Question 1

which cells express tissue factor?

Accepted Answer

stromal fibroblasts and leukocytes/

Question 2

what does antithrombin inhibit?

Accepted Answer

Antithrombin (AT) is a circulating serine protease inhibitor (SERPIN). It neutralizes most of the enzymes in the clotting cascade, especially thrombin (factor IIa), factors Xa, and IXa; as well as factor XIIa and factor XIa.

Question 3

Absence of factor 12 hmwk and kallikrein will u have a bleeding disorder?

Accepted Answer

No extrinsic compensates

Question 4

What activates protein c and what does it do?

Accepted Answer

thrombin and inactivates factor 8 and 5 with help of protein s

Question 5

what increases antithrombin adhesion? what activates it?

Accepted Answer

heparan sulfate and nothing its constantly active.

Question 6

what main enzymes are responsible for fibrinolysis? what 2 enzymes produce it?

Accepted Answer

plasmin, urokinase and tissue plasminogen activator

Question 7

Whats donor rbc lifespan? nornal rbc lifespan?

Accepted Answer

60 days . 120 days

Question 8

Name the main rhesus antigens?

Accepted Answer

D, C, c E, e

Question 9

Name 8 complications of blood transfusions?

Accepted Answer

Iv haemolysis and DIC shock Acute haemolytic reactions - donors rbc destroyed by recipent antibodies (ones in low conc - kell or duffy antibs) non haemolytic febrile transfusion reaction- antibs against donor lymphocytes. urticaria bacterial infection - shock iron overload TRALI - HLA antibodies in donors blood directed against recipents hla. antigen antibody reaction activates neutrophils in lungs - releasing proteases and oxidases - damaging blood vessels and making them leak

Question 10

What is minimum haem conc for humans?

Accepted Answer

4-5g/L. 8g/L offers safety margin

Question 11

Name 4 reasons for coagulopathy?

Accepted Answer

dilution of coagulation factors, thrombocytopenia, hypothermia, acidosis.

Question 12

What is INR?

Accepted Answer

Ratio of patients prothrombin time to a normal (control) sample raised to power of ISI value (International sensitivity index) to account for differences in tissue factor used.

Question 13

Define acute abdomen?

Accepted Answer

Undiagnosed abdo pain that has been present for less than a week. The term acute abdomen represents the rapid onset of severe symptoms that may indicate potentially life-threatening intra-abdominal pathology that requires urgent surgical intervention. Abdominal pain is usually a feature, but a pain-free acute abdomen can occur, particularly in older people, in children, in the immunocompromised, and in the last trimester of pregnancy. These patient groups need to be paid special attention as they can present atypically. Abdominal pain lasting more than 48 hours is less likely to require surgery than pain of shorter duration. The enlargement of the uterus, which displaces and compresses intra-abdominal organs, together with the laxity of the abdominal wall, makes it difficult to localise pain and can blunt peritoneal signs. Pregnant patients may sometimes have a mild physiological leukocytosis, so this finding is non-specific in these patients.

Question 14

What does explosive pain onset suggest? and rapid? Aetiology of acute abdomen?

Accepted Answer

Perforation and acute inflammation. AETIOLOGY (more common to less common): Obstruction (Adhesions are the most common cause of obstruction in industrialised countries, with incarceration of hernias the second leading cause: hernia incarceration is the most common cause of bowel obstruction in patients without prior abdominal surgery. Other causes of obstruction include volvulus, gallstones, and intussusception. Less common causes include congenital anatomical abnormalities, gastrointestinal neoplasm, and inflammatory bowel disease.) peritonitis (secondary to infection (e.g., pelvic infection, appendicitis), haemorrhage (e.g., ectopic pregnancy, ruptured aortic aneurysm), ischaemia (e.g., ovarian torsion, mesenteric ischaemia) or processes associated with contamination by GI contents (e.g., perforated duodenal or gastric ulcer)). Inflammatory causes may include cholecystitis, appendicitis, acute pancreatitis, and acute diverticulitis and Meckel diverticulitis. Ulcerative colitis and Crohn's disease may present with abdominal pain secondary to the inflammatory process or due to the complication of obstruction. Female patients presenting with an acute abdomen should always have a pregnancy test to rule out ectopic pregnancy. Other pathologies involving the female reproductive organs include ruptured ovarian cyst, ovarian torsion, pelvic inflammatory disease, and endometriosis. Vascular pathologies may result in intra-abdominal haemorrhage such as abdominal aortic dissection, ruptured aortic aneurysm, and ruptured splenic artery aneurysm. Ischaemic causes include acute mesenteric ischaemia and infarction, ischaemic colitis, splenic infarct. Vaso-occlusive episodes in sickle cell crises also can present with abdominal pain. Budd-Chiari syndrome involves hepatic venous outflow obstruction and the abdominal pain may present with hepatomegaly and ascites. Abdominal wall haematoma may occur spontaneously or secondary to trauma, exercise, coughing, or a procedure. Infective processes may involve intra-abdominal organs or structures such as the liver (hepatic abscess or hepatitis), and the gastrointestinal tract (gastroenteritis, infectious colitis, typhilitis [neutropenic enterocolitis; inflammation of the caecum]) Psoas abscess is more commonly due to a tuberculous abscess, which has extended from the lumbar vertebra into the psoas muscle. Fitz-Hugh Curtis syndrome, a complication of pelvic inflammatory disease, comprises right upper quadrant abdominal pain associated with perihepatitis. It involves liver capsule inflammation leading to the creation of adhesions. Right upper quadrant (RUQ) abdominal pain is aggravated by breathing, coughing or laughing, which may be referred to the right shoulder. Metabolic causes of acute abdomen include uraemia, diabetic ketoacidosis, Addisonian crisis and hypercalcaemia. Inherited metabolic disorders include acute intermittent porphyria and hereditary Mediterranean fever. Heavy metal poisoning may be caused by medical/environmental/occupational exposure to, for example, mercury, lead, or arsenic. Narcotic withdrawal from opioids may result in abdominal cramping pain. In men, testicular torsion should be considered. Others: radiological enterocolitis.

Question 15

Name 6 signs of peritonitis

Accepted Answer

prostration - bowing positon. shock. lying still. Positive cough test. No bowel sounds. Board like rigidity. rebound tenderness, guarding.

