High Yields 2018 Qs Flashcards

Question 1

Q

How does the PD-1/PD-L1 interaction relate to tumor growth?
TEST QUESTION

Answer

A

PD-L1 expressed on many cells, including cancer cells
PD-1 expressed on B and T cells.
PD-1 is the negative regulator of cell activation.
The tumor microenvironment up-regulates PD-1 on tumor reactive T cells, and contributes to impaired antitumor immune responses.

Question 2

Q

what are Interferons?

Answer

A

non specific immune modulators named for interfering with viral machinery

Question 3

Q

what part of the Her2 receptor is the target of intervention? (ie: Intracellular, tyrosine kinase, extracellular, transmembrane)

Answer

A

extracellular portion

Question 4

Q

What is the other name for protein Ca125?

Answer

A

MUC16 or mucin16

Question 5

Q

What distinguishes PSTT from choriocarcinoma?

Answer

A

1.INTERMEDIATE trophoblasts
2.Human Placenta Lactogen
3. Lower betaHCG

*all of these

Question 6

Q

What distinguishes endometrial stromal nodule (ESN) from low grade endometrial stromal sarcoma (LG-ESS)?

A ESS has more mitoses
B ESS has more atypia
C presence of spiral arterioles
D absence of LVSI in ESN

Answer

A

No LVSI is the correct answer choice

The histologic features of ESN are identical to LG-ESS but ESN has a circumscribed, noninfiltrating border without evidence of myometrial or vascular invasion

B&H: Because diagnosis is based on complete circumscription and absence of lymphovascular invasion, the distinction between stromal nodule and stromal sarcoma can usually be made only at the time of hysterectomy.

Question 7

Q

Ratio of tumor markers for ovca and colon cancer?

Answer

A

CA125/CEA (this one, 25:1), HE4/CEA

Question 8

Q

Picture of pap serous uterine cancer histology

Answer

A

pap serous
other test options that are wrong: LMS, endometrioid

Architecture:
Papillary with or without appreciable fibrovascular cores; micropapillary pattern can be seen
Slit-like spaces
Gland-like spaces may be observed
Psammoma bodies may be present in up to 33% of cases
Cytoplasm usually scant but can be abundant with eosinophilia or clearing
Tumor cells can colonize existing endometrial glands
Tumor cells can appear discohesive
Nuclei are typically high grade with pleomorphism, hyperchromasia, prominent nucleoli and frequent mitotic figures (including atypical mitotic figures)

Question 9

Q

Napsin A (IHC stain)

Answer

A

clear cell carcinoma

Question 10

Q

POLE mutated (group 1)

Answer

A

excellent prognosis regardless of grade POLE (why? high tumor mutation burden, tumor neoantigen production, and tumor infiltrating T cells)

Question 11

Q

MSI hypermutated (group 2)

Answer

A

Most common methylation of MLH1; also can have mutated MLH1, MLH2, MSH6, PMS2; MLH1 + PMS2, MSH2 + MSH6 form dimers so if one degraded the other is; immunotherapy candidates if recurrent; radiation beneficial

Question 12

Q

MSS/copy number low (group 3 - PTEN, ARID1A, PIK3CA mut, ER/PR pos)

Answer

A

Good prognosis; respond to hormonal therapy; PI3K/mTOR inhibitors for metastatic disease

Question 13

Q

Copy number high (group 4) of endometrial cancer molecular subgroup is most likely what histology?

Answer

A

serous; p53 mutated; poor prognosis; trastuz if HER2 +/ERBB2 amp

Question 14

Q

what are the most common MMR defects in Hnpcc?

Answer

A

MLH1/MSH2 (this one); PMS2, MSH6

MLH1 and MSH2 genes are by far the most commonly mutated in Lynch syndrome patients accounting for ~70% of the mutations identified (32% in MLH1 and 38% in MSH2)

Question 15

Q

KRAS associations?

Answer

A

Type 1 ovary tumors, mucinous histology ; also recurrent low grade serous carcinoma (unlike BRAF)

Question 16

Q

Integrin role in cancer?

Answer

A

metastases role (cell invasion and migration)
adhesion of leukocytes to endothelial cells

Question 17

Q

Mechanism of ERBB2 oncogenicity?

Answer

A

AMPLIFICATION of oncogene producing HER2 protein

Question 18

Q

How do kinases work?

Answer

A

Phosphorylation

Question 19

Q

Which of the following is a tumor site not included in risk for HNPCC ?

