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Ccs 401: GENEL CERRAHİ + ANESTEZİ > Ccs 401 Genel Cerrahi 1 > Flashcards

Ccs 401 Genel Cerrahi 1 Flashcards

1
Q

yaralara nasıl müdahele edilir

A

Cleansing (nötrofil ve nk lenfosit), closure (fibroblast) ve protection (kabuk bağlama)

Dipnot: Closure kısmında ikinci kez debridman yaparız duruma göre.

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2
Q

Irrigation ne demek

A

Bir cleansing yöntemi. Basınçlı ılık saline ile yara temizleme.

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3
Q

Cleansing/ debridement yöntemleri

A

Irrigation, mechanical scrubbing, pearls (povidone iodine 10%)

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4
Q

Yara iyileşmesi süreci hücre bazında nasıl gerçekleşir?

A

1) platelet (coagulation) 1 saat
2) Nötrofil (iflammation) 1 gün
3) macrophage (inflammation) 2 gün
-aslında bu kısma monosit de eklenebilir-
4) Fibroblast (inflam + proliferation)
-Proliferation başlangıcında zirve yapıyor, proliferation’ın başrolü)
5) lenfositler (infalmmation evresinin bittiğini gösterirler, proliferationa geçiş olur)
-Özellikle T lenfositler-

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5
Q

Yara enfeksiyonu yapan ajanlar

A

Staphylococcus species
Coagulase negative streptococcus
Enterococci
E coli

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6
Q

Yara iyileşmesini etkileyen faktörler

A

advanced age
hypoxia, anemia, hypoperfusion
Steroids (inhibition of inflam phase)
Chemotherapeutic drugs
Diabetes
Uremia
Obesity
A vitamini ve çinko (iyi etkilerler)
Arginine, glutamine ve c vitamini (çok elzemler)

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7
Q

Ameliyat öncesi prophylaxis için hangi antibiyotik tercih edilmeli?

A
  1. Ve ardından 3. kuşak cephalosporin
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8
Q

Definition of acute abdomen

A

Sudden, spontaneous, nontraumatic, severe abdominal pain typically less than 24 hours

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9
Q

Epidemiology info regarding acute abdomen

A

5 to 10% of ED visits.
Undifferentiated abdominal pain diagnosis: 25% of patients discharged from ED and 35-41% of patients admitted to hospital. However, 80% of this diagnosis’ patients improve or become pain free within 2 weeks.

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10
Q

Visceral vs Parietal pain

  • Hasta acılı yerini parmağı ile gösteremiyorsa visceraldir. Bir de ağrı muayene ile artıp azalmaz. Writhing pain. Colic.

Hastaya el bastırdıktan sonra ağrıya alışamıyorsa : visceral
alışıyorsa: parietal. (ör periton irritasyonu). Motionless bearing. Appendicitis de örnek.

A

Visceral pain: Merkezi SS. Sensation is mediated by afferent C fibers. Elicited by distention, inflammation or ischemia. Felt in midline. Talamusta sonlanır. Gerilme reseptörü.

Parietal pain: Mediated by both C and A delta nerve fibers (miyelinli, cortexte sonlanır). Elicited by irritation. Sharp and well localized. Cortexte sonlanır. Basınç sıcaklık vs reseptörleri.

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11
Q

Sindirim kanalını oluşturan 3 yapıdan biri olan foregut hakkında bilgi.

A

Foregut: Medulla spinalisten ayrı bunun organlarına sinir gitmez. Tüm foregut organları aynı acıyı verir. Parietal acıya dönüşene dek acının hangi organdan kaynaklandığını anlayamayız.

OK–> kötü: visceral acı–> parietal

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12
Q

Eşleştirme: Mid epigastirum, mid abdomen, lower abdomen organları

A

Mid epigastirum: stomach, duodenum, hepatobiliary system, pancreas
mid abdomen: jejenum ileum
lower abdomen: colon, internal reproductive organs

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13
Q

Causes of RUQ abdominal pain

Biliary, hepatic

A

Biliary: biliary colic, acute cholecystitis, acute cholangitis, sphincter of oddi dysfunciton (nadir)

Hepatic: Acute hepatitis, perihepatits (fitz hugh curtis sendromu) -ılımlı transaminaz artışı olur-, Budd-chiari syndrome (nadir), portal vein thrombosis

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14
Q

Causes of epigastric abdominal pain

A

Acute MI
Acute pancreatitis
Chronic pancreatitis
Peptic ulcer disease
GERD
gastritis/ gastropathy
Functional dyspepsia
Gastroparesis

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15
Q

Causes of LUQ abdominal pain

A

Splenomegaly
Splenic infarct
Splenic abscess
Splenic rupture

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16
Q

Causes of Lower abdominal pain

A

Appendicitis
Diverticulitis
Nephrolithiasis
Pyelonephritis
Acute urinary retention
Cystitis
Infectious colitis

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17
Q

Emergency differential diagnosis (hepsi acil durum + ölümcül) for abdomen
(Patlayıcı ağrıların başta olması acil duruma işaret eder.)
(İskemi şiddetli ağrıya sebep olur.)

A

Abdominal aortic aneurysm
Mesenteric ischemia (en kötü visceral ağrılardan biri. Ağrı kesici ulaşamıyor. Pat diye başlar. İskemi ağrısı çok kötü.)
Perforation of gis tract, including pepctic ulcer bowel esop or appendix
Acute bowel obstruction
Volvulus
Ectopic pregnancy
Placental abruption
MI (patlayıcı ağrı)
Splenic rupture (patlayıcı ağrı)

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18
Q

Common differential diagnosis for abdomen

A

Appendicitis, biliary disease, pancreatitis, diverticular disease, peptic ulcer disease, incarcerated hernia, gastroenteritis and other infectious causes, inflammatory bowel disease, UTI pyelonephritis, nephrolithiasis, adnexal torsion, PID, ruptured ovarian cyst, Tubo ovarian abscess, Fitz hugh curtiz syndrome (perihepatits), endometriosis

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19
Q

Abdominal acı konusunda yüksek riske sahip hasta grupları

A

65+, immunocompromised, alcholism, Cardiovascular disease, major comorbidities, prior surgery, recent GI instrumentation, early pregnancy, diabetes

pain: Sudden onset, maximal at onset, pain then subsequent vomiting, constant pain of less than two days duration (48+ saat ise detaylı tetkik yapabiliriz)

Exam findings: Tense or rigid abdomen, involuntary guarding, shock signs, vital fonksiyon bozukluğu, oskültasyonda metalik ses

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20
Q

Patlayıcı ağrının en sık sebepleri

A

1) Vasküler sebepler (AAA)
2) Perforasyon
3) Lithiasis (ürolithiasis) (biliary colic)

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21
Q

Aggravating and alleviating factors of abdominal pain

A

Peptik ülser yemekten sonra iyileşirken biliary colic kötüleşir.
Pankreatit hastaları dik oturunca iyileşirken yatınca kötüleşir
Peritonit hastaları haraketsiz yatmaya çalışır ve öksürmek onları kötüleştirebilir.
Nephrolithiasis hastaları ise huzursuzdur ve rahat bir pozisyon bulmakta zorlanırlar.

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22
Q

Steps of abdominal examination

A

1- global assessment, vital signs
2- Inspection
3- Auscultation
4- cough tenderness
5- percussion
6- palpation
7- Special signs (guarding or rigidity, local palpation, rebound tenderness, deep tenderness, bump tenderness)
8- external hernias and male genitelia
9- rectal exam
10- pelvic exam

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23
Q

Signs that suggests major intra abdominal hemorrhage

A

Etreme pallor, hpotension, hypothermia, tachycardia, tachypnea, diaphoresis.

Indication for emergency laparatomy

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24
Q

Characteristics of mid- small and late bowel obstruction on auscultation

A

Middle + (early acute pancreatitis)–> peristaltic rushes synchronous with colic
Late + (diffuse peritonitis)–> silent except for infrequent tinkly or squeky sounds

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25
Q

Rebound tenderness ile eşlenik olabilecek bulgu nedir?

A

Cough tenderness.
Bu sayede peritonit hastalarında özellikle hastaya acı daha az vermiş oluruz.
Peritonitin parietal acısının aksine kolik acı viseral acıdır o nedenle derin nefes veya öksürük ile kötüleşmez.
Cough tenderness olan kısım acıyan kısımdır (parietal acı). O ksıımdan uzakta başlanır.

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26
Q

Well demarcated tenderness, poorly localized tenderness unaccompanied by guarding, little or vaguely localized tenderness.
Bu üç bulgu hangi hastalıklara ya da durumlara başlıca işaret eder?

A

Well demarcated tenderness–> acute cholecystitis, appendicitis, diverticulitis, acute salpingitis

Poorly localized tenderness unaccompanied by guarding–> gastroenteritis, inflammatory intestinal process without peritonitis

Little or vaguely localized tenderness–> uncomplicated hollow viscus obstruction

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27
Q

Rectus muscle rigidity is formed due to??

A

Peritoneal inflammation

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28
Q

Unlike peritonitis, renal colic induces spasm confined to ipsilateral rectus muscle

A

Renal colic NOT PERİTONİTİS

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29
Q

Apandisitte görülebilen signlar

A

İlopsoas sign
Obturator sign
Rovsing’s sign
Target sign?