Question 16

Define ischaemic bowel disease? Classification? Pathophysiology?

Accepted Answer

Ischaemic bowel disease encompasses a heterogeneous group of disorders caused by acute or chronic processes, arising from occlusive or non-occlusive aetiologies, which result in decreased blood flow to the gastrointestinal tract. It is classified into 3 main types: Acute mesenteric ischaemia, Chronic mesenteric ischaemia and Ischaemic colitis (colonic ischaemia). Ischaemic colitis and mesenteric ischaemia are different disorders, but are classified under the same umbrella. Pathophysiology: Several collateral arteries exist between the SMA and the IMA, including the marginal artery of Drummond (connects SMA and IMA) and the arc of Riolan (Connects Middle and Left colic A). The splenic flexure and the recto-sigmoid junction are 2 watershed areas where collateralisation of blood flow may be limited. Segments of bowel which do not cause acute necrosis or perforation can heal with stenosis or stricture. Thromboembolic events that lead to mesenteric ischaemia usually involve the SMA instead of the other mesenteric arteries (IMA and coeliac artery). This is because of the anatomical position of the SMA; the SMA is positioned vertically while the other vessels form more oblique angles from the aorta.

Question 17

Describe Acute Mesenteric ischaemia?

Accepted Answer

It encompasses the following: Superior mesenteric artery embolus, Superior mesenteric artery thrombosis, Non-occlusive mesenteric ischaemia (NOMI), Superior mesenteric vein thrombosis, Focal segmental ischaemia. All have impaired blood supply to intestine, and passage of bacteria back to sterile tissue and a SIRS response. USUALLY AFFECTS OLD PEOPLE. AETIOLOGY: Vasculitis, embolus (AF), atherosclerosis, Malignancy, Shock, HF (hypoperfusion), Pancreatitis, appendicitis, diverticulitis, abscess, venous stasis due to portal HTN (cirrhosis). Hypercoagulability disorders (eg, protein C and S deficiency, Factor V leiden). Recent surgery Such as aortic aneurysm repair, aorto-iliac bypass, colectomy, colonoscopy. Pregnancy. COCP. DRUGS: vasopressin, vasopressors. epinephrine. pegylated interferon, methamphetamines, and cocaine. sumitriptan. Digoxin. polycythaemia vera, phaeochromocytoma, carcinoid syndrome. PRESENTATION: PAIN OUT OF PROPORTION TO SIGNS. In early stages no signs of peritonism. occlusion of sma or smv Triad - Acute severe pain, no abdo signs, rapid hypovolemia(shock). Constant central or RIF pain, acidosis, tachcardia, INVESTIGATIONS: wbc increased. ANgio is gold standard. Abdo X ray: may show SBO, or ileus, or other DD. CT: gas in portal vein, bowel wall or mucosal oedema. may show solid organ infarct. MANAGEMENT: MEDICAL: IV fluids, oxygen. Medical options include papaverine (to relieve vasospasm) or thrombolytics infused through an angiogram catheter, and heparin for MVT. SURGERY: Angioplasty to the superior mesenteric artery, Embolectomy, Aortomesenteric bypass and resection of bowel if gangrene develops.

Question 18

Describe Chronic mesenteric ischaemia?

Accepted Answer

This is a chronic atherosclerotic disease of the vessels supplying the intestine. Usually all three major mesenteric arteries are involved. AVERAGE AGE IS 60. RISK FACTORS ARE THOSE FOR ATHEROSCLEROSIS: smoking, hypertension, diabetes mellitus and hyperlipidaemia. PRESENTATION: VARIABLE. MOD to SEVERE COLICKY, CONSTANT ABDO PAIN. weight loss, postprandial pain ('intestinal angina') and a fear of eating. Nausea, vomiting, bowel irregularity. EXAMINATION: mild tenderness, abdo bruit, CVD signs. INVESTIGATIONS: arteriography is gold standard. Mesenteric duplex ultrasonography. FBC, UandE, LFTs may reflect malnutrition. MANAGEMENT: MEDICAL if unfit for surgery: Nitrate therapy, anticoagulation. Once the decision to operate has been taken, intra-arterial papaverine should be administered to reduce vasospasm. SURGERY: angioplasty, stenting, Transaortic endarterectomy of the coeliac or superior mesenteric artery. Retrograde bypass from the external iliac artery. Anterograde bypass, which provides the best orientation of the graft to the aorta.

Question 19

extra abdo causes of acute abdomen? 6

Accepted Answer

lower lobe pneumonia, inferior MI, DKA, sickle crisis, herpetic neuralgia, haemolysis.

Question 20

describe 4 things that would make you think testicular torsion?

Accepted Answer

swollen, tender testis. reddening of scrotal skin. Lifting of testis over symphysis increases pain. Bell clapper deformity.

Question 21

13 tests could do in acute abdo?

Accepted Answer

fbc - malignancy, wbc - infection, u+e, amylase, lft, ABG - metabolic a with no other signs may indicate mesenteric infarct. urinalysis - haematuria - renal stones, infection, dka. preg test - human beta chorionic gonadotropin. ECG - MI. CXR(erect) AXR - obstruction. AAA. US - appendix, gallstones. endoscopy - peptic ulcers.

Question 22

Describe Ischaemic colitis?