A breast
B gastric
C pancreatic
D urethral
E brain

Answer

A

“breast // does include endometrial, colon, gastric, ovarian, pancreatic, urethral, brain (glioblastoma), small intestinal,
sebaceous gland adenomatous polyps, keratoacanthomas

Question 20

Q

Histopath of leiomyosarcoma?
List 3

Answer

A

-prominent cellular atypia
-abundant mitoses (≥10 per 10 high power fields)
-areas of coagulative necrosis

Question 21

Q

Grade 1 endometrioid, young, normal weight - tumor most likely to express:

A MSH2
B CK7
C ER
D PR

Question 22

Q

Germ cell tumor least likely to have elevated AFP

Answer

A

Dysgerminoma and choriocarcinoma both not elevated

Question 23

Q

Germ cell tumor least likely to have elevated AFP

Answer

A

Dysgerminoma and choriocarcinoma both not elevated

Question 24

Q

Genetic mut associated with type I endometrial cancer

Answer

A

PTEN (PTEN tumor suppressor is the most important negative regulator of PI3K signaling)

Question 25

Q

How does Loss of heterozygosity occur (two mechanisms)

Answer

A

Deletion (most common), or methylation

*Loss of heterozygosity: refers to a type of mutation that results in the loss of one copy of a segment of DNA

Question 26

Q

High LET has what effect on cancer cells?

Answer

A

Tumor necrosis, higher LET is more direct damage

*Linear energy transfer (LET) average amount of energy lost per unit track length in tissue by a type of radiation

*High LET radiation: particles with substantial mass and charge such as alpha particles or neutrons

*Low LET radiation: X-rays, gamma rays

Question 27

Q

Elevated CA19-9 and CEA

Answer

A

mucinous tumor

Question 28

Q

Downstream effect of VEGF receptor binding

Answer

A

Capillary permeability (THIS ONE), increased intratumor pressure, other options

Question 29

Q

Cowden
What is the germline mutation?
Clinical picture (non-cancer)?
Screening?

Answer

A

PTEN
Clinical picture: GI polyps, thyroid disease, benign breast disease, mucocutaneous lesions

Cancer risk: breast, thyroid, endometrial

Screening for breast cancer: breast self awareness from 18yo, clinical breast exam q6-12mo from age 25 (or 5-10 years before earliest family dx), annual MMG+MRI from 35yo (or 10 years before earliest family dx) per NCCN 6/2023
Screening for colon: start c/scope age 35-40 or 5-10yr before earliest family dx)
Screening for endometrial cancer: start 35yo. prompt eval of AUB. consider q1-2yr EMB per NCCN 6/2023

Question 30

Q

Cowden most common GYN cancer

Answer

A

Endometrial cancer (lifetime risk 19-28%)

Question 31

Q

Cowden most common cancer

Question 32

Q

What causes invasion through the basement membrane?

Answer

A

MMP

Matrix metalloproteinases

Question 33

Q

Function of integrins?

Answer

A

migration and invasion

Question 34

Q

What tumor is associated with FOXL2 mutation?

Answer

A

Granulosa cell tumor

Question 35

Q

Which common medication inhibits the mTOR pathway?

Answer

A

Metformin

Question 36

Q

Which of the following is an oncogene: listed choices were PTEN, P53, BRCA and c-myc?

Question 37

Q

CA 125 is also known as?

Answer

A

MUC 16

*Direct questions

Question 38

Q

BRAF mutation in which ovarian tumor?

Answer

A

low grade serous

Question 39

Q

What type of endometrial cancer is associated with p53 and her2neu?

Answer

A

Type II endometrial cancer

Question 40

Q

Kras mutation in which ovarian histology- mucinous, serous, clear cell, endometrioid?

Answer

A

MUCINOUS

*Direct question: also low grade serous, this was 2 different questions on the exam

Question 41

Q

First step in carcinogenesis of ovarian cancer: p53 mutation, fallopian tube stic, a few other options - which one?

Answer

A

p53 mutation

Question 42

Q

MC germline mutation in ovarian cancer?

Question 43

Q

Mutation most common in p53?

Answer

A

Missense mutation

Question 44

Q

How do you protect vulva skin during radiation?

anti fungal
estrogen cream
positioning (frogleg)
cold packs
Using a diluted water/H2O2 rinse

Answer

A

positioning (frogleg)
Based on MCG RadOnc text consult

Question 45

Q

How does HDR differ from LDR?

