

Basic because tubules unable to excrete H+ ions. In contrast with RTA Type II in which bicarb can’t be reabsorbed, BUT DCT can still excrete H, hence pH < 5.5

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119
Q

Efficacy of pentoxyfylline for Intermittent Claudication in PAD?

A

COCHRANE REVIEW OCT 2020

Conclusion: There is a lack of high-certainty evidence for the effects of pentoxifylline compared to placebo, or other treatments, for IC. There is low-certainty evidence that pentoxifylline may improve PFWD and TWD compared to placebo, but no evidence of a benefit to ABI or QoL (moderate-certainty evidence).

Broderick C, Forster R, Abdel-Hadi M, et al. Pentoxifylline for intermittent claudication. Cochrane Database Syst Rev. 2020 Oct 16;10:CD005262. doi: 10.1002/14651858.CD005262.pub4.

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120
Q

Convalescent plasma for COVID RCT?

A

BMJ Oct 2020
PLACID Trial

RCT Phase II Trial

Patients: Indian; confirmed moderate covid-19 (partial pressure of oxygen in arterial blood/fraction of inspired oxygen (PaO2/FiO2) ratio between 200 mm Hg and 300 mm Hg or a respiratory rate of more than 24/min with oxygen saturation 93% or less on room air

Intervention: two doses of 200 mL convalescent plasma, transfused 24 hours apart

NOTE: neutralizing ab NOT measured prior

MAIN OUTCOME MEASURE: Composite of progression to severe disease (PaO2/FiO2 <100 mm Hg) or all cause mortality at 28 days post-enrolment.

CONCLUSION: Convalescent plasma was not associated with a reduction in progression to severe covid-19 or all cause mortality

Agarwal A, Mukherjee A, Kumar G, et al. Convalescent plasma in the management of moderate covid-19 in adults in India: open label phase II multicentre randomised controlled trial (PLACID Trial). BMJ. 2020 Oct 22;371:m3939. doi: 10.1136/bmj.m3939.

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121
Q

Tocilizumab RCT for COVID - effective?

A

JAMA OCT 2020

Prospective, open label RCT - 1st for Tocilizumab

Who: COVID-19 pneumonia documented by imaging, partial pressure of arterial oxygen to fraction of inspired oxygen (Pao2/Fio2) ratio between 200 and 300 mm Hg, and an inflammatory phenotype defined by fever and elevated C-reactive protein.

Patients: 60 vs 66 patients

Intervention: Tocilizumab 8mg/kg (max 800) x 2 doses (12 hours apart)

Outcome: composite outcome was defined as entry into the intensive care unit with invasive mechanical ventilation, death from all causes, or clinical aggravation documented by the finding of a Pao2/Fio2 ratio less than 150 mm Hg, whichever came first

Results: Seventeen patients of 60 (28.3%) in the tocilizumab arm and 17 of 63 (27.0%) in the standard care group showed clinical worsening within 14 days since randomization (rate ratio, 1.05; 95% CI, 0.59-1.86)

Conclusion: The trial was prematurely interrupted after an interim analysis for futility. Tocilizumab provided no benefit on disease progression was observed compared with standard care.

Salvarani C, Dolci G, Massari M, et al. Effect of Tocilizumab vs Standard Care on Clinical Worsening in Patients Hospitalized With COVID-19 Pneumonia: A Randomized Clinical Trial. JAMA Intern Med. 2020 Oct 20. pii: 2772186. doi: 10.1001/jamainternmed.2020.6615.

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122
Q

What are the vessels that a transcranial Doppler can evaluate?

A

MCA, PCA, ACA, Vertebrobasilar flow and ICA!

ALL the arteries you’d be interested in and that a CTA or MR Angiography could evaluate

TCD can detect acute MCA occlusions with high (> 90%) sensitivity, specificity, and positive and negative predictive values.40–43TCD can also detect occlusion in the ICA siphon, vertebral, and basilar arteries with reasonable (70 to 90%) sensitivity and positive predictive value and excellent specificity and negative predictive value (> 90%

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123
Q

What is the difference between what part of the brain is affected by P1 stroke vs P2 stroke from a PCA stroke?

A

P1 – Midbrain stroke

P2 – occipital and temporal lobe involvement

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124
Q

How does the hemianopia between PCA stroke vs MCA stroke differ?

A

MCA stroke – spares the macula

PCA stroke does NOT spare the macula since P2 segment perfuses the calcarine cortex

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125
Q

What is the characteristic presentation of an ischemic stroke due to embolism to the top of the basilar artery?

A

Acute onset of bilateral signs:

  • Bilateral ptosis
  • Pupillary asymmetry
  • Somnolence (few strokes cause somnolence)
  • Posturing
  • Myoclonic jerks that look like seizures
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126
Q

What part of the brain is supplied by the PICA?

A

Review: PICA comes from the vertebral artery

Lateral medulla AND inferior part of the cerebellum

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127
Q

How do the different parts of the vertebral artery differ in how strokes are produced?

A

Review: 4 parts of the vertebral artery
- V1 and V4 and the most common part disposed to strokes
- V1 and V4 atherothrombotic which can lead to thrombotic occlusion and extension OR embolism
V2 and V3 dissection

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128
Q

What are the possible arteries involved in if patient presents with medial medullary syndrome? Lateral medullary syndrome?

A

Medial medullary: Vertebral artery (or branch of vertebral artery or lower basilar artery)

Lateral medullary syndrome: any of the following 5 vessels

  • Vertebral
  • PICA
  • Superior, middle or inferior lateral medullary arteries
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129
Q

What is the presentation of lateral medullary syndrome?

A

AKA Wallenberg’s Syndrome

TIP: NO hemiparesis; Deficits are mainly from the neck above; brainstem heavy presentation

Horner syndrome
Double vision 
Hoarseness
Dysphagia
Dysarthria 
Vertigo 
Numbness of ipsilateral face and CONTRA lateral limbs

Picmonic:
- Horse with a horn like a unicorn; wearing glasses and crossed eyes, on a skate board, wearing a muzzle (dysarthria), half of face black and half of body black like a jester

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130
Q

What is the relationship between a cerebellar infarction and respiratory depression and cardiac arrest?

A

Cerebellar edema leads to ICP and closure of the aqueduct of Sylvius and 4th ventricle leading to hydrocephalus

NUS emergency! But easy fix if caught

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131
Q

Framework concept/question:

What is the presentation of brainstem strokes?

A

PICMONIC

Clinical tip: brainstem strokes can come from any variety of vessels that supply the brainstem, AKA any of the posterior cerebral circulation, hence vertebral, PICA, medullary arteries, basilar arteries and their branches, etc, but brainstem strokes tend to have the following presentation in common:

  • Vertigo
  • Dysarthria
  • Diplopia
  • Hyperacusis/Tinnitus
  • Ataxia
  • Coma
  • Word salad
  • Cranial nerve involvement

Hence, lateral medullary syndrome, since it involves the vertebral artery, or PICA or medullary arteries, can have above findings on presentation

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132
Q

What part of the brainstem is most affected by a basilar artery stroke?

A

PONS

Why: basilar artery first starts at the medullarpontine junction, spans the pons and ends at the midbrain pontine junction

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133
Q

What is the presentation of complete basilar occlusion?

A

EASY:

  • Bilateral long tract signs (motor/sensory),
  • cranial nerve involvement
  • cerebellar involvement

Basilar artery supplies mostly the PONS, hence presentation of a basilar artery stroke should represent pontine ischemia

Since basilar artery supplies the anterior part of the pons and that is where corticospinal tracts run through, the sx are bilateral and motor/sensory

Ataxia due to cerebellar involvement

TIP: Asymmetry but bilaterality of neurologic signs is the rule AKA one side is predominantly affected, but both sides are always affected to some extent

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134
Q

What is the purpose of non-contrast CT Head in ALL patients with CVA (stroke or TIA)?

A

Since stroke is a clinical diagnosis, CT head is NOT needed for diagnosis. However, it aids in clarifying the diagnosis - looking for masqueraders and determining if the stroke is hemorrhagic.

CT is helpful as part of treatment, as a hemorrhage would make TPA contraindicated

Masqueraders: tumors, abscess, extraparenchymal hemorrhage

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135
Q

What does MRI brain provide that CT Head does not in regards to stroke?

A

MRI scan shows extent and location of infarction in ALL areas of brain

CT: does not show posterior fossa well; does not show infarct in the first 24-48 hours

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136
Q

What is the gold standard image to evaluate the intracranial and extracranial vessels in the setting of stroke?

A

CT Angiography is the GOLD standard

WATCHOUT: gold might be X ray angiography

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137
Q

How does CT Angiography compare to MR Angiography in regards to evaluating intra/extracranial vessel disease in setting of stroke? When is one used as opposed to the other?

A

CT Angiography

MR Angiography: Highly sensitive for extra and intracranial stenosis of LARGE vessels; Can also evaluate for dissections like CTA; However, overestimates the degree of stenosis in instances of higher grade stenosis compared to CTA.

In acute stroke protocols, CTA is used. MRI, being time consuming, is used most often OUTSIDE the acute period.

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138
Q

When is MRI Head used in regards to stroke evaluation?

A

AFTER the acute period given its limitations of availability and timing

  • Clearly defining the extent of tissue injury and discriminating old from new regions of infarction
    TIA patients as it allows identification of new infarction
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139
Q

Framework concept: acute stroke imaging

A

In acute stroke, CT remains the main imaging modality given ease, availability, speed and efficacy

  • Non-contrast CT Head
  • Then, CT Angiography of head/neck to evaluate for stenosis

All others are used in the post stroke period – MRI and Ultrasound

Clinical tip: AHA/ASA
- Suggest CT head OR MRI head first to eval for intracranial hemorrhage
- Following the above, suggest either CTA OR MRA with DWI (with or without perfusion) to eval if patient candidate for thrombectomy
TLDR: both CT and MRI are both kosher

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140
Q

What is “perfusion” in regards to CT or MRI?

A

CT Angiography OR MR Angiography does NOT imply perfusion.

Perfusion is a technique that can be added to CT (SPECT) or MRI (perfusion) that reports relative cerebral blood flow and ultimately increases sensitivity of detecting ischemia

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141
Q

Does addition of PSCK9 to current active LDL lowering therapy lead to improved CVD outcomes?

A

Cochrane OCT 2020

No to patients with active LDL lowering therapy - low certainty evidence

Yes to patients NOT on active therapy

Outcomes: CVD events, stroke, MI, all cause mortality

24 studies with 60,997 participants.

18 trials alirocumab and 6 to evolocumab.

Alirocumab compared with placebo

Alirocumab reduces CVD events, mortality, MI and stroke when compared to placebo all with high certainty evidence, but when compared to active treatments showed no difference in all outcomes with low certainty evidence

Evolocumab reduces CVD events, not mortality, yes MI and stroke when compared to placebo all with high certainty evidence, but but when compared to active treatments showed no difference in all outcomes (stroke unable to measure) with low to very low certainty evidence

TLDR: PSCK9 inhibitors are clearly beneficial for patients not actively being treated with LDL lowering therapy, but there is no evidence to demonstrate that would be helpful as additional therapy for people already on LDL lowering therapy

Schmidt AF, Carter JL, Pearce LS, et al. PCSK9 monoclonal antibodies for the primary and secondary prevention of cardiovascular disease. Cochrane Database Syst Rev. 2020 Oct 20;10:CD011748. doi: 10.1002/14651858.CD011748.pub3.