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30
Q

Akut abdomen hastalarınad görülebilen signlar

A

İlopsoas sign
Obturator sign
Rovsing’s sign (bu üçü apandisit)
Bump tenderness
Murphy s
Kehr s
Carnett s

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31
Q

The presence of pyuria, proteinuria + hematuria suggests…

A

Uti and also acute appendicitis or any other inflammatory process adjacent to either ureter.
Nearly half of the patients with appendicitis have blood leukocytes or bacteria in their urine.

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32
Q

Lab tests that should be made for:
Clinically significant upper or mid abdominal pain–>
“” epigastric–>
Chronic pancreatitis–>

A

Clinically significant upper or mid abdominal pain–> liver + pancreatic ezyme concentrations
“” epigastric–> amylase (ilk o yükselir)
Chronic pancreatitis–> lipase (2 3 hafta yüksek kalır)

Not: Amilaz elevasyonu ne sensitif ne de spesifiktir pankreas için ve mezenterik iskemi ya da bağırsak perforasyonu gibi daha kötü bir tabloya işaret ediyor da olabilir

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33
Q

Akut abdomenli hastalara ağrı kesici verilebilir mi?

A

Evet. Morfin veya fentanil kullanabiliriz

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34
Q

Appendix’in anatomik olarak bulunma ihtimalinin en yüksek olduğu yer neresi?

A) pelvik B) retrocecal C) subcecal D) paracecal E) pre-ileal/ post ileal F) Promontoric.

A

Retrocecal.

Çoktan aza: retrocecal (%63)
pelvic (%33)
subcecal (%2)
paracecal
pre-ileal/ post ileal (%1%1)
Promontoric

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35
Q

Target sign nedir?

A

Thickened, inflamed and fluid filled appendix. Gerçekten hedef tahtasına benziyor. (Daha fazla bilgi araştırıp yaz)

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36
Q

Appendix’in anomalileri nelerdir?

A

Absence, duplication, diverticulum

(Apendiks divertikülü akut apandisitin çok nadir bir nedenidir.)
(Divertikül: Sindirim sisteminde yer alan küçük şişkin keseciklerdir. En çok kalın bağırsağın alt kısımlarında görülür)

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37
Q

What is the most common acute surgical condition of the abdomen?

A

Acute appendicitis

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38
Q

What is the peak incidence of acute appendicitis? (by age group + population + gender)

A

early adulthood
7-10% of population develop acute appendicitis
M > F

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39
Q

Common etiologies (neden geliştiği) of acute appendicitis

A

% 66–> Obstruction of the lumen (iç boşluk)
ex: fecalith (hardened stool), hypertrophy of lymphoid tissue, food seeds, intestinal worms, inspissated barium (baryum taşı ya da yoğunlaşmış baryum. Görüntüleme amaçlı verilen baryumun feces ile birleşmesi.), tumor (primer, metastatic, carcinoid), parasite (ascaris -bağırsak solucanı-)

% 33–> Without luminal obstruction
ex: Generalized infection (respiratory ti)
Senility (impaired circulation)

EN SIK NEDEN FECALITH

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40
Q

How does the pathogenesis (nasıl geliştiği ) of acute appendicitis occur?

A

Proximal obstruction
Distal distention (şişkinlik)
Compromised blood supply
Progression to gangrene and perforation
Peritonitis

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41
Q

How does the obstruction cause acute appendicitis? (anlamadıysan video seyredebilirsin)

A

Mucus + inflam exudation–> increases intraluminal P –> obstruction of lymphatic drainage –> Edema + mucosal ulceration + bacterial translocation to submucosa –> venous obstruction due to further distension –> stasis + edema –> arterial obs –> ischemia –> bacterial invasion –> acute appendicitis

+++ Apandisit denilen organ, kalınbağırsağa açılan ağzının tıkanması sonucunda şişmeye başlar. Ağzı tıkanmış olan apandisitin şişmesi devam eder, bir aşamadan sonra buradaki lenfatik akın kan dolaşımı durur ve apandisitin duvarında nekrozlar (çürüme) oluşarak duvar bütünlüğü bozulmaya başlar. Eş zamanlı ağzı tıkalı olan apandisit içerisindeki sıvıdaki mikroplar hızla çoğalmaya başlarlar ve apandisiti daha da şişirirler. Apandisitin bu aşamadan sonra tanı ve tedavisindeki gecikme ile orantılı olarak apandisit içerisindeki mikroplar kan yolu ile vücuda geçmeye başlar ve bunun sonunda vücutta karın ağrısı yanında ateşte olmaya başlar. Laboratuvar bulgularında da iltihap bulguları görünmeye başlar. Bu aşamadan sonrada tedavide gecikilmesi durumunda içerisi tamamen şişmiş olan ve duvarında kan akımının azalması sonrasında çürümelerin olduğu bir alandan apandisit patlar ve tüm mikrop dolu olan içeriği karın içerisine akmaya başlar. Halk arasında apandisiti patlamış ve zehirlemiş dedikleri karın içi sepsis tablosu oluşur.

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42
Q

What are the visceral and somatic/ parietal pain an acute appendicitis patient experiences?

A

Visceral –> distention of the appendix causes it. Abdominal pain.

Parietal –> right lower quadrant pain due to parietal peritoneum.

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43
Q

Mcburney noktası anatomik lokalizasyonu?

A

Ant sup iliac spine ile göbek deliğini birleştiren çizgiyi 3e bölüp göbek deliğine 2/3 uzaklıkta kalan noktadır.

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44
Q

Mcburney noktasında hassasiyet neye işaret eder?

A

McBurney noktasındaki derin hassasiyet , McBurney belirtisi olarak bilinir ve akut apandisitin bir belirtisidir.

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45
Q

How does perforation occur in acute appendicitis

A

If fever> 38.5 + wbc> 18000–> ıf ischemia continue –> necrosis of the appendicular wall –> gangrenous appendicitis –> perforation with free bacterial contamination of peritoneal cavity

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46
Q

What are the morphologies of acute appendicitis?

A

acute catarrhal appendicitis
acute suppurative appendicitis
acute gangrenous appendicitis

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47
Q

What are the most common bacterial agents of acute appendicitis and also peritonitis

A

Bacteroides fragilis, E coli –> %100
Peptostroptococcus –> %80
Pseudomonas, Bacteroides splanc –> %40

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48
Q

Akut apandisitin semptomları nelerdir?

A

Pain (%100)
Anorexia (iştahsızlık)
Nausea
Vomiting
Pain migration (%50) –> göbekten sağ alt kadrana göç de söz konusu, mcburney noktasına yani.
Fever

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49
Q

Akut apandisitin işaretleri nelerdir?

A

Temperature
Peritoneal irritation signs: Mcburney (rebound/ defence), rebound tenderness (blumberg), rovsing, psoas (retrocecal), obturator, ten-horn, dunphy, rosenstein, aaron

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50
Q

Lab findings of acute appendicitis?

A

Leukocytosis > 10.000 per mm3, neutrophilia
Elevated CRP, 0,8 mg per dl
Urine analysis: pyuria, hematuria proteinuria

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51
Q

Imaging studies for acute appendicitis?

A

X-ray –> appendicolith varsa görürüz (apandisit taşı)
USG –> target sign! (abscesses or plastron first)
CT –> gold standard.
MR –>
Barium enema –> çok kullanmıyoruz

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52
Q

Plastron nedir?

A

Bazı apandisit hastalarında apandisit iltihabı ilerleyip delinme-patlama aşamasına doğru giderken karın içi örtü tabakası (omentum) ve çevre organlar apandisi sararak enfeksiyonu sınırlamaya çalışır. Sonuçta karın sağ alt tarafta bir sertlik ve kitle oluşturur. Buna plastron denir.

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53
Q

Differential diagnosis’ of acute appendicitis?

A

Acute mesenteric adenitis**(most frequent mistake)
Acute gastroenteritis
Meckel’s diverticulum!!
Intussusception
Regional enteritis
Perforated peptic ulcer
Acute cholecystitis
Urinary tract disorders!
PID
Ruptured Grafian follicule!!
FMF! (familial Mediterranean fever)

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54
Q

Complications of acute appendicitis

Treatment–> appendectomy only. Open or lap. Ama hasta bilinçli biriyse antibiyotik vererek takip de edebiliriz

A

Perforation(most frequent)**
(Overall:%25,<Age 10:%50,Age 10-50:%10,>Age 50:%30)
Peritonitis
Appendiceal abscess
Phylephlebitis (with liver milier abscess-most mortal complication)
Plastron appendicitis(best imaging studie CT***)

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55
Q

A.app en sık neden—
Obstruksiyonun en sık nedeni—
A.app a yol açan parazit—
A.app en sık komplikasyon—
A.app tanıda en yararlı tetkik—
Ayırıcı tanı ve komplikasyon ayırımında en yararlı tetkik—
A.app komplikasyon kliniğine sarılık eklenirse—
A.app en mortal komplikasyon—
Acil cerrahi için tek kontrendikasyon—
Gebelerde en sık yapılan cerrahi —
2 cm den küçük karsinoid tm—
2 cm den büyük karsinoid tm—

A

A.app en sık neden—luminal obstr.
Obstruksiyonun en sık nedeni—Fekalit
A.app a yol açan parazit—Askariazis
A.app en sık komplikasyon—Perforasyon
A.app tanıda en yararlı tetkik—BT
Ayırıcı tanı ve komplikasyon ayırımında en yararlı tetkik—BT
A.app komplikasyon kliniğine sarılık eklenirse—Pyeloflebit(portal venlerin septik embolisi)
A.app en mortal komplikasyon—Pyeloflebit
Acil cerrahi için tek kontrendikasyon—Plastron varlığı
Gebelerde en sık yapılan cerrahi —apendektomi
2 cm den küçük karsinoid tm—apendektomi
2 cm den büyük karsinoid tm—sağ hemikolektomi

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56
Q

Alvarado skalası nedir?

