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Internal Medicine > February/March 2021 > Flashcards

February/March 2021 Flashcards

1
Q

When do antibodies develop for Cocci infection?

A

During symptoms, which normally occur between 7 to 21 days after having been exposed

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2
Q

What does the presence of IgM and/or IgG Ab to Cocci signify in regards to timeline of infection? (e.g. past, previous, etc)?

A
  • IgM and/or IgG signify recent or active. IgG does NOT last forever. It will appear close to the time IgM appears, hence they both can signify recent infection. IgG can last for several months though
  • KEY: Very different from many other infections in which IgG tends to be lifelong. Easy to think that IgM/IgG have NO meaning in Cocci. They both mean the same thing – recent/active infection
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3
Q

Suspicion for Cocci PNA is high, but EIA Ab test is negative for IgM and IgG. What is the next step?

A
  • Repeat EIA in 2-3 weeks; 1st week of disease 50% positive, 3rd week of disease 90% positive
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4
Q

What is the preferred initial screening tetss for Cocci?

A
  • Serology (IgM/IgG) via EIA
  • Negative test does NOT need confirmation
  • Positive test needs confirmation
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5
Q

If patient has disseminated Cocci, how does that change the value of the serologies?

A
  • Patients who have already developed extrapulmonary coccidioidal lesions nearly always exhibit anticoccidioidal antibodies in their serum, regardless of whether tested by EIA for IgG or by IDCF (aka IgG testing via immunodiffusion), and higher CF ab titers
  • Lesson: Serology testing in Cocci seems to be very much connected to disease course, that is, the timing and extent. They reflect organism activity
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6
Q

Which serology test for Coccidioides is commonly used to measure disease activity?

A
  • Complement fixation provides antibody titers
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7
Q

What is the triad that is indicative of cardiac tamponade?

A
  • The three principal features of tamponade (Beck’s triad) are hypotension, soft or absent heart sounds, and jugular venous distention with a prominent x (early systolic) descent but an absent y (early diastolic) descent
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8
Q

How much pericardial fluid is there normally?

A
  • From 10ml ot 50 ml
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9
Q

Does the amount of pericardial fluid determine the risk for tamponade?

A
  • Not really. As little as 200ml can cause tamponade if accumulates quickly. If slowly, the pericardial space can hold up to 2 L WITHOUT tamponade.
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10
Q

Explain pulsus paradoxus and what disease dose it indicate?

A
  • During inspiration, the negative intra-thoracic pressure results in an increased right venous return, filling the right atrium more than during an exhalation. The increased blood volume dilates the right atrium, reducing the compliance of the left atrium due to their shared septum. Lower left atrial compliance reduces the left atrium venous return and as a consequence causes a reduction in left ventricular preload. This results in a reduction in left ventricular stroke volume, and will be noted as a reduction in systolic blood pressure in inspiration. Pulsus paradoxus is therefore an exaggeration or an increase in the fall of systolic BP beyond 10 mmHg during inspiration.

TIP: there is nothing “pulsus” nor “pardoxical” about pulsus paradoxus. It is more like “pressure” “exaggeratus”

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11
Q

What are the most common malignancies - primary and secondary - associated with malignant pericardial effusions?

A

Most common primary malignancy to cause: Mesothelioma
- TIP: INCURABLE

Secondary Malignancies:

  • Lung
  • Breast
  • Lymphoma/Leukemia
  • Melanoma
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12
Q

How to conceptualize the cause of pathologic gynecomastia in males?

A

Testosterone/Estrogen ratio is DESCREASED
o Decrease of T:
Primary testicular failure
o Increase of E:
- HCG/LH stimulate testicles to make E e.g. Lung/germ cell tumors can make HCG (HCG is similar to LH)
- Androstenedione peripheral conversion (aromatization) e.g. Adrenal tumor
- Decreased clearance due to liver disease

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13
Q

What age is osteoporosis screening recommended for women?

A

> 65 yo (after menopause is key as estrogen deficient states increase risk for osteoporosis)

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14
Q

What is the strongest risk factor for RCC?

A

Smoking

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15
Q

What histologic cell type for RCC is the most common?

A

Clear cell carcinoma makes up 60% of the cases

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16
Q

What is the most common way RCC is diagnosed?

A

Incidental imaging for other reasons

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17
Q

What is RCC’s known response to chemotherapy

A

Characteristically known to be resistant to chemotherapy amongst the cancers

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18
Q

Between non-treponemal and treponemal serologic tests, which remains life long in patient’s having had syphilis, regardless of treatment status and stage of dissease?

A

Treponemal tests last forever REGARDLESS of the test e.g. TPPA, FTA-ABS, etc

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19
Q

What serologic test for syphilis is used for treatment response?

A

Non treponemal tests i.e. RPR

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20
Q

What are nontreponemal tests measuring?

A
  • Cardiolipin, lecithin and cholesterol
  • Interesting: the thought is that syphilis, causing damage to cells, causes the release of phospholipids
    What are the available treponemal tests?
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21
Q

What is the most sensitive treponemal test to confirm early infection ?

A

FTA ABS

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22
Q

What are the available treponemal tests?

A

TPPA – treponemal pallidum particle agglutination

FTA – ABS – Fluorescent Treponemal Antibody-Absorption Assay

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23
Q

What is the difference between the following terms referring to fungi:

  • Yeast
  • Mold
  • Hyphae
  • Pseudohyphae
  • Mycelium
A
  • Yeast: single cell fungi
  • Mold: multicellular fungi
  • Hyphae: filamentous form of fungi (AKA hyphae = filament) – can be septated or nonseptate
  • Pseudohyphae: Chains of fungal cells. “Pseudo” because they look hyphae, but in reality, each new cell buds from another and they are marked by constrictions as opposed to septa at each junction
    Mycelium: the tangled network of hyphae
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24
Q

TIPS can lead to higher incidence of PSE. Does the use of Rifaximin prevent PSE (primary ppx) in patients with TIPS (for ascites; no history of PSE)?