Accepted Answer

Ischaemic colitis occurs when there is an acute, transient compromise in blood flow, below that required for the metabolic needs of the colon. This leads to mucosal ulceration, inflammation, and haemorrhage. AETIOLOGY: Systemic: Heart failure, (SIRS), atherosclerosis, Embolic: Atrial fibrillation, Thrombotic: Concurrent malignancy and haematological disorders. IATROGENIC: DRUGS: Chemotherapy, sex hormones, interferon therapy, pseudoephedrine, cardiac glycosides, diuretics, statins, non-steroidal anti-inflammatory drugs (NSAIDS), immunosuppressive drugs, vasopressors. SURGERY: Abdominal aortic aneurysm repair. Endoscopic: Colonoscopy and bowel preparation media for colonoscopy. PRESENTATION: DIARRHOEA, rRECTAL BLEEDING, COLICKY ABDO PAIN. Examination typically reveals a soft abdomen with tenderness and voluntary guarding over the affected segment of colon. The presence of peritonitis suggests full thickness ischaemia, perforation, or alternative diagnosis. INFLAMMATORY OR INFECTIVE HAS A MORE INSIDIOUS ONSET. ISCHAEMIC IS FASTER ONSET. IT may cause a SIRS response. INVESTIGATE URGENTLY: CT is diagnostic investigation of choice (portal vein gas, pneumatosis (gas in the wall), wall thickening, ascites) It suggests diagnosis need colonscopy to confirm. Colonoscopic evaluation is recommended within 48 hours to visualise mucosa and confirm diagnosis (Petechial haemorrhages, Oedematous and fragile mucosa, Segmental erythema, Scattered erosions, Longitudinal ulcerations (colon single stripe sign). USS and X RAYs waste of time dont do. INVESTIGATIONS: U and E. CRP. FBC. Lactate (normal does not exclude full thickness infarct). CLotting studies. TREATMENT: IV fluids. ABG. Usually conservative management. SUrgery may be needed if repeated transfusions required, perforation, peritonitis. SUrgery includes: segmental resection and colostomy formation.

Question 23

what age can appendicitis occur?

Accepted Answer

Any age highest incidence is between 10-20years - more infections. Also higher in elderly due to constipation and faecoliths. This condition is most commonly seen in patients aged between early teens and late 40s.

Question 24

Can kids get appendicitis?

Accepted Answer

Rare. appendix is cone shaped - larger lumen. So less likely to happen.

Question 25

What are faecoliths?

Accepted Answer

Stone made of faeces - central matrix of dry faeces and calcium salts and fibre around the outside.

Question 26

Decribe the pathogenesis of appendicitis?

Accepted Answer

The lumen distal to the obstruction starts to fill with mucous and acts as a closed-loop obstruction. This leads to distension and an increase in intraluminal and intramural pressure. As the condition progresses, the resident bacteria in the appendix rapidly multiply. The most common bacteria in the appendix are Bacteroides fragilis and Escherichia coli. Distension of the lumen of the appendix causes reflex anorexia, nausea and vomiting, and visceral pain. As the pressure of the lumen exceeds the venous pressure, the small venules and capillaries become thrombosed but arterioles remain open, which leads to engorgement and congestion of the appendix. The inflammatory process soon involves the serosa of the appendix, hence the parietal peritoneum in the region, which causes classical right lower quadrant pain. Once the small arterioles are thrombosed, the area at the anti-mesenteric border becomes ischaemic, and infarction and perforation ensue. Bacteria leak out through the dying walls and pus forms (suppuration) within and around the appendix. Perforations are usually seen just beyond the obstruction rather than at the tip of the appendix. Gut organisms invade wall after lumen obstruction - lymphoid hyperplasia (IBD) or infection (measles, mononucleosis) faecoliths or filarial worms.

Question 27

name 5 general signs of appendicitis?

Accepted Answer

fever, furred tongue, coughing hurts, shallow breaths, foetor oris (or halitosis) (bad breath)

Question 28

Describe how pain symptoms change in appendicitis? Describe how location of the pain may vary depending on the location of the appendix?

Accepted Answer

Dull ache pain around umbilicus then sharp pain at mcburneys point. If it continues - nausea, vomiting and anorexia may occur. Pain typically starts at the mid-abdominal region and later (1 to 12 hours) shifts to the right lower quadrant. Pain is usually constant in nature and with intermittent abdominal cramps and is usually worse on movement and coughing. Location of the pain may vary depending upon the location of the appendix: Retrocaecal appendix may cause flank or back pain, Retroileal appendix may cause testicular pain due to irritation of the spermatic artery or ureter, Pelvic appendix may cause suprapubic pain, A long appendix with tip inflammation in the left lower quadrant may cause pain to that region.

Question 29

without what feature is appendicitis unlikely?

Accepted Answer

Anorexia

Question 30

name 2 atypical symptoms of appendicitis?

Accepted Answer

diarrohea if lies near rectum and uti if near bladder

Question 31

what happens after appendix bursts?

Accepted Answer

Day 3 mass forms. day 5 abscess - hr fast and swinging pyrexia.

Question 32

Name clinical signs found in appendicitis?

Accepted Answer

Rovsing's sign may be positive: palpation of the left lower quadrant increases the pain felt in the right lower quadrant. This pressure stretches the entire peritoneal lining, and so causes pain in any location where the peritoneum is irritating the muscle. psoas sign - pain on extending hip if appendix is retrocaecal. Cope sign - pain on flexion and internal rotation if near to obturator internus. Other methods to demonstrate an inflamed appendix include: the psoas test (extend the hip and abduct the thigh with the patient on the left side) and the obturator test (flex and internally rotate the right hip).A retrocaecal or pelvic appendix may be missed. Rectal examination may reveal localised tenderness as the only sign of an inflamed retrocaecal or pelvic appendix.

Question 33

Describe the approach to assessment of a patient with suspected appendicitis?