A

Apandisit tanısında kullanılan klinik bir skorlama sistemidir. Alvarado skorlaması, klinik bir tahmin aracı olarak yerini büyük ölçüde Apandisit İnflamatuar Tepki skoru almıştır.

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57
Q

Info about parietal and visceral pleura

A

Parietal layer lines the abdominal and pelvic cavities and the abdominal surface of the diaphragm.
- loosely connected with the body Wall,seperated from it by an adipose layer,tela subsero

Visceral layer covers the abdominal and pelvic viscera and includes the mesenteries.
-Visceral peritoneum is usually tightly attached to the organs it covers.

Not: Erkeklerde peritoneal cavity kapalı iken kadınlarda uterine tubelar ile dışa açılmaktadır.

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58
Q

What are the intra and retroperitoneal organs?

A

Intra–> Completely covered by visceral peritoneum.
Stomach, 1st part of duodenum, jejenum, ileum, transverse colon, sigmoid colon, liver, spleen

Retro–> Partially covered by peritoneum
Kidneys, ureters, suprarenal glands, rectum.

primary retroperitoneal: aorta abdominalis + vena cava inf, kidney ureter, suprerenal fland, cisterna chyli, truncus symphaticus

Sec retp: colon ascendens + descendens, duodenum except 1st part, pancreas

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59
Q

What are lesser and greater omentum?

A

Lesser o: arises from the lesser curvature of the stomach and extends to the liver

Greater o: Given off from the greater curvature of the stomach, forms a large sheet that lies over the intestines, then converges into parietal peritoneum.

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60
Q

Pain sensations of visceral and parietal peritoneum
+ innervations

A

Obvious, vis–>vis and par–>par

Anyway, parietal p: T7, T12-L1 Nerve + phrenic nerve (diyaframı da innerve eder). In the pelvis: obturator nerve

visceral p: anatomic afferent nerves
+ akut ileus, kolesistit –> visceral peritoneum yüzünden acı çekeriz çünkü periton gerilir.

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61
Q

Functions of peritoneum

A

It suspend the organs within the peritoneal cavity.
It fixes some organs within the abdominal cavity.
Storage of large amount of fat in the peritoneal ligaments(e.g.. Greater omentum)
Peritoneal covering of intestine tends to sick together in infection.
Greater omentum is called the policeman of abdomen to prevent spread of infection
It secretes the peritoneal fluid.

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62
Q

Tomosynthesis mammography nedir?

A

Normal dijital iki boyutlu mamografilerde üç boyutlu bir objenin(memenin) iki boyutlu, dokuların imajlarının üst üste düştüğü bir imajı elde edilmekte idi. Son yıllarda geliştirilen mamografide Dijital Tomosentez teknolojisi ile meme dokusu 3 boyutlu olarak taranabilmektedir. Bu yöntemle değişik açılarla çok sayıda görüntü alınmakta ve bu görüntüler bilgisayar sistemiyle aynı bilgisayarlı tomografilerde olduğu gibi meme dokusunun bir mm lik kesitler seklinde 3 boyutlu olarak görüntüsü elde edilmektedir.

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63
Q

Meme görüntülemesinde en çok tercih edilen görüntüleme yöntemleri nelerdir?

A

1) Breast USG
2) Tomosynthesis mammography
3) Mammography
4) Breast MRI

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64
Q

Classification of breast pain

A

Cyclical, noncyclical, extramammary pain

En sıktan en nadire

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65
Q

Etiologies of cyclical, noncyclical, extramammary pain

A

Cyclical–> Hormonal fluctuations. Usually a week before menses, most severe in upper outer quadrant, bilaterally.

Noncyclical–> Large pendulous breasts, Diet, lifestyle, Hormone replacement therapy, Breast cysts, Ductal ectasia, Mastitis, Inflammatory breast cancer, Hidradenitis suppurativa, Other etiologies of breast pain include pregnancy, thrombophlebitis (Mondor’s disease), trauma, macrocysts, prior breast surgery, and a variety of medications (hormones as well as some antidepressants, cardiovascular agents, and antibiotics)

Extramammary–> Chest wall pain, Spinal and paraspinal disorders, Trauma, Postthoracotomy syndrome

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66
Q

What are the arteries that supply breast?

A

Thoracoacromial arter superiorly
Lateral thoracic artery and internal mammary artery lateral and medially
Intercostal perforator arteries inferiorly, they penetrate the breast.

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67
Q

What are the steps on diagnosing a women who presents with breast pain?

A

Women presents with breast pain –> Are there any findings suggestive mastitis
Painful, red swollen breast, fever?

If yes: Evolution and treatment of mastitis
If no: Are there any findings suspicious for breast cancer?

If yes: Breast Cancer evaluation and treatment
If no: True breast pain or pain from another source? If yes, extrammamary pain treatment.
If no, it could be diffuse or locale true breast pain.

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68
Q

Treatment of breast pain?

A

First-line therapy for breast pain is conservative.

Second-line therapy— patients who still have breast pain that diminishes quality of life despite first-line therapy for six months.
Tamoxifen, Danazol,Postmenopausal hormone therapy that causes breast pain should be decreased or discontinued.

Bromocriptineis a dopamine agonist that inhibits prolactin release

Investigational therapies

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69
Q

What are benign breast lesions? + most common ones

A

Type 1 + 2 cyst
Papilloma
Ductal hyperplasia
Sclerosing adenitis
Fibrocystic
Fibroadenoma

Breast Cysts
Fibroadenoma
Fat necrosis
Nipple discharge
Ductal Ectasia = Dilatation
İntraductal Papilloma
Lactational mastitis
Idiopathic Granulomatous Lobular Mastitis
(sıktan nadire)

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70
Q

Classification of benign breast lesions

A

Nonproliferative Lesions
Simple breast cysts
Galactocele
Papillary apocrine change
Mild hyperplasia of the usual type

Proliferative Lesions Without Atypia
Usual ductal hyperplasia
Intraductal papillomas
Solitary lesions
Sclerosing adenosis
Radial scars
Fibroadenomas: Simple fibroadenomas, Complex fibroadenomas,Giant fibroadenomas, Juvenile fibroadenomas
Adenomas
Pseudoangiomatous stromal hyperplasia

Proliferative Lesions With Atypia
atypical ductal hyperplasia (ADH),
atypical lobular hyperplasia (ALH),
lobular carcinoma in situ (LCIS)
Flat epithelial atypia (FEA)

Miscellaneous Benign Lesions Of The Breast
Lipoma
Fat necrosis
Diabetic mastopathy
Hamartoma
Idiopathic granulomatous mastitis
Sarcoidosis

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71
Q

Info about breast cyst?

A

A breast cyst is a fluid-filled round or ovoid mass derived from the terminal duct lobular unit (TDLU)
cysts were identified in 37.5 percent of all women screened, with the peak incidence between 35 and 50 years of age.
A breast cyst is suspected by either physical finding of a palpable breast mass or an abnormal imaging finding (most commonly a mammogram).
A breast cyst is diagnosed by breast ultrasound. Breast ultrasound also provides information about whether the breast cyst is simple, complicated, or complex

Anahtar kelimeler: TDLU, 37.5%, 35-50 years, breast ultrasound

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72
Q

What is the classification + management of a breast cyst?

A

Simple complicated and complex

Simple–> A simple cyst is benign, and no further intervention is necessary. Clustered simple microcysts are also benign, and no further intervention is required.

Complicated–> Most complicated cysts are BI-RADS 2, which does not require any further intervention. Occasionally, complicated cysts can be BI-RADS 3. Complicated cysts classified as BI-RADS 3 should undergo repeat ultrasound imaging and mammography (if the lesion was visualized on mammography) and clinical examination in SIX MONTHS.

Complex–> A complex cyst identified by ultrasound must be confirmed to be a benign or malignant lesion by image-guided CNB. FNA is not sufficient, because a sample of the solid component or thickened septa needs to be obtained, not just cyst fluid.

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73
Q

What is FNA (Fine needle aspiration) and CNB (core needle biopsy) ?

A

FNA: ince bir iğne kullanarak vücuttaki kitlelerden sıvı veya hücre örnekleri almak için yapılan bir biyopsi yöntemidir. Genellikle memedeki kistler, lenf düğümleri, tiroid nodülleri ve bazı tümörlerin tanısında kullanılır. .
FNA’nın Yapılış Amacı:
Bir kitle veya nodülün benign ya da malign olup olmadığını belirlemek.
Sıvı dolu kistlerin içeriğini boşaltmak ve tanı koymak.

FNA, kanser teşhisinde yeterli olabilir, ancak tümörün tam yapısını veya derecesini belirlemek zor olabilir.
Hücreler dışında stromal ve çevresel doku hakkında bilgi sağlamaz.

CNB–> Daha kalın bir iğne kullanılarak, kitleden silindir şeklinde bir doku örneği (daha büyük bir biyopsi örneği) alınması işlemidir.