A

Annals of Internal Medicine 2020
RCT, double blind, multicenter

Yes!

RESULTS: An episode of overt HE occurred in 34% (95% CI, 25% to 44%) of patients in the rifaximin group (n = 93) and 53% (CI, 43% to 63%) in the placebo group (n = 93) during the postprocedure period (odds ratio, 0.48 [CI, 0.27 to 0.87]). Neither the incidence of adverse events nor transplant-free survival was significantly different between the 2 groups.

CONCLUSION: In patients with cirrhosis treated with TIPS, rifaximin was well tolerated and reduced the risk for overt HE. Rifaximin should therefore be considered for prophylaxis of post-TIPS HE.

Bureau C, Thabut D, Jezequel C, et al.The Use of Rifaximin in the Prevention of Overt Hepatic Encephalopathy After Transjugular Intrahepatic Portosystemic Shunt : A Randomized Controlled Trial.Ann Intern Med. 2021 Feb 2. doi: 10.7326/M20-0202.

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25
Q

What antihypertensive, given after AMI in patients with heart failure, lead to longer life expectancy?

A

Ramipril

CONCLUSION: For patients with clinically defined heart failure following AMI, ramipril results in a sustained survival benefit, and is associated with an extension of life of up to 14.5 months for, on average, 13 months treatment duration.

Wu J, Hall AS, Gale CPLong-term survival benefit of ramipril in patients with acute myocardial infarction complicated by heart failure.Heart. 2021 Jan 15. pii: heartjnl-2020-316823. doi: 10.1136/heartjnl-2020-316823.

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26
Q

What serologic test is best used to indicate that a patient has had a syphilis infection any time in their life?

A

Treponemal antibodies appear earlier than nontreponemal antibodies and usually remain detectable for life, even after successful treatment

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27
Q

What are the steps of the reverse algorithm for syphilis screening/testing?

A
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28
Q

In the reverse algorithm for syphilis testing, what are the possible explanations for a discordant test result?

I.e. Treponemal Ab POS/Non treponenal Ab NEG

A

Discordant testing results could be caused by

1) previous syphilis infection, treated or untreated, with persistence of treponemal antibodies but seroreversion of nontreponemal antibodies
2) a false-positive treponemal test result

or

3) early primary syphilis in a person who has yet to develop nontreponemal antibodies.

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29
Q

Framework Question:

What is the pathogenesis of ascites from portal hypertension (for example, cirrhosis)?

A

Simply, portal hypertension and the resultant renal salt and water retention that is a result but also a exacerbating factor, are the causes of ascites. Portal hypertension is hydrostatic pressure. Since albumin can’t cross the vasculature, fluid shifts from portal system to peritoneal space, hence the albumin in the peritoneal space becomes less concentrated compared to the serum.

Portal hypertension, plainly, increased pressure in the portal system is a product of resistance. Ohm’s law describes pressure = resistance x flow (P=FR, “puffer”).

It is the increased resistance that leads to portal hypertension. 3 causes:

1) Hepatic fibrosis which defines cirrhosis
2) Hepatic stellate cells activativation lead to vasoconstriction of the smooth muscle cells as well as their fibrosis
3) Decreased eNOS causes increased hepatic vasocontriction

Renal salt and water retention is caused by systemic vasodilation and ineffective circulating blood volume:

  • Cirrhosis leads to systemic NO
  • Vasodilation especially in the splanchnic circulation
  • Pooling of blood in the splanchnic circulation
  • Body interprets as a state of hypovolemia
  • RAAS and ADH system respond by renal salt and water retention, worsening the ascites
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30
Q

Explain how SAAG >1.1 is indicative of portal hypertensive causes of ascites

A

Simply, portal hypertension and the resultant renal salt and water retention are the causes of ascites. Portal hypertension is hydrostatic pressure. Since albumin can’t cross the vasculature, fluid shifts from portal system to peritoneal space, hence the albumin in the peritoneal space becomes less concentrated compared to the serum.

Serum Albumin - Serum Ascites > 1.1

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31
Q

What is the mechanism of action of ascites in non portal hypertensive cases?

A

Causes include malignancy, infections and pancreatic diseases.

In the case of malignancy, the tumor cells produce protein rich fluid, which draws fluid from extracellular spaces into the peritoneum (oncotic pressure)

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32
Q

What are general causes of non portal hypertensive ascites?

A

Cardiac ascites

Malignancy (secondary and primary)

Infections (tuberculosis, chlamydia)

Intraabdominal pathologies (pancreatic disease, renal disease, biliary disease)

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33
Q

Paracentesis of a patient with ascites is performed. TG > 1000. What are the possible causes of chylous ascites?

A

Biliary trauma or disruption from any cause

  • Cirrhosis
  • Tumor
  • Tuberculosis
  • Congenital abnormalities

Clinical Tip: MRCP to eval for biliary structure

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34
Q

Paracentesis of a patient with ascites is performed. The fluid is BLACK. What are the possible causes?

A

Melanoma

Pancreatic necrosis

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35
Q

What does the SAAG represent physiologically?

A

Think of it as amount of portal HTN. It is reflective of the pressure within the hepatic sinusoids.

The greater the difference between serum albumin and ascitic albumin, the greater the portal hypertension.

SAAG >1.1

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36
Q

Can the interpretation of SAAG be affected by diuresis?

