Surgery Flashcards
what are the factors predisposing to gastrooesophageal disease
Pregnancy, obesity, diet (fat, chocolate, alcohol, coffee, large meals), smoking, drugs (anticholinergics, tricyclics, nitrates, ca channel blockers), systemic sclerosis, treatment for achalasia, hiatus hernia
which drugs predispose to gastrooesophageal disease
(anticholinergics, tricyclics, nitrates, ca channel blockers)
symptoms of hiatal hernia
For most people, a hiatal hernia by itself causes no symptoms.
Chest pain or pressure Heartburn Difficulty swallowing Coughing Belching Hiccups
what types of hiatal hernia are there? prevelence?
Sliding, 30% adults over 50, oesopheal-gastric junction slides above hiatus.
Rolling, part of fundus of stomach slides alongside oesophagus. Approx 5-15% of hiatus hernias are this type
Risk factors for hiatus hernia
age, obesity, and smoking
What advice could be given to pts experiencing GORD symptoms
Lose any excess weight
Stop smoking
Avoid bending or stooping
Raise the head of your bet
Avoid large meals - particularly hot and spicy foods
Avoid any foods that you notice cause heartburn
Avoid fats and chocolates, cut down on alcohol
Avoid pressure on the stomach - for example from tight clothes like corsets
what are the features of a barium swallow/meal
The barium meal X-ray, also called the barium swallow test, is one of the most effective ways of identifying a hiatus hernia.
As part of the test you will be asked to drink some barium solution. Barium is a non-toxic chemical that shows up clearly on an X-ray. Once the barium moves down into your digestive system a series of X-rays will be taken to identify any problems.
If you need to have a barium meal X-ray, you will not be able to eat or drink anything for at least six hours before the procedure so that your stomach and duodenum (top of the small intestine) are empty. You may be given an injection to relax the muscles in your digestive system.
You will be given a white, chalky liquid containing barium to drink while lying down. This means your specialist will be able to see your stomach on an X-ray monitor more easily, as well as any ulcers or abnormal growths. Your bed may be tipped slightly during the test so that the barium fills all the areas of your stomach.
A barium swallow usually takes about 15 minutes to perform. Afterwards you will be able to eat and drink as normal, although you may need to drink more water to help flush the barium out of your system.
You may feel slightly sick after a barium meal X-ray and the barium may cause constipation. Your stools may also be white for a few days afterwards as the barium passes through your system.
What medication can somebody with GORD be treated with
Medication
A number of different medications can be used to treat symptoms of hiatus hernia. These are described below.
Antacids
Antacid medicines can relieve some of the symptoms of hiatus hernia. They come in liquid or tablet form and can be swallowed or chewed. They help neutralise stomach acid when they reach the oesophagus and stomach by making it less acidic. eg gaviscon/milk of magnesia
Antacids should not be taken at the same time as other medicines because they can stop other medicines from being properly absorbed by your body. They may also damage the special coating on some types of tablets. Ask your GP or pharmacist for advice.
Alginates
Alginates are an alternative medicine to antacids. They work by producing a protective coating that shields the lining of your stomach and oesophagus from the effects of stomach acid. eg gaviscon
H2-receptor antagonists
In some cases, a medicine known as an H2-receptor antagonist (H2RA) may be recommended if a hiatus hernia is causing GORD. Examples of H2RAs include cimetidine, famotidine and ranitidine.
H2RAs block the effects of the chemical histamine, which your body uses to produce stomach acid. H2RAs therefore help reduce the amount of acid in your stomach.
Side effects of H2RAs are uncommon. However, possible side effects may include diarrhoea, headaches, tiredness and a rash.
Some H2RAs are available over the counter at pharmacies. These types of HR2As are taken in a lower dosage than the ones available on prescription. Ask your GP or pharmacist if you are not sure whether these medicines are suitable for you.