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142
Q

Should patients with anti-phospholipid syndrome be treated with secondary prevention with either anticoagulation or antiplatelet therapy or both?

A

October 2020 Cochrane review

8 RCTs total with 811 patients total

Conclusion: Interestingly, a lot of the treatments were associated with an increased risk of thromboembolic events

  • VKA vs NOAC
  • VKA with antiplatelet vs VKA alone
  • no placebo trials

Bala MM, Celinska-Lowenhoff M, Szot W, et al. Antiplatelet and anticoagulant agents for secondary prevention of stroke and other thromboembolic events in people with antiphospholipid syndrome. Cochrane Database Syst Rev. 2020 Oct 12;10:CD012169. doi: 10.1002/14651858.CD012169.pub3

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143
Q

What is the penumbra?

A

The dysfunctional tissue that surrounds the core of infarction in a stroke that is defined as “ischemic but reversible”

Clinical tip: the acute treatment of stroke is focused on saving the penumbra

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144
Q

How does hyperglycemia affect patients with acute stroke?

A

Worsens the brain injury, hence it is essential to control the hyperglycemia if present

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145
Q

Patient presents with acute stroke – what to do about VTE chemical prophylaxis?

A

Essential to prevent VTE as acute ISCHEMIC stroke patients have high morbidity from VTE. Hence, if no contraindication, start chemical ppx for VTE

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146
Q

Where does the pain in osteoarthritis come from?

A

Because cartilage is aneural, cartilage loss in a joint is not accompanied by pain.

Thus, pain in OA likely arises from structures OUTSIDE the cartilage. Innervated structures in the joint include the synovium, ligaments, joint capsule, muscles, and subchondral bone.

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147
Q

Patient with possible OA, but also presentation that may be indicative of inflammatory arthritis – how will synovial fluid analysis help?

A

If > 1000 WBC, likely inflammatory

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148
Q

What patients in the US (or developed countries) are at risk of Vitamin C deficiency?

A

Elderly
Alcoholics
Autistic children

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149
Q

What is treatment for IPF?

A

Nintedanibis an intracellular tyrosine kinase inhibitor that inhibits several growth factors including vascular endothelial growth factor, fibroblast growth factor, and platelet-derived growth factor.

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150
Q

What is the most common form of familial amyloidosis?

A

The most common form of familial amyloidosis is ATTRm in the updated nomenclature, caused by mutation of the abundant plasma protein transthyretin (TTR, also known asprealbumin)

More than 100 TTR mutations are known, and most are associated with ATTR amyloidosis

151
Q

When to suspect familial amyloidosis?

A

ATTR amyloidosis warrants consideration in the differential diagnosis of African American patients who present with concentric cardiac hypertrophy and evidence of diastolic dysfunction, particularly in the absence of a history of hypertension

152
Q

What is the purpose of the modified Duke Criteria? What is considered definitive diagnosis?

A

To provide a clinical and definitive diagnosis of endocarditis

2 Major
1 Major and 3 minor
5 Minor

153
Q

What is the minor criteria for the modified Duke criteria?

A

1) Fever
2) Predisposing condition: IV drug user or heart condition
3) Vascular phenomenon: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions

TIP: vascular means bleeding, clots or aneurysms

4) Immunologic phenomenon: glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor
5) Positive blood cultures

154
Q

Review the major criteria of the modified Duke Criteria

A

Major criteria:

  • Blood culture positive for IE
  • Evidence of endocardial involvement

Blood culture positive for IE can be any of the following:

  • 1 blood culture for Coxiella burnetii, or positive Q fever serology (anti-phase 1 immunoglobulin G antibody titer > 1:800)
  • 2 separate blood cultures positive for typical organisms (Staphylococcus aureus, Enterococcus without primary focus, Streptococcus viridans, Streptococcus bovis, HACEK group)
  • Microorganism consistent with IE in ≥ 2 blood cultures drawn > 12 hours apart or on all of 3 blood cultures or most of ≥ 4 separate blood cultures, with first and last samples drawn ≥ 1 hour apart

TIP: “1, 2, 3, 4 rule”

  • 1 coxiella or
  • 2 blood cultures consistent with typical organisms 12 hours apart or
  • 3 positive blood cultures or
  • most of 4 positive blood cultures (first and last cultures are 1 hour apart)

Evidence of endocardial involvement:

  • Oscillating intracardiac mass on valve or support structure in path of regurgitant jets or on implanted material
  • Abscess
  • New partial dehiscence of prosthetic valve

TIP: new or worsening murmur is NOT enough

155
Q

Patient has WPW as shown in their EKG – What are some EKG findings that localize the bypass tract to the right ventricle vs the left ventricle?

A

Right ventricle bypass tract:

  • LBBB morphology (as seen in I and aVL) since impulse goes to RV via tract and then sweeps toward the LV just like LBBB
  • PR interval shorter (then PR interval in LV bypass tract) since SA node is VERY close to RV, the impulse travels from atria to RV faster than atria to LV tract
  • QRS is wider (than compared to LV bypass tract) because I imagine the atria impulse travels so quickly to the RV that depol starts from RV and sweeps over to the LV. If bypass tract was in the LV, impulse has time to go down the His Purkinje system and hence have a more narrow QRS
156
Q

Explain the different doses of Vit D supplementation and when to use each?

A

800 IU/day of Vit D3 for daily dietary intake

2000 IU/day of Vit D3 for Vit D def

50,000 IU of D2 (or D3) weekly for 8 weeks to achieve 25OH Vit D >30, then 2000 IU/day of Vit D3 for severe Vit D deficiency

157
Q

What is the MOA by which AK002 Lirentelimab, an anti-Siglec-8 antibody, treats eosinophilic gastritis/duodenitis?

A

Depletes eosinophils and inhibits mast cells

158
Q

AK002 (lirentelimab) is an anti-Siglec-8 antibody – does it work for eosinophilic gastrititis/duodenitis?

A

NEJM Oct 2020

RCT, Phase 2

Yes

Patient: 43 patients vs 22 placebo
Intervention: Lirentelimab, 4 monthly infusions
Outcome: The primary end point was the change in gastrointestinal eosinophil count from baseline to 2 weeks after the final dose; Secondary end points were treatment response (>30% reduction in total symptom score and >75% reduction in gastrointestinal eosinophil count) and the change in total symptom score.

Phase 2 trials – showed reduction of eosinophils compared to placebo and improved patient symptoms scores

Dellon ES, Peterson KA, Murray JA, et al.Anti-Siglec-8 Antibody for Eosinophilic Gastritis and Duodenitis.N Engl J Med. 2020 Oct 22;383(17):1624-1634. doi: 10.1056/NEJMoa2012047.

159
Q

In post mortem studies, what was found in lung pathology of patients who had died from COVID 19?

A

Chest Oct 2020
Systematic Review

  • diffuse alveolar damage in 88%
  • pulmonary microthrombi in 57%
  • organizing fibrosis in 52%
  • superimposed pneumonia in 32%
  • pulmonary thrombosis in 15
  • acute fibrinous and organizing pneumonia in 4%
  • end-stage fibrosis in 1%
160
Q

What imaging technique can demonstrate the location and extent of penumbra?

A

CT or MRI “with perfusion”

161
Q

Dosing of tPA for acute stroke?

A

0.9 mg/kg, 10% bolus, followed by remaining infusion over 60 minutes

162
Q

What window of time does tPA lead to neurological benefit?

A

Within 3 to 4.5 hours

163
Q

What is considered time of stroke onset? What if patient awoke with stroke?

A

The time of stroke onset is defined as the time the patient’s symptoms were witnessed to begin or the time the patient was last normal.

If awakens with stroke, onset is defined as when patient went to bed

164
Q

What is considered “endovascular therapy” for stroke?

A
  • Mechanical thrombectomy

- Intra-arterial thrombolysis

165
Q

What vessels, if involved in stroke, may endovascular treatment be considered?

A

MCA - M1 segment
Internal carotid artery

Explication: the larger the clot burden, the likelihood that systemic TPA will not be successful

166
Q

Intra-arterial thrombolysis vs thrombectomy - which one?

A

Mechanical thrombectomy is FDA approved, but not intra-arterial thrombolysis, hence mechanical thrombectomy is preferred over intra-arterial thrombolysis

167
Q

What is the only antiplatelet therapy used for acute stroke?

A

Aspirin

168
Q

What is the dosing of ASA in the acute setting of acute ischemic stroke? What if patient received TPA?

A

300mg x 1 on the first day, followed by 81 mg/day

If received TPA: wait 24 hours following TPA to start ASA

169
Q

What benefits do patients receive from ASA in the acute setting for acute ischemic stroke?

A
  • Recurrent ischemic stroke
  • Early mortality
  • Dependency/disability at discharge

CAST TRIAL

170
Q

What role does anticoagulation play in acute ischemic stroke?

A

No role - increases risk of brain hemorrhage

171
Q

What percentage of stroke remain unexplained?

A

30%!

172
Q

What is the ONE key lab to evaluate prior to administration of tPA?

A

Blood glucose level

Hypoglycemia can present with stroke-like symptoms

173
Q

Patient presents with acute ischemic stroke in this arterial distribution which implies cardioembolic stroke - what distribution?

A

Intracranial internal carotid artery

MCA

PCA

(infrequently ACA)

TIP: I wonder if this is how UofL decided on TEE vs TTE. For example, if patient presented with lacunar stroke, likely more related to HTN, but still need to rule out embolism, hence TTE. If MCA stroke, TEE for more definitive eval of atria

174
Q

What is the most common cause of embolic stroke?

A

Atrial fibrillation

175
Q

What is the relationship between recent MI and stroke?

A

Recent MI, especially affecting the anteroapical ventricular wall can predispose to clot formulation that leads to stroke.

176
Q

What is the work up to demonstrate that the cause of stroke is from a pulmonary AVM?

A

Transcranial doppler with insonation of the MCA which shows bubbles immediately following the injection of agitate saline

Especially when ECHO with bubble study fails to show a a right to left cardiac shunt

177
Q

How do large intracranial arteries and carotid arteries with underlying atherosclerosis cause stroke?

A

Thrombus formation on atherosclerotic plaques may embolize to intracranial arteries producing artery-to-artery embolic stroke

TIP: unlike coronary arteries, it is less likely that local thrombosis with acute occlusion be the mechanism of stroke

178
Q

What part of the carotid artery is most likely to form atherosclerosis (and hence, cause embolic stroke)?

A

Common carotid bifurcation

Proximal internal carotid artery (part that comes soon after bifurcation)

Carotid siphon (portion within the cavernous sinus)
TIP: makes sense since it is a cramped and tortuous space
179
Q

What is the relationship between the degree of carotid stenosis and stroke?

A

Generally, the more stenotic the carotid artery, the more atherosclerosis there is, which increases the risk of thombosis and subsequent embolism.