A

NO

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37
Q

What is the differential diagnosis of SAAG > 1.1

A

KEY: SAAG is representative of portal hypertension in the hepatic sinusoids. NOT just cirrhosis

Once SAAG> 1.1, the differential diagnosis is predominantly focused on causes of portal HTN

Diff Diag:

  • Cirrhosis
  • Hepatic venous thrombosis (Budd Chiari)
  • Liver with massive mets
  • Sinusoidal obstructive syndrome
  • Cardiac ascites
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38
Q

What does ascitic protein represent physiologically? How does it aid in further refining the differential diagnosis?

A

Represent the integrity of the hepatic sinusoids. If ascitic protein > 2.5, this means that the hepatic sinusoids are normal AND hence, allow for the passage of protein into the ascites.

If protein > 2.5:

  • Cardiac ascites
  • SOS
  • IVC obstruction
  • Early Budd Chiari Syndrome

If protein < 2.5:

  • Cirrhosis
  • Late Budd chiari
  • Massive liver metastasis
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39
Q

What ascitic fluid findings are consistent with perforated viscus?

A

Low Glucose

Elevated LDH

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40
Q

What ascitic fluid findings are consistent with pancreatic ascites?

A

Elevated amylase

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41
Q

What ascitic fluid findings are consistent with tuberculous peritonitis?

A

ADA (highest sensitivity)
AFB Smear
AFB culture

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42
Q

What is the most common cause of pediatric periodic fever syndrome

A

PFAPA the most commonpediatric periodic fever syndrome in the general population

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43
Q

What age group does PFAPA tend to occur in ?

A

The first symptoms of PFAPA syndrome most often begin between the ages of 11 months and 5 years

In large cohorts, only10% to 20% of PFAPA patientsexperience their first symptoms after 5 years of age.

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44
Q

Are all the sx of PFAPA present during fever flares?

A

It should be noted that not all subjects with PFAPA have the full spectrum of clinical findings embodied in the acronym. In areview of a large number of PFAPA patients,

  • 60% to 90% of the patients had pharyngitis
  • 53% to 93% cervical lymphadenitis,
  • 27% to 57% aphthous stomatitis
  • 40% tonsillitis
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45
Q

Describe the characteristic fever of PFAPA

A

The most distinctive feature of PFAPA is the clockwork periodicity of fevers with afebrile intervals of approximately 24 days. Most untreated fevers last 2–3 days and have average highs of 39.3– 40.1°

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46
Q

First line treatment in aborting fever during a fever flare from PFAPA

A

Low-dose corticosteroids are the most used first-line treatment in children with PFAPA and are very effective in reducing the duration of febrile episodes.

With the administration of asingle dose of corticosteroid(prednisone 1–2 mg/kg/dose, up to 25–60 mg, or betamethasone 0.1–0.2 mg/kg/dose) given early during the fever flare, fever will disappear within a FEW HOURS in more than 90% to 95% of patients, though some fatigue may remain for hours or days.

TIP: could be helpful diagnostically

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47
Q

Natural history of PFAPA

A

While most affected children will spontaneously recover from PFAPA over time, the effects of the illness on lifestyle and overall well-being usually require that medical management be instituted

Nolong-term complicationsof PFAPA have been reported so far.

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48
Q

Differential diagnosis of patient suspected to have PFAPA

A

Monogenic autoinflammatory fever syndromes (MAIDS), such as Familial Mediterranean Fever (FMF), tumor necrosis factor receptor-associated periodic syndrome (TRAPS), and cryopyrin-associated periodic syndrome (CAPS) are important entities to be considered in the differential diagnosis of PFAPA.

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49
Q

How to dist between PFAPA and Monogenic autoinflammatory fever syndromes (MAIDS)?

A

Monogenic autoinflammatory syndromes are very rare, often life-long and chronic, and are progressive disorders associated with significant morbidity.

While associated with fevers, the fever pattern is usually irregular in those with FMF, TRAPS, and CAPS.

All three have detectable genetic abnormalities and, unlike PFAPA, have more prominent abdominal pain, diarrhea, vomiting, cutaneous rashes, and arthralgia.

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50
Q

What non-medical treatment can cure PFAPA?

A

In 2019, a Cochrane review of the benefits of surgery was published (see Abstract). The review observed that the risk ratio (RR) for the resolution of symptoms after surgery was 4.38 (95% confidence interval [CI] 0.64 to 30.11 [moderate-certainty evidence]).

There was no evidence that the addition ofadenoidectomyto tonsillectomy provided any greater benefit.

The role of routine tonsillectomy is a hotly debated topic even though the procedure has a high chance of “curing” the patient. T

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51
Q

What is the general difference between treponemal antibody tests and nontreponemal antibody tests in regards to what phase of the disease they may appear?

A

TIP: They are the opposites! They make up for what the other lacks!

Non treponemal: negative early in disease, late in disease and after treatment can seroconvert

Treponemal: present early in disease (earlier than nontreponemal), late in disease and even after treatment – LIFE LONG

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52
Q

What is considered a “discordant” test when using the reverse algorithm for syphilis testing?

A

Reverse algorithm means you start with a treponemal antibody test (EIA/CIA) then followed by a nontreponemal test (RPR or VDRL)

Discordant refers to POSITIVE treponemal test (EIA), but NEGATIVE nontreponemal test

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53
Q

What does the presence of “discordant” sera mean in regards to syphilis infection?

A

Basically, the 4 possibilities of a negative RPR

1) Previous treated infection in which the nontreponemal test has seroconverted
2) Early infection in which patient has not yet developed RPR Ab
3) Late infection in which patient has not been treated
4) False positive Treponemal Ab test

Remember:

TIP: They are the opposites! They make up for what the other lacks!