Proton-pump inhibitors (PPIs)
Your GP may prescribe a medication called a proton-pump inhibitor (PPI). PPIs work by reducing the amount of acid produced by your stomach. Examples of the PPIs you may be prescribed include omeprazole, lansoprazole, rabeprazole and esomeprazole.
Most people tolerate PPI well and side effects are uncommon. When they do occur they are usually mild and may include headaches, diarrhoea, feeling sick, or constipation.
To minimise any side effects, your GP will prescribe the lowest possible dose of PPIs they think will be effective. You should let your GP know if the prescribed dose of PPIs doesn’t work. A stronger dose may be needed.
Prokinetics
If your symptoms are not responding to other forms of treatment, your GP may prescribe a short-term dose of a prokinetic. Examples of prokinetic medicines include domperidone and metoclopramide.
what surgical options are available to treat hiatus hernia/gord
Surgery is usually only recommended for a sliding hiatus hernia if the problem fails to respond to lifestyle changes and medication.
You may also wish to consider surgery if you have persistent and troublesome symptoms but do not want to take medication on a long-term basis.
Prior to surgery you may need further investigations to check how well the oesophagus moves (manometry) and how much acid is being refluxed (24-hour oesopageal pH studies).
Laparoscopic nissen fundoplication (LNF)
A procedure called a laparoscopic nissen fundoplication (LNF) is one of the most common surgical techniques used to treat GORD and sliding hiatus hernias.
LNF is a type of keyhole surgery that involves making a series of small cuts in your abdomen. Carbon dioxide gas is used to inflate your abdomen to give the surgeon room to work in.
During LNF, the stomach is put back into the correct position and the diaphragm around the lower part of the oesophagus is tightened. This should prevent any acid moving back out of your stomach.
LNF is carried out under general anaesthetic, so you will not feel any pain or discomfort. The surgery takes 60 to 90 minutes to complete.
After having LNF, most people can leave hospital once they have recovered from the effects of the general anaesthetic. This is usually within two to three days. Depending on the type of job you do, you should be able to return to work within three to six weeks.
For the first six weeks after surgery it is recommended you only eat soft food, such as mince, mashed potatoes or soup. Avoid eating hard food that could get stuck at the site of the surgery, such as toast, chicken or steak.
Common side effects of LNF include difficulties swallowing (dysphagia), belching, bloating and flatulence.
These side effects should resolve over the course of a few months. However, in about 1 in 100 cases they can be persistent. In such circumstances, further corrective surgery may be required.
what are the clinical features of GORD
HEARTBURN/INDIGESTION worse on bending over/lying down, worse on drinking hot liquids/alcohol, relieved by antacids
Regurg of food/acid, worse when bending/lying
Belching
Acid/bile regurg
waterbrash (sudden filling of mouth with saliva, often accompanying dyspepsia
odynophagia (painful swallowing)
recent weight gain
woken at night, regurg fluid irritating larynx
atypical chest pain, distal oesophageal muscle spasm
Can contribute to asthma and cause nocturnal wheeze/cough
What are the red flags/indications for endoscopy in a patient presenting with GORD
>55 >4 weeks symptoms dysphagia persistent symptoms despite treatment relapsing symptoms weight loss
what further investigations additional to endoscopy could be performed on a patient with GORD?
barium swallow, demonstrate hernia
24 hour luminal pH monitoring combined with manometry will diagnose GORD when endoscopy normal. Do prior to surgery to exclude dysmotility
Risk factors for inguinal hernia
Children prematurity, male
In adults: male sex, obesity, constipation, chronic cough, heavy lifting.
Complications hernia surgery
Recurrence: 1.0% - most happening within five years of operation. Recurrence rate increases:
In children aged younger than 1 year
In elderly patients
After incarcerations
In those with ongoing increased intra-abdominal pressure
Where there is growth failure
With prematurity
Where there are chronic respiratory problems
In girls with sliding hernias
Infarcted testis or ovary with atrophy.
Wound infection.
Bladder injury.
Intestinal injury.
A hydrocele from fluid accumulation in the distal sac usually resolves spontaneously but sometimes requires aspiration.