However, near occlusive disease is NOT associated with increased risk of stroke. TIP: so occlusive that there is no room for thrombosis to occur

180
Q

“Painful stroke”

A

Dissection of the ICA or vertebral arteries

SAH

181
Q

What is the common trigger or inciting factor for a carotid or vertebral dissection?

A

Trauma, usually a MVA or a sports injury, can cause carotid and vertebral artery dissections. Spinal manipulative therapy, such as osteopathic med maneuvers, care also associated

182
Q

What is a “lacunar stroke”? What is the pathophysiology of a “lacunar stroke”?

A

Lacunar comes from the word “lacune” which means lakes. Now called “small vessel strokes”, what was previously called lacunar strokes was called this because of the autopsy findings.

Small vessel strokes are strokes of the penetrating arteries caused by thrombotic OR lipohyalinotic occlusions

TIP: stands out because it is one of the few strokes in which thrombotic occlusion is the main mechanism as opposed to embolism

183
Q

What are the main risk factors for small vessel strokes?

A

HTN

Age

184
Q

What are the most common syndromes of small vessel strokes?

A
  • Pure motor hemiparesis: face, arm and leg almost ALWAYS involved
    • Cause: posterior limb of internal capsule or the pons
  • Pure sensory stroke
    • Cause: Ventral thalamus
  • Ataxic hemiparesis: AKA ataxia and hemiparesis of the same side of the body
    • Cause: Vental pons or internal capsule
  • Dysarthria and clumsy hand (AKA clumsy speech, clumsy hand syndrome):
    • Cause: Ventral pons or the genu of the internal capsule
185
Q

Should patients with small vessel strokes be evaluated with ECHOcardiography?

A

Yes, though the main mechanism is from either atherothrombosis or lipohyalinotic occlusion, a larger vessel source may manifest itself as a small vessel stroke or infarction

186
Q

Why is it rare for GCA (Giant cell arteritis) to cause stroke?

A

Predilection for the EXTERNAL carotid artery - NOT internal

187
Q

Why is RCVS (reversible cerebral vasoconstriction syndrome) on the differential diagnosis for subarachnoid hemorrhage?

A

Both present with sudden, severe headache

188
Q

What is the preferred imaging to diagnosis RCVS (reversible cerebral vasoconstriction syndrome)?

A

Conventional X Ray angiography which would demonstrate changes in the vascular caliber thoughout the hemispheres that appears vasculitic, but is noninflammatory

189
Q

What type of strokes are characteristic of CADASIL?

A

Small vessel strokes (anterior temporal lobes)

190
Q

What are the risk factors for stroke?

A
Age
DM
Smoking 
HTN 
Cholesterol (low HDL, high LDL)

Clinical tips:

  • HTN is the most important factor
  • DM likely the most important modifiable factor to reduce stroke
191
Q

What is the single most significant risk factor for strokes?

A

Hypertension

192
Q

Is statin therapy effective in stroke prevention if the patient has normal lipid profile?

A

Yes, even in patients WITHOUT elevated LDL or low HDL

Clinical tip: SPARCL trial

193
Q

What is likely the most effective primary and secondary prevention of stroke?

A

Prevention of DM

194
Q

What are the effective antiplatelets available for stroke prevention?

A

1) Aspirin daily 81-325 mg daily
2) Aspirin + Dipyridamole ER
3) Clopidogrel 75 mg daily

Clinical tip: ASA/Dipyridamole ER is effective as demonstrated by the ESPS II trial, but costs 100 monthly at Costco

195
Q

How do antiplatelet medications prevent stroke?

A

Preventing platelet aggregation prevents the formation of atherothrombosis which can cause occlusive thrombosis or emboli

196
Q

FRAMEWORK QUESTION:

Explain the MOA of ASA and how it prevents stroke?

A

Aspirin, like other NSAIDs, are COX inhibitors

ASA inhibits COX irreversibly by acetylating the COX enzyme

This irreversibly inhibits (8 days) the formation of TXA2, thromboxane. Thromboxane normally causes both vasoconstriction and platelet aggregation

No platelet aggregation, no atherothrombotic events

197
Q

Aspirin, by blocking the COX, will lead to the inhibition of Prostacyclin. Prostacyclin causes vasodilation and inhibits platelet aggregation. Explain how ASA doesn’t lead to platelet aggregation.

A

The effect on prostacyclin is transient

198
Q

What is the only scenario in which ASA and Clopidogrel will be used in combination in stroke?

A

Following TIA, ASA/Clopidogrel can be used for 21 days and has shown a reduced risk of stroke within a 90 day window without increasing bleeding risk

199
Q

Taken as a whole, taking any antiplatelet for stroke prevention will reduce stroke by what margin?

A

25- 30% reduction in stroke risk

Clinical tip: 25% reduction in all vascular events taken together

200
Q

What is the yearly risk of having stroke recurrence for those with TIA or stroke?

A

8-10% yearly

Clinical tip: Hence the importance of taking secondary prevention like ASA!

201
Q

What confers a higher risk of stroke - paroxysmal atrial fibrillation or permanent atrial fibrillation?

A

SAME risk! Hence, in cryptogenic stroke, it is always a good idea to have ambulatory monitoring for 3-4 weeks for TIA or cryptogenic stroke

202
Q

What is the MOA of dipyridamole?

A

1) Prevents the uptake of adenosine by the endothelial cells. The accumulated adenosine acts as an inhibitor of aggregation.
2) Inhibits phosphodiesterase of the platelets which leads to accumulation of cAMP. cAMP also inhibits aggregation by potentiating the effects of NO and prostacyclin.

A lot of cAMP outside platelets, a lot of adenosine outside the enthodelial cells => inhibits aggregation

203
Q

What degree of stenosis, in a patient with symptomatic carotid stenosis, benefits from surgical therapy?

A

> 70%

204
Q

What is the indication for surgical therapy for a patient with carotid stenosis?

A

Perform carotid endarterectomy (CEA) for patients with

  • symptomatic carotid stenosis
  • that’s caused a TIA/ NON DISABLINGstroke within the last 6 months
  • caused by either ipsilateral severe (70%-99%) stenosis documented by noninvasive imaging or ipsilateral moderate (50%-69%) stenosis documented by catheter-based imaging
  • and a perioperative morbidity and mortality risk estimated to be < 6%

NASCET

205
Q

When should a patient undergo surgery for symptomatic carotid stenosis?

A

within 2 weeks of TIA/Stroke

206
Q

Patient with TIA found to have ipsilateral carotid stenosis (70%) - Carotid artery stenting or endarterectomy?

A

Endarterectomy

Carotid stenting is as effective as endarterectomy in preventing recurrent stroke in symptomatic carotid stenosis but associated with a higher risk of periprocedural stroke or death than endarterectomy.

Combining procedural safety and long-term efficacy in preventing recurrent stroke favours endarterectomy.

Stenting for asymptomatic carotid stenosis carries a small increase in the risk of periprocedural stroke or death compared with endarterectomy.

COCHRANE REVIEW 2020

207
Q

Symptomatic intracranial atherosclerosis and symptomatic carotid artery disease are very different in regards to treatment

A

Symptomatic intracranial atherosclerosis

  • Stenting -> harmful (SAMMPRIS trial)
  • Anticoagulation -> harmful (WASID trial)

Symptomatic carotid artery disease
- Stenting and CEA -> beneficial

208
Q

When to start a statin for a patient who presents with an acute ischemic stroke, but wasn’t on a statin prior to presentation?

A

The consensus of the committee is that it would be safe to start statins after 48hours.
NICE Guidelines 2019

209
Q

What is the only proven scenario in which ASA and Clopidogrel combination can be used for stroke prevention?

A

Following TIA, the combination of Clopidogrel and ASA for 21 days decreased risk of recurrent stroke within 90 days without increasing risk of bleeding

TIP: Mulitple studies have shown that ASA/Clopidogrel combination for stroke prevention shows no benefit over ASA alone and only increases bleeds (CAPRIE, MATCH, CHARISMA trials)

210
Q

What is the difference between “fixed effect meta-analysis” and “random effect meta-analysis”?

A

Meta-analyses use either a fixed effect or a random effects statistical model.

A fixed effect meta-analysis assumes all studies are estimating the same (fixed) treatment effect. This assumes all studies are estimating the same (common) treatment effect. In other words, there is no between study heterogeneity in the true treatment effect.

Whereas a random effects meta-analysis allows for differences in the treatment effect from study to study. assumes the observed estimates of treatment effect can vary across studies because of real differences in the treatment effect in each study as well as sampling variability (chance).

211
Q

What is better in regards to treatment of variceal hemorrhage - shunts vs endoscopic therapy +/- medical therapy?

A

COCHRANE REVIEW OCT 2020

TLDR: who knows; low evidence and high bias

27 studies, 1828 participants
Shunts: total shunts, distal splenorenal shunts and TIPS
Endoscopic therapy: sclerotherapy, banding

High risk of bias
Very low certainty of evidence ((i.e. the true effects of the results are likely to be substantially different from the results of estimated effects)
Very low evidence

CONCLUSIONS: Evidence on whether portosystemic shunts versus endoscopy interventions with or without medical treatment in people with cirrhosis and previous hypertensive portal bleeding have little or no effect on all-cause mortality is very uncertain. Evidence on whether portosystemic shunts may reduce bleeding and mortality due to bleeding while increasing hepatic encephalopathy is also very uncertain. We need properly conducted trials to assess effects of these interventions not only on assessed outcomes, but also on quality of life, costs, and length of hospital stay.

Simonetti RG, Perricone G, Robbins HL, et al. Portosystemic shunts versus endoscopic intervention with or without medical treatment for prevention of rebleeding in people with cirrhosis. Cochrane Database Syst Rev. 2020 Oct 22;10:CD000553. doi: 10.1002/14651858.CD000553.pub3.

212
Q

What is under the umbrella of “MACE”?

Major Adverse Cardiovascular Events

A

The so-called “classical 3-point MACE” is defined as a composite of nonfatal stroke, nonfatal myocardial infarction, and cardiovascular death

213
Q

What is Whipple’s triad? Purpose?

A

1) Hypoglycemia (as obtained by serum BG)
2) Symptoms consistent with hypoglycemia
3) Reversal of symptoms with resolution of BG

Purpose: connect specific symptoms with episode of hypoglycemia

214
Q

What is the definition of hypoglycemia?

A

BG < 80, decreased insulin secretion
BG of 70 is the lower limit of normal fasting glucose
- Hence BG < 70 is considered hypoglycemia (my own logic)
BG < 55 stop the 72 hour fast
BG < 45 stop the 72 hour fasting test

Normal fasting glucose is < 70 to 100
Normal post-prandial < 140

215
Q

What organs are especially sensitive to dysfunction from hypoglycemia?

A

The brain, as its main source of energy is glucose and it has limited stores of glycogen (few minutes) and CANNOT synthesize its own glucose.

Hence practically needs continuous supply of glucose. Reason why strokes present acutely

216
Q

What is the normal range of glucose that the body attempts to maintain?

A

BG 70-110 mg/dL

217
Q

How many hours of fasting can be sufficiently supported by hepatic glycogen stores?