Answer

A

decreased treatment time

Question 46

Q

How does cisplatin augment radiation?

Answer

A

inability to repair DNA

Question 47

Q

What radiation source the longest half-life?

Answer

A

Radium

-cesium 137 - 30 years
-irdium 192 - 74 days (SHORTEST)
-radium 226: very long like 1600 years
-colbalt 60 - 5 years

Question 48

Q

What is the half life of cesium?

Question 49

Q

What type of radiation is produced by cobalt ?

Question 50

Q

What is most sensitive to side effects from pelvic radiation?

Answer

A

ileum

*2 questions on this topic

Question 51

Q

What do you call the area around the gross tumor volume that might have microscopic tumor?

Answer

A

clinical target volume

Question 52

Q

Inverse square law, if you go from 2 cm to 1 cm how much does dose increase?

Answer

A

400%

*this is on every year

The radiation inverse square law specifies that: the intensity of the radiation goes down by the square of the distance from the source. For instance if you move twice as far from the source the intensity of the radiation will decrease by a factor of 4.
Intensity = 1 / (distance ^2)

Question 53

Q

Adjuvant treatment for positive right inguinal lymph node?

Answer

A

bilateral radiation to nodes and pelvic field

Question 54

Q

XRT vs brachy - which symptom is shared?

Answer

A

FATIGUE (answer)
-wrong answers: vaginal stenosis, 2 other

Question 55

Q

Which chemo causes delayed bone marrow suppression?
TEST QUESTION

Answer

A

mitomycin C
Marrow suppression at 28 to 42 days with recovery 40 to 60 days after treatment

And Melphalan and chlorambucil

Question 56

Q

Which drug do you need to dose reduce for renal insufficiency?

A bev
B vinca
C taxol
D etoposide

**TEST QUESTION **

Answer

A

Etoposide

A BICC THE MMP require renal dosing modifications
ActD,
Bleo, ifos, cytoxan, capecitabine,
Topo, hydroxyurea, etopo,
mtx/pemetrexed, melphalan, platinum (carbo/cis, oxali)

Question 57

Q

Dose limiting toxicity of carbo?

**TEST QUESTION **

Answer

A

thrombocytopenia

Question 58

Q

What drug is most likely to cause constipation?
a. Paclitaxel
b. Vincristine
c. Cisplatin
d. Gemcitabine

**TEST QUESTION **

Answer

A

Vincristine

FYI per the SGO chemo book, vinblastine&raquo_space;> vincristine

Question 59

Q

What is the mechanism of action of Capecitabine?
a. Inhibits topoisomerase I
b. Creates DNA crosslinks
c. Prodrug, converted to 5-FU in the tumor tissue
d. Prodrug, converted to 5-FU in the liver

**TEST QUESTION **

Answer

A

c. Prodrug, converted to 5-FU in the tumor tissue

converted initially to another intermediate in the liver but the final step is conversion intercellularly in tumoral tissue

Question 60

Q

What is the mechanism of action of gemcitabine?
a. Prodrug, converted to 5-FU
b. Creates ss DNA breaks
c. Stabilizes microtubules
d. Prodrug, converted to a fraudulent base pair

**TEST QUESTION **

Answer

A

d. Prodrug, converted to a fraudulent base pair

Also important that it requires active transport

Question 61

Q

How does liposomal doxorubicin differ in mechanism of action from doxorubicin
a. Liposomal coating creates a more basic tumor microenvironment
b. Liposomal coat causes increased receptor affinity with the tumor cells
c. Liposomal coat causes slower drug release which decreases toxicity
d. Liposomal coat causes increased hepatic metabolization

**TEST QUESTION **

Answer

A

c. Liposomal coat causes slower drug release which decreases toxicity

Question 62

Q

How to reduce thrombocytopenia in patient getting taxol/carbo?

**TEST QUESTION **

Answer

A

Dose reduce carbo
Carbo causes thrombocytopenia
Taxol causes neutropenia

Question 63

Q

Imatinib: MOA, target, drug class

** TEST QUESTION **

Answer

A

BCR-ABL Tyrosine Kinase Inhibitor

Bcr-Abl tyrosine kinase is the constitutive abnormal gene product of the Philadelphia chromosome in chronic myeloid leukemia (CML).
Inhibition of this enzyme blocks proliferation and induces apoptosis in Bcr-Abl positive cell lines.
Also inhibits tyrosine kinase for platelet-derived growth factor (PDGF), stem cell factor (SCF), c-kit, and cellular events mediated by PDGF and SCF.