Accepted Answer

Usually diagnosed via history or examination. CT or US can help if diagnosis is uncertain or atypical presentation. Women of childbearing age should have a pelvic examination to rule out other pelvic pathology. Pregnant women presenting with right-sided abdominal pain, with nausea and vomiting, pose an even greater challenge and should proceed to ultrasound examination, followed by MRI or CT scan if needed. HISTORY: SOCRATES, Anorexia is another important symptom almost always associated with acute appendicitis. Without anorexia the diagnosis of acute appendicitis is in question. Nausea and vomiting are also present in 75% of patients. Vomiting usually occurs only once or twice. Severe constipation is a late feature. Complicated appendicitis (perforation or intra-abdominal abscess) is more likely the greater the duration of symptoms and in older patients (over 50 years). EXAMINATION: In patients presenting with a high-grade fever, another diagnosis should be considered. Usually not much change in vital signs. A classic sign is right lower quadrant abdominal tenderness (McBurney's sign) and localised rebound tenderness, if appendix is anterior. There may also be pain in the right lower quadrant after compressing the left lower quadrant (Rovsing's sign). Pain may be elicited with the patient lying on their left side and slowly extending the right thigh to cause a stretch in the iliopsoas muscle (psoas sign) or by internal rotation of the flexed right thigh (obturator sign). Bowel sounds may be reduced, particularly on the right side compared with on the left. Classical abdominal findings may not be present if the appendix is in an atypical position. Patients with perforation may present acutely unwell with hypotension, tachycardia, and a tense, distended abdomen with generalised guarding and absent bowel sounds. A palpable mass may be felt if the appendiceal perforation has been contained by the omentum, resulting in a peri-appendiceal abscess. INVESTIGATIONS: FBC (mild leukocytosis may be present) Patients with a palpable abdominal mass should also have either an ultrasound or an abdominal CT. In patients with equivocal clinical findings, imaging by ultrasound or CT scan of the abdomen is indicated. Women, in particular, benefit from preoperative imaging. Ultrasound has the advantage of being readily available, rapid, and able to be performed at the bedside. If a normal appendix is visualised in its full length, then acute appendicitis can be excluded. However, this is rarely the case, and the greatest utility for ultrasound is to detect alternative causes of abdominal pain. Appendiceal CT scan is increasingly used as the initial diagnostic test for acute appendicitis. A urinalysis should be performed to exclude possible urinary tract infection or renal colic. Sexually active women of childbearing age should have a urinary pregnancy test. CRP may be raised but a normal level does not exclude a diagnosis of appendicitis. May also do U+E and laparacopy. Ultrasound is Indicated in atypical presentations, including appendicitis with intra-abdominal abscess. However, a CT scan is often required as well. It has a sensitivity and specificity of 86% and 81%, respectively.

Question 34

How is diagnosis made in appendicitis?

Accepted Answer

on clinical signs, CT can be useful if diagnosis is unclear.

Question 35

What incision is made at 90 degrees to mcburneys point?

Accepted Answer

girdiron incision.

Question 36

Tx in appendicitis? DD?

Accepted Answer

DD: Acute mesenteric adenitis, Viral gastroenteritis, Meckel's diverticulum, PUD, crohns, UTI, PID, Mittelschmerz, etopic pregnancy, ovarian torsion. Management: In uncomplicated: Once the diagnosis of acute appendicitis is made, patients should be given nil by mouth. Maintenance IV fluids, such as lactated Ringer's solution, should be started. Use of prophylactic antibiotics post op. Appendectomy should be performed without delay. If complicated: Complications of acute appendicitis occur in 4% to 6% of patients and include gangrene with subsequent perforation or intra-abdominal abscess. Initial management includes keeping the patient nil by mouth and starting maintenance IV fluids. If the patient is in shock, they should be given a bolus of IV fluid, such as 0.9% normal saline or lactated Ringer's solution, in order to maintain a stable pulse rate and BP. Intravenous antibiotics should be started immediately and continued until the patient becomes afebrile and the leukocytosis is corrected. In patients with acute peritonitis, appendectomy should be performed without delay. Patients presenting with right lower quadrant abscess should be managed with IV antibiotics and drainage either by interventional radiology (CT-guided drainage) or by operative drainage. If there is clinical improvement and the signs and symptoms are completely resolved, then there is no need for interval appendectomy. Interval appendectomy is performed after 6 weeks if the symptoms are not completely resolved. appendicectomy: open: girdiron incison or Lanz incision: Lanz is more horizotal better scar as in langers lines. Appendix located at convergence of teniae coli. If appendix is normal meckels diverticulum is looked for. open appendectomy is considered to be the safest approach in pregnant women, whereas a laparoscopic approach is considered safest in obese patients.

Question 37

prognosis of appendicitis?

Accepted Answer

1% mortality in perforated appendix

Question 38

Name 5 causes of mass in RIF?

Accepted Answer

psoas abscess, ovarian cyst, ileocacal carcinoma, appendix mass, crohns, mucocele of gallbladder

Question 39

what are 4 positions of the appendix?

Accepted Answer

paracaecal, retrocaecal, post ileal, pre ileal

Question 40

Define gallstones?

Accepted Answer

Cholelithiasis is the presence of cystalline deposits in the gallbladder. Gallstones form in the gallbladder but may exit into the bile ducts (choledocholithiasis). Symptoms ensue if a stone obstructs the cystic or the bile duct. 5 Fs - fair, fat, forty, fertile, female. 90% asymptomatic. Classification of stones: Cholesterol (80%), Pigment (10%), calcium or mixed (10%).

Question 41

Describe the pathophysiology of gallstones? Aetiology of gallstones? 4 things?

Accepted Answer

Cholelithiasis transpires as a result of 3 principal defects: bile supersaturated with cholesterol, accelerated nucleation, and gallbladder hypomotility retaining this abnormal bile. Cholesterol supersaturation of gallbladder bile occurs primarily when the liver secretes excessive amounts of cholesterol, compared to its solubilising agents, bile salts and lecithin. The next stage is precipitation of cholesterol microcrystals in the gallbladder, initiated by the presence of nucleating agents (primarily biliary glycoproteins such as mucin). Impaired gallbladder contractility then facilitates retention, providing time for these microcrystals to agglomerate in a mucin scaffold and grow into overt gallstones. Ninety percent of gallstones are composed of cholesterol; these form in the gallbladder. Some risk factors for the development of cholesterol gallstones are modifiable, such as obesity, total parenteral nutrition, rapid weight loss after bariatric surgery, and medications (e.g., oestrogen, octreotide, clofibrate, ceftriaxone). Others, such as age, genetic factors, and female sex, are immutable. These cholesterol stones that form in the gallbladder can migrate into the common bile duct, as occurs in 10% to 15% of patients presenting for cholecystectomy. Approximately 2% of all gallstones are black pigment stones. The pigment material consists of polymerised calcium bilirubinate. Patients with chronic haemolytic anaemia, cirrhosis, cystic fibrosis, and ileal diseases are at highest risk of developing black pigment stones.Brown pigment gallstones form de novo in bile ducts as a result of stasis and infection. They consist of calcium bilirubinate, calcium salts of long-chain fatty acids, cholesterol, and mucin (glycoproteins primarily from bacterial biofilms). Bacterial infection, biliary parasites (Clonorchis sinensis, Opisthorchis species, and Fasciola hepatica), and stasis (from partial biliary obstruction) are key factors, particularly in Asian people. In developed countries, such bile duct stones more commonly result from biliary strictures, either inflammatory or neoplastic. Aetiology: Obesity - increased hepatic synthesis of cholesterol, Pregnancy - increased oestrogen causes cholestasis. Ileal disease ore resection - bile salt loss. Total parenteral nutrition - gallbladder stasis. Symptoms and complications of cholelithiasis result when stones obstruct the cystic and/or bile ducts. Transient obstruction of the cystic duct results in biliary pain. More persistent obstruction leads to acute cholecystitis. Uncommonly (in 1% of cholecystectomies), a large gallstone becomes impacted in the cystic duct or the neck of the gallbladder, compresses the common bile duct, and causes obstruction and jaundice. Clofibrate – A fibrate drug, this lowers plasma cholesterol by increasing cholesterol secretion in bile.