A

8 hours

The hepatic glycogen stores can maintain plasma glucose levels for about 8 hours. BUT it can be shorter if there is greater demand (illness/exercise) or stores have been depleted prior (pre-existing starvation)

218
Q

FRAMEWORK PRINCIPLE: Glucose metabolism

A

Glucose making factories: liver and kidney
- Via gluconeogenesis

Glucose delivery centers: liver and kidney
- Via glycogenolysis

Glucose natural resources: Adipose and muscle

  • Via proteinolysis -> lactate, AA, glutamine, alanine
  • Via lipolysis -> Glycerol and FFA
219
Q

What is the first line of defense for acute hypoglycemia?

A

Decreased secretion of insulin

Which leads to glycogenolysis and gluconeogenesis, that is, liver and kidney release glycogen stores as well as make glucose with “spare parts”

220
Q

What is the first line of defense for acute hypoglycemia?

Second line?

Third line?

A

First line: decreased insulin secretion
- glycogenolysis and gluconeogenesis

Second line: glucagon release
- glycogenolysis and gluconeogenesis

Third line: epinephrine release

  • glycogenolysis and gluconeogenesis
  • via the “sympathoadrenal” response; sympathetic system produces NE/cholinergic that leads to the neuroglycopenic and behavioral response; adrenal glands leads to Epinephrine
221
Q

What is the role of cortisol and growth hormone in acute hypoglycemia?

A

NO ROLE!

When hypoglycemia is prolonged beyond 4 hours, cortisol and growth hormone are secreted. Growth hormone works 20% as powerful as Epinephrine to maintain glucose levels

222
Q

At what level of hypoglycemia do counterregulatory hormones start to react to maintain normoglycemia?

A

BG < 80, insulin secretion is decreased

TIP: Not even what we would considered “hypoglycemia”. Remember, fasting BG is between 70-100, so BG <70 would be considered hypoglycemia

223
Q

How does the level of hypoglycemia influence the secretion or decreased secretion of counterregulatory hormones?

A

BG < 80: insulin secretion is decreased

BG < 65

  • triggers glucagon secretion
  • triggers Epinephrine secretion
  • triggers Cortisol/growth hormone secretion

Clinical tip: these thresholds are dynamic. E.g. a diabetic with persistent hyperglycemia may experience sx at relative hypoglycemia (which may be technically in the normal range)

224
Q

Can patients experience hypoglycemia symptoms with BG > 80?

A

Clinical tip: these thresholds are dynamic. E.g. a diabetic with persistent hyperglycemia may experience sx at relative hypoglycemia (which may be technically in the normal range)

225
Q

What is the relationship between ACS and hypoglycemia?

A

Hypoglycemia actually activates pro-inflammatory, pro-coagulant, pro-atherothrombotic responses in diabetic (type I and 2) and non-diabetic individuals which encourages platelet aggregation and reduce fibrinolysis.

226
Q

FRAMEWORK QUESTION:

Why may long standing diabetes lead to higher risks of recurrent hypoglycemia?

A

Due to both hypoglycemia associated autonomic failure (HAAF, possibly reversible) and diabetic autonomic neuropathy (irrevesibile)

HAAF: caused by iatrogenic or preceding hypoglycemia

Diabetic autonomic neuropathy: actual pathology of the autonomic system and inability to produce a normal sympathetic response in the face of hypoglycemia

Long standing Type I and II DM leads to failure of the Beta cell and subsequent insulin deficiency. In the face acute hypoglycemia, there is NO first line defense - no insulin means no decreased secretion of insulin. And patient likely on exogenous insulin. There is also NO second line of defense, as glucagon is secreted only when insulin is decreased, which can’t occur if there is no insulin and patient receiving exogenous insulin.

227
Q

What is the morbidity of hypoglycemia in diabetics?

A

Up to 10% of TIDM will die because of hypoglycemia!!!

6-10%

228
Q

What is the difference between the prevalence of hypoglycemia between TIDM and TIIDM?

A

Absolute numbers, there are more episodes hypoglycemia in TIIDM because there are simply more TIDM

229
Q

What are the antidiabetic drugs that pre-dispose to hypoglycemia?

A

Insulins, Sulfonyureas and Glinides

TIP: easier to remember the few that cause hypoglycemia since the rest DO NOT!

230
Q

What is the pathophysiologic basis for hypoglycemic risk factors in diabetic patients?

A

The vast majority of risk factors leading to hypoglycemia in diabetes are identified on the basis of the premise that a relative or absolute insulin excess is the sole determinant of the risk

1) Insulin (or insulin secretagogue) doses are excessive, ill-timed or of the wrong type
2) Influx of exogenous glucose is reduced (e.g., during overnight fast, periods of temporary fasting, or after missed meals or snacks)
3) insulin-INDEPENDENT glucose use is inclrease (e.g., during exercise)
4) Sensitivity to insulin is increased (e.g. with improved glycemic control, in the middle of the night, late after exercise, or with increased fitness and weight loss)
5) Endogenous glucose production is decreased (e.g. after alcohol ingestion)
6) insulin clearance is reduced (e.g. in renal failure)

231
Q

Explain how absolute endogenous insulin deficiency leads to recurrent hypoglycemia or hypoglycemia risk

A

Long standing Type I and II DM leads to failure of the beta cell and subsequent insulin deficiency. In the face acute hypoglycemia, there is NO first line defense - no insulin means no decreased secretion of insulin. And patient likely on exogenous insulin. There is also NO second line of defense, as glucagon is secreted only when insulin is decreased, which can’t occur if there is no insulin and patient receiving exogenous insulin.

TLDR: absolute insulin def indicates that insulin levels will NOT decrease and glucagon levels will NOT increase as plasma glucose levels fall

232
Q

What is the cause of hypoglycemia associated autonomic failure?

A

Recent antecedent iatrogenic hypoglycemia

233
Q

What is the cause of “hypoglycemia unawareness”? What is its relationship with “hypoglyemia associated autonomic failure (HAAF)”?

A

Iatrogenic hypoglycemia leads to an attenuated sympathoadrenal response. Hence, not much NE/Epi are being produced. This leads to less behavioral manifestations as these manifestations are dependent of NE/Epi

234
Q

How is hypoglycemia unawareness treated?

A

Avoidance of hypoglycemia, that is scaling back on insulin. This allows the sympathoadrenal response to be recalibrated

235
Q

How does intense glucose control affect macrovascular disease vs microvascular disease?

A

Decreases incidence of microvascular disease

Has NO effect on macrovascular disease (e.g. myocardial infarction)

236
Q

What is the goal BG level in the inpatient setting?

A

140-180

Clinical tip:

  • NICE SUGAR
  • ACCORD TRIAL
  • VADT TRIAL
  • ADVANCE TRIAL
237
Q

How does alcohol lead to hypoglycemia? What is the timing?

A

SUPER INTERESTING!

Alcohol blocks gluconeogenesis, NOT glycogenolysis

Hence, the timing of hypoglycemia usually follows a several day binge, during which little food is ingested, and during which glycogen stores are depleted. Then when gluconeogenesis is required to respond to hypoglycemia, it is inhibited by alcohol.

238
Q

In critically ill patients, what are the 3 key organs, if damaged, place patients at risk and can lead to hypoglycemia?

A

Liver, renal and heart failure

Liver failure: source of glucose production (gluconeo/glycogenolysis)

Renal failure: source of gluconeogenesis, decreased clearance of insulin

Heart failure: uncertain MOA

239
Q

What is the pathophysiology of sepsis and hypoglycemia?

A

In sepsis, cytokines are being produced by macrophages in major organs such as liver, spleen and spleen which utilize glucose as source of energy. In sepsis, the glucose utilization surpasses the supply.

Macrophages, during sepsis, use glucose to carry out their duties

240
Q

What is the pathophysiology of how starvation leads to hypoglycemia?

A

In starvation, the brain utilizes alternative fuels such as ketones, lactate and pyruvate, so there is only a modest neuroendocrine and autonomic nervous system response

My guess: maybe the body, having an alternative source of energy, doesn’t respond as robustly to hypoglycemia

241
Q

What is the pathophysiology of the hypoglycemia from cortisol deficiency?

A

Cortisol deficiency is associated with impaired gluconeogenesis and low levels of gluconeogenic precursors; these associations suggest that substrate-limited gluconeogenesis, IN THE SETTING OF GLYCOGEN DEPLETION, is the cause of hypoglycemia

242
Q

What type of tumors, considered “non-islet cell tumor”, cause hypoglycemia? What is the general pathophysiology of hypoglycemia?

A

Mesenchymal or epithelial tumors such as hepatomas, adrenocortical carcinomas and carcinoids

Most hypoglycemia is mediated by the over production of an unprocessed insulin like growth factor II (“big IGF II”) that does not complex normal with circulating binding proteins and thus more readily gains access to target tissues

243
Q

What are helpful labs to obtain if concerned for hypoglycemia due to “non-islet cell tumor”

A
  • High IGF II to IGF I ratio
  • Free IGF II
  • High pro IGF II
244
Q

FRAMEWORK PRINCIPLE:

Categorizing causes of hypoglycemia

A

2 broad categories:

1) Relative or absolute excess of insulin

2) Hormone related causes of hypoglycemia:
A) Excess hormones e.g
- insulin
I) Primary B cell disorder
- which can be a primary B cell tumor
- or functional B cell disorder such as B cell hypertrophy/plasia (nesidioblastosis)

         II) Antibody to insulin or to the insulin receptor 
             - Autoimmune hypoglycemia

         III) B cell secretagogue

         IV) Ectopic insulin secretion 
      - IGF II
 B) Hormone deficiency e.g. GH and Cortisol deficiency

Tip: obviously an overlap exists

245
Q

What causes of hypoglycemia fall under the category of “endogenous hyperinsulinism”?

A

1) Primary B cell disorder
- which can be a primary B cell tumor
- or functional B cell disorder such as B cell hypertrophy/plasia (nesidioblastosis)

2) Antibody to insulin or to the insulin receptor
- Autoimmune hypoglycemia

3) B cell secretagogue
4) Ectopic insulin secretion

246
Q

Insulinoma - benign or malignant?

A

Benign in 90% of the cases!

247
Q

What is the fundamental pathophysiologic feature of hypoglycemia caused by “endogenous hyperinsulinism”?

A

Failure of insulin secretion to fall to very low levels despite the presence of hypoglycemia

248
Q

Patient presents with hypoxemia and concomitant hypercapnia. What can aid in distinguishing whether the hypoxia is due to hypoventilation as opposed to V/Q/Shunt/diffusion defect?

A

The alveolar-arterial oxygen (A-a O2) difference can be helpful in distinguishing hypoventilation (elevated partial pressure of carbon dioxide [PCO2]) as a cause of hypoxemia.

The A-a O2 difference on room air should be less than 15 mmHg in a young adult and typically increases slightly with age.

The A-a O2 difference cannot easily be interpreted when the fraction of inspired oxygen (FiO2) is greater than 0.21.