Question 64

Q

What do tyrosine kinase receptors do?
a. Increase the membrane action potential by increasing flow through ion channels
b. Activate cell replication machinery
c. Activate DNA repair mechanisms
d. Activate/phosphorylate proteins through signal transduction cascades

**TEST QUESTION **

Answer

A

Activate/phosphorylate proteins through signal transduction cascades

Answer 59

A

Screen for Lynch with IHC testing first

Answer 60

A

High fidelity, template, dependent DNA repair mechanism for double stranded DNA breaks

Steps:
1. dsDNA breaks are recognized by the MRN complex and checkpoint proteins
2. 5’-3 exonuclease generates 3’ overhangs, which are coded with replication protein a
3. BRCA1/RAD51 forms a complex.
4. RAD51 assembles onto single stranded ends.
5. Homology search, strand invasion, and DNA synthesis.
6. Links between DNA strands (double holliday junctions) resolved to produce exchange between chromosomes or no exchange.

Answer 61

A

NK cells release granzymes & perforins

NK cells secrete preformed secretory lysosomes called lytic granules (LGs) directly toward bound target cells, a process known as cell-mediated cytotoxicity

True granules released by: mast cells, basophils, neutrophils, eosinophils (granulocytes)

Answer 62

A

Notes say: I picked something about effects on PI3K pathway

Lit review: Statins can stimulate inflammatory responses and anticancer immune surveillance via phosphorylated Akt and downregulation of the mammalian rapamycin target protein (mTOR). statins have antiproliferative and antimetastatic effects,

PI3K —> PIP3 —> PDK —> AKT—> mTOR

Answer 63

A

Tamoxifen increases PR expression which sensitizes to Megace

Answer 64

A

After ligand binding, EGFR (ErbB-1) dimerizes with itself or with its homologs ErbB-2, ErbB-3, or ErbB-4 and consequently increases its intracellular tyrosine kinase activity. This activates signaling cascades that have many effects: cell proliferation, reduced apoptosis, and angiogenesis.

RAS —> RAF —> MEK —> MAPK [—> to nucleus] —> promote transcription of genes involved in tumor growth (e.g., MYC, JUN, FOS).
-or-
PI3K —> PIP3 —> PDK —> AKT —> mTOR

Answer 65

A

IGF‐1 is known to promote cancer development by inhibiting apoptosis and stimulating cell proliferation.
(Insulin like growth factor)

Binding to IGRF1 stimulates PI3K —> PIP3 —> PDK —> AKT —> mTOR

Answer 66

A

Clear cell ovarian cancer > Endometrioid ovarian cancer

Endometriosis related cancers

Tumor, suppressor gene, participates in DNA repair through interaction with checkpoint kinase ATR

Answer 67

A

Routine screening

Answer 68

A

50%; however, this has recently been called into question on lit review

Answer 69

A

Pneumonia after 65, but yes if weak immune sys.

All 60yo need shingles.
*new shingles vaccine is dead = shingrix
*old shingles vax is live = zostavax

Answer 70

A

long-term NGT suctioning

Notes says: NG tube. two most common causes of metabolic alkalosis in general are loss of gastric acid (vomiting, NG drainage) and diuretics (specifically furosemide and thiazides)

Answer 71

A

Methadone

Answer 72

A

●Intravenous calcium to antagonize the membrane actions of hyperkalemia (if electrocardiogram (ECG) changes consistent with hyperkalemia are present)

Answer 73

A

Flattening of T waves,
depression of ST segment,
prominent U waves,
prolongation of QT interval —> can lead to torsades

Answer 74

A

Long PR, QRS
Peaked T waves initially —> flatten at higher concentrations

QT prolongation —> torsades de pointes

Answer 75

A

Shortening of QT interval

Answer 76

A

Prolonged QT interval —> torsades de pointes

Answer 77

A

Peaked T waves,
flattened P waves,
Prolonged PR
Short QT
prolonged QRS complexes —> sine wave —> ventricular fibrillation / cardiac arrest

Answer 78

A

Pancreatic fistula

Loss of bicarbonate-rich pancreatic fluid via a pancreatic fistula can result in a hyperchloraemic or normal anion gap metabolic acidosis.