Question 42

3 types of stone ?

Accepted Answer

mixed 80% - cholesterol bile pigments and calcium salts pigmented - 10% - calicum bilirubinate- associated with haemolytic disorders - malaria cholesterol - 10% large

Question 43

What the name of the triangle associated with gallstones? Preventive strategies for gallstones?

Accepted Answer

Admirand's Triangle - increase risk of stone if decrease lecithin, bile salts and increase cholesterol. Preventative medical therapy employs ursodeoxycholic acid (UDCA) to lower cholesterol saturation in bile and so lessen the short-term risk of stone formation in obese individuals undergoing rapid weight loss through dietary caloric restriction or bariatric surgery.

Question 44

Step by step approach to Gallstones?

Accepted Answer

History: Typical biliary pain occurs in the RUQ or epigastric area, sometimes after consumption of food. This constant pain increases in intensity and lasts for several hours. Pain of short duration (less than 30 minutes) is not biliary colic, while that of long duration (over 12 hours) suggests cholecystitis or another major complication. It is often accompanied by nausea. Choledocholithiasis is most commonly accompanied by jaundice. Tenderness to palpation in the RUQ/epigastric area is the most common abdominal examination feature in patients with symptomatic cholelithiasis. In acute cholecystitis, Murphy’s sign with inspiratory arrest when palpating the gallbladder fossa has a good sensitivity (97%) for acute cholecystitis, but poor specificity (48%). INVESTIGATIONS: FBC, Amylase and LFT, are usually normal with an episode of simple biliary pain. An elevated WBC count suggests acute cholecystitis, cholangitis, or pancreatitis. Obstructive choledocholithiasis is most commonly associated with ALP and bilirubin elevations. The INITIAL TEST OF CHOICE in ALL patients with suspected biliary pain is abdominal USS = GOLD STANDARD. If suspect common bile duct stones (obstructive jaundice picture) then should do EUS or MRCP. An unremarkable abdominal ultrasound in the presence of biliary pain warrants an abdominal CT scan to evaluate for alternative diagnoses. If choledocholithiasis is suspected, magnetic resonance cholangiopancreatography (MRCP) is an excellent non-invasive imaging method with a sensitivity of 92% and specificity of 97%. Endoscopic ultrasound scan (EUS) and MRCP have similar accuracies for the detection of bile duct stones. MRCP, however, has a reduced sensitivity (65%) to detect small (less than 5 mm) biliary stones. ERCP is the preferred intervention for patients with high risk of bile duct stones (positive imaging, symptoms, and/or blood tests). It offers both diagnosis and therapy, removing the stones. ERCP – this is not normally used in uncomplicated gallstone disease. It is often used where the history is very suggestive of gallstones, but no stones can be seen on ultrasound.

Question 45

what % of gallstones are radioopaque?

Accepted Answer

10%

Question 46

what % of stones remain in gallbladder or cystic duct?

Accepted Answer

90

Question 47

what is biliary colic?

Accepted Answer

steady right upper quadrant abdominal pain lasting more than half an hour. stones in biliary duct- causing episodic RUQ pain. Not colicky pain - progressive then constant for 1-4hour until stone passes and is relieved. Pain radiates to back/r shoulder. provoked by fatty foods. nausea and vomiting. acute cholecystitis can occur if infection develops. Unable to get comfortable. Colic is defined as a severe paroxysmal abdominal pain, waxing and waning in intensity, due to spasm, obstruction, or distension of one of the hollow viscera. Biliary colic however is not colicky; the intensity of the pain rises to a crescendo over a period of minutes to an hour and then persists as a constant severe, pain for between one and twenty four hours before resolving. It can wake patients up at Night.

Question 48

What is acute cholecystitis? what is common organism? difference from biliary colic? what clinical sign?

Accepted Answer

impacted stone in hartmanns pouch. E coli. Has inflammatory component (peritonism, fever) epigastric or RUQ pain radiating to shoulder tip. Nausea and vomiting with tachycardia. Murphy's sign. Radiological signs of acute cholecystitis on USS include a thickened gallbladder wall (over 4 mm), an enlarged gallbladder (long axis diameter over 8 cm, short axis diameter over 4 cm), or fluid collection around the gallbladder.

Question 49

whats murphys sign?

Accepted Answer

- 2 fingers over RuQ - pain when inhales stops when exhale(+ve if no pain on Left side). Indicates; cholecystitis.

Question 50

describe histology in chronic cholecystitis? and characteristics?

Accepted Answer

fibrosed and enlarged GB, atrophic mucosa. Fat intolerance, vague abdo discomfort, distension, nausea, flatulence.

Question 51

whats acalculous cholecystitis? 3 causes?

Accepted Answer

inflammed gb without stone. Sepsis, diabetes, burns or fever (increased viscosity)

Question 52

Whats mirrizi's syndrome?

Accepted Answer

Stone impacted in cystic duct- causes GB swelling and CD swelling - compresses CBD - obstructive jaundice

Question 53

name 4 complications of stones in the cbd?

Accepted Answer

obstructive jaundice ascending cholangitis gallstone pancreatitis, gallstone ileus

Question 54

4 signs of obstructive jaundice

Accepted Answer

dark urine, pale stools, pruritus, jaundice

Question 55

What is the key thing for identifying ascending cholangitis? Define ascending cholangitis? Aetiology? Pathophysiology?