The A-a O2 difference elevated: ventilation-perfusion (V/Q) mismatch, shunt, or diffusion defect

Normal A-a O2 difference normal: hypoventilation

249
Q

How to calculate the A-a O2 difference (or gradient?

A

PAO2 – PaO2

PAO2 = PiO2 – PaCO2/0.8

PiO2 = 0.21 x (760 – 47) – sea level

PiO2 = 150mmHg

PAO2 = 150 – PaCO2/0.8

PAO2 – PaO2 = (150 – PaCO2/0.8) – PaO2

Normal: difference < 15 (for young adult and increases as one ages)

KEY: must be FiO2 of 21%

250
Q

What are physical exam findings characteristic of cirrhosis due to alcohol?

A

Palmar erythema
Gynecomastia
Testicular atrophy

251
Q

What type of MRI technique is best used to evaluate suspected metastatic brain disease?

A

MRI with T2 and Flair

252
Q

What is the difference between T1 and T2 imaging? FLAIR?

A

TLDR: T1 good for fat and subacute hemorrhage

TLDR: Flair and T2 are related; FLAIR is a subset of T2

TLDR: T2O, hence, higher intensity with substances that have water like CSF and edema (metastatic brain disease)

253
Q

What is the difference between T1 and T2 imaging? FLAIR?

A

Magnetic resonance imaging (MRI) is generated from the interaction between the hydrogen protons in biologic tissues, the magnetic field, and the radiofrequency (Rf) of waves generated by the coil placed next to the body part of interest. The Rf pulses transiently excite the protons of the body with a subsequent return to the equilibrium energy state, a process known as relaxation. During relaxation, the protons release Rf energy creating an echo that is then transformed via Fourier analysis to generate the MRI. The two relaxation rates that influence the signal intensity of the image are T1 and T2. T1 refers to the time in milliseconds that it takes for 63% of protons to return to their baseline state. T2 relaxation is the time for 63% of protons to become dephased due to interactions among nearby protons. The intensity of the signal is also influenced by the interval between Rf pulses (TR) and the time between the Rf pulse and the signal reception (TE). T1-weighted images are produced by keeping both TR and TE relatively short, whereas T2-weighted images require long TR and TE times. Fat and subacute hemorrhage have relatively short TR and TE times and thus appear more bright on T1-weighted images. Conversely, structures with more water such as CSF or edema have long T1 and T2 relaxation times, resulting in higher signal intensity on T2-weighted images. T2 images are also more sensitive for detecting demyelination, infarction, and chronic hemorrhage.
Fluid-attenuated inversion recovery (FLAIR) is a type of T2-weighted image that suppresses the high-intensity signal of CSF. As a result, images created by the FLAIR technique are more sensitive to detecting water-containing lesions or edema than the standard spin images

254
Q

This patient has an asymptomatic microcytosis and hypochromia, as evidenced by a low MCV and low MCH, but is not anemic. What disease is characteristic for this?

A

This is typical of individuals with α-thalassemia trait.

α-Thalassemia trait results when there is a defect in two of the α-globin genes (-α/-α or –/αα)

Overall, the production of the α-globin is adequate to yield a normal hemoglobin and not result in excessive hemolysis. However, microcytosis and hypochromia are seen. Hematocrit is normal or only minimally reduced while RBC count may be increased.

In addition, to microcytosis and hypochromia, the characteristic finding on peripheral smear is the target cell

255
Q

What is the populations usually affected by alpha-thalassemia?

A

α-Thalassemias are most common in individuals of African, Asian, Middle Eastern, or Mediterranean descent.

256
Q

What patients are at risk of surreptitious hypoglycemia?

A

Heath care workers!
- CLINICAL TIP: the patient being a healthcare worker is NOT necessarily good. Gut instinct to trust and be relieved that patient is a healthcare worker should be tempered knowing that healthcare workers are the very patients who have factitious disorder

Patients with diabetes

Relatives of patients with diabetes

History of factitious disorder

257
Q

How long can the hypoglycemia last for in sulfonylurea ingestion?

A

Hours or even DAYS

TIP: Don’t rule it out so quickly when hypoglycemia lasts for days

258
Q

How does the administration of glucagon raise blood glucose levels?

A

Via glycogenolysis

Clinical tip: hence, in patient’s with depleted glycogen stores, such as alcoholics, glucagon will have little to no effect

259
Q

Dosing and administration of glucagon?

A

1 mg IM dose of glucagon (adult dose)

260
Q

What category of disease, more often seen in pediatric patients, can be a cause of hypoglycemia in adults?

A

Inborn errors of metabolism

261
Q

Why can fructose drinks cause diarrhea?

A

Fructose is absorbed by facilitated diffusion and there is a limited capacity. When capacity is reached, there is malabsorption

Review:

Facilitated diffusion is the PASSIVE movement of molecules across the cell membrane via the aid of a membrane protein (carrier protein or channel protein)

262
Q

What is the mechanism of diarrhea from lactase deficiency?

A

Lactose is a Disaccharide, which must be split. Retained disaccharides cause an osmotic retention of fluid in the intestine and bacteria ferment it into gases

263
Q

What is the purpose of calculating the stool osmotic gap?

A

Further characterizing watery diarrhea: secretory vs osmotic

264
Q

What is the stool osmotic gap equation? Explain the result?

A

290 mOsm/kg − 2 × (stool Na + stool K)

Gap > 75, means there is a lot of unmeasured non-electrolyte is contributing to the fecal osmolality hence, osmotic diarrhea

Gap < 50, secretory diarrhea

265
Q

What is the first line empiric treatment for chronic diarrhea?

A

Opioid

Loperamide which as a mu receptor acts specifically on the intestines and has low abuse potential

266
Q

Aside from Loperamide (opioids), what are other possible medications for the empiric treatment of chronic diarrhea?

A

Bile acid resins such as cholestyramine, colestipol and colesevelam. Though effective in (BAM), bile acid malabsorption, there is a constipating effect

267
Q

What is the MOA of antidiarrheal effect of clonidine in patients with DM?

A

DM can lead to “diabetic diarrhea”

Clonidine, alpha 2 adrenergic agonist, can stimulate absorption and and slow transit. In DM there is a LOSS of noradrenergic innervation int he gut

268
Q

Antibiotic choices for SIBO?

A

Antibiotics to selectively target bacterial strains causing SIBO syndrome if possible

  • Rifaximin, with usual dose 1,200 mg/day or 1,600 mg/day for 7-10 days as one treatment course or as cyclic therapy, has the largest experience base
  • other options include tetracycline, neomycin, norfloxacin, amoxicillin/clavulanate, erythromycin
269
Q

What are sites in which Enterococcus can cause infection in the body? (e.g. UTI)

A

Heart infections: endocarditis

Blood infections: bacteremia from catheter or hepatobiliary

GI infections: complication of intestinal, pelvis or biliary tract surgery, cholangitis, peritonititis

GU infections: UTIs most commonly from catheter or instrumentation

CNS infections: meningitis, but in the setting NUS or head trauma

Skin infecions: surgical wounds, especially GI, and decubitus ulcers; diabetic foot infections

270
Q

What are sites in which Enterococcus can cause infection in the body? (e.g. UTI)

A

Heart: endocarditis

Blood: bacteremia from catheter or hepatobiliary

GI: complication of intestinal, pelvis or biliary tract surgery, cholangitis

GU: UTIs most commonly from catheter or instrumentation
NOTE: bacteremia from enterococcal UTI is uncommon

Intraabdominal: peritonitis, intraabdominal infection, pelvic infection (tends to be mixed with other flora)

CNS: meningitis (in the setting of neurosurgery)

Skin/Soft tissue: surgical wounds (especially GI), decubitus ulcers

271
Q

What is the general duration of treatment of bacteremia without any endocarditis?

A

10-14 days

SANFORD

272
Q

What type of prognosis is portended for patients that have malignant pleural effusion regardless of the specific primary?

A

Typically signifies advanced stage cancer and usually indicates that death will likely occur within an average of four to seven months

UTD 11/11/2020

273
Q

What one procedure will control malignant pleural effusions in almost all patients and prevent reaccumulation?

A

Pleural abrasion or pleurectomy

274
Q

What are options for the treatment of malignant pleural effusions?

A

Observation

Therapeutic thoracentesis

Chest catheter drainage only

Chest catheter drainage with chemical pleurodesis (eg, talc slurry)

Thoracoscopy with talc insufflation

Long-term indwelling pleural catheter

Long-term indwelling pleural catheter with talc instillation

Pleural abrasion or pleurectomy

Pleuroperitoneal shunt

Chemotherapy

Radiotherapy

275
Q

What are options for the treatment of malignant pleural effusions?

A

Observation

Therapeutic thoracentesis

Chest catheter drainage only

Chest catheter drainage with chemical pleurodesis (eg, talc slurry)

Thoracoscopy with talc insufflation

Long-term indwelling pleural catheter

Long-term indwelling pleural catheter with talc instillation

Pleural abrasion or pleurectomy

Pleuroperitoneal shunt

Chemotherapy

Radiotherapy

276
Q

What is the concern about observing a malignant effusion that is asymptomatic for too long?

A

Concern exists that prolonged observation of these effusions without drainage results in a nonexpandable lung that may complicate palliative benefit from later drainage, AKA lung entrapment

277
Q

First line treatment for malignant pleural effusion?

A

Therapeutic thoracentesis is the first-line treatment for symptomatic MPE and is typically performed using a needle/catheter under ultrasound guidance.

278
Q

How does renal insufficiency affect the interpretation of serum (and urine) free light chains?

A

The normally rapid renal clearance of serum FLCs is reduced in the presence of renal insufficiency (eg, creatinine clearance <60 mL/min). As a result, serum FLC concentrations rise as the glomerular filtration rate falls, and may be 20 to 30 times normal in end-stage renal failure

279
Q

Empiric treatment for abdominal source abscess or infection?

A
280
Q

Empiric antibiotics for hepatic abscess?

A

Refer to SIS Guideline 2017

Hepatic abscess is a type of intra-abdominal abscess

Hence empiric treatment depends on the category of patient

  • Low risk community acquired IAI
  • High risk community acquired IAI
  • Health care-associated IAI
281
Q

What is the most appropriate timing of antibiotics for patient with either suspected or confirmed intra-abdominal infection?

A

Immediately

TIP: osteomyelitis is one of the only, if not the only, infection in which antibiotics are held until cultures are obtained and organism identified

282
Q

What is the best imaging modality to evaluate for a fistulizing enteric source?

A

CT with oral contrast

283
Q

What are the major pathogens in community acquired intra-abdominal infections?

A

Coliforms (Enterobacteriaceae, especially E.
coli) and anaerobes (especially B. fragilis)

Organism found in at least 30% of the cases

  • E. Coli
  • Bacterioides
  • Clostridium species
  • Streptococcus specis
284
Q

What is an aerobic bacteria? Anaerobic? Facultative?

A

An aerobic organism or aerobe is an organism that can survive and grow in an oxygenated environment. In contrast, an anaerobic organism (anaerobe) is any organism that does not require oxygen for growth

Facultative anaerobes can grow with or without oxygen because they can metabolise energy aerobically or anaerobically. They use dissolved oxygen (DO) or oxygen obtained from food materials such as sulfate or nitrate ions, or some can respire through glycolysis. The bacteria can live under aerobic, anoxic, or anaerobic conditions.