Ddx groin swelling
Skin (sebaceous cyst) Subcut (benign growths eg lipoma/fibroma) Arterial (femoral aneurysm) Venous (saphena varix) Muscle (psoas abscess) Other hernia Ectopic testes
What are the surgical treatment options for hernia repair
Open hernia repair. During an open hernia repair, a health care provider usually gives a patient local anesthesia in the abdomen with sedation; however, some patients may have
sedation with a spinal block, in which a health care provider injects anesthetics around the nerves in the spine, making the body numb from the waist down
general anesthesia
The surgeon makes an incision in the groin, moves the hernia back into the abdomen, and reinforces the abdominal wall with stitches. Usually the surgeon also reinforces the weak area with a synthetic mesh or “screen” to provide additional support.
Laparoscopic hernia repair. A surgeon performs laparoscopic hernia repair with the patient under general anesthesia. The surgeon makes several small, half-inch incisions in the lower abdomen and inserts a laparoscope—a thin tube with a tiny video camera attached. The camera sends a magnified image from inside the body to a video monitor, giving the surgeon a close-up view of the hernia and surrounding tissue. While watching the monitor, the surgeon repairs the hernia using synthetic mesh or “screen.”
People who undergo laparoscopic hernia repair generally experience a shorter recovery time than those who have an open hernia repair. However, the surgeon may determine that laparoscopy is not the best option if the hernia is large or if the person has had previous pelvic surgery.
Symptoms diverticulosis. How does it differ in definition from diverticular disease
Often no symptoms although commonly unexplained painful cramps, bowel movement disturbances(more often constipation than diarrhoea) and painless blood in the stool. Diverticular disease is diverticulosis with symptoms
Symptoms diverticulitis
pain in the abdomen, usually in the lower left side; bleeding, bright red or maroon blood may appear in the toilet, on the toilet paper, or in the stool. Bleeding is often mild and usually stops by itself; however, it can become severe fever; nausea; vomiting; chills; and constipation (less often, diarrhea). Palpable mass/abdo distension
Which symptoms could suggest a serious complication of diverticulitis
worsening abdominal pain;
persistent fever;
vomiting (no food or liquid can be tolerated);
constipation for an extended period of time;
burning or pain during urination/air in urine
bleeding from the rectum.
Treatment of diverticulitis
High-fiber diet: Some health care practitioners recommend a fiber supplement to prevent constipation.
Clear fluids
Mild pain medications
Treatment for diverticulitis depends on the severity of the condition.
Simple cases can be treated by a health care practitioner at his or her office.
Treatment for uncomplicated cases usually consists of antibiotics and bowel rest. This usually involves two to three days of bowel rest, taking in only clear fluids (no food at all), so the colon may heal without having to work.
Complicated cases typically involve severe pain, fever, or bleeding. If an individual has any of these symptoms, he or she will probably be admitted to the hospital. Treatment consists of IV antibiotics, bowel rest, and possibly surgery.
What are the possible complications of diverticulitis
Perforation: A hole in the intestine caused when the diverticular pouch bursts because of increased pressure and infection within the intestine.
Peritonitis: A more serious infection of the abdominal cavity that often occurs after perforation, when the contents of the intestine leak out into the abdominal cavity (peritoneum) outside of the intestine.
Abscess: A pocket of infection that is very difficult to cure with antibiotics.
Fistula: An abnormal connection between the colon and another organ that occurs when the colon damaged by infection comes in contact with another tissue, such as the bladder, the small intestine, or the inside of the abdominal wall, and sticks to it. Fecal material from the colon can then get into the other tissue. This often causes a severe infection. If fecal material gets into the bladder, for example, the resulting urinary tract infection can become recurrent and very difficult to cure. Symptoms of uti and air in urine
Blockage or obstruction of the intestine
Prevalence of diverticulosis
A smal percentage of Americans over the age of 40 have diverticulosis. As we age, the condition becomes more prevalent. Over half of people older than 60 years of age develop the condition, and about two-thirds of individuals older than 80 years of age are believed to have diverticulosis.