Accepted Answer

Ascending cholangitis is the historical term for the condition currently referred to as acute cholangitis or simply as cholangitis. It is an infection of the biliary tree, most commonly caused by obstruction. In its less severe form, there is biliary obstruction with inflammation and bacterial seeding and growth in the biliary tree. It is estimated that 50% to 70% of these patients present with right upper quadrant pain, fever, and jaundice. In the more severe, life-threatening form, known as toxic cholangitis or cholangitis with sepsis, patients have purulent biliary tree contents, as well as evidence of sepsis, hypotension, multi-organ failure, and mental status changes. Cholangitis is relatively uncommon, presenting as a complication in about 1% of cases of cholelithiasis. The median age of presentation is between 50 and 60 years. AETIOLOGY: The most common aetiology of acute cholangitis is cholelithiasis leading to choledocholithiasis and biliary obstruction. Iatrogenic biliary duct injury, most commonly caused via surgical injury during cholecystectomy, can lead to benign strictures, which can in turn lead to obstruction (with or without secondary sclerosing cholangitis). Other causes of benign biliary stricture include chronic pancreatitis (with stenosis and stricture of the distal common bile duct, which has an intrapancreatic course), radiation-induced biliary injury, or biliary injury as a complication of systemic chemotherapy (e.g., fluorodeoxyuridine). Sclerosing cholangitis (primary and secondary) has been shown to cause up to 24% of cases of acute cholangitis. Less common causes of acute cholangitis are acute pancreatitis, parasite entry into the bile ducts (Ascaris lumbricoides or Fasciola hepatica), extrinsic compression of the biliary tree due to adenopathy, fibrosis of the papilla, blood clots, and sump syndrome (a rare complication that can develop following the creation of a choledochoduodenostomy where the distal common bile duct can trap food particles and become a source of biliary infection).Malignant strictures are much less likely to be associated with the development of acute cholangitis, but this can still occur, especially if there has been prior instrumentation of the biliary tree. Malignant biliary strictures most commonly arise due to primary biliary tumours (cholangiocarcinoma), primary gallbladder cancer, ampullary cancer, pancreatic cancer, and, rarely, primary small bowel cancer. PATHOPHYSIOLOGY: Obstruction of the common bile duct initially results in bacterial seeding of the biliary tree, possibly via the portal vein, and when combined with bacterial contamination, can lead to acute cholangitis. Additionally sludge forms, providing a growth medium for the bacteria. As the obstruction progresses, the bile duct pressure increases. This forms a pressure gradient that promotes extravasation of bacteria into the bloodstream. If not recognised and treated, this will lead to sepsis. Charcots triad - rigors(fevers and chills) obstructive jaundice and RUQ pain.

Question 56

Describe the presentation and approach to assessment of patients with ascending cholangitis? 2 complications of ascending cholangitis?

Accepted Answer

It is diagnosed based on typical history and laboratory findings and confirmed by imaging, ERCP, or percutaneous biliary drainage in patients who cannot undergo ERCP. Patients with acute cholangitis are usually over 50 years of age. Their past medical history may be positive for gallstones, prior ERCP, surgical or radiological biliary tree intervention, and/or HIV. A current history of acholic stools, pruritus, and jaundice is often found. Fever and RUQ pain are present in 65% to 90% of patients, though fever can be absent in older patients (those over 60 years old); 65% of patients will have RUQ tenderness. Jaundice is present in 60% to 70% of patients. Hypotension is present in 30% of patients. Mental status changes occur in about 15% of patients. Hypotension and mental status changes are indicative of severe disease and are associated with a poor prognosis. Tests: FBC (WCC is increased), CRP is increased. LFTs: hyperbilirubinaemia is almost always present and, if absent, cholangitis is less likely to be the true diagnosis. Abnormal liver tests are usual findings, with raised serum alkaline phosphatase and transaminases being typical. Urea and creatinine: raised renal function parameters are more common in severe disease states. Electrolytes plus magnesium: possible decreases of serum potassium and magnesium. Coagulation profile: abnormalities can include decreased platelets and raised prothrombin time. ABG analysis (additional if there is concern about systemic sepsis): metabolic acidosis is common in severe disease states. Blood culture: positive blood culture rates among patients with acute cholangitis range from 21% to 71%. Bacteria are usually gram-negative, but gram-positive bacteria and anaerobes are also implicated in cholangitis. Transabdominal ultrasound should be ordered in all patients presenting with RUQ pain and suspected cholangitis. It is a quick, easy, and inexpensive test for use as the initial diagnostic imaging modality in this circumstance. Accuracy of detecting common bile duct (CBD) dilation is over 90%, although the diameter of the CBD becomes a less useful parameter in patients who have previously undergone cholecystectomy, as physiological dilation of the CBD can occur in this setting. Transabdominal ultrasound has a poor sensitivity for detecting mid to distal CBD stones. Abdominal CT scan with intravenous (IV) contrast should be ordered if there is high clinical suspicion of cholangitis and ultrasound is negative. It provides better anatomical detail of the biliary tree than transabdominal ultrasound. It is particularly useful to visualise the distal part of the CBD. If neoplasm is suspected as the cause of cholangitis, this test is a better initial imaging choice. Patients with a history of biliary disease, an indwelling biliary prosthesis, or other predisposing factors should be considered for early ERCP for rapid diagnosis and therapy. If ERCP is not available or impossible to perform (e.g., post-Roux-en-Y gastric bypass, presence of oesophageal, pyloric or duodenal stricture), percutaneous trans-hepatic cholangiography (PTC) can provide direct evaluation of the biliary tree. Abdominal MRI with MRCP represents another non-invasive imaging modality with good sensitivity and specificity for the diagnosis of biliary obstruction. It should be ordered if ultrasound and CT are negative and a high clinical suspicion remains for cholangitis. Endoscopic ultrasound (EUS) is as accurate as MRI with MRCP for the detection of choledocholithiasis. Complications: liver abscess, acute pancreatitis and septicaemia. Life threatening urgent decompression needed with ercp or surgery.

Question 57

What is gallstone that causes gastric outlet obstruction called? Management of ascending cholangitis?