Non treponemal: negative early in disease, late in disease and after treatment can seroconvert

Treponemal: present early in disease (earlier than nontreponemal), late in disease and even after treatment – LIFE LONG

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54
Q

What is the solution to “discordant sera” when testing for syphilis?

Discordant:
- Treponemal Test (EIA/CIA) POSITIVE
Non treponemal Test (RPR/VDRL) NEGATIVE

A

Another treponemal Ab test like FTA-ABS or TPPA

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55
Q

What is the preferred treponemal test for “discordant sera” when testing for syphilis?

A

TPPA

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56
Q

Framework question:

Why is there an ammonia build up in HE?

A

3 major organs: Liver, Kidney and Muscle

Natural process: colonic bacteria break down protein -> nitrogen-containing compounds -> metabolized into ammonia in GI tract -> Ammonia enters liver -> urea cycle -> water soluble and non-toxic urea is excreted

In cirrhosis, 1) decreased hepatic function 2) decreased access to hepatocytes due to fibrotic sinusoids and 3) portosystemic shunting of ammonia rich blood away from gut/liver all lead to ammonia build up

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57
Q

How are the kidneys and muscles contributing to the pathogenesis of hepatic encephalopathy?

A

Kidneys need glutamine for 2 functions: acid base homeostasis and eukalemia.

In the setting of either acidosis or hypokalemia, the kidney uses glutamine to correct these disturbances. Glutamine, however, leads to ammonia as a byproduct.

Hence, any of these disturbances in the setting of liver failure, will add ammonia to the blood stream, in the setting of an already high ammonia state

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58
Q

Where is ammonia normally produced in the body?

A

In the gut as a normal part of digestion

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59
Q

Is asterixis pathognomic for HE?

A

NO

Occurs in uremia too

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60
Q

What other neurologic diseases does HE NOT mimic?

A

Stroke

Seizures

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61
Q

What neurogenerative disease can HE mimic?

A

Parkinson given the extrapyramidal dysfunction such as hypomimia (lack of facial expression), bradykinesia, muscle rigidity, tremor

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62
Q

What exactly is going on in asterixis?

A

It is NOT a tremor, but rather, a negative myoclonus, that is, loss of postural tone.

Hence when assuming an extended posture at the wrist, the flap is the loss of postural tone

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63
Q

Is HE an indication for liver transplant?

A

Yes, but only, recurrent and intractable HE.

Interesting: it would be difficult to pin a patient’s AMS’s only on HE and push toward transplant

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64
Q

How to use Ammonia blood level in the diagnosis of HE?

A

A high ammonia level does not add anything to the diagnosis of HE, but a low ammonia level brings into question the diagnosis of HE

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65
Q

How does Lactulose treat HE?

A

In addition to laxative effect, factors that may improve hepatic encephalopathy include prebiotic effects (nonabsorbable disaccharide is a prebiotic which promotes growth of beneficial microbiota), reduction (acidification) of colonic pH, reduced breakdown of nitrogen-containing compounds by bacteria, and interference with mucosal uptake of glutamine/ammonia in gut

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66
Q

What is the dosing and frequency of lactulose to treat overt HE?

A

25 ml lactulose every 1-2 hours until 2 soft BM’s are produced

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67
Q

Can rifaximin alone be used to treat HE?

A

No

Always used with lactulose

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68
Q

What is the first line treatment for HE?

A

Lactulose

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69
Q

Can any laxative be used to treat HE?

A

No

They lack the pre-biotic properties of lactulose and other disaccarhides

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70
Q

What are alternatives to treat HE if lactulose and Rifaximin are not working?

A

Branch chained amino acids

IV LOLA (L-ornithine L-aspartate)

Neomycin

Metronidazole

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4
5
Perfectly
71
Q

What is the informal name given infection by Coccidioides?

A

Valley Fever

72
Q

What are the 2 species of Coccidioides? What is the difference between them in regards to clinical disease

A

Coccidioides immitis

Coccidioides posadasii

Both are identical in both clinical disease and routine lab media

73
Q

Where does the “valley” in Valley Fever come from?

A

“Valley” refers to the San Joaquin Valley in which the southern part of the San Joaquin Valley is endemic for Coccidioides

74
Q

What part of California is Coccidioides endemic?

A

Southern part of San Joaquin Valley (think Bakersfield)

75
Q

What general area (that is, states) is Coccidioides endemic?

A

Southwestern US generally

California
New Mexico 
Nevada 
Arizona 
Texas 
Utah
76
Q

Outside of the US, what other countries is Coccidioides endemic?

A

Northern Mexico (makes sense as it is part of the Southwestern part of the US)

Localized parts of central and south america

77
Q

Why are Coccidioides outbreaks associated with archaeologic excavations?

A

Interestingly, Coccidioides is located at a specific depth of soil - 2-20 cm below the ground. Any deeper, Coccidioides does not exist. Nor is it found in cultivated soil (high up)

78
Q

What part of the immune system is key in controlling Coccidioides infections?

A

Cellular immunity

Clinical tip: Hence, uncontrolled HIV patients that are at great risk for symptomatic and disseminated Coccidioides

79
Q

What non-disease related risk factor is related to high probability of symptomatic disease from Coccidioides?

A

Age

80
Q

What are the expected symptoms of primary pulmonary Coccidioides?

A 
Fever
Cough
Pleuritic chest pain 
Night sweats
PROFOUND fatigue
81
Q

What radiographic findings, if present, is uncommon for Coccidioides?

A

Pleural effusions

82
Q

What are expected radiographic findings of Acute Coccidioides?