FNA’dan daha iyi teşhis ve grading yapmayı sağlar çünkü doku incelemesi yapabilir, sadece hücrelerle sınırlı değildir.

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74
Q

Info about primary peritonitis

A

AKA spontaneus bacterial peritonitis. Not related to intraabdominal abnormality
S. Pneumonia–> commonest for children
E.coli, K. Pneumonia–> adult

1) Cirrhosis (ascites getting infected) 2) Lupus –> adult
1)NS –> children

Gold standart is paracentesis
Abd pain + fever + leukocytosis + pozitif paracentesis = diagnosis

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75
Q

Secondary peritonitis

A

Due to spillage of gı or gu organisms into peritoneal space (perforation!) Because of breach of öucosal barrier

E coli + bacteriodes fragilis

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76
Q

Sec peritonitis etiology

A

İçi boş olup da delinebilecek her şey etiyoloji olabilir

Ör: biliary colic, perforated duodenal ulcer, meckel’s diverticulum, acute perforative appendicitis, ruptured ovarian cyst, acute salpingitis, perforated gastric ulcer, acute pancreatitis, acute intestinal obstruction, acute diverticulitis, torsion of ovary, ectopic pregnancy

Yani: perforation of viscus, trauma, infected intraperitoneal blood, foreign bodies, pancreatitis, strangulating intestinal obstruction, vascular catastrophes (mesenteric thrombosis or embolism), IUD (long lastinf), gonococcus and chlamydia (sexually active women), anastomotic dehiscence, peritoneo ischemic shunts, drains, barium, meconium, peritoneal dialysis

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77
Q

Symptoms of peritonitis

A

Abdominal pain, abdominal tenderness, fluid in abdomen, silent abdomen (no gas or feces out), distended abdomen, fever, low urine output, nausea + vomiting, point tenderness, thirst, peristalsis absence

Severe: tenderness occur all over the abdomen, vomiting, high fever

+ The loss of fluids into the peritoneal cavity and bowel leads to severe dehydration and electrolyte disturbances
Adult respiratory distress syndrome also develops rapidly.
Kidney failure, liver failure, and disseminated intravascular coagulation follow

78
Q

Complications of peritonitis

A

Intraabdominal abscess (intraperitoneal and or hepatic abscess)

Intraabdominal adhesions and bands (Abdominal adhesions are bands of scar-like tissue that form inside your abdomen.)

+band to designate an adhesion that causes bowel obstruction, reserving the term adhesion to describe the phenomenon of abnormal union between peritoneal surfaces. The term synechia would be equivalent, although it has fallen into disuse in surgery.

++ Stricture: a narrowing of the bowel that could be caused by inflammation or scar tissue. Adhesion: a band of scar tissue that may form after surgery or due to inflammation.

79
Q

What is an intraabdominal adhesion?

+ adhesion vs band?

A

bands of scar-like tissue that form inside the abdomen. The bands form between two or more organs or between organs and the abdominal wall.

+The term band is to designate an adhesion that causes bowel obstruction, reserving the term adhesion to describe the phenomenon of abnormal union between peritoneal surfaces. The term synechia would be equivalent, although it has fallen into disuse in surgery.

Intraabdominal band olan hastaların bağırsak çapları (?) artar, defekasyon gerçekleşemez ve cerrahi mecburi bir hal alır.

80
Q

What is ileus?

A

Despite of the
reason, all of the bowel obstructions are defined
as ileus. It is classified as acute, subacute and
chronic according to the progress rate

81
Q

What is Boerhaave’s syndrome?

A

Forceful vomiting with a full stomach may cause esophageal rupture (Boerhaave’s syndrome), which is the most serious type of emetic injury. Pain in the left upper quadrant, left chest, or shoulder after any of these occurrences should alert the physician to order an immediate meglumine diatrizoate (Gastrografin) swallow.

82
Q

What causes one of the most serious cases of peritonitis?

A

Perforated gastric or duodenal ulcer.

Tends to cause the one of most serious cases of peritonitis; the mortality rate is nearly 20%.

Mild onset.

There may be a history of peptic ulcer disease, but in about 33% of cases, the first symptom is a sudden attack of severe epigastric pain.
A patient examined shortly after onset may be relatively free of pain and show only mild tenderness and diminished or absent peristalsis. However, within a few hours, vomiting, tenderness, and spasm, either in the epigastrium or over the whole abdomen, develop.

83
Q

What is the most common cause of peritonitis?

A

Perforated appendix.

It can occur at any age but is the most common cause of peritonitis in children and young adults.
In children, because of a poorly developed omentum, peritonitis is likely to be generalized;
in adults, local peritonitis and abscess formation are more common.
Tenderness in the right lower quadrant or over the entire abdomen indicates the extent of inflammation.

84
Q

Info about perforated colon

+ most common reason of peritonitis from a perforated colon?

A

Perforated colon is caused obstruction, diverticulitis, inflammatory diseases, and toxic megacolon.

Patients receiving prednisone or immunosuppressive drugs are also in an increased risk of perforation.

Crohn’s disease, ulcerative colitis
Acute necrotizing enterocolitis patients too. (bundan emin değilim)

+ Perforated diverticulitis of the sigmoid or right colon is the most common cause of peritonitis from a perforated colon.

85
Q

Info abt vascular lesions of the intestine or colon. (and of course, its relationship with peritonitis)

A

Usually, the superior mesenteric distribution is involved, but the area supplied by the inferior mesenteric artery can be devitalized by division of this artery during resection of an aortic aneurysm.

A history of abdominal angina for weeks or months preceding an acute onset of peritonitis suggests thrombotic occlusion of the superior mesenteric artery or its branches in association with atherosclerotic disease of these vessels.
Alternatively, a history of recent atrial arrhythmia, MI, or endocarditis
Strongly suggests embolization to the superior mesenteric artery and its resultant intestinal ischemia

Mesenteric venous thrombosis

86
Q

perforated gallbladder or biliary tree and peritonitis?

A

Acute cholecystitis can lead to perforation of the gallbladder, which usually leads to a local abscess but occasionally to generalized peritonitis.

Operation should include cholecystectomy. The common cause of bile peritonitis arising from the bile ducts is iatrogenic damage during cholecystectomy or EST (endoscopic shinchterectomy probably)

Cholecystitis acalculosa, poor blood supply of gallbladder (Acalculous cholecystitis is inflammation of the gallbladder without gallstones. Causes of acalculous cholecystitis are severe trauma or burn, surgery, long-term starvation, cytomegalovirus, cryptosporidiosis, systemic infection such as Typhoid and severe underlying diseases (Diabetes Mellitus, Cardiovascular disease).)

Key note: Iatrogenic damage

87
Q

Info abt nonocclusive intestinal ischemia

A

is the partial- or full-thickness necrosis of intestine in the absence of obvious organic vascular occlusion.

It may be caused by ++prolonged shock or cardiopulmonary bypass++, during which mesenteric blood flow decreases.
In cases in which this diagnosis is considered, ++arteriography++ must be performed.
Demonstration of an organic vascular lesion will lead to operation, whereas diffuse spasm may respond to vasodilator therapy.
Transmural bowel necrosis and peritonitis must be treated by bowel resection.

88
Q

Pancreatitis and peritonitis?

A

can cause an exudate that at first is retroperitoneal but soon involves the peritoneal cavity.

It is a +chemical peritonitis+, initially with a high level of amylase in the exudate; later, contamination with organisms from the GI tract may occur. +Infected pancreatitis+.

If the diagnosis seems certain and trauma was not a factor, laparotomy usually is avoided and reserved for the complications of pancreatic necrosis, abscess, or pseudocyst.

However, failure to improve may be an indication for earlier operation.

89
Q

What is the most common agent of fungal peritonitis? How do we treat these patients?

A

Candida.

Genelde post op hastalarda antibiyotikle tedavi edilmiş ısrarcı peritonitis varsa görülür.

IV amphotericin ile tedavi edebiliriz ancak çok kötü prognoz.

90
Q

Periton diyalizi nedir?

Bunun peritonitis ile ilişkisi nedir?

A

Periton diyalizi, hastanın karın boşluğuna küçük bir ameliyat ile yerleştirilen kateter aracılığı ile verilen özel olarak hazırlanmış bir solüsyon ile, hastanın kendi peritonu kullanılarak hastanın kanının zararlı maddelerden arındırılması ve vücuttaki sıvı dengesinin sağlanması işlemidir.

+ Frequently is complicated by peritonitis; cloudy effluent may indicate its presence.
Inlying catheters or shunts used for ascites can lead to bacterial invasion, notably by Staphylococcus epidermidis and Staphylococcus aureus.
Treatment is with antibiotics, as determined by culture and sensitivity; removal of shunts, if necessary; or hemodialysis, as a last resort.

91
Q

Tubo-ovarian abscess info

A

Develops in about 15% of women with salpingitis. (Salpenjit, Jinekolojide Fallop tüplerinin iltihaplanması. Salpenjit, yalnız Fallop tüplerinde olabileceği gibi yumurtalıklara da yayılabilir. İltihap ikisinde birden olursa salpengoovarit dölyatağına kadar yayılırsa metrosalpenjit adını alır.)

It can accompany acute or chronic infection and may require prolonged hospitalization, sometimes with surgical percutaneous drainage.