What is courvoiser’s law?
Courvoisier’s law states that, in the presence of jaundice, an enlarged gallbladder is unlikely to be due to gallstones; rather carcinoma of the pancreas or the lower biliary tree is more likely.
This may be explained by the observation that the gallbladder with stones is usually chronically fibrosed and so, incapable of enlargement.
The converse of Courvoisier’s law is not true; the cause of jaundice in a patient with a non-palpable gallbladder is not necessarily gallstones as 50% of dilated gallbladders are impalpable
How can you tell the difference between an enlarged kidney/enlarged spleen?
In the upper abdomen the main areas percussed are the liver and spleen. Note that percussion over the kidneys which are retroperitoneal organs with bowel gas anterior to them will be resonant and this can help the examiner differentiate between an enlarged left kidney and spleen. Dullness over the suprapubic region is usually due to an enlarged bladder
What are the stigmata of CLD?
. Jaundice
chronic liver disease
jaundice – in chronic liver disease
2. Fetor hepaticus ; also known as breath of the dead or hepatic foetor
- asterixis : flapping tremor
asterixis, flapping tremor - spider naevi
spider naevi, web spider, chronic liver disease
5. palmar erythema palmar erythema palmar erythema 6. clubbing 7. gynaecomastia gynaecomastia gynaecomastia 8. testicular atrophy 9. splenomegaly 10. bruises
causes of splenomegaly
Removal of defective RBCs spherocytosis thalassemia hemoglobinopathies nutritional anemias early sickle cell anemia Immune hyperplasia
Response to infection (viral, bacterial, fungal, parasitic)
mononucleosis, AIDS,[5] viral hepatitis subacute bacterial endocarditis, bacterial septicemia splenic abscess, typhoid fever brucellosis, leptospirosis, tuberculosis histoplasmosis malaria, leishmaniasis, trypanosomiasis ehrlichiosis[6] Disordered immunoregulation
rheumatoid arthritis Systemic lupus erythematosus serum sickness autoimmune hemolytic anemia sarcoidosis drug reactions Extramedullary hematopoiesis
myelofibrosis marrow infiltration by tumors, leukemias marrow damage by radiation, toxins Organ Failure cirrhosis Vascular
hepatic vein obstruction portal vein obstruction Budd–Chiari syndrome splenic vein obstruction Infections
hepatic schistosomiasis
hepatic echinococcosis
What are the causes of jaundice?
f an infection or medical condition makes the red blood cells break down sooner than usual, bilirubin levels rise. This is known as pre-hepatic jaundice.
Conditions which may trigger this include malaria, sickle cell anaemia, thalassaemia, Gilbert’s syndrome, hereditary spherocytosis and Crigler-Najjar syndrome.
Intra-hepatic jaundice
If the liver is damaged, it may be less able to process bilirubin. This causes what doctors call intra-hepatic jaundice.
The liver damage may be a result of causes that include hepatitis, alcoholic liver disease, glandular fever, liver cancer, illegal drug use including ecstasy, and paracetamol overdose.
Obesity and non-alcoholic fatty liver disease can be a cause of cirrhosis of the liver and jaundice.
Post-hepatic jaundice
Gallstones, pancreatitis, pancreatic cancer and cancers of the gallbladder or bile duct may also disrupt the bilirubin removal process leading to jaundice. This is called post-hepatic jaundice.
Eating a high-fat diet can raise your cholesterol levels and increase the risk of having gallstones.