A
  • Most commonly focal consolidation
  • Pleural effusion (< 10% of the time)
  • Mediastinal and hilar adenopathy
  • Pulmonary nodules
83
Q

What are expected radiographic findings of Chronic Coccidioides?

A

Nodules

Cavities

84
Q

What patient population is more likely to develop disseminated disease from Coccidioides?

A

KEY: cellular immunity is key to controlling Coccidioides infections

  • African Americans and Filipinos
  • Pregnant women who acquire disease in 2nd or 3rd trimester or soon after delivery
  • Untreated HIV
  • Chronic Glucocorticoid
  • Solid Organ Transplant
  • TNF alpha
85
Q

What extrapulmonary Coccidioides infection is fatal without treatment?

A

Coccidioides Meningitis

86
Q

What are characteristic findings on blood count that point toward Coccidioides?

A

Peripheral eosinophilia

87
Q

What scenario would it be best to use Amphotericin as initial treatment for Coccidioides?

A

Diffuse primary pulmonary Coccidioides

Severe disseminated Coccidioides

Meningitis that has failed triazole therapy

88
Q

What is the first line drug class to treat Coccidioides?

A

Triazoles (e.g. Fluconazole, Itraconazole, Posaconazole)

89
Q

Do ALL patients with Coccidioides Pneumonia require treatment?

A

NO, most patients with primary focal pulmonary Coccidioides do NOT need treatment

KEY: ALL extrathoracic Coccidioides requires treatment

90
Q

Which patients with primary pulmonary Coccidioides gets treatment?

A

Those with underlying cellular immunodeficiencies

Prolonged symptoms

Diffuse primary pulmonary Coccidioides because they tend to be very sick

91
Q

What is the usual duration of therapy for primary pulmonary Coccidioides?

A

6 months

92
Q

Which type of Coccidioides infection requires lifelong treatment?

A

Meningitis because 80% recurrence upon discontinuation of drug

93
Q

In patient’s receiving PLEX for TTP, what is the goal platelet count prior to stopping TTP?

A

150k x 2 days

Clinical tip: NOT all patients with TTP are critically ill. Hence, in patients with BOTH anemia/thrombocytopenia, do the full work up - CBC, Retic, DAT, Haptoglobin, Peripheral smear, Bili.

94
Q

Patient has necrotic ulcer in the lower extremities. What part of the presentation would be characteristic of calciphylaxis?

A

Extreme pain. Pain out of proportion

95
Q

What is the must common valvular abnormality in patients with ankylosing spondylitis?

A

Aortic stenosis

96
Q

What bacteria characteristically targets the jaw and causes infection there when there is underlying abnormalities such as osteonecrosis?

A

Actinomyces. Actinomyces is a classic oral organism with a propensity to infect the jaw, particularly when the bone is abnormal usually due to radiation or osteonecrosis

97
Q

What is the relationship between Actinomyces and bisphosphonates?

A

Osteonecrosis of the jaw due to bisphosphonates is an increasingly recognized risk factor for Actinomyces infection

98
Q

What are “sulfur granules”?

A

Sulfur granules are an in vivo concretion of Actinomyces bacteria, calcium phosphate, and host material

99
Q

Outside of “hemolytic attacks”, what should the lab work (CBC and Retic count) of patient’s with G6PD Deficiency?

A

CBC and Retic is normal in ALMOST ALL patients with G6PD deficiency.

Clinical tip: when evaluating patients with anemia at baseline, G6PD deficiency should NOT be on the differential diagnosis

100
Q

What pain can accompany a “hemolytic attack” from G6PD Deficiency?

A

Lumbar pain or abdominal pain

101
Q

Characteristic peripheral smear findings for a patient with G6PD def “hemolytic attack”?

A

The peripheral blood smear shows bite cells (arrow in Figure III-58), anisocytosis, and spherocytes.

102
Q

Why is the sclera of patients with OI blue?

A

Another common clinical feature of type 1 OI includes blue sclera, which is thought to be due to the thinness of the collagen fibers of the sclerae, allowing the choroid layers to be seen

103
Q

Inheritance pattern of OI?

A

Autosomal dominant

Picmonic: Monster truck running over skeletons

104
Q

What lab is the single most powerful predictor of prognosis for multiple myeloma?

A

Serum β2-microglobulin is the single most powerful predictor of survival and can substitute for staging. Patients with β2-microglobulin levels <0.004 g/L have a median survival of 43 months, and those with levels >0.004 g/L have a survival of only 12 months

105
Q

What labs are used for staging in multiple myeloma?

A

Combination of serum β2-microglobulin and albumin levels forms the basis for a three-stage International Staging System (ISS) that predicts survival

106
Q

In all scenarios of PE/VTE (regardless of the cause), what is the minimal duration of AC treatment?

A

The minimum
duration of anticoagulant therapy for DVT or PE is
usually 3 months; this period of treatment is referred
to as “long-term therapy.”1 A decision to treat patients
for longer than 3 months, which we refer to as
“extended anticoagulant therapy,” usually implies that
anticoagulant therapy will be continued indefinitely.

107
Q

What is the suggested maximum volume of fluid to remove in one single thoracentesis?

A

1.5 L per BTS 2010

108
Q

What is the definition of pleurodesis?

A

pleurodesis. : obliteration of the pleural cavity

109
Q

What is the most common cause of malignant pleural effusion in men? Women?

A

Lung cancer in men
Breast cancer in women
Together, these make up at least 50% of ALL malignant pleural effusion s

110
Q

“Massive pleural effusions” which are described as pleural effusions that completely opacify the hemithorax are often due to what etiology?

A

Malignant pleural effusions

111
Q

What is the best way to effectively manage a malignant pleural effusion?

A

Malignant pleural effusions
are often most effectively managed by complete
drainage of the effusion and instillation of a sclerosant
to promote pleurodesis and prevent recurrence
of the effusion.