285
Q

What is an obligate anaerobic bacteria?

A

Obligate anaerobes are organism which can only live in environments which lack oxygen. Unlike the majority of organisms in the world, these organisms are poisoned by oxygen. Obligate anaerobes are typically bacteria, and live in a variety of places naturally.

286
Q

Empiric treatment for intra-abdominal infections all should cover what categories of organisms?

A

Antibiotics used for empiric treatment of community acquired intra-abdominal infection should be active against:

Enteric gram-negative aerobic and facultative bacilli and enteric gram-positive streptococci

287
Q

How to decide what empiric regimen of antibiotics to treat patient with intra-abdominal infection?

A

Low risk vs high risk

Community acquired vs “health care-associated intraabdominal infection”

288
Q

What is the definition of “Health care-associated intra-abdominal infection”?

A

“Health care–associated infection” includes “community onset” and “hospital-onset.”

Community-onset health care–associated infection includes cases involving patients with at least 1 of the following health care risk factors:

(1) presence of an invasive device at time of admission
(2) history of MRSA infection or colonization
(3) history of surgery, hospitalization, dialysis, or residence in a long-term care facility in the 12 months preceding the culture date.
4) Hospital-onset infection includes cases involving patients with positive culture results from a normally sterile site obtained 48 h after hospital admission.

Clinical tip: “Health care associated” is commonly caused by more resistant flora

IDSA 2010

289
Q

What is an “investigator initiated trial”?

A

A clinical trial in which the investigator conceives the research, develops the protocol, and serves as sponsor investigator

As opposed to an industry initiated trial

290
Q

What is more effective in treating acute symptomatic hyponatremia?

A

JAMA OCT 2020

RCT

Objective: To compare the risk of overcorrection in rapid infusion bolus (RIB) and slow continuous infusion (SCI) with hypertonic saline in patients with symptomatic hyponatremia.

Design, Setting, and Participants: This prospective, investigator-initiated, multicenter, open-label, randomized clinical trial

  • 178 patients
  • Na < 125

Interventions: RIB or SCI of hypertonic saline( 3%, for 24 to 48 hours)

Main Outcome: The primary outcome was overcorrection at any given period, defined as increase in the sNa level by greater than 12 or 18 mmol/L within 24 or 48 hours, respectively.

Results: mean Na concentrations, 118.2

  • RIB group (n = 87) vs SCI group (n = 91).
  • Overcorrection 15 of 87 (17.2%) and 22 of 91 (24.2%) patients in the RIB and SCI groups, respectively (absolute risk difference, -6.9% [95% CI, -18.8% to 4.9%]; P = .26).
  • The RIB group showed lower incidence of relowering treatment than the SCI group (36 of 87 [41.4%] vs 52 of 91 [57.1%] patients, respectively; absolute risk difference, -15.8% [95% CI, -30.3% to -1.3%]; P = .04; number needed to treat, 6.3).
  • Groups did not differ in terms of efficacy in increasing sNa concentrations nor improving symptoms
  • RIB, when compared with SCI, showed better efficacy in achieving target correction rate within 1 hour P = .02

Conclusions and Relevance: This randomized clinical trial found that both RIB and SIC therapies of hypertonic saline for treating hyponatremia were effective and safe, with no difference in the overcorrection risk. However, RIB had a lower incidence of therapeutic relowering treatment and tended to have a better efficacy in achieving sNa within 1 hour than SCI. RIB could be suggested as the preferred treatment of symptomatic hyponatremia, which is consistent with the current consensus guidelines.

Baek SH, Jo YH, Ahn S, et al. Risk of Overcorrection in Rapid Intermittent Bolus vs Slow Continuous Infusion Therapies of Hypertonic Saline for Patients With Symptomatic Hyponatremia: The SALSA Randomized Clinical Trial. JAMA Intern Med. 2020 Oct 26. pii: 2772353. doi: 10.1001/jamainternmed.2020.5519.

291
Q

Bromhexine for COVID?

A

RCT, open-label

Small study in Iran: 39 patients vs 39 pateints
Bromhexine TID
Outcome: ICU admissions, Intubations and deaths
Results:
- There was a significant reduction in ICU admissions (2 out of 39 vs. 11 out of 39, P = 0.006)
- intubation (1 out of 39 vs. 9 out of 39, P = 0.007)
- death (0 vs. 5, P = 0.027) in the bromhexine treated group compared to the standard group.

Conclusion: Bromhexine, in a small study, showed decreased, ICU admissions, intubations and deaths in COVID patients

Background: bromhexine (international) is a known mucolytic

Ansarin K, Tolouian R, Ardalan M, et al. Effect of bromhexine on clinical outcomes and mortality in COVID-19 patients: A randomized clinical trial. Bioimpacts. 2020;10(4):209-215. doi: 10.34172/bi.2020.27. Epub 2020 Jul 19.

292
Q

What FDA approved treatment for mild to moderate COVID exists?

A

Bamlanivimab

As of Nov 2020
Efficacy based on BLAZE-1 clinical trial

293
Q

MOA of Bamlanivumab?

A

Bamlanivimab is a recombinant neutralizing human IgG1k monoclonal antibody that binds to spike protein of SARS-CoV-2 virus, which prevents SARS-CoV-2 from attaching to human ACE2 receptors

Efficacy based on BLAZE-1 clinical trial

294
Q

Bamlanivumab as a treatment for COVID - what is the dosing?

A

Dosing: 700 mg single IV infusion over ≥ 60 minutes
give bamlanivimab as soon as possible after positive test result and within 10 days of symptom onset monitor patients during infusion and observe for ≥ 1 hour after infusion

Efficacy based on BLAZE-1 clinical trial

295
Q

What category of patients will benefit from Bamlanivumab?

A

Mild-to-moderate COVID-19 in adults and children ≥ 12 years old weighing ≥ 40 kg who are at HIGH RISK of progressing to severe COVID-19 and/or hospitalization

Bamlanivimab is associated with poor clinical outcomes when given to hospitalized patients with COVID-19 who require high flow oxygen or mechanical ventilation

Not authorized for use in patients who are hospitalized, require oxygen therapy, or are on pre-existing chronic oxygen therapy requiring increase in baseline oxygen flow rate

Efficacy based on BLAZE-1 clinical trial

296
Q

Efficacy of Bamlanivumab for mild to moderate COVID?

A

Based on nonclinical outcome in prespecified interim analysis of randomized trial

Patients:

  • 467 adults (median age 45 years, 54% women)
  • mild (76%) or moderate COVID-19
  • not hospitalized
  • ≥ 1 risk factor for severe disease

Intervention: single infusion of bamlanivimab 700 mg vs. 2,800 mg, vs. 7,000 mg vs. placebo

Results: follow-up 29 days
Note: decrease in log viral load of 3.81 corresponds to elimination of > 99.97% of viral RNA

  • mean decrease in log viral load at 11 days
    • 3.67 with 700 mg (not significant vs. placebo)
    • 4 with 2,800 mg (p = 0.02 vs. placebo)
    • 3.38 with 7,000 mg (not significant vs. placebo)
    • 3.47 with placebo

Hospitalization at 29 days in 1.6% vs. 6.3% (no p value reported) !!!

297
Q

What is the recommended DAPT for ACS with PCI?

A

Ticagrelor and ASA

298
Q

What is the one RCT that has demonstrated Ticagrelor/ASA efficacy over Clopidogrel/ASA in ACS with PCI?

A

PLATO trial

Tip: most of the guideline recc for Ticagrelor is really from 1 major RCT, the Plato Trial

299
Q

What is the pharmacologic profile of NPH?

A

Intermediate-acting insulins, such as neutral protamine
Hagedorn is known as NPH or lente (means slow in spanish!) insulin

  • delayed onset of action ranging between 2 to 4 hours
  • approximately 6 to 7 hours to reach peak concentration
  • duration of action: up to 20 hours

Clinical tip: This leads to a distinct peak and trough effect, and therefore, when used as basal insulin,
2 or MORE injections are often required each day to
minimize the daily excursions of insulin levels

300
Q

What is the relationship between NPH and short acting insulin such as lispro?

A

NPH is treated like a long acting, and hence, it’s use is for basal insulin coverage

So, just like any typical basal bolus regimen, NPH acts as the basal and rapid acting acts as the meal time and correctional

Ex:

  • Basal: NPH 30 U BID
  • Meal time: 3U lispro TID w/ meals
  • Correctional: SSI with lispro

Ex:

  • Basal: Lantus 40 nightly
  • Meal time: 3U lispro TID w/ meals
  • Correctional: SSI with lispro

BOTH are functional basal bolus regimens

301
Q

What is the relationship between NPH and 70/30 Humulin/Novolin?

A

NPH can be administered alone, simply NPH

OR

It can be administered in what is called “premixed conventional insulin”.

Ex: 70/30 Humulin/Novolin means (70% NPH, 30% regular)
- The regular insulin can be either Humulin or Novolin - they both are regular insulin

302
Q

What is the difference between these 2 groups of pre-mixed insulins?

Humulin 50/50 (Eli Lilly, Indianapolis, Indiana)
Humulin 70/30 (Eli Lilly)
Novolin (70/30) (Novo Nordisk, Bagsvaerd, Denmark)

Humalog mix 75/25 (Eli Lilly)
Humalog mix 50/50 (Eli Lilly)
Novologmix 70/30 (Novo Nordisk)

A

The first group is called “conventional premixed human insulins” and the 2nd group is called “Insulin analogue mixes”.

The conventional premixed human insulins are a mixture of NPH and Regular insulin

The insulin analogue mixes are a mixture of intermediate acting (ex: insulin lispro protamine) and rapid acting insulin (ex: lispro)

Pharmacokinetically, the analogues have a faster onset and peak, but BOTH groups have the same duration of action

Conventional premixed human insulins have an onset
of action of approximately 0.5 to 2 hours, usually plateau
at 3 to 6 hours, and last up to 24 hours. Insulin analogue
mixes have an onset of action of approximately 15 minutes,reach a peak biological action at 1 to 4 hours, and last up to 24 hours (24)

303
Q

HumuLIN vs HumuLOG - which is regular and which is rapid?

A

LIN is regular

Linhs are regular people

LOG is rapid

Think of log rolling down a hill

304
Q

What is the difference between the dose adjustment for renal function when using Apixaban for VTE vs Atrial Fibrillation?

A

Deep vein thrombosis and/or pulmonary embolism treatment: NO dosage adjustment is recommended by the manufacturer for any degree of reduced kidney function.

For Nonvalvular Atrial Fibrillation:

If Cr <1.5: no dose adjustment
- UNLESS >80 yo AND weight < 60kg: 2.5mg BID

If Cr > 1.5 AND one of the following

  • > 80 yo
  • <60kg

Then adjust to 2.5mg BID

Otherwise, no adjustment

305
Q

What does “Bence Jones” protein refer to?

A

Bence Jones proteins is the other name to refer to Free Light Chains, that is, the kappa or lamda light chains that are NOT attached to heavy chains, hence they are FREE

306
Q

What is the clinical relevance of evaluating Free Light Chains (serum and/or urine) when evaluating a patient with possible plasma cell dyscrasia?