92
Q

Are abscess’ rupture an emergency?

A

Yes.
It is a surgical emergency, rapidly progressing from severe lower abdominal pain to nausea, vomiting, generalized peritonitis, and septic shock.

93
Q

What is pyosalpinx?

A

1 or 2 fallopian tubes getting filled by pus.

Pyosalpinx ciddi bir durum olup acil tedavi, hastanede yatış ve gerekli hallerde ameliyat gerektirebilen bir enfeksiyondur. Nedeni ne olursa olsun, tüplerin tıkanık olması gebelik oluşumunu engeller.

Sıvısı steril olabilir ancak WBCler predomine halde olur.

94
Q

Post op peritonit nedenleri

A

Operative injury, anastomotic dehiscence, retaiend foreign objects

Gossypiboma: hastada içerde bir şey unut mak

95
Q

Tetriary peritonitis nedir?

A

Klinik peritonitin ya da peritonitin sistemik signlarının 2ndary peritonitis tedavisinden sonra da devam etmesidir.

Genelde düşük virülanslı organizmalar izole edilir ya da etiyoloji organizmalardan kaynaklanmıyordur.

96
Q

Diagnosis of peritonitis

A

ANAMNESIS, PHYSICAL EXAMINATION!!

Laparotomy or laparoscopy is the most important diagnostic measure. Altın standart.

Cxray ve USG diff dg için önemli.

Chest x-rays: diff.dg ( pneumonia )
The presence of gas beneath the diaphragm points to a perforation of the GI tract. If the diagnosis is in doubt, (Gastrografin/ bir kontrast) passed into the stomach through an inlying nasogastric tube will demonstrate the perforation.

Ultrasound: Can help in differential diagnosis.( gallstone, measurement of gallbladder wall, localisation and amount of intraabdominal fluid collection, sign of tumors, kidney stone )

97
Q

Laparotomy vs laparoscopy?

A

Laparotomy –> Açmak
laparoscopy–> kamera ile bakmak. Bu sayede hastayı çok açmaya gerek kalmıyor

(Bundan emin ol, hataı olabilir)

98
Q

Clinical features of peritonitis

A

Pain, ileus signs, systemic shock signs

Pain: Constant and severe, Worse on movement, Eased by lying still

Signs of ileus: (generalised peritonitis>localised peritonitis), distension, Vomiting, Tympanic abdomen with reduced bowel sounds

Signgs of systemic shock: Tachycardia,tachypnoea,hypotension,low urine output, More prominent with generalised than localised peritonitis

99
Q

Investigation of peritonitis?

A

Localized p: blood test, cxray, ecg
(localized emergency mi?)

Generalized p: SURGICAL EMERGENCY
Blood test, amylase, crp, LDH, AST, d-dimer, WBC, Cxray, CT

LDH: Kanda Laktat Dehidrogenaz (LDH) yüksekliği, organ veya bir tür doku hasarı olduğu anlamına gelir. Bu hasarın nedeni genellikle ciddi bir hastalık, enfeksiyon veya yaralanmadan kaynaklanır. Bazende aşırı egzersiz, travma, enjeksiyon, kan alınması ve bazı ilaçların kullanımı da LDH yüksekliğine yol açabilir.

100
Q

Treatment of peritonitis

A

Treat the underlying cause.

General therapy includes antibiotics, nasogastric intubation and suction, respiratory care, and fluid and electrolyte replacement.

Third-generation cephalosporins are effective and probably safest. A combination of gentamicin and clindamycin is effective but dangerous if renal function is diminished.

101
Q

Management of 2ndary peritonitis

A

Surgery management.

Elimination of the source of infection
Reduction of bacterial contamination of the peritoneal cavity
Prevention of persistent or recurrent intra-abdominal infections
.
.
Could be combined with fluid resuscitation, antibiotics and ICU management
Source control achieved by closure or exteriorisation of perforation
Bacterial contamination reduced by aspiration of faecal matter and pus
Recurrent infection prevented by the used of:
Drains
Planned re-operations
Leaving the wound open / in case of serious pancreatitis

102
Q

Fibrokistik Meme ve Kistik Meme Arasındaki Farklar?

A

Fibrokistik meme: Memedeki fibrotik dokuların ve kistlerin bulunduğu, ağrı ve hassasiyet ile seyreden hormonlara bağlı bir durumdur. Genellikle tedavi gerektirmez, ancak ağrı yönetimi ve semptom kontrolü önemlidir.

Kistik meme: Sıvı dolu kistlerin olduğu, genellikle zararsız bir durumdur. Kistler büyükse veya rahatsızlık veriyorsa, sıvısı boşaltılabilir.

103
Q

Info about fibroadenoma?

A

EN SIK görülen benign meme lezyonudur! Biyopsilerin yarısını oluşutrmaktadır. Sıvı içerikli fibrokistlerin aksine solid yapıdadır.

In 20 percent of cases, multiple fibroadenomas occur in the same breast or bilaterally.
The etiology of fibroadenomas is not known, but a hormonal relationship is likely since they persist during the reproductive years, can increase in size during pregnancy or with estrogen therapy, and usually regress after menopause.
They are most commonly found in women between the ages of 15 and 35 years

Simple fibroadenomas
Complex fibroadenomas
Giant fibroadenomas
Juvenile fibroadenomas

104
Q

Information about simple fibroadenomas?

A

benign solid tumors containing glandular as well as fibrous tissue.
It is NOT necessary to excise all biopsy-proven simple fibroadenomas.
If a biopsy-proven simple fibroadenoma is asymptomatic, then it can be left in place, although some women wish to have the mass excised so that they will not worry further.
Disadvantages of excisional surgery include SCARRING at the incision site, DIMPLİNG of the breast from the removal of the tumor, DAMAGE to the breast’s duct system, and MAMMOGRAPHIC CHANGES (eg, architectural distortion, skin thickening, increased focal density).

Biyopsi yapmak zorunlu ama almak değil. Takip edilebilir.

105
Q

What are the indications for excision of fibroadenomas?

A

In women over 40 years of age,

The growth rate is high,

It is over 2cm

Family history of breast cancer.

memeden çıkardığımız bütün dokuları bütün olarak çıkarıyoruz.

106
Q

Info abt fat necrosis?

A

A benign condition that occurs as the result of breast trauma or surgical intervention.

Can be confused with a malignancy on physical examination and may mimic malignancy on imaging.

It is sometimes necessary to biopsy these lesions to confirm the diagnosis, however, a lesion might represent fat necrosis based on mammographic and USG findings such as oil cysts (collections of liquefied fat).

Excision is not necessary, there is no increased risk of breast cancer.

107
Q

Info abt nipple discharge

A

Nipple discharge is categorized as normal (lactation), galactorrhea (physiologic), or pathologic based on the characteristics of presentation. Most nipple discharge is benign in origin.

108
Q

What is physiological nipple discharge, AKA galactorrhea?

A

It is characterized by bilateral, non-bloody discharge regardless of color.

Galactorrhea is often caused by hyperprolactinemia secondary to medications, endocrine tumors (pituitary adenoma), or endocrine abnormalities, among other medical conditions.

Hiperprolaktinemi düşündürmelidir.

109
Q

What is pathological nipple discharge?

A

Pathologic discharge is characterized by unilateral or blood discharge, or discharge with an associated mass or skin change.

An intraductal papilloma is the most common cause of pathologic discharge, followed by duct ectasia and malignancy.

110
Q

Low risk nipple discharge vs high risk nipple discharge?

A

Low–> provocation, bilateral, milky or green, premenopausal

High–> Spontaneous, unilateral, bloody and serous, postmenopausal.

111
Q

What are the modalities that can be used to screen nipple discharge?

A

Begin with breast ultrasonography and/or mammography depending on the age and sex of the patient

Breast MRI may follow if mammogram and ultrasound are negative.

Suspicious lesions should undergo core needle biopsy and clip placement.

112
Q

Info abt ductal ectasia AKA dilatation?

A

Large and medium sized ducts.
It is filled with desquamated epithelium and secretion
Palpable lesion
Periductal inflamation can be accompanied.
More common in postmenopausal women.
Serous or bloody nipple discharge.
Differential diagnosis: Breast cancer.
No malignant potential

113
Q

Info abt intraductal papilloma?

A

Kanlı meme akıntısının EN SIK sebebi.

Solitary (central) intraductal papillomas:
They are arising major lactiferous ductus.
Ages 30-50.
These lesions are generally <1cm and
usually 3-4mm tumors within the dilated duct.
Pathologic nipple discharge
Excision of the relevant duct

Multiple (peripheral) papillomas:
Younger patient, peripherally and bilaterally
Less commonly nipple discharge.
Malignant potential is high.

114
Q

What is infectious diseases of breast?

A

Age: 18-50 years old
Commonly benign.
When an abscess occurs, it is the only benign disease of the breast that requires urgent intervention (sepsis!).
Differential diagnosis is difficult from breast cancer
In infections that do not respond to treatment, biopsy is absolutely necessary to rule out malignancy.

Breast abscess is an emergency!

115
Q

What are some common sites and types of breast infection?

A

Skin associated abscess, lactational abscess, central or subareolar abscess, peripheral parenchymal abscess

116
Q

Info abt lactational mastitis?

A

Lactational mastitis is inflammation of the breast tissues associated with breastfeeding.