Accepted Answer

Bouveret's syndrome. Management: acute: 1st IV antiBs and usually managed in the intensive care setting. Patients with a deteriorating status despite initial antibiotic treatment and intensive medical management require these decompression interventions be undertaken in an emergent manner, within the first 12 to 24 hours following admission. Signs of status worsening include: persistent abdominal pain or hypotension despite intravenous (IV) fluid administration, fever over 39°C (102°F), or a worsening confusional state. For those patients responsive to initial treatment (i.e., not evidencing the signs of deterioration noted above), these interventions can be undertaken in a less urgent timeframe, the following 24 to 48 hours, lessening the risks of adverse consequences associated with the procedure. Biliary decompression and drainage are necessary to allow for antibiotic delivery. ERCP with sphincterotomy, duct clearance, and/or stenting is the first-line therapy for ascending cholangitis. Percutaneous trans-hepatic cholangiography (PTC) is performed initially for those who are poor ERCP candidates (e.g., status post-Roux-en-Y gastric bypass, presence of oesophageal stricture) or in those who do not obtain relief of bile duct obstruction from ERCP performance. Nasobiliary catheter insertion by ERCP with decompression by aspiration is an option for patients too unwell to undergo either ERCP with sphincterotomy or PTC, or for those who do not obtain adequate drainage subsequent to performance of one or the other of those procedures. For bile duct stones that are large or difficult to remove, endoscopic lithotripsy may be performed. opoid analgesia are used. 2nd Line: surgical decompression: If adequate biliary decompression/drainage is not accomplished via non-operative means, choledochotomy with T-tube placement or cholecystectomy with common bile duct exploration may need to be performed.

Question 58

Tx of gallstones?

Accepted Answer

If symptomatic then cholecystectomy. Choledocholithiasis with or without symptoms then 1st line is ERCP. Because: The combination of biliary pain and abnormal liver biochemistry (particularly an elevated bilirubin) suggests that a stone may have migrated into the common duct. Documented bile duct stones on ultrasonography, evidence of acute cholangitis, a dilated common duct (over 6 mm), or a markedly elevated bilirubin (over 68 µmol/L or over 4 g/dL) indicates choledocholithiasis. Documented bile duct stones warrant treatment since they are associated with developing serious complications such as acute cholangitis, pancreatitis, or hepatic abscesses. ERCP with biliary sphincterotomy and stone extraction is the treatment of choice. In about 10% to 15% of patients, sphincterotomy with standard extraction techniques is not successful, usually due to the characteristics of the stone, being large (over 1.5 cm), impacted, or located proximal to a stricture. These circumstances require lithotripsy (fragmentation), papillary balloon dilation, and long-term biliary stenting. Laparoscopic common bile duct exploration, though technically difficult, is as effective as ERCP performed prior to or after cholecystectomy with regards to stone clearance, and has similar rates of mortality and morbidity. Laparoscopic common bile duct exploration should be considered in patients with surgically altered anatomy (e.g., gastric surgery) or failed ERCP. For those at an intermediate risk of a common duct stone (abnormal liver biochemistry with more modest bilirubin elevations; biliary pancreatitis; and age over 55 years), initial cholecystectomy with intraoperative cholangiography and common duct exploration may shorten hospitalisation without increasing complications. If ongoing asymptomatic cholelithiasis 1st line is observational, but Prophylactic cholecystectomy in asymptomatic individuals might be considered in 2 situations: a heightened risk of developing gallbladder carcinoma (either harbouring large gallstones [over 3 cm] or possessing a calcified 'porcelain' gallbladder) or when the risk of gallstone formation and its complications are high (the severely obese undergoing bariatric surgery and those with sickle cell disease). Lifestyle: decrease fatty foods, increase exercise. Cholecystectomy is the ultimate as many patients have recurrence of symptoms. The timing of cholecystectomy in patients with acute cholecystitisis also controversial. Although the traditional belief was to allow the inflammation to settle and perform laparoscopic cholecystectomy after a period of at leastsix weeks, a systematic review on this topic has shown that early laparoscopic cholecystectomy performed within one week of onset of symptoms can avoid further complications from gallstones while waiting for surgery.

Question 59

tx of biliary colic?

Accepted Answer

early cholecystectomy

Question 60

conservative tx of gallstones? 4 things

Accepted Answer

fluid managemant, nbm, AntiB, analgesia.

Question 61

ERCP indications?

Accepted Answer

Choledocholithiasis, Acute pancreatitis due to biliary obstruction, sphincter of Oddi dysfunction or idiopathic, recurrent cases. Detection of pancreatic divisum (more common in patients who develop pancreatitis but may not necessarily be causal). Diagnosis of pancreatic and biliary malignancy. Endoscopic ultrasound provides an acceptable option in many cases and can be used as a triage procedure to determine which patients should proceed to ERCP (see below). Palliative therapy for inoperable pancreaticobiliary malignancies - eg, drainage procedures. Dilatation of benign strictures - eg, following orthoptic liver transplantation. Chronic pancreatitis - very controversial but there may be a role for dilatation of strictures or stent insertion. Manometry measures in sphincter of Oddi dysfunction. Emergency procedure if ascending cholangitis is suspected and need to remove ductal stones

Question 62

Define Acute cholecystitis? Describe the Epideems. Aetiology? Approach to assessment?