Causes of hepatomegaly
An infection such as a from a virus or abscess
Certain medications
Toxins
Certain types of hepatitis, including alcoholic hepatitis
Autoimmune disease
Metabolic syndrome
Genetic disorders that cause fat, protein, or other substances to build up
Abnormal growths may cause an enlarged liver. This may result from:
Cysts
Tumors that start or spread to the liver
A problem with blood flow can cause the liver to enlarge. This may be due to a variety of conditions such as:
Congestive heart failure, a condition where the heart fails to pump blood well
Hepatic vein thrombosis, a blockage of veins in the liver
Veno-occlusive disease, a blockage of small veins in the liver
what are the treatment options for varicose veins
Self-help
Your doctor may suggest some self-help measures you can take to relieve your symptoms. These may include losing any excess weight and doing light to moderate physical activity, such as swimming or walking. Try not to stand for long periods of time as this may make your symptoms worse. If you rest your legs up on a stool, it may ease any discomfort. .
Non-surgical treatments
There are a number of non-surgical procedures available to treat varicose veins. If you have complications of varicose veins, you may be able to have these on the NHS. If you want treatment for cosmetic reasons, it’s unlikely you will be able to have this on the NHS. However, you can choose to pay for treatment privately.
Endothermal ablation
Endothermal ablation procedures include radiofrequency ablation and endovenous laser ablation. In these procedures, your doctor uses either an electrical current (radiofrequency ablation) or a laser (endovenous laser ablation) to heat the inside of your varicose vein. This damages the vein and causes it to close.
Endothermal ablation procedures are less invasive alternatives to traditional surgery for varicose veins and for this reason, will now usually be offered to you first. They can be carried out under local anaesthetic and you may have less bruising and swelling after these procedures than after surgery. However, it’s still common to have some side-effects from these procedures, such as bruising and tightness in your legs. Common complications also include some inflammation, darkening or reddening of your skin and pins and needles in your legs.
There is evidence to show that these procedures may help to reduce your symptoms for up to three years after the procedure. However, as they are relatively new treatments, longer term data isn’t yet available. As with any treatment for varicose veins, you may need to have further treatment if your varicose veins come back.
Foam sclerotherapy
If endothermal procedures are unsuitable for you, your doctor may recommend you have foam sclerotherapy. This treatment involves injecting a foam into your varicose veins. This damages your veins and causes them to close.
Foam sclerotherapy may help to get rid of your varicose veins. Like the endothermal procedures, it is less invasive than surgery and can be done under local anaesthetic. However, there is a possibility that your varicose veins may come back and you may need further treatment.
Your doctor will talk to you about the risks involved in this procedure to make sure you are aware of the potential complications. There have been reports of mild complications after foam sclerotherapy, such as chest tightness, headaches, coughing and problems with vision. However, these aren’t common and are usually only temporary. More serious complications such as stroke, nerve damage, seizures and heart attack have occasionally been reported in some people after having sclerotherapy. However these complications are rare and may be due to existing health problems.
Another type of sclerotherapy, called liquid sclerotherapy, is sometimes used in the treatment of smaller varicose veins. It’s usually used alongside other treatments. However, there is little evidence to confirm how well liquid sclerotherapy works.
Surgery
If less invasive procedures are unsuitable for you, your doctor may suggest you have varicose vein surgery. In varicose vein surgery, your surgeon will remove any superficial veins that have become varicose veins. The veins that are situated deep within your legs will take over the role of the damaged veins.
This most common technique for varicose vein surgery is called ligation and stripping. This is usually carried out under general anaesthesia. In this operation, your surgeon will tie off the faulty vein (ligation) to stop blood flowing through it and then remove it (stripping). You may have a procedure called phlebectomy with ligation and stripping to remove the smaller surface veins that lie under your skin. In this operation, your surgeon will use hooks to pull out your varicose veins through small cuts in your leg.
Surgery is considered to be beneficial and relatively safe over the long term. However, it’s still common to have some side-effects, such as bruising and pins and needles in your legs. More serious side-effects are uncommon, but can include deep vein thrombosis (DVT) and pulmonary embolism. Although many people won’t need any further treatment after surgery, it’s possible that new varicose veins can form.