112
Q

What are the 2 DOAC’s that have been approved for cancer associated VTE?

A

Edoxaban and Rivaroxaban

113
Q

What is the MOA of aminoglycosides (TIP: MOA of a few other classes of abx are similar)

A

Aminoglycosides bind irreversibly to the 16S ribosomal RNA of the 30S ribosomal subunit to prevent protein synthesis. (review: 16s is rRNA, 30S is the ribosome itself. Ribosome = RNA + Protein) This class of medication can also cause misreading of messenger RNA codon.

Tobramycin, gentamicin, and amikacin are commonly used aminoglycosides.

Tetracyclines also bind to the 16S ribosomal RNA of the 30S ribosomal subunit, but in contrast to aminoglycosides, the binding is reversible.

114
Q

Aminoglycosides: bacteriostatic vs bacteriocidal?

A

These drugs bind within the bacterial ribosome and are most commonly bacteriostatic, although aminoglycoside antibiotics are bactericidal

115
Q

Patient with recurrent hypotension in dialysis _ management?

A

Midodrine

116
Q

Patient presents with a mole, and the biopsy confirms melanoma. What is the best predictor of metastatic potential?

A

The best predictor of metastatic risk in melanoma is Breslow thickness, which defines the absolute extent of tumor extension into the tissue

TIP: the deeper the melanoma, the higher likelihood of metastatic disease

117
Q

What are the characteristics of neuropathic pain?

A

unusual burning, tingling, or electric shock–like quality and may be triggered by very light touch, allodynia/hyperpathia (exaggerated pain from light touch)

118
Q

What are sources of secondary peritoneal carcinomatosis?

A

GU and GI sources, e.g. colon cancer or ovarian cancer

119
Q

What is a Krukenberg tumor?

A

Metastatic disease TO the ovary

120
Q

What are some vascular complications of Behcets?

A

DVT, Superficial venous thrombosis, Cerebral venous thrombosis

Pulmonary artery vasculitis, which may be mistaken for PE

Arterial thrombosis

121
Q

In the process of diagnosing brain death, what are tests to demonstrate absent brainstem reflexes?

A

Pupillary light reflex

Corneal reflex

Oculocephalic test

Tracheal (or phayryngeal reflex) tracheal suctioning past carina doesn’t lead to cough response

122
Q

What are the 3 essential parts of diagnosing brain death?

A

1) irreversible unresponsive coma
2) absent brainstem reflexes
3) apnea

123
Q

If a patient has renal solid mass diagnosed and presumed RCC, what subtype is more likely if metastatic disease is present as well?

A

> 80% of metastatic disease in RCC is due to clear cell

124
Q

First line treatment for patient with advanced RCC?

A

Sunitinib (PO med!), Tyrosine Kinase Inhibitor

125
Q

What age group is often affected by pulmonary alveolar proteinosis?

A

Pulmonary alveolar proteinosis is a rare disorder that usually presents between ages 30 and 50 years.

Clinical tip: subacute shortness of breath in a relatively young person

126
Q

Treatment for pulmonary alveolar proteinosis?

A

Whole lung lavage

127
Q

CT Scan findings consistent with Pulmonary Alverolar 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

128
Q

Role of antibiotics in necrotizing pancreatitis?

A

Several trials over the last several decades have demonstrated that there is no role for prophylactic antibiotics in the management of either interstitial or necrotizing pancreatitis

129
Q

What is the difference or the relationship between EIA and ELISA?

A

ELISA is a type of EIA

EIA: An assay that uses an enzyme-bound antibody to detect antigen. The enzyme catalyzes a color reaction when exposed to substrate.

ELISA (enzyme-linked immunosorbent assay) is a PLATE-BASED assay technique designed for detecting and quantifying soluble substances such as peptides, proteins, antibodies, and hormones.

130
Q

What is FENO a marker of in regards to asthma?

A

FeNO is a biomarker of the pulmonary type 2 inflammation seen in asthmatics. FeNO can easily be measured in exhaled breath. Type 2 inflammation, also known as eosinophilic inflammation in the airway, is characterized by airway immune responses that are mediated primarily by eosinophils, mast cells, basophils, type 2 helper T lymphocytes, group 2 innate lymphoid cells, and immunoglobulin E (IgE)–producing B cells.

131
Q

How may FENO be used to predict response to steroid treatments?

A

In clinical practice, FeNO <25 ppb in adults and <20 ppb in children is considered a normal value. FeNO values >50 ppb in adults and >35 ppb in children are likely to be associated with airway eosinophilic inflammation and are used to predict a response to anti-inflammatory therapy with corticosteroids, while low FeNO <25 ppb (<20 ppb in children) correlates with less eosinophilic inflammation and poorer responsiveness to corticosteroids

132
Q

What factors can influence FENO results?

A

Confounding factors include a patient’s race/ethnicity, sex, weight and height, diet and drugs such as anti-inflammatory medications. The presence of atopy, drinking alcoholic beverages and smoking influences FeNO levels. Allergen exposure in atopic individuals raises levels of FeNO. Alcohol ingestion and active and passive smoking may lower FeNO levels regardless of allergy status.

TIP: demographic factors can affect FENO - age, (not sex), race, weight/height

133
Q

How does race affect the FENO results?

A

Races other than white tend to have higher FENO

Asians
Hispanics
Blacks

They HOT (inflammation)

134
Q

What is the purpose between the 2 lumens in a Salem sump catheter?

A

Used for aspiration in one lumen, and venting in the other

135
Q

What is the purpose of having a separate lumen for venting in a Salem Sump?