A

16 % patients with Multiple Myeloma produce only Bence Jones proteins, that is, only FLC

Hence the SPEP and Serum Immunofixation may be negative, but the FLC would catch the multiple myeloma

307
Q

What is the definition of “non-secretory multiple myeloma”?

A

Monoclonal plasma cells ≥10% in the bone marrow and by negative results on serum and urine electrophoresis and immunofixation studies.

308
Q

How does renal insufficiency affect the FLC, specifically the level of kappa, level of lamda, the kappa/lamda ratio?

A

Increase level of kappa and lambda

Conflicting results in regards to the ratio per studies

Clinical tip: Kappa/lamda ratio > 3 is too abnormal for renal insufficiency alone

309
Q

What Kappa/Lamda Ratio is helpful to indicate that the ratio is NOT solely explained by renal insufficiency, that is, there may be a plasma dyscrasia that needs to be evaluated

A

Kappa/lambda ratios >3.0 are unlikely to be due to renal insufficiency alone

310
Q

CLINICAL TIP:

How to use SPEP/Serum immunofixation/serum FLC in relation to UPEP/Urine immunofixation?

A

The serum tests may obviate the initial need for urine protein studies in the initial evaluation for monoclonal gammopathies when serum FLC analysis is performed along with serum protein electrophoresis and serum immunoelectrophoresis [43].

If a monoclonal protein is found, electrophoresis and immunofixation of an aliquot from a 24-hour urine collection should then be performed.

311
Q

What are the different categories or populations which fall under the category of intra-abdominal infections that can aid in determining the empiric antibiotics/route?

A

Low risk vs high risk

Community acquired vs “health care-associated intraabdominal infection”

312
Q

According to the Surgical Infection Society Guidelines, what is considered a “low risk” vs “high risk” patient?

A

High Risk

APACHE II score > 10

Or 2 of the following:

  • Advanced age (‡ 70 y)
  • Malignancy
  • Significant cardiovascular compromise, liver disease or cirrhosis or renal disease
  • Diffuse, generalized peritonitis
  • Hypoalbuminemia
  • Extent of infection/adequacy of initial source control
  • Elevated MPI score
  • Delayed initial source control
  • Inability to achieve adequate source control
  • Microbiologic characteristics
  • Suspected infection with resistant pathogens
313
Q

According to the Surgical Infection Society Guidelines, what is considered a “health care-associated intra-abdominal infection” patient?

A

Infection developing greater than 48 h after initial source control.

Hospitalized for greater than 48 h during current admission or within the previous 90 d.

Residence in a skilled nursing or other long-term care facility within the previous 30 d.

Home infusion therapy, home wound care, or dialysis within the preceding 30 d.

Use of broad-spectrum antimicrobial therapy for 5 d or more during the preceding 90 d.

TIP: all the risk characteristics that help define “health care-associated” are simply places that are healthcare associated and whether the patient has been exposed between 30 to 90 days

314
Q

According to the Surgical Infection Society Guidelines, what is the empiric therapy for intra-abdominal infections for “low risk” patients?

A

Cefotaxime PLUS Metro (Grade 1-A).

Cetriaxone PLUS Metro (Grade 1-A).

Cipro PLUS Metro (Beta lactam allergy)

Monotherapies:

  • Ertapenem
  • Moxifloxacin (Beta lactam allergy)
315
Q

When should empiric antifungal therapy be used for treatment of intra-abdominal infection?

A

Critically ill patients, such as ICU patients

316
Q

According to the Surgical Infection Society Guidelines, what is the empiric therapy for intra-abdominal infections for “high risk” patients?

A

Piperacillin-tazobactam MONO (Grade 2-A)

Doripenem MONO (Grade 2-A)

Imipenem-cilastatin MONO (Grade 2-A)

Meropenem MONO (Grade 2-A)

Cefepime PLUS Metro (Grade 2-A)

Ceftazidime PLUS Metro (Grade 2-B).

TIP: notice that that “high risk” patients can get dual or monotherapy

TIP: notice that the dual therapies have different cephalosporins compared to “low risk” empiric therapy

317
Q

According to the Surgical Infection Society Guidelines, what is the empiric therapy for intra-abdominal infections for “Health care-associated intra-abdominal infection” patients?

A

TIP: Same as high risk community acquired intra-abdominal infection

Use the broader-spectrum agents recommended for higher-risk patients with CA-IAI for initial empiric therapy of patients with HA-IAI.

318
Q

According to the Surgical Infection Society Guidelines, what is the recommended duration of antibiotic treatment for intra-abdominal infections?

A

TIP: depends on source control

1 day if small bowel perforation but operated within 12 hours, gastroduodenal perf operated on within 24 hours

4 days in source control

5-7 days without definitive source control

7 days if secondary bacteremia

319
Q

What is the difference between Enterobacteriaceae and Enterobacter?

A

Enterobacteriaceae is the group (or family) and Enterobacter species is the species

320
Q

What are some bacteria (species) that fall under the group Enterobacteriaceae?

A

E. Coli

Klebsiella

Shigella

Salmonella

Proteus

Citrobacter

Enterobacter

321
Q

Framework Concept:

“Enteric organisms”

vs

“Enterobacteriaceae”

vs

“Enterobacter”

A

“Enteric organisms” are gram negative organisms part of the normal intestinal flora and can include gram positive organisms too

Under the Enteric organisms are “groups” or “families” such as Enterobacteriaceae, Vibrionaceae, Pseudomaceae and Bacterioidaceae

Enterobacter or E. Coli are “species” under the groups, and in this case, Enterobacteriaceae

322
Q

Compared to community acquired intra-abdominal infections, what organisms can make up the cause of “health care-associated intra-abdominal infections”?

A

In addition to the enteric flora (gram negative aerobic/facultative and anaerobic organisms)

Incidence of other Enterobacteriaceae, such as Enterobacterspp., as well as lactose-negative gram-negative bacilli, such as P. aeruginosa and Acinetobacter spp., have increased.

Gram positive micro-organisms, particularly Enterococcus spp., Staphylococci, both coagulase-negative species and Staphylococcus aureus are also identified more frequently in patients with HA-IAI

323
Q

What are the adult outcomes from childhood and adolescent HTN?

A

Systematic Review
JAMA Nov 2020

Objective: To update the evidence on screening and treatment of hypertension in childhood and adolescence for the US Preventive Services Task Force.
Study selection: English only, RCT, cohort and meta-analysis

Results

  • 43 studies, N>12,400
  • 13 RCTs and 1 Meta-analysis showing reduction of BP with ACEi and ARB, but NOT with CCB, BB or Mineralocorticorticoid blocker
  • No studies looking at adult outcomes
  • 20 observational studies showing association of childhood HTN with adult
  • No conclusion in regards to accuracy of BP measurements in office setting

Gartlehner G, Vander Schaaf EB, Orr C, et al.Screening for Hypertension in Children and Adolescents: Updated Evidence Report and Systematic Review for the US Preventive Services Task Force.JAMA. 2020 Nov 10;324(18):1884-1895. doi: 10.1001/jama.2020.11119.

324
Q

Following CABG with SVG, does the addition of Ticagrelor to Aspirin prevent occlusion of graft at 1 year?

A

RCT Nov 2020

CIRCULATION
POPular CABG Trial

Type: investigator-initiated, randomized, double-blind, placebo-controlled, multicenter trial

Patients:

  • 500 patients: 220 vs 223, 1:1
  • Male, 70 years of age, 30% for ACS

Outcome: SVG occlusion at 1 year by CT Angiography
-Secondary: 1-year SVG failure, which was a composite of SVG occlusion, SVG revascularization, myocardial infarction in myocardial territory supplied by a SVG, or sudden death.

Results:

  • SVG occlusion rate in the ticagrelor group was 10.5% (51 of 484 SVGs) versus 9.1% in the placebo group (43 of 470 SVGs), odds ratio, 1.29 [95% CI, 0.73-2.30]; P=0.38.
  • SVG failure occurred in 35 (14.2%) patients in the ticagrelor group versus 29 (11.6%) patients in the placebo group (odds ratio, 1.22 [95% CI, 0.72-2.05]).

Conclusion: NO, addition of ticagrelor to standard aspirin did not reduce SVG occlusion at 1 year after CABG

Willemsen LM, Janssen PWA, Peper J, et al.Effect of Adding Ticagrelor to Standard Aspirin on Saphenous Vein Graft Patency in Patients Undergoing Coronary Artery Bypass Grafting (POPular CABG): A Randomized, Double-Blind, Placebo-Controlled Trial.Circulation. 2020 Nov 10;142(19):1799-1807. doi: 10.1161/CIRCULATIONAHA.120.050749. Epub 2020 Aug 31.

325
Q

What percent of SVG are occluded at 1 year after CABG?

A

15%

326
Q

In the IDSA guidelines for endocarditis, what is the definition of “persistent bacteremia?”?

A

“Persistently positive blood cultures” defined as follows:

1) at least 2 positive cultures of blood samples drawn >12 h apart
2) or all 3
3) or a majority of ≥4 separate cultures of blood (with first and last sample drawn at least 1 h apart)

TIP: “2,3,4” Rule

327
Q

What is the recommendations in regards to obtaining blood cultures in pateints suspected of having endocarditis?

A

At least 3 sets of blood cultures obtained from different venipuncture sites should be obtained, with the first and last samples drawn at least 1 hour apart (Class I; Level of Evidence A).

Clinical tip: the modified Duke criteria makes more sense – the Major Criteria

Blood culture positive for IE
Typical microorganisms consistent with IE from 2 separate blood cultures: Viridans streptococci, Streptococcus bovis, HACEK group, Staphylococcus aureus; or community-acquired enterococci in the absence of a primary focus,

OR

Microorganisms consistent with IE from persistently positive blood
cultures defined as follows: at least 2 positive cultures of blood samples
drawn >12 h apart or all 3 or a majority of ≥4 separate cultures of blood (with
first and last sample drawn at least 1 h apart)

OR

Single positive blood culture for Coxiella burnetii or anti–phase 1 IgG
antibody titer ≥1:800

IDSA 2015

328
Q

What is the major criteria regarding blood cultures of the Modified duke criteria?

A

Blood culture positive for IE
Typical microorganisms consistent with IE from 2 separate blood cultures: Viridans streptococci, Streptococcus bovis, HACEK group, Staphylococcus aureus; or community-acquired enterococci in the absence of a primary focus,

OR

Microorganisms consistent with IE from persistently positive blood
cultures defined as follows: at least 2 positive cultures of blood samples
drawn >12 h apart or all 3 or a majority of ≥4 separate cultures of blood (with
first and last sample drawn at least 1 h apart)

OR

Single positive blood culture for Coxiella burnetii or anti–phase 1 IgG
antibody titer ≥1:800

329
Q

Framework Question:

What is the basic taxonomy schema for bacteria?

A

Domain

Phylum

Class

Order

Family

Genus

Species

DPCOFGS

Dirty People Carry Old, Festering, Gross Sicknesses

330
Q

What are the expected findings on gram stain consistent with enterococcus?