Compression stockings
If the treatments above aren’t suitable for you, your doctor may suggest you try compression stockings. You may also be offered compression stockings to wear after having a procedure or surgery. Compression stockings can help the blood in your veins flow up towards your heart. The stockings may relieve the swelling and aching in your legs. However, there is no evidence to show whether they help to stop your varicose veins getting worse, or more varicose veins from developing.
Red flags for bowel ca 2ww
Refer urgently if red flag symptoms or signs are present.
In particular, refer people who meet the following criteria, under 2-week wait rules for suspected colorectal cancer:
Symptoms suggestive of colorectal or anal cancer.
Aged 40 years or older, reporting rectal bleeding with a change of bowel habit towards looser stools and/or increased stool frequency persisting for 6 weeks or more.
Presenting with a right lower abdominal mass consistent with involvement of the large bowel.
Presenting with a palpable rectal mass (intraluminal and not pelvic).
Aged 60 years or older, with a change in bowel habit to looser stools and/or more frequent stools persisting for 6 weeks or more with or without rectal bleeding.
Men of any age with unexplained iron deficiency anaemia and a haemoglobin level of 11 g/100 mL or less.
Non-menstruating women with unexplained iron deficiency anaemia and a haemoglobin level of 10 g/100 mL or less.
tests for chronic diarrhoea
Full blood count — to detect anaemia or raised platelet count suggesting inflammation.
Liver function tests, including albumin level.
Tests for malabsorption:
Calcium.
Vitamin B12 and red blood cell folate.
Iron status (ferritin).
Thyroid function tests.
Amylase (chronic panc)
ESR (erythrocyte sedimentation rate) and CRP (C-reactive protein) — elevated levels may indicate inflammatory bowel disease.
Antibody testing for coeliac disease — immunoglobulin (Ig)A tissue transglutaminase antibody (tTGA), or IgA endomysial antibody (EMA).
Consider stool sample ovum cysts parasites (3 samples 2-3 days apart) consider stool sample for c diff
Presentation of chronic pancreatitis
Abdominal pain. Classically, epigastric pain radiating into the back. The pathogenesis of this pain is not understood but pancreatic duct obstruction from one of the complications of chronic pancreatitis may be one cause.[1] Usually the pain is very severe, which often requires opiates in the acute setting. In some cases pain may not be the major feature.
Nausea and vomiting.
Decreased appetite.
Exocrine dysfunction. Malabsorption with weight loss, diarrhoea, steatorrhoea (pale, loose, offensive stools that are difficult to flush) and protein deficiency.
Endocrine dysfunction. Diabetes mellitus and its associated morbidity and mortality.
Examination can be largely unremarkable apart from tenderness in the abdomen.
Risk factors for c diff infection
The main risk factors for Clostridium difficile infection are [National Clostridium difficile Standards Group, 2003]:
Advanced age — the rate of positive C. difficile assay results in people older than 65 years of age is 20–100 times greater than the rate in people 10–20 years of age.
Antibiotic treatment — although none can be excluded, the most commonly implicated antibiotics are:
Clindamycin.
Cephalosporins — in particular second- and third-generation cephalosporins (such as cefuroxime axetil, cefixime, ceftriaxone, and cefotaxime).
Fluoroquinolones (such as ciprofloxacin, norfloxacin).
Co-amoxiclav.
Ampicillin and amoxicillin (which may relate mainly to the volume of their use rather than being high risk).
Underlying morbidity such as abdominal surgery, cancer, chronic renal disease, and tube feeding.
Current use of a proton pump inhibitor (such as omeprazole and lansoprazole) or other acid-suppressive drugs (such as H2-receptor antagonists).
Other risk factors for C. difficile infection include:
Hospitalization — rates of colonization are about three times higher in hospitalized people than in those treated as outpatients.
Exposure to other cases — C. difficile infection can occur in outbreaks.
Long duration of antibiotic treatment.
Multiple antibiotics prescribed concurrently, or multiple antibiotic courses prescribed.
Inflammatory bowel disease.
History of C. difficile infection — approximately 20% of people experience recurrence of symptoms after the initial episode of C. difficile has resolved.