A

The blue sump port (pigtail) allows atmospheric air to enter the patient’s stomach and equalize the pressure in the stomach and atmosphere which prevents the creation of negative pressure that can occur with active suction.

Negative pressure can lead to stomach wall collapsing on the suction port and subsequent mucosal injury. Secondly, it can lead to inefficient suctioning.

136
Q

What is the main function of a Salem sump catheter?

A

Drainage of the stomach and decompression such as in the case of an SBO

137
Q

What is the main advantage of using a Salem sump catheter for suction/drainage/decompression compared to a Levin catheter?

A

Salem sump catheter is a dual lumen catheter while the Levin is a single lumen catheter. Both can be used for suction.

However, using a single lumen catheter for suction can lead to suction against the stomach mucosa AFTER the stomach has been emptied, a risk for mucosal injury

Using a dual lumen catheter, in which one of the lumens is used purely for venting, that is, allowing the pressure in the stomach to equalize with the pressure in the stomach, prevents the negative pressure that can be created when stomach contents are emptied and the stomach collapses on itself.

138
Q

Patient has a Salem sump in place for gastric decompression. There is minimal output recorded - How do you verify that a stomach is truly fully decompressed from a Salem sump as opposed to the stomach lining simply having collapsed over the holes of the tip of the catheter.

A

Introduce air into the sumping port (the lumen used for venting)

If the stomach is truly empty, that air will then be suctioned by the suction tubing and air bubbles will be seen in the tubing and wall suction

If the stomach is actually still full and the mucosa has instead covered the distal holes of the suction tubing, air introduced through the sump port will push the mucosa away, enter the gastric contents and bubble to the top of the fluid and NOT be seen in the suction tubing

139
Q

Patient has a Salem sump in place for gastric decompression. What can be done to prevent the stomach lining from intermittently collapsing over the holes of the tip of the catheter?

A

Low intermittent suction allows the mucosa to be released from the negative pressure of the suction tube

140
Q

The disadvantage of low intermittent suction is that it may not be the most efficient in removing all the gastric contents. What can be done instead?

A

Continuous suction

Periodic (Q4h) injection of air into the sump port and water into the suction lumen will push the gastric mucosa away from the suction catheter/sump port holes

141
Q

What is the main purpose of a Dobhoff tube?

A

Enteral feeds

142
Q

What is the difference between a Dobhoff tube and a traditional NGT?

A

Dobhoff Tubes are types of NGT

Dobhoffs are NGT with weighted ends and are inserted using a stylet and are supposed to be post-pyloric to ideally prevent aspiration

143
Q

Cavitary lesion in a patient with TB is often found in which type of pulmonary TB, primary pulmonary TB vs post primary pulmonary tuberculosis (AKA reactivation TB)?

A

Cavitary lesions are more common in reactivation TB (up to the 45%) than in primary TB

144
Q

What is the most common radiographic finding of primary TB in pediatric patients?

A

The more striking finding, especially in children, is that of ipsilateral hilar and contiguous mediastinal (paratracheal) lymphadenopathy, usually RIGHT-sided. This pattern is seen in over 90% of cases of childhood primary TB, but only 10-30% of adults

145
Q

What are possible radiographic findings of primary TB?

A

Patchy areas of consolidation and even lobar consolidation

146
Q

What findings on radiograph help distinguish between primary vs reactivation TB?

A

Upper lobe involvement more common in reactivation TB

Middle or lower lobe involvement more common in primary TB

147
Q

Miliary TB is a presentation of primary vs post primary TB?

A

BOTH. It can occur in both.

Represents hematogenous spread of uncontrolled TB

148
Q

What factor radiologically distinguish between “cyst” and a “cavity” in regards to lung imaging?

A

Wall less than 3 mm is cyst, also surrounded by normal lung

Wall > 4mm is cavity, surrounded by pulmonary consolidation/mass/nodule

149
Q

What is the differential diagnosis of patient presenting with a cavitary lung lesion? (conceptual framework)

A

Large umbrellas
- Infectious vs non infectious
-> Infectious
&raquo_space; TB vs NTM
&raquo_space; Bacterial
&raquo_space; Fungal - all the endemic fungal infections such as crypto, histo, blasto, pjp, Coccidioides
&raquo_space; Parasitic - Echinococcus
-> Non-infectious (smaller list): NSCLC, Pulmomary sarcoid, GPA, septic emboli and RA

150
Q

What are some pyogenic bacteria that could be possible causes of lung abscesses? AKA What organisms can cause monomicrobial lung abscess formation?

A
  • Staphylococcus aureus
  • Klebsiella pneumoniae
  • Pseudomonas aeruginosa
  • Streptococcus pyogenes
  • Burkholderia pseudomallei
  • Haemophilus influenzae type b,
  • Legionella
  • Nocardia
  • Actinomyces
151
Q

Most common preceding factor leading to lung abscess?

A

Aspiration

152
Q

What is the difference between “necrotizing pneumonia” and “lung abscess”?

A

Necrosis and multiple small abscesses is characteristic of necrotizing pneumonia

153
Q

Monomicrobial vs polymicrobial - what’s more common in lung abscess?

A

Polymicrobial since most common cause is aspiration and oral microbio is polymicrobial

Clinical tip: empiric treatment is broad

154
Q

What is the most common leukemia in adults?

A

CLL

Clinical tip: If you had to learn about one leukemia in adults, this would be it

155
Q

What is the differencebetween CLL vs SLL (vs MBL)

A

KEY: Absolute clonal lymphocyte count alone establishes CLL. It’s only when the clonal count is lower than 5000 are the other subtypes possible

CLL:
Absolute Clonal Lymphocyte > 5000
+/- BM (cytopenia) involvement
+/- LN/tissues (organomegaly) involvement

SLL:
Absolute Clonal Lymphocyte < 5000
LN/other tissue involvement
NO BM involvement

MBL:
Absolute Clonal Lymphocyte < 5000
NO LN/tissues involvement
NO BM involvement

Basically it is the precursor to ALL CLL/SLL

156
Q

Framework Question:

What is CLL?