Lactational mastitis has been estimated to occur in 2 to 20 percent of breastfeeding patients

Episodes are most common in the first four to six weeks of breastfeeding

The primary event appears to be ductal narrowing that leads to poor drainage and subsequent inflammation, edema, and compression of additional milk ducts.

117
Q

How does lactational mastitis occur + what are the pathogens that causes the disease?

A

Breast milk can contain bacteria; incomplete breast emptying may result in organisms growing and proliferating into infectious mastitis.

Microbiology– Most episodes of infectious lactational mastitis are caused byStaphylococcus aureusorStreptococcusspecies. Methicillin-resistantS.aureus(MRSA) has become an important pathogen.

118
Q

What are the clinical presentation of lactational mastitis?

A

Patients mostly present with a swollen and tender region of the breast, which may also be red in patients with lighter skin tone.
Systemic complaints may include myalgia, chills, malaise, and flu-like symptoms.

119
Q

How can we treat lactational mastitis?

A

Non severe infection + no MRSA risk: Dicloxacillin, cephalexin and flucloxacillin. 500mg x4, orally.

MRSA risk or beta lactam intolerance: trimethoprim-sulfamethoxazole(TMP-SMX)orclindamycin. TMP-SMX 1 double strength x2, clindamycin 450mg x 3, orally.

Severe infection: IV vancomycin AND either ceftriaxone or piperacilin-tazobactam

120
Q

What should we do if a lactational mastitis turns into an abscess?

A

Superficial (painfull, erythematous and fluctuating mass)
Deep (tenderness and edema) Breast USG!

Treatment: Abscess aspiration or abscess drainage (nipple evacuation or percutaneous or open incisional +/- irrigation accompained antibiotic therapy).

Percutaneous abscess aspiration and irrigation under USG as an alternative to surgical drainage

If there is a risk of malignancy, biopsy from the abscess cavity.

En iyisi, tercihen cerrahi drenaj.

121
Q

Info about Idiopathic Granulomatous Lobular Mastitis

A

Chronic mastitis, common in patients of young childbearing age.

It is mostly thought to be of AUTOIMMUNE origin and/or previous infection and trauma

It can be confused with breast Ca (especially inflammatory type breast Ca)

Biraz endişelendirir. Net bir tedavisi yoktur.

122
Q

What is the pathology of Idiopathic Granulomatous Lobular mastitis?

A

Epithelioid cell granuloma (biyopsi alıyoruz) , Langhans giant cell, lymphohistiocytic aggregate (+).

Non-caseous granuloma and microabscess (+/-), Caseous granulomas in tuberculosis.

123
Q

What is the treatment of Idiopathic Granulomatous Lobular mastitis?

A

Tuberculosis and malignancy should be excluded.

Conservative approach in localized cases: observation and/or anti-inflammatory treatment

Abscess drainage and wide excision in refractory localized cases

Corticosteroid therapy or immunosuppressive therapy in widely localized or diffuse multicentric cases

Wide excision in cases if it becomes localized disease

Treatment-resistant cases should be reviewed for tuberculosis and fungal infection

124
Q

En sık görülen kanser çeşidi nedir?

A

Meme kanseri. 2. akciğer, 3. ise prostat kanseridir.

125
Q

Meme kanserinin 5 yıllık hayatta kalıp oranı nedir?

A

%90

(stages)
Lokalize–> 99.3%
Regional–> 86.3%
Unknown–> 70.2%
Distant–> 31%

126
Q

What are the risk factors for breast cancer?

A

*Increasing age is the most important risk factor for most cancers.
Other risk factors:
*Family health history.
*Major inheritance susceptibility. Germline mutation of the BRCA1 and BRCA2 genes and other breast cancer susceptibility genes.
*Alcohol intake.
*Breast tissue density (mammographic).
*Estrogen (endogenous). Menstrual history (early menarche/late menopause).

127
Q

What is Gail model and IBIS/Tyrer-Cuzick model

A

Age-specific risk estimates are available to help design screening strategies for women with and without a family history of breast
cancer.
Regarding this, Gail model and IBIS/Tyrer-Cuzick model are among the most commonly used models for that

128
Q

What does the “classic” characteristics of a cancerous lesion include, in breast?

A

a hard, immovable, single dominant lesion with irregular borders.

However, these features cannot reliably distinguish a benign from a malignant tumor.

129
Q

What are some signs that suggests breast carcinoma?

A

Nipple retraction/ inversion, Breast dimpling, Redness and inflammation in the breast (suggests Inflammatory breast carcinoma), Peau d’orange view, Breast skin ulceration

130
Q

How is the BIRADS classification made?

A

Breast Imaging Reporting & Data System (BI-RADS) has 0 to 6 classification.

0–> not defined, need evaluations
1–> negative
2–> benign
3–> probably benign
4–> suspicious abnormality
5–> highly suggestive of malignancy
6–> proven malignancy (+ biopsy)

131
Q

How is the diagnosis of breast carcinoma made?

A

Fine Needle Aspiration Biopsy (FNAB)
* Core Needle Aspiration Biopsy (CNAB)

…

Ultrasound guided breast biopsy (core biopsy)
MRI guided breast biopsy
Stereotactic (Mammogram-Guided) tru-cut biopsy

…

Others: * Vacuum Associated Biopsy
* Wire Localization Biopsy
* Radioguided Occult Lesion Localization (ROLL) and
* Sentinel node and Occult Lesion Localization (SNOLL)
* İncisional biopsy
* Excisional biopsy

(Çok yapılmıyor) (Bu karttaki bilgiler düzensiz ya da yanlış olabilir)

132
Q

Why Tru-cut Biopsy (Core Biopsy) should be chosen for diagnosis?

A

Pathological tissue evidence
* Tumor type
* Immunohistochemical staining: ER Status, PR Status, cerbB2, Ki67, p53
* Molecular subtypes

These can be known by using tru cut biopsy.

133
Q

Histopathological classification of breast cancer, info.

A

1) In situ carcinoma
1-a) Ductal: Comedo, Cribiform, micropapillary, papillary, solid
1-b) Lobular: Low histological variation

2) Invasive (infiltrating carcinoma): tubular, ductal lobular, invasive lobular, mucinous (colloid), medullary, infiltrating ductal

These can be well, moderately or poorly differentiated. (this is based on nuclear pleomorphism, glandular/ tubular formation and mitotic rate.)

134
Q

Molecular subtypes of breast carcinoma?

A

Luminal A: HR+ (ER+ and/or PR+), HER2-

Luminal B: HR+ (ER+ and/or PR+), HER2+/-

Her2-enriched: HR- (ER-, PR-), HER2+

Triple negative: HR- (ER- , PR-), HER2-

135
Q

What should be done when breast cancer is diagnosed?

A

Systemic Staging:
* Lung X-Ray
* Abdominal USG
* Torax CT
* Abdominal CT
* Bone Scintigraphy
* PET/CT

Hereditary Breast Cancer:
* Genetic Conseling,
* BRCA1 and BRCA2 gene mutation analiysis

136
Q

What are the stages of breast cancer?

A

1A–> T <2cm
1B–> clusters of cancer cells in lymph nodes +- T <2cm
2–> daha fazla lenf yayılımı (1-3) ve daha büyük tümör, 2-5 arası ya da >5
3A–>Daha da fazla lenf yayılımı (4-9) ve daha büyük tümör, >5
3B–> Infammatory bc buna girer!
3C–> No tumor or tumor is any size, ya ln yayılımı daha çok, >10 ya da daha axilla veya sternuma doğru, uzak.
4–> Metastaz.

137
Q

Hereditary breast cancer syndromes?

A
  • BRCA1 ve BRCA2
  • PALB2
  • Ataxia-Telangiectasia: ATM (tumor suppressor gene)
  • CHEK2 geni
  • Li Fraumeni: p53
  • Cowden Syndrome: PTEN
  • Peutz-Jeghers Syndrome: STK11
138
Q

Which pts need genetic testing?

A
  • Female breast cancer diagnosed ≤45.
  • Triple-negative breast cancer, any age.
139
Q

Management of breast cancer?

A

*Upfront Surgery
*Neoadjuvant Systemic Therapy
*Metastatic Disease

140
Q

Some techniques for breast surgery?

A

Racket Incision, Round-Block Technique (Benelli), Batwing Incision, V-Mammoplasty,

NOT: Mastectomy and breast conserving surgery has EQUAL fayda rate.

141
Q

Info abt upfront surgery?

A

‘Upfront surgery’ refers to surgical resection as the initial treatment without prior radiation therapy or chemotherapy.

Can be used in early stage bc pts with nipple areola complex (-). (NAC - ne demek anlamadım)

Breast surgery–> Mastectomy (+/- reconstruction), BCS –> breast conserving surgery (oncoplastic surgery)

Axillary surgery–> SLNB (Sentinel Lenf Nodu Biyopsisi ), ALND (Aksiller lenf nodu diseksiyonu) TAS (targeted axillary surgery), no touch

142
Q

Complications of ALND (Aksiller lenf nodu diseksiyonu)?

A

Lost or decreased sensation in the back of the arm or armpit. …
*Tingling, numbness, stiffness, weakness, or LYMPHEDEMA (swelling of the arm). …
*Inflammation of the arm veins as they pass through the armpit region. …
*Winged scapula. …
*Increased risk of infection in the surgical area.

143
Q

Axillary Lymph Node Staging in Early Breast Cancer?