A

Gram positive cocci, diplococci, short chains or long chains

TIP: one cocci, then 2, then 3, then 4

331
Q

What are the basic characteristics of Enterococcus? (that is, the chemical characteristics that distinguish it from other organisms)

A

Facultative, anaerobic, gram positive bacteria found in the colon

Hydrolyze esculin in the presence of 40% bile salts

Grows/lives at high salt concentration (6.5%) and high temperatures (46 degrees)

Non-hemolytic

332
Q

What chemical property helps in distinguishing enterococcus from streptococcus gallolyticus species?

A

Vast majority of enterococcus can hydrolyze PYR – pyrrolidonyl-beta-naphthylamide

333
Q

What are the 2 major enterococcus species that cause the majority of disease?

A

Enterococcus Faecalis

Enterococcus Faecium

TIP: 18 species of enterococcus total

334
Q

Is enterococcus normally found as part of the human body?

A

Normal inhabitants of the LARGE bowel, but it only makes up <1% of the organisms

335
Q

Explain why the history of antibiotic use is a key factor in both the colonization and subsequent infections by Enterococcus?

A

Most antibiotics used normally don’t target enterococcus, rather, target the gram negative organisms and anaerobes of the gut. Since enterococcus only makes up <1% of the colonic bacteria, exposure to antibiotics wipe out other colonic bacteria, allowing enterococcus to move into the open niche

336
Q

What is the relationship between enterococcus colonization and infection?

A

They go hand in hand, the former is part of the pathogenesis of the latter. Those colonized are the ones who get disease

337
Q

What are the 3 main virulence factors of enterococcus?

A

1) ”Enterococcal secreted factors” are factors released outside of the bacterial cell wall. The main ones are hemolysin/cytolysin/serine protease which destroy cells/tissue
2) ”Enterococcal surface compounds” that are adhesins. Important one is “aggregation substance of Enterococcus faecalis”.
3) ”Stress protein GLS24” which yields resistance to bile salts

338
Q

How common is enterococcus in regards to hospital acquired infections? What is more common between the 2 enterococcus species?

A

2 organism recovered from hospital acquired infections after Staph (MSSA/MRSA)

Faecalis is much more common historically, but now both are just as even

339
Q

What is the general difference in the resistance patterns between enterococcus faecalis and enterococcus faecium?

A

E. Faecalis susceptible to ampicillin and vanc

E. Faecium 90% resistant to ampicillin and 80% resistant to vancomycin

340
Q

What is the “critical step” in developing an enterococcal infection?

A

Colonization

341
Q

What part of the world is there a high prevalence of VRE?

A

US/Asia > Europe > Latin America

342
Q

What is the #1 type of enterococcal infection?

A

UTI

343
Q

Does Enterococcal UTI often lead to bacteremia? In what case would that be more likely?

A

No

However, chronic prostatitis can lead to recurrent enterococcal bacteremia

344
Q

Patient presents with enterococcal bacteremia. What are the more common sources of enterococcal bacteremia?

A

Gastrointestinal, hepatobiliary, intra-abdominal abscess, pelvic

Intravascular source

Less commonly, UTI, wound infections and bone infections

345
Q

In what scenario is enterococcus a common cause of endocarditis?

A

In hospital acquired endocarditis, it is the second most common cause!

346
Q

What cardiac complication is commonly associated with enterococcal endocarditis?

A

Heart failure and hence valve replacement may be needed

347
Q

What is the definition of “tolerance” to antibiotics?

A

Defined as the lack of killing at concentrations 32 times higher than the MIC

348
Q

Enterococcal endocarditis – monotherapy?

A

No, always dual therapy for synergistic effect

349
Q

Explain how synergism works in the treatment of enterococcal endocarditis with Cell wall active agent /Aminoglycoside?

A

2 different mechanisms of action:

-The Beta lactam or glycopeptide is a cell wall active agent that creates a way for the aminoglycoside to enter for better penetration

350
Q

In beta-lactam susceptible enterococcal species, what are the most active agents?

A

Aminopenecillins (ampicillin/amoxicillin)/Ureidopenecillins (piperacillin/tazobactam) > Penicillin G and Imipenem

351
Q

What are the antibiotics that are active against VRE?

A
LineZOLID
TediZOLID
TelaVANCIN
OritaVANCIN
DaptoMYCIN
FosfoMYCIN
Quiniprisin/Dalfopristin
Tigelcycline

Clinical tip: Though active, not all the antibiotics are FDA approved or beneficial in all clinical scenarios

352
Q

Review the resistance of Enterococcus to cephalosporins

A

Enterococcus species are resistant to ALL cephalosporins

353
Q

Which enterococcus species tends to be resistant to aminopenicillins? MOA?

A

Enterococcus faecium

The penicillin binding protein of the species is called PBP5 which has a LOW affinity for the ampicillin so the bacteria can continue to grow cell wall in the presence of aminopenicillin

354
Q

What is the MOA of vancomycin?

A

Like beta lactams, it is a cell wall agent.

It works in the step prior to that of beta lactams

It targets and binds to D-ala D-ala of the peptidoglycan of the cell wall and prevents transpeptidylation

355
Q

What is the MOA of vancomycin resistence in VRE?

A

D-ala D-ala is replaced with D-lactate or D-serine, hence changing the very target of vancomycin

Secondary MOA of resistence is that enterococcus can produce substances that literally destroy the D-ala D-ala

356
Q

What are the 2 aminoglycosides used in enterococcal infections for synergstic effects?

A

Gentamicin and Streptomycin

357
Q

What is the MOA of how Naltrexone is used for alcohol abstinence?

A

Naltrexone is an opioid antagonist that can be administered orally or as a monthly injection. It is thought to act by decreasing activity in the dopamine-rich ventral tegmental area of the brainstem and subsequently decreasing the pleasurable feelings associated with alcohol consumption.

358
Q

What is the MOA of how Acamprostate is used to treat alcohol withrawal sx long term?

A

Acamprosate inhibits NMDA receptors, decreasing symptoms of prolonged alcohol withdrawal.

359
Q

Disulfuram - MOA for alcohol abstinence and what patients is it contraindicated to give this medication?

A

Disulfiram is an aldehyde dehydrogenase inhibitor that has been used for many years in the treatment of alcoholism

The primary mechanism by which it acts is to create negative effects of vomiting and autonomic nervous system hyperactivity when alcohol is consumed concurrently with use of the medication. Because it inhibits an enzyme that is part of the normal metabolism of alcohol, it allows the buildup of acetaldehyde, which creates these unpleasant symptoms.

As a result of the autonomic side effects, it is contraindicated in individuals with hypertension, a history of stroke, heart disease, or diabetes mellitus

360
Q

What are the expected findings characteristic of HCC on US?

A

An ultrasound examination of the liver is an excellent screening tool.

The two characteristic vascular abnormalities are hypervascularity of the tumor mass (neovascularization or abnormal tumor-feeding arterial vessels) and thrombosis by tumor invasion of otherwise normal portal veins.

361
Q

What Clostridial species, if found in bacteremia, warrant a search for primary GI tumor?

A

Clostridium septicum is seen often in conjunction with GI tumors.

362
Q

Most common bacterial pathogen to cause infection in CNS shunt?

A

Probably because of its ubiquity and ability to stick to foreign surfaces, S epidermidis is the most common cause of infections of CNS shunts as well as an important cause of infections on artificial heart valves and orthopedic prostheses

363
Q

Framework question:

How to conceptualize the pathophysiology of gynecomastia to guide work up?

A

Testosterone to estrogen ratio

Pathologic gyecomastia occurs when there is a decrease in the testosterone to estrogen ratio:

1) Decreased testosterone production
2) Increased Estrogen production
- E production: HCG stimulating Leydig cells to produce E, Carney syndrome, Peutz Jegher or Sertoli cell tumor
- Increased conversion of androgens to estrogens: Hyperthyroid, adrenal tumors
- Decreased clearance: liver disease

364
Q

Medications associated with gynecomastia?

A

A variety of drugs, including diethylstilbestrol, heroin, digitalis, spironolactone, cimetidine, isoniazid, and tricyclic antidepressants, also can cause gynecomastia.

365
Q

Difference between statin induced myopathy vs myositis due to antibodies to HMG CoA?

A

Mild statin-induced myopathy is noninflammatory and usually resolves with discontinuation of therapy. In rare patients, however, muscle weakness continues to progress even after the statin is withdrawn; in these cases, a diagnostic muscle biopsy is indicated and search for antibodies to 3-hydroxy-3 methylglutarylcoenzyme A reductase (HMGCR) is suggested

The latter has persistent elevation of CK after discontinuation

366
Q

Anti Jo Ab are indicative of what disease? What organs are involved?

A

Antisynthetase Syndrome

Myositis + Lung disease

367
Q

What is the effect of iodonated contrast in a patient with Graves disease?

A

Patients with Graves disease produce thyroid-stimulating immunoglobulins. They subsequently produce higher levels of T4 compared with the normal population. As a result, many patients with Graves disease are mildly iodine deficient, and T4 production is somewhat limited by the availability of iodine. Exposure to iodinated contrast thus reverses iodine deficiency and may precipitate worsening hyperthyroidism by replenishing the iodine supply. Additionally, the reversal of mild iodine deficiency may make iodine-125 therapy for Graves disease less successful because thyroid iodine uptake is lessened in the iodine-replete state.

368
Q

Convalesent plasma in COVID 19 - effective?

A

NOV 2020
NEJM RCT

The primary outcome was the patient’s clinical status 30 days after the intervention, as measured on a six-point ordinal scale ranging from total recovery to death.

Results:

At day 30 day, no significant difference was noted between the convalescent plasma group and the placebo group in the distribution of clinical outcomes according to the ordinal scale (odds ratio, 0.83 (95% confidence interval [CI], 0.52 to 1.35; P = 0.46). Overall mortality was 10.96% in the convalescent plasma group and 11.43% in the placebo group, for a risk difference of -0.46 percentage points (95% CI, -7.8 to 6.8).

CONCLUSIONS: No significant differences were observed in clinical status or overall mortality between patients treated with convalescent plasma and those who received placebo.

Simonovich VA, Burgos Pratx LD, Scibona P, et al. A Randomized Trial of Convalescent Plasma in Covid-19 Severe Pneumonia. N Engl J Med. 2020 Nov 24. doi: 10.1056/NEJMoa2031304

369
Q

What invasive mold can often be found in blood cultures?

A

Fusarium species

370
Q

What is the first line treatment for invasive or disseminated fusarium infection?

A

Voriconazole + Liposomal Amphotericin

371
Q

What organs can be affected in disseminated Fusarium infection?

A

Affected organs may include

Skin
sinuses
lungs
joints
retina
liver
spleen
kidneys
372
Q

What population of patients are at highest risk fusarium infection?

A

Blood malignancy and stem cell transplant

373
Q

What is the characteristic look of Fusarium under microscopy?

A

Fusarium filaments were hyaline, septate and 3- to 8-mcm in diameter, typically branching at acute or right angles

Tip: Blue bananas hanging off of a stalk at acute and right angles