Historically between 20–50% of recurrences have been reinfections and not relapses caused by the same strain of C. difficile.
Signs of hyperthyroidism
Being restless, nervous, emotional, irritable, sleeping poorly and ‘always on the go’.
Tremor of your hands.
Losing weight despite an increased appetite.
Palpitations.
Sweating, a dislike of heat and an increased thirst.
Diarrhoea or needing to go to the toilet to pass faeces more often than normal.
Shortness of breath.
Skin problems such as hair thinning and itch.
Menstrual changes - your periods may become very light or infrequent.
Tiredness and muscle weakness may be a feature.
A swelling of your thyroid gland (a goitre) in the neck may occur.
Eye problems if you have Graves’ disease. (See below under ‘What are the causes of hyperthyroidism?’.)
Which drugs can cause diarrhoea
Other drugs (for example allopurinol, angiotensin-II receptor blockers, antibiotics, digoxin, colchicine, cytotoxic drugs [such as methotrexate or chemotherapy], H2-receptor antagonists, magnesium-containing antacids, metformin, nonsteroidal anti-inflammatory drugs, proton pump inhibitors, selective serotonin reuptake inhibitors, statins, theophylline, thyroxine, and high-dose vitamin C).
What are the features of whipples disease
Whipple’s disease is a rare infection of the small intestine, caused by bacterium Trophermyma whippleii. It mainly affects white men between 30-60 years of age, living in North America and Europe. Main symptoms are diarrhea, inflamed joints, skin darkening, and weight loss. Diagnosis is by investigation of a sample of duodenal mucosa taken during upper endoscopy. Disease is progressive and may be fatal if not treated; antibiotic treatment is usually successful (1). Disease may recur.
What are the commonest causes of diarrhoea
Acutely infectious, chronically functional (irritable or chrons)
Differences between clinical presentation of chrons and uc
Many symptoms of ulcerative colitis and Crohn’s disease are similar, but there are some subtle differences. ulcerative colitis patients tend to have pain in the lower left part of the abdomen, while Crohn’s disease patients commonly (but not always) experience pain in the lower right abdomen. With ulcerative colitis,
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bleeding from the rectum during bowel movements is very common, and bleeding is much less common in patients with Crohn’s disease.
Pattern of inflammation
The pattern that each form of IBD takes in the digestive tract is very distinct. Ulcerative colitis tends to be continuous throughout the inflamed areas. In many cases, ulcerative colitis begins in the rectum or sigmoid colon, and spreads up through the colon as the disease progresses. In Crohn’s disease, the inflammation may occur in patches in 1 or more organs in the digestive system . For instance, a diseased section of colon may appear between two healthy sections.
What are the indications that surgery will be likely in uc
Stool frequency of more than eight per day
Pyrexia
Tachycardia
An abdominal X-ray showing colonic dilatation
Low albumin, low haemoglobin, high platelet count or CRP >45 mg/L
Common causes of small bowel obstruction
May be due to adhesions, strangulated hernia, malignancy or volvulus or chrons (rarely). The majority (75%) of small bowel obstructions are attributed to intra-abdominal adhesions from prior operations.[1]
Malignancy usually means a tumour of the caecum, as small bowel malignancies are very rare.[2]
features of volvulus
Regardless of cause, volvulus causes symptoms by two mechanisms:[citation needed]
One is bowel obstruction, manifested as abdominal distension and vomiting.
The other is ischemia (loss of blood flow) to the affected portion of intestine.
Depending on the location of the volvulus, symptoms may vary. For example, in patients with a cecal volvulus, the predominant symptoms may be those of a small bowel obstruction (nausea, vomiting and lack of stool or flatus), because the obstructing point is close to the ileocecal valve and small intestine. In patients with a sigmoid volvulus, although abdominal pain may be present, symptoms of constipation may be more prominent.