Other non AG: renal tubular acidosis, diarrhea, pancreatic leak

Rhabdo —> lactic acidosis

High AG metabolic acidosis
MUD PILES, representing Methanol, Uraemia, Diabetes, Paraldehyde, Iron (and Isoniazid), Lactate, Ethylene glycol, and Salicylate.

Answer 79

A

hyperchloremic metabolic acidosis

The mechanism of the development of hyperchloremic acidosis When urine is in contact with the bowel wall, ammonia, hydrogen and chloride are reabsorbed

Answer 80

A

cefepime

Other choices: cefepime + growth factors, other abx choices

Answer 81

A

methadone

Answer 82

A

Fentanyl

Per B& H: Fentanyl or methadone
- Buprenorphine, remifentanil also ok

Morphine and codeine are not recommended, because the accumulation of their metabolites may cause neurotoxic symptoms

Answer 83

A

Cryoprecipitate, also called “cryo” (1 unit = 10 to 20 mL)
Indicated for DIC

Notes were unsure of cryo vs concentrated fibrinogen.

Fibrinogen concentrates: prepared from pooled human plasma and are available as lyophilized powders… reconstituted in a small volume. More for prevention, off label for DIC.

https://www.ncbi.nlm.nih.gov/books/NBK537184/

FFP higher volume (1 unit = 200 to 300 mL) indicated for DIC, not good for CHF

Answer 84

A

anti platelet factor 4 antibodies (actual answer is serotonin release assay which wasn’t an option, anti PF4 is second best)

The solid-phase ELISA, most widely used. detects the presence of anti-platelet factor 4 (PF4)/heparin antibodies in patient serum. Sensitivity 91->97%, but low specificity

Serotonin release assay is considered the gold standard among diagnostic tests for HIT; sensitivity+specificity >95%

Answer 85

A

obesity

anti-Xa monitoring may be warranted to ensure safe and effective anticoagulation where optimal dosing is less predictable: renal or hepatic insufficiency, extremes of body weight (≤ 40 kg or ≥150 kg), newborns, children, pregnancy, prolonged therapy (≥7–10 days), and advanced age

Answer 86

A

Standard dosing (40mg/daily)

CrCl 30 to 50 mL/minute: No dose adjustment necessary for most indications.

BMI ≥40 kg/m2:
- 40 mg twice daily or 0.5 mg/kg twice daily (based on actual body weight)

BMI >50 kg/m2,
- 60 mg twice daily or 0.5 mg/kg twice daily (based on actual body weight)

Answer 87

A

Skinny answer: LMWH + Rivaroxaban

lovenox, nadroparin: requires renal dose reduction
Dalteparin: likely requires renal dose reduction
Tinzaparin: likely requires renal dose reduction
Fondaparanux: likely requires renal dose reduction

Xarelto/Rivaroxaban, Edoxaban: requires renal dose reduction
Eliquis/Apixiban: likely requires renal dose reduction, but less dependent on kidney function than other DOACs

Warfarin: likely requires renal dose reduction, but probably ok to use

Heparin: NO DOSE REDUCTION
Argatroban: NO DOSE REDUCTION

Answer 88

A

Transitioning from UFH continuous infusion to fondaparinux: Start fondaparinux within one hour after UFH continuous infusion has been stopped

Option for anticoagulation treatment in the setting of HIT

Answer 89

A

argatroban (Parenteral direct thrombin inhibitor) is probably best option

Others:
Bivalirudin (Parenteral DTI)
Danaparoid (Parenteral inhibitor of thrombin and factor Xa (indirect, heparinoid)
Fondaparinux (parental Xa inhibitor)
Apixaban, Edoxaban, Rivaroxaban (PO Xa inhibitor)
Dabigatran (ODTI)
Warfarin (CANNOT BE USED INITIALLY)

Answer 90

A

a life-threatening complication of exposure to heparin (ie, unfractionated heparin, low molecular weight [LMW] heparin) that occurs in up to 5% of patients exposed, regardless of the dose, schedule, or route of administration.

HIT results from an autoantibody directed against platelet factor 4 (PF4) in complex with heparin (referred to as a HIT antibody).

HIT antibodies activate platelets and can cause catastrophic arterial and venous thrombosis (50% those with HIT, venous > arterial).