A

Standard Axillary Staging is Sentinel lymph node biopsy (SLNB).
* Survival, disease-free survival and regional control are similar to
axillary dissection.
* Complications such as limitation of movement, edema, pain and loss
of sensation are significantly lower.

Anladığım kadarıyla SLNB > ALND ama emin olmak lazım

144
Q

How do we do lymphoscintigraphy?

A

With Nanocolloid injection of isosulfan blue/ patent blue.

SLNB uses this technique (isosulfan blue + radiocolloid)

145
Q

Info abt neodjuvant systemic therapy

A

+Can turn inoperable tumors into operable ones.
+Facilitates breast conservation.
+Treatment response provide important prognostic information, particularly in patients with TNBC or HER-2
positive breast cancer. BU kanser hastalarında hastalık kalmışsa relaps riskini düşürmek için adjuvan kemoterapi planlamamıza yardımcı olur.
+May allow SLNB alone if initial cN(+) becomes cN0 after preoperative therapy.
+Allows time for genetic testing

146
Q

Who should be the Candidates for Neoadjuvant Systemic Therapy?

A
  • Patients with inoperable breast cancer:
    Inflammatory breast cancer
    Bulky or matted cN2 axillary nodes
    cN3 nodal disease
    cT4 tumors
  • Operable breast cancer
    Preoperative systemic therapy is preferred for:
    ◊ HER2-positive and TNBC, if ≥cT2 or ≥cN1
    ◊ Large primary tumor relative to breast size in a patient who desires
    breast conservation.
147
Q

What could be the responses of a tumor to neoadjuvant systematic therapy?

A

A) Concentric tumor shrinkage
B) Scattergun/ honeycomb response (ne anlama gelir???)

148
Q

What are the pathological complete responses of molecular subtypes of breast cancer to neoadjuvant chemotherapy?

A

Luminal A: HR+ (ER+ and/or PR+), HER2- –> 20%

Luminal B: HR+ (ER+ and/or PR+), HER2+/- –>55%

Her2-enriched: HR- (ER-, PR-), HER2+ –> 78%

Triple negative: HR- (ER- , PR-), HER2- –> 44%

149
Q

Which of the molecular subtypes of breast cancer has the best response to neoadjuvant chemotherapy?

A

Her2- enriched.

150
Q

Which of the molecular subtypes of breast cancer has the least response to neoadjuvant chemotherapy?

A

Luminal A.

151
Q

What is the definition of shock?

A

A life-threatening condition in which tissue perfusion is not capable of sustaining aerobic metabolism.
Perfüzyon sadece kan alımı demek değildir, hücrenin beslenmesi ve oksijenlenmesi anlamındadır.
Kanser, CO zehirlenmesi ve aniden parçalanmayan tüm canlıların sonu şoktan kaynaklanır.
Kısacası, Anything leading to a lack of oxidative phosphorylation in the cellular level can cause shock.

152
Q

What happens during shock on a cellular level?

A

*Na/ k pumps stop (sodium enters the cell, Water follows sodium, cellular swelling / vacuolar degeneration occurs, membrane integrity gets disrupted)
*Cellular edema begins (loss of absorption surface. Microvilli smoothing. Ribosomes detach from RER. Deformation of the cytoskeleton)
*Calcium channels open–> Enzyme activation: Proteases, Endonucleases, Phospholipases (+lactic acid), Increase in the permeability of the mitochondrial membrane–> Cytochrome C - apoptosis
Cytochrome C apoptoz red flagidir.

153
Q

Şok sonucunda neler olur hücresel düzeyde?

A

Loss of membrane integrity
Cytokines and cellular debris into the circulation
Worsening of the microcirculation
Sistemik etki parakrin (–> dolaşım) etkiden kaynaklanır. TNF gibi sitokinler ya da her sinyal molekülü hücre dışına çıkınca orada kalmaz. Diğer hücrelere girip de (insult sürüyorsa) artıp sonra dolaşıma katılabilirler.

154
Q

What are the shock types?

A

Lack of perfusion: Hypovolemic shock, Cardiogenic shock (kan var kalp iptal. Obstructive shock türü), Distributive shock (kan ve kalp var. Periferde göllenme olur. Septik şok örnek.)

Lack of oxygen (cytopathic shock): Cyanide, Carbon monoxide, Rotenone

155
Q

Most common causes of shock?

A

Blood loss: Every kind of bleeding
Fluid loss:
Burns, Diarrhea, Pancreatitis, Overt vomiting, Bowel obstructions, Increase in insensible loss (fever) –> bunların bir kısmının niye su kaybettirdiğini anlamdadım. Öğren

156
Q

Vücudun şok için verdiği savaşta hangi sistemler önemlidir?

A

The Central Nervous System–> ilk tepki veren sistem. Diğerleri daha geriden gelseler de daha uzun ve sağlam bir yanıta sebep olurlar.
The Endocrine System
The Immune System
The Coagulation System

157
Q

CNS in shock response?

A

The fastest response
Through the afferent and efferent signals. Baroreseptör!

Hypotension, Pain, Hypoxemia, Hypercarbia, Acidosis, Hyperthermia
Sympathetic tone.

158
Q

Sympathetic tone in shock response?

A

Şok sırasında sempatik tone artar.
Bu, kendisini vasoconstriction, tachycardia ve norepinephrine ve epinehrine hormonlarının salgılanması ile gösterir.
Vasoconstriction–> alpha1 adrenergic receptors regüle eder, periphery (skeletal m + skin), splanchnic area.
Tachycardia–> beta1 adrenergic receptors
Hormon secretion–> ikisinin de hem alpha hem beta reseptör etkileri var

159
Q

Splanchnic alan nedir?

A

Sindirim sistemine giden vasküler sistemdir. Abdominal aortun üç ana dalını içerir: çölyak arter, superior mezenterik arter ve alt mezenterik arter.

160
Q

Endocrine system in shock response?

A

Later activated. Longer lasting effects. Activation of the hypothalamic-pituitary-adrenal axis

Hypothalamus: CRH
Pituitary: ACTH (CRH uyarır), ADH
Kidney: Cortisol (ACTH), aldosterone (ACTH), Renin (ACE2)
Liver: Angiotensinogen–> Angiotensin1 (Renin)
Lung: Angiotensin 2

161
Q

Innate immune system in shock response?

A

PAMPs (patojen) and MAMPs (hasar). They recognize: Lipopolysaccharides of gram – and Lipoteichoic acid of gram + and Double s rna of viruses.
Alarmins (DAMPs): HMGB1 (high mobility group box). HSP (heat shock protein). (ikisi nükleik hasar belirteçleridir.)
Septik şok–> PAMP uyarımı
Hipovolemik şok–> DAMP uyarımı
Hızlı etki eder, adaptive aksine.

162
Q

Şoklardan hangisinde cardiac output değişmez?

A

Distributive shock.

163
Q

Complement system işlevi nedir?

A

Microbiolysis. Platelet activation. Histamine relaese. Chemotaxis. Opsonization. Promotes phagocytosis and degranülation.
Non spesiffik ve spesifik immün hücrelerinin tanınmasını kolaylaştırır. İmmün yanıtı arttırır. Fagositoz ve homeostaziyi (?) kolaylaştırır.
Innate IS ye dahildir

164
Q

Adaptive immune system in shock response?

A

TNF alpha and IL-1 are main regulators+ IL6.
CD4 T helper – IFN gamma -> main macrophage activator
Prolonged insult -> more systemic response
Increased metabolic demand from inflammatory cells
İnsult sonrası sitokin fırtınası olabilir. Kötüleşme proliferasyon sonrasında olur, sitokin fırtınası ile. Çünkü immün sistem gecikerek çok fazla pro inflammatory cytokine salgılar.

165
Q

What are the Proinflammatory and anti inflammatory cytokines?

A

Proinflammatory–> Interleukin-1, Interleukin-2, Interleukin-6, Interleukin-8, Interferon, TNF, PAF
1 2 6 8

anti inflammatory–> Interleukin-4, Interleukin-10, Interleukin-13, Prostaglandin E2, TGFβ
4 10 13

166
Q

TNF görevleri nelerdir?

A

TNF–> Yara iyileşmesinin orkestra şefi. Source: Macrophage, T cells, Fibroblasts, Endothelial cells. T ½ 20 min. Release of proinflammatory cytokines. Increased vascular permeability. Increased chemotaxis. Hypercoagulability. CRH secretion. Fever, anorexia. APP (acute phase pt–> CRP örnek) production.
TNF-alpha diğer adı kaşeksin. TNF ve IL6yı arttıran her şey CRPyi de arttırır.

167
Q

IL1 ve IL6 görevleri nelerdir?

A

IL1–> Source: macrophage, endotel. T ½ 6 min. Major pyrogen, hyperalgesia. En kısa ömürlü cytokine.

IL6–> Induced by TNF. Peaks at 48 hours. B and T lymphocyte differentiation. NK and and neutrophils. APP production. Longer t1/2. Artması kötü prognoz gösterir.

168
Q

Insult sonrası cytokine seviyeleri zamanla nasıl değişmelidir normal şartlar altında?

A

Cytokines peak after 48 hours of insult returns normal around 7- 10 days.
İlk 2 gün inflammatory ağrı yapar. İnsult durduysa 2 günden sonra azalır. Azalmaz ise sıkıntı.