Volvulus causes severe pain and progressive injury to the intestinal wall, with accumulation of gas and fluid in the portion of the bowel obstructed.[2] Ultimately, this can result in necrosis of the affected intestinal wall, acidosis, and death. This is known as a closed loop obstruction because there exists an isolated (“closed”) loop of bowel. Acute volvulus often requires immediate surgical intervention to untwist the affected segment of bowel and possibly resect any unsalvageable portion.[2]
Volvulus occurs most frequently in middle-aged and elderly men.[2] Volvulus can also arise as a rare complication in persons with redundant colon, a normal anatomic variation resulting in extra colonic loops.[4]
Sigmoid volvulus is the most-common form of volvulus of the gastrointestinal tract[5] and is responsible for 8% of all intestinal obstructions.[citation needed] Sigmoid volvulus is particularly common in elderly persons and constipated patients. Patients experience abdominal pain, distension, and absolute constipation.
Cecal volvulus is slightly less common than sigmoid volvulus and is associated with symptoms of abdominal pain and small bowel obstruction.
Volvulus can also occur in patients with Duchenne muscular dystrophy due to the smooth muscle dysfunction.[citation needed]
signs/symptoms of small bowel obstruction
Obstruction can be characterized as either partial or complete versus simple or strangulated. Abdominal pain, often described as crampy and intermittent, is more prevalent in simple obstruction. Usually, pain that occurs for a shorter duration of time and is colicky and accompanied by bilious vomiting may be more proximal. Pain that lasts as long as several days, is progressive in nature, and is accompanied by abdominal distention may be typical of a more distal obstruction.
Some signs and symptoms associated with SBO include the following:
Nausea
Vomiting - Associated more with proximal obstructions
Diarrhea - An early finding
Constipation - A late finding, as evidenced by the absence of flatus or bowel movements
Fever and tachycardia - Occur late and may be associated with strangulation
Previous abdominal or pelvic surgery, previous radiation therapy, or both - May be part of the patient’s medical history
History of malignancy - Particularly ovarian and colonic malignancy
causes of illeus
Chest infection Acute myocardial infarction Stroke Acute kidney injury Puerperium Trauma Severe hypothyroidism Electrolyte disturbance Diabetic ketoacidosis
Causes of acute limb iscaemia
Embolism: for example, left atrial thrombus in patients in atrial fibrillation, mural thrombus after myocardial infarction, prosthetic and abnormal heart valves, aneurysm (aorta, femoral, or popliteal), proximal atheromatous stenosis, malignant tumour, or foreign body.
Thrombosis: most cases of leg ischaemia result from the presence of thrombus at sites of atherosclerotic narrowing; presentation of ischaemia may be:
Acute, as a result of emboli from rupture of proximal atherosclerotic plaque or thrombus.
Chronic, usually resulting from gradual extension of thrombus with development of collateral vessels.
Trauma.
Raynaud’s syndrome.
Compartment syndrome: this occurs when perfusion pressure falls below tissue pressure in a closed anatomical space; causes include:
Orthopaedic (tibial or forearm fractures).
Vascular: haemorrhage, phlegmasia caerulea dolens (massive thrombosis in the major veins of the limbs, causing gross swelling that obstructs arterial flow).
Soft tissue injury (prolonged limb compression, crush injury, burns).
Congenital causes of early-onset leg ischaemia - eg, aortic hypoplasia.
Ischaemia of the arm is most often embolism of cardiac origin, but may also be due to damage to the subclavian artery or thoracic outlet syndrome.
Treatment of critical limb ischaemia
Vascular team review straight away
thrombolysis with unfractionated heparin (in debate, no mention by nice guidance)
Offer angioplasty/bypass where possible
Stent if complete aorto/illeal obstruction
Pain relief (paracetamol and strong/weak opiates)
Amputation as last resort
What investigations should be performed in a patient with critical limb ischaemia
Hand-held Doppler ultrasound scan may help demonstrate any residual arterial flow.
Blood tests
FBC (ischaemia is aggravated by anaemia).
ESR (inflammatory disease - eg, giant cell arteritis, other connective tissue disorders).