THROMBOSIS (can lead to skin necrosis, limb gangrene, organ infarction)

mortality rate as high as 20%, with improved recognition and early intervention, mortality rates below 2 percent have been reported.

plt drop usu >50% baseline, occurs 5-10d after exposure (could be earlier if recently exposed to heparin). resolution after stopping heparin is usually 7d

Answer 91

A

If choose just one, NAAT

two-step approach beginning with a test for glutamate dehydrogenase (GDH), followed by a toxin test and/or a nucleic acid test.
Alternatively, in institutions where established clinical algorithms guide testing, a nucleic acid test alone is acceptable.

Best is combination of EIA GDH then EIA for toxins A&B or NAAT

Cdiff tests:
●NAAT: specific for toxigenic strains but do not test for active toxin protein production and are capable of detecting asymptomatic carriers of C. difficile

●Enzyme immunoassay for C. difficile GDH: GDH antigen enzyme is produced by all C. difficile isolates; but cannot distinguish between toxigenic and nontoxigenic strains… useful as an initial screening step in a multistep approach

●Enzyme immunoassay for C. difficile toxins A and B: sensitivity of EIA for toxins A and B is on average about 75 percent, specificity ~99%).high false-negative rate since 100-1000 pg of toxin must be present for the test to be positive. used together with toxin EIA

●Cell culture cytotoxicity assay: sensitive and specific but resource intensive and time consuming. Not routine

●Selective anaerobic culture: useful for epidemiologic studies but is generally too slow and labor intensive for routine use

Answer 92

A

4-factor prothrombin complex concentrate (PCC, contains Factors II, VII, IX, and X). [these are vit K dependent factors 2+7=9, 10]

A plasma product such as thawed plasma or FFP (approximately 10 mL/kg, depending on INR) can be used as an alternative if PCC is not available.

Vitamin K (intravenous)

Hold warfarin

Recheck the prothrombin time (PT)/INR at approximately 30 minutes following PCC administration, and periodically thereafter, with the frequency determined by the severity of bleeding.

Answer 93

A

Intravesicular pressure

Answer 94

A

excess calories due to sugar

Answer 95

A

The most common presenting symptom is dyspnea followed by chest pain (classically pleuritic but often dull) and cough

Answer 96

A

ETCO2 (~40)

Waveform capnography is the most reliable tool to confirm placement of an advanced airway, both for endotracheal (ET) tubes and supraglottic-airway devices. When a device is placed correctly, a waveform and end-tidal CO2 (ETCO2) reading appear within seconds after the first ventilation is delivered to the patient

Answer 97

A

Likely getting at air embolus:
- tx is Trendelenburg and left lateral decubitus position

desufflation of the abdomen
The Durant or Trendelenburg position is used to direct the gas bubble into the right ventricle apex and away from the pulmonary artery.
Ventilation with 100% oxygen could be used to wash out CO2, reduce ventilation-perfusion mismatch, and improve hypoxemia.
Hyperventilation is also used to help eliminate CO2

Second thought is massive bleeding, but seems less likely

Answer 98

A

STK11 mutations only account for about half of PJS cases, and a second disease locus has been proposed at chromosome segment 19q13.4 on the basis of genetic linkage analysis in one family. We identified a t(11;19)(q13;q13.4) in a PJS polyp arising from the small bowel in a female infant age 6 days.

PJS associated with Ovarian sex cord tumor with annular tubules

granulosa: FOXL2 is a point mutation).
Though translocation in a case report:
https://www.sciencedirect.com/science/article/abs/pii/016546089290231V

Answer 99

A

Dobutamine: is not a vasopressor but rather is an inotrope that causes vasodilation

Vasopressors elevate blood pressure
Inotropes enhance cardiac output

Inotropes:
- dopamine: dose dependent. Inotropic and vasopressor
- dobutamine
- Isoproterenol: primarily an inotropic and chronotropic agent rather than a vasopressor.

Vasopressors:
- epinephrine: dose dependent. Inotropic and vasopressor
- norepinephrine: both Inotropic and vasopressor
- phenylephrine: vasopressor only
- vasopressin: antidiuretic hormone, vasopressor
- Ephedrine: mostly vasopressor. For epidural hypotension

Answer 100

A

low dose 1 to 2 mcg/kg per minute
- dopamine-1 receptors in the renal, mesenteric, cerebral, and coronary beds, resulting in selective vasodilation.

medium dose 5 to 10 mcg/kg per minute
- also stimulates beta-1 adrenergic receptors and increases cardiac output, predominantly by increasing stroke volume with variable effects on heart rate

high dose >10 mcg/kg per minute
- stimulate alpha-adrenergic receptors and produce vasoconstriction with an increased SVR

Answer 101

A

Septic shock. Low SVR, splanchnic vasoconstriction, increased cardiac output, characterize the hyperdynamic phase of shock.