A

Accumulation of mature malignant monoclonal B cells in blood

It is a cancer of the mature B cells

157
Q

CLL Picmonic

A

Old fairy (chronic, lymphocytic) cleaning up broken plates/red cells (AIHA). Zangief holding large spleen and causing earthquakes (Richter transformation)

  • Tyrosine Kinase Inhibitor -
158
Q

Does ALC < 5000 rule out CLL?

A

Yes, technically, CLL has ALC > 5000

BUT SLL and MBL can have ALC <5000, but still show monoclonal B cell in flow cytometry

Clinical tip: patient with LN and organomegaly can still have SLL even if the ALC < 5000. Still worth it to do cell flow cytometry

159
Q

What is Richter transformation of CLL?

A

Histologic transformation to more aggressive diseases - CLL can transform to diffuse large B-cell lymphoma (DLBCL), classical Hodgkin lymphoma, or progression of CLL with increased prolymphocytes or expanded proliferation centers

Picmonic: Richter scale, imagine earthquake and out of the ground is large LN, spleen, liver, blood

Richter is to CLL as Blast phase is to CML

160
Q

When to even suspect Richter transformation?

A

New onset B symptoms

Enlarging LN

Elevated tumor markers

161
Q

First line treatment of CLL?

A

Tyrosine Kinase Inhibitor

TIP: TKI’s are also first line for CML

162
Q

Amongst the lymphomas, how common are B symptoms in CLL?

A

10 %, not very common

163
Q

What is the main presentation of CLL?

A

1 asymptomatic, diagnosed bc lab showed ALC > 5000

164
Q

How to diagnose CLL?

A

Peripheral flow cytometry demonstrating monoclonal mature b cell proliferation

Flow cytometry will confirm monoclonal B lymphocyte count > 5000

And the immunophenotype typical of CLL: CD19, the T-cell antigen CD5, and CD23

165
Q

Is CLL curable?

A

INCURABLE

But! Not all patients need treatment. Only symptomatic, active disease. Actually, 1/3 patients do not need treatment ever

166
Q

From a CBC standpoint, what is the most common abn that should be suspicious for CLL?

A

ALC > 5000

167
Q

What is the key indication for starting treatment for CLL?

A

“Symptomatic active disease.”

Actually, 1/3 patients do not need treatment ever

This is the indication for treatment regardless of where the patient is in his disease - initial, recurrent

168
Q

What is considered “symptomatic active disease” in CLL

A

KEY: this determines treatment

♣ B symptoms such as fatigue, weight loss, night sweats and fever without infection

♣ Rest of the disease has more to do with growth of disease

   - Cytopenias
   - Bulky LN leading to end organ damage
   - Bulky disease such as splenomegaly
169
Q

What are the range of stool consistencies for C diff infection?

A

SOFT, unformed, loose, watery

170
Q

What is essential in C diff strains to be able to cause CDI?

A

Not all strains ofC difficileare equipped with the gene that produces toxin, and bacteria that do not produce toxin are not pathogenic [1]. Furthermore, EVEN toxigenic strains ofC difficilecan live harmlessly in the colon without producing toxin.

171
Q

What determines if a patient with a toxigenic strain of C difficile actually produces toxin which leads to CDI?

A

A complex balance of host factors, including immune function, exposure to medications such as antibiotics or immunosuppressants, and the host microbiome, mediates whether a toxigenic organism actively produces toxin

172
Q

How prevalent is C diff colonization? How does that compare to the rates of true CDI?

A
  • 10 % community
  • 18% inpatient
  • 20 % longterm care

Colonization is 5-10x more common than CDI

173
Q

What do the tests for C diff actually test for?

A

Is there bacteria: ELISA for GDH (aka antigen test, glutamate dehydrogenase) which is a component of toxigenic, nontoxigenic strain as well as other bacteria

Is there C diff with toxin producing capability: NAAT (or PCR) for the tdcB gene and tdcC, but not if toxin is actively being produced

Is there toxin being produced: ELISA for toxin, but not sensitive, so can produce false negatives

Is there toxin causing damage: cell culture cytotoxin test, which would be considered the gold standard

174
Q

What are the MAJOR risk factors for C diff infection?

A

Antibiotic, age and hospitalization

175
Q

What are the 3 essential events that lead to C diff infection?

A

1) Exposure to abx
2) Acquisition to C diff, either toxigenic or nontoxigenic
3) Variable what the 3rd factor is: but possibly inadequate IgG response to toxin A

176
Q

Patient presents with a pontine stroke. What are the vessels, that if involved, could lead to pontine stroke? (AKA what are the main vessels that supply the pons?)

A

Depends on the level of the pons: superior, mid or inferior. Also whether medial vs lateral

  • Superior, medial: paramedian artery of the basilar artery
  • Superior, lateral: superior cerebellar artery
  • Midpons, medial: paramedian artery of the basilar artery
  • Midpons, lateral:short circumferential artery
  • Inferior, medial: paramedian artery of the basilar artery
  • Inferior, lateral: anterior inferior cerebral artery
  • TIP: ALL medial syndromes of the pons, regardless of superior, mid or inferior, is due to penetrating arteries from the basilar artery
  • TIP: vast majority of pons is supplied by the basilar artery through both the penetrating arteries of the paramedian arteries and the short circumferential artery

Internal Medicine (6 decks)

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