Accepted Answer

Acute cholecystitis is acute gallbladder inflammation, and one of the major complications of cholelithiasis. In most cases (90%), it is caused by complete cystic duct obstruction usually due to an impacted gallstone in the gallbladder neck or cystic duct. In 5% of cases, bile inspissation (due to dehydration) or bile stasis (due to trauma or severe systemic illness) can block the cystic duct, causing an acalculous cholecystitis. Acute acalculous cholecystitis accounts for 5% to 14% of cases of acute cholecystitis. The incidence is higher in the intensive-care population, particularly in patients in burn and trauma units. AETIOLOGY: At least 90% of patients with the condition have gallstones. Helminthic (parasitic worms) infection is one of the major causes of biliary disease in Asia, southern Africa, and Latin America. AIDS-related cholecystitis and cholangiopathy may be secondary to CMV and Cryptosporidium organisms. Various micro-organisms can be identified early in the onset of disease. These include Escherichia coli, Klebsiella, enterococci, Pseudomonas, and Bacteroides fragilis. It has been suggested that this bacterial invasion is not a primary perpetrator of injury, because in over 40% of patients no bacterial growth is obtained from surgical specimens. Generally, bacterial infection is a secondary feature and not an initiating event. Occasionally, acute cholecystitis occurs in the absence of gallstones. Starvation, total parenteral nutrition, narcotic analgesics, and immobility are predisposing factors for acalculous acute cholecystitis. Secondary infection with gram-negative flora occurs in most cases. PATHOPHYSIOLOGY: The pathophysiology of acalculous cholecystitis is poorly understood, but it is probably multi-factorial. Functional cystic duct obstruction is often present and related to biliary sludge or bile inspissation caused by dehydration or bile stasis (due to trauma or systemic illness). Occasionally, extrinsic compression may play a role in the development of bile stasis. CLASSIFICATION: calculous, and acalculous. Can also get Oedematous (occurs first 2 to 4 days: Gallbladder tissue is intact histologically, with oedema in the subserosal layer). Necrotising: 3 to 5 days: Oedema with areas of haemorrhage and necrosis. Necrosis does not involve the full thickness of the wall. Suppurative: 7 to 10 days: WBCs present within the gallbladder wall, with areas of necrosis and suppuration: Intra-wall abscesses involving the entire thickness of the wall. Chronic: Occurs after repeated episodes of mild attacks: Mucosal atrophy and fibrosis of the gallbladder wall. Emphysematous: Air appears in the gallbladder wall due to infection with gas-forming anaerobes. Often found in diabetic patients. HISTORY: Patients typically complain of nausea and pain that lasts more than 3 to 6 hours, which is unremitting and may be associated with fever. The pain is severe and steady. The duration of pain can be shorter if the gallstone returns into the gallbladder lumen or passes into the duodenum. EXAMINATION: Physical examination may reveal RUQ tenderness or a palpable mass. A positive Murphy's sign (the examiner's hand rests along the costal margin and deep inspiration causes pain) has a specificity of 79% to 96% for acute cholecystitis. Persistent pain, fever, chills, and more severe localised or generalised tenderness may indicate complicated disease (e.g., abscess formation or gallbladder perforation). Acalculous cholecystitis is more difficult to diagnose clinically, as it often occurs in critically ill patients who may not be able to express pain. Patients receiving total parenteral nutrition are at increased risk. Fever, jaundice, vomiting, abdominal tenderness, leukocytosis, and hyperbilirubinaemia should lead to a high index of clinical suspicion. Typically acalculous cholecystitis is a diagnosis of exclusion. TESTS: FBC and C-reactive protein (CRP) should be assessed to look for evidence of an inflammatory process. Liver function tests (LFTs) may show elevated bilirubin, alkaline phosphatase, and gamma-GT. IMAGING: RUQ ultrasound should be the first test ordered and can be performed at the patient's bedside. Detection of gallstones alone does not definitively diagnose the condition. To make an accurate diagnosis, there must be stones and an ultrasonographic Murphy's sign. About 92% of patients with a positive Murphy's sign in the presence of gallstones have the condition. Scintigraphy with hepatobiliary iminodiacetic acid (HIDA) scan should be obtained if ultrasound results are equivocal. Abdominal CT scan is inferior to ultrasound in assessing acute biliary disease, but it is useful when obesity or gaseous distension limits ultrasound interpretation. It is also indicated for evaluation of suspected complications (such as abscess) and concurrent intra-abdominal conditions. Abdominal MRI is appropriate for pregnant patients with abdominal pain.

Question 63

name 4 complications of ercp?

Accepted Answer

perforation of duodenum or biliary tree, haemorrhage, acute pancreatitis, cholangitis. Pancreatitis - 2-9% of patients will develop pancreatitis and it is seen especially in endoscopic sphincterotomy for sphincter of Oddi dysfunction. It is the most common complication.

Question 64

Treatment of cholecystitis?

Accepted Answer

TREATMENT: When a diagnosis of acute cholecystitis is suspected, medical treatment, including NPO, intravenous fluids, antibiotics, and analgesia, together with close monitoring of blood pressure, pulse, and urinary output, should be initiated. Simultaneously, the grade of severity needs to be established. Mild (grade I): Defined as acute cholecystitis in a healthy patient with no organ dysfunction and mild inflammatory changes in the gallbladder; responds to initial medical treatment. Supportive Medical treatment above may be sufficient, and urgent surgery may not be required. Oral antiBs can be used. Non-steroidal anti-inflammatory drugs (NSAIDs) such as diclofenac or indomethacin are recommended as part of the medical treatment for their analgesic effects and their inhibition of prostaglandin release from the gallbladder wall. For patients with mild cholecystitis, the Tokyo guidelines state that early laparoscopic cholecystectomy (ELC) is the preferred treatment. ELC (within 72 hours of onset of symptoms) has a clear benefit compared with delayed cholecystectomy (over 6 weeks after index admission) in terms of complication rate, cost, quality of life, and hospital stay. If medical management fails, and patients are poor surgical candidates (e.g., medically not fit for surgery), a percutaneous cholecystostomy tube should be considered. Moderate (grade II): Defined as acute cholecystitis associated with any one of the following: elevated white blood cell count (over 18,000/microlitre), palpable tender mass in the right upper abdominal quadrant, duration of complaints over 72 hours, and marked local inflammation (gangrenous cholecystitis, pericholecystic abscess, hepatic abscess, biliary peritonitis, emphysematous cholecystitis). Same supportive measures as above plus IV antiBs should be used and NSAIDS. Early Laparoscopic cholecystectomy or percutaneous cholecystostomy with delayed cholecystectomy should be done if don't respond to medical treatment. Moderate-grade cholecystitis usually does not respond to the initial medical treatment. Severe (grade III): Defined as organ dysfunction in at least any one of the following organs/systems of cardiovascular (hypotension requiring treatment with dopamine over or equal to 5 micrograms/kg per minute, or any dose of noradrenaline [norepinephrine]), CNS (decreased level of consciousness), respiratory (PaO2/FiO2 ratio 176.8 micromols/L [over 2.0 mg/dL]), hepatic (INR over 1.5), or haematological (platelet count renal (oliguria, creatinine over 176.8 micromols/L [over 2.0 mg/dL]), hepatic (INR over 1.5), or haematological (platelet count less than 100,000 cells/microlitre), and/or severe local inflammation. Intensive supportive care is required to monitor and treat organ dysfunction. Requires urgent management of severe local inflammation by percutaneous gallbladder drainage (i.e., percutaneous cholecystostomy tube) followed where indicated by delayed elective cholecystectomy 2 to 3 months later, when the patient's general condition has improved.

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