Low SVR - hypotension
High CO - tachycardia

Add photo

https://journals.lww.com/aoca/Fulltext/2015/18040/Pharmacologic_agents_for_acute_hemodynamic.14.aspx

Answer 102

A

Inc venous capacitance
Low SVR, splanchnic vasoconstriction, increased cardiac output, characterize the hyperdynamic phase of shock.

Venous capacitance is increased and results in diminished effectiveness of the circulating the blood volume.

Answer 103

A

Berlin Definition of ARDS all of the following
●Respiratory symptoms begun within one week of a known clinical insult.
●Bilateral opacities on chest imaging.
●respiratory failure must not be fully explained by cardiac failure or fluid overload.
●A moderate to severe impairment of oxygenation must be present, as defined by the ratio of arterial oxygen tension to fraction of inspired oxygen (PaO2/FiO2). The severity of the hypoxemia defines the severity of the ARDS:
•Mild ARDS – The PaO2/FiO2 is >200 mmHg, but ≤300 mmHg.
•Moderate ARDS – PaO2/FiO2 >100 mmHg, but ≤200 mmHg.
•Severe ARDS – The PaO2/FiO2 is ≤100 mmHg

Notes say: b/l infiltrates vs PaO2/FIO2 ratio <200 (we all put different answers)
- b/l infiltrates is non specific

By definition, arterial blood gas (ABG) analysis shows hypoxemia, which is often initially accompanied by acute respiratory alkalosis, and an elevated alveolar-arterial oxygen gradient

Answer 104

A

1 most important- low tidal volume with permissive hypercapnia (limitation of tidal volume (6 ml/kg predicted body weight) ** higher tidal volumes result in barotrauma.

Answer 105

A

Systemic vascular resistance (SVR) =
80 x ([MAP – CVP or RAP]/CO)

CO =SV x HR

Normal SVR is 700 to 1,500 dynes/seconds/cm-5

right atrial pressure (RAP)
central venous pressure (CVP)
mean arterial pressure (MAP)
cardiac output (CO)

These indices can be obtained from an accurately placed pulmonary artery catheter (PAC):
●Central venous pressure (CVP)
●Right-sided intracardiac pressures (right atrium, right ventricle)
●Pulmonary arterial pressure (PAP)
●Pulmonary artery occlusion pressure (PAOP; pulmonary capillary wedge pressure [PCWP]; pulmonary artery wedge pressure [PAWP])
●Cardiac output (CO)
●Mixed venous oxyhemoglobin saturation (SvO2)

Answer 106

A

Decreases FIO2 requirement

Mechanism for improving oxygenation
Physiologic PEEP is 4 cm H2O
Increasing PEEP is preferred for improving oxygenation opposed to increasing the FIO2 for postop pts
Addition of PEEP recruits collapsed alveoli, improves oxygenation and lung compliance

Answer 107

A

Adenomatous (tubular adenoma) About 70 percent of all polyps are adenomatous, making it the most common type of colon polyp

Adenomas are the most frequently observed neoplasms. By definition adenomas are benign lesions but there is a relationship to the development of invasive cancer (Vogelstein 1990). There are three forms of colonic adenomas: tubular, villous, and mixed.

Answer 108

A

Pleural effusion: possible complication of debulking diaphragmatic disease

Pneumonia: 48 to 72 hours after hospital admission
PE: 3-20d postop

Answer 109

A

Strep pyogenes - aka erysipelas (this one),

strep > staph

Lymphangitis most often results from an acute streptococcal infection of the skin. Less often, it is caused by a staphylococcal infection. The infection causes the lymph vessels to become inflamed. Lymphangitis may be a sign that a skin infection is getting worse

Answer 110

A

Decreased postoperative complications

Answer 111

A

POD#0 feeding > POD Ambulation (MLH I think)

Answer 112

A

Anastomosis <5cm from anal verge

Answer 113

A

loop ileostomy

Answer 114

A

primary closure

Primary closure is best suited to small lesions (1 cm or less) that are a result of cold or sharp injury. However, thermal injury sustained via electrosurgical devices induces delayed tissue damage beyond the visible edges of the immediate defect, and surgeons should consider a resection of bowel to at least 1 cm beyond the immediately apparent injury site.