169
Q

Şoktaki bir hastanın klinik belirtileri nelerdir?

A

Pale skin, dry mucus membrane, distended jugular veins (venöz geri dönüşü arttırmak için. Sadece kalbin üstündeki damarlarda distension olur.), slow capillary refill time, tachycardia, hypotension.

170
Q

Shock index nedir ve nasıl hesaplanır?

A

Heart rate / Systolic Blood Pressure >0.9 olarak hesaplanır.
Normal range of 0.5 to 0.7 in healthy adults.
Ortalama arter basıncı= (sistol + diastol)/2. Bu değer <60 => hipotansif şok vardır. Aynı zamanda, böbrek fonksiyonlarını etkileyecek bir hipotansiyon da hipotansif şok demektir.

171
Q

Levels of shock info? (Level 1 ve 2)

A

Level 1–> <15% volume loss. Vitals are not altered much. Capillary refill <3sn. Bunda narrowed pulse pressure yok. Overcompensation yüzünden. Hipertansiyon görmek bile mümkündür bu evrede.

Level 2–> %15 – 30 volume loss. HR > 100 beats/min. Tachypnea. Cold and moist skin. Decrease in systolic pressure: Orthostatic. Narrowed pulse pressure (SP azalır, DP artar. SP-DP diye hesaplandığından değerler yaklaşmış olur). Agitation.

172
Q

Levels of shock info? (Level 3 ve 4)

A

Kan verilmeli.
Level 3–> %30 – 40 volume loss. Marked tachycardia. Low systolic pressure: At rest. Narrowed pulse pressure. Decreased urine output: < 0.5 ml/kg/h

Level 4–> > %40 volume loss. Continuous tachycardia. Diastolic pressure may be ABSENT. Oliguria or anuria. Life threatening acidemia

173
Q

Laboratory and Imaging diagnosis of shock?

A

Lab–> Complete blood count. Electrolytes. Urea / Creatinine. Arterial gas / pH / Base deficit. Coagulation tests. Cross match. Beta HCG (neden??)

Imaging–> Chest X ray. Ultrasound: Abdomen + Echo. CT / MRI

174
Q

First aid and hospital care for shock patients?

A

First aid–> Trauma pad. Collar. IV access. Oxygen: 2 l/m cannula + 5 l/m mask. Trendelenburg (bacakları yukarı kaldırma. Sadece 1 ve 2 lvl için işe yarar.)

Hospital care–> Monitorization. Bladder catheterization. Central Venous access? / Cut – down? (bunu kaçırdım :( ). Arterial catheterization

175
Q

Fluid resuscitation for shock patients info.

A

How much?–> 1 – 2 liter for adults. 20 ml/kg for children
What–> Isotonic saline. Lactated ringer solution. Bunlar kristalloid sıvılar. Fazla verirsek akciğer başta olmak üzere ödeme sebep olabilir.

176
Q

Şok hastalarına hangi ilaçları vermeliyiz?

A

Alpha ve beta adrenerjik + dopamin vermeliyiz.

A adr–> noradrenaline. Hem alfa1 ve beta1 etkisi olsa da daha çok alfadır. Septik şokta tercih ederiz. Can increase the duration of the contraction without increased chronotrophy.

B adr–> adrenaline. Potent b1 ama az da olsa b2 ve a1 etkisi vardır. Norepten sonra septik şokta tercih ederiz. Mediate increases in inotrophy and chronotrophy with minimal vasoconstriction.

Dopamine–> Böbreğe özgü! Vazodilasyon yapar. Dopamine1 reseptörlere etki ederek düşük doz verildiğinde selektif vazodilasyon yapar. daha fazla verirsek b1 etki ile CO arttırır. Daha da fazla versek a1 etkisi ile vasocons yapar.

177
Q

Üst ve alt GIS kanamayı nasıl ayırt ederiz?

A

Upper–> Above the ligament TREITZ. Esop, stomach, proximal duodenum.

Lower–> Below the ligament TREITZ. distal duodenum to rectum.

178
Q

What are the symptoms of GIS bleeding?

A

Hematemesis–> kan kusma. Üst GI kanamasına işaret eder.
Melena–> Siyah gaita. Çoğu üst gis kanamasından kaynaklanır. (BENCE BU DOĞRU DEĞİL)
Hematochezia–> Parlak kırmızı kanlı gaita. Genelde kolonun sonuna doğru olan alt gis kanamalarıdır.

179
Q

Upper GI bleeding etiology?

A

Gastric and duodenal ulcers. Severe or erosive esophagitis, gastritis or duodenitis.
Esophagogastric varices. Portal hypertensive gastropathy.
Angiodysplasia aka vascular ectasia
Mass lesions (Polyps + cancers)
No lesion identified (%10-15)
Mallory Weiss syndrome–> yüksek karın içi basınçların Mallory-Weiss yırtığı adı verilen mukozada yırtılma ve kanamaya neden olduğu bir durumdur

180
Q

Lower GI bleeding etiology?

A

Diverticular bleeding
Vascular–> angiodysplasia (yumak halindeki damar kanamaya yatkındır), ishcemic, radiation induced)
Inflammatory, Neoplastic, After therapeutic intervention.

181
Q

Hangi ilaçlar GI kanama riskini arttırabilir?

A

Asprin and other NSAIDs, including COX2 inhibitors.
Anticoagulants (ex: warfarin) and antiplatelet (P2Y12) agents.

182
Q

1) Peptic ulcer 2) esophageal ulcer 3) Mallory weiss tear 4) Variceal hemorrhage or portal hypertensive gastropathy 5) Malignancy
Bu 5 durumun kardinal semptomlarını söyle.

A

1) Peptic ulcer–> Upper abdominal pain.
2) esophageal ulcer–> Odynophagia, GERD, dysphagia
3) Mallory weiss tear–> Emesis, retching, coughing prior to hematemesis
4) Variceal hemorrhage or portal hypertensive gastropathy –> Jaundice, abdominal distension (ascites!)
5) Malignancy–> Dysphagia, early satiety, involuntary weight loss, cachexia (daha fazla kalori almakla durdurulamayan kilo ve kas kaybı)

183
Q

Stool color can indicate where in the colon is bleeding. So, what does black, maroon and red stools indicate?

A

Black–> Proximal to hepatic flexure
Maroon–> Proximal to splenic flexure
Red–> Distal to descending colon

184
Q

How does Triage (öncelik belirleme) of GI bleeding is made?

+ what is the initial assessment of GI bleeding patients?

A

Glasgow- batchford score.

+ ABC! Asses the degree of hypovolemic shock

185
Q

General support for GI bleeding patients info

A

NOTHING per mouth. Two large caliber peripheral IV catheters or a central venous line.
Elective endotracheal intubation: * High-risk for aspiration
* Massive upper GI bleeding * Altered mental status

Treat hypovolemic shock:
* Restrictive transfusion strategy for hemodynamically stable
* Avoid over transfusion in patients with suspected variceal bleeding

186
Q

Lab tests and their results that indicate GI bleeding?

A

Lab tests–> CBC, serum chemistries, liver tests, coagulation studies, blood group + cross match

Initial hemoglobin may be normal. As blood is absorbed through the small bowel patients may have decreased renal perfusion. BUN- to creatinine and Urea- to creatinine ratios; the higher they are the more likely the bleeding is from a upper GI source.

+ kan bağırsakta kaldıkça enfeksiyona açık hale gelir.

187
Q

Nasogastrik tüpün faydaları ve kullanım alanları nelerdir?

A

Most useful situation: patients with severe hematochezia, and unsure if UGIB vs. LGIB
* Positive aspirate (blood/coffee grounds) indicates UGIB

Can provide prognostic info:
* Red blood per NGT – predictive of high risk endoscopic lesion
* Coffee grounds – less severe/inactive bleeding
* Negative aspirate – not as helpful; 15-20% of patients with UGIB have negative NG aspirate

188
Q

Upper GI bleeding management? (General support kartında yazanlar management dahilindedir ondan onları tekrarlamıyorum.)

A

Give PPI for bleeding, early endoscopy is recommended.
If there is suspected esophagogastric variceal bleeding and/ or cirrhosis–> somatostatin or its analogue, IV antibiotic (ex: ceftriaxone, fluoroquinolone)
Baloon tamponade!
Acid suppression: * Bolus (eg, esomeprazole 80 mg)
Prokinetics to improve gastric visualization: * Metoklopramid (10 - 30 mg iv)
Vasoactive medications: * Octreotide, and terlipressin

189
Q

Tekrar GI kanamanın ne kadar mümkün olduğunu gösteren sınıflandırmanın adı nedir?

A

Forrest classification. 3 seviyeden oluşur.

190
Q

Lower GI bleeding Diagnosis and Treatment?

A
  • Endoscopy–> Diagnostic / therapeutic
  • Colonoscopy
  • Scintigraphy–> not specific but sensitive, küçük kanamaları bile tespit eder.
  • CT angiography–> More effective during active bleeding.
  • Angiography–> Focus detection success: Bleeding rate + Blood pressure
  • Surgery–> Son çare olarak başvurulur. Pre-operative detection of bleeding focus çok önemlidir. Intraoperative enteroscopy. 10-25% mortality.

Stable patient: Early colonoscopy
Unstable patient: CT angiography –> Therapeutic
angiography/Surgery

Ccs 401: GENEL CERRAHİ + ANESTEZİ (6 decks)

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