If appropriate antibiotic prophylaxis for colonic surgery has not been given prior to skin incision, it should be administered once the colotomy is identified.

Answer 115

A

gracilis (not tram/vram)

Maylard incision: deep inferior epigastric vessels are isolated, clamped, transected, and ligated.

TRAM (transverse rectus abdominus muscle) and vertical rectus abdominis myocutaneous (VRAM) flap both use deep inferior epigastric vessels as pedicles

Answer 116

A

VRAM or TRAM best based on the below, if not option, gracillis

For full thickness defects, a variety of reconstructive options
Fasciocutaneous and myocutaneous flaps are probably the most commonly used options for reconstruction of partial and circumferential vaginal defects. These have the advantage of providing a large quantity of pliable tissue, which can be used as soft tissue filler in the pelvis, in addition to tissue for vaginal reconstruction. The neovagina also tends to retain its caliber over time, and does not stenose. However, the lack of natural lubrication often necessitates the use of supplemental lubricants during sexual intercourse. Other disadvantages include incidence of partial or complete flap necrosis. However, the incidence of this is relatively low.
Flap specific complication rates are lowest for vertical rectus abdominis myocutaneous (VRAM) flaps compared with gracilis and Singapore flaps.

Answer 117

A

Right Hepatic vein

Answer 118

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CK7- CK 20+ metastatic colon cancer

Ovarian mucinous CK7+ CK20+
Endometrial CK7+ CK20-

Answer 119

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2 wks (2 questions one was 14 days and the other gave options of 0-10days v. 2-4weeks)

UTD:
In order to optimize the immune response to vaccination, we vaccinate patients at least 2 weeks, and ideally 10 to 12 weeks, prior to splenectomy when possible. When vaccines cannot be given at least two weeks prior to splenectomy, we vaccinate two weeks following the procedure.

Answer 120

A

bleeding, thrombosis, and infections.

Notes say: thrombocytosis. This seems to be incorrect based on below

UTD:
The major postoperative risks, infection and venous thromboembolism (VTE), appear to be increased following splenectomy regardless of the initial indication for splenectomy. absolute risk of VTE has ranged from 3 to 7 percent. Malignancy and myeloproliferative neoplasms and increased platelet count postoperatively appeared to be associated with greater risk.

Operative mortality is declining but remains a concern. Perioperative complications include bleeding, thrombosis, and infections. Late complications include a lifetime increased risk of infection and sepsis, especially with encapsulated organisms; venous thromboembolism; and possibly thrombocytosis. Risks that are less well established include cardiovascular disorders, recurrence of primary disease, cancer, and possibly pulmonary arterial hypertension

Answer 121

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Urinary tract
Notes said: we all put different things but right answer is probably bowel

Answer 122

A

The single most important pathogen is S. pneumoniae. This organism accounts for approximately 40 to 60 percent of cases of severe infection and overwhelming sepsis in splenectomized patients [10,13,14]. Although the overall incidence of S. pneumoniae infections is declining because of widespread pneumococcal vaccination [29,30], patients with impaired splenic function are still at higher risk for S. pneumoniae infection and poorer outcomes when compared with patients who have normal splenic function

Answer 123

A

Direct comparisons of enteral nutrition with parenteral nutrition in critically ill patients from randomized trials indicate that outcomes in patient receiving enteral or parenteral nutrition are comparable

Probably not a fair question. Notes say: Mortality vs caloric requirements

UTD: Earlier evidence suggests early parenteral nutrition may increase the risk of infection. Data since then refutes these findings, and better safety practices may account for comparable outcomes between enteral nutrition and parenteral nutrition.

Answer 124

A

OR start time?

UTD: Contributing factors include poor communication, failure to use site markings, incorrect patient positioning, multiple procedures on the same patient, emergency operations, surgeon fatigue, presence of multiple surgeons, unusual time pressures, and/or unusual patient anatomy

Answer 125

A

uterine serous carcinoma

Architecture:
Papillary with or without appreciable fibrovascular cores; micropapillary pattern can be seen
Slit-like spaces
Gland-like spaces may be observed
Psammoma bodies may be present in up to 33% of cases
Cytoplasm usually scant but can be abundant with eosinophilia or clearing
Tumor cells can colonize existing endometrial glands
Tumor cells can appear discohesive
Nuclei are typically high grade with pleomorphism, hyperchromasia, prominent nucleoli and frequent mitotic figures (including atypical mitotic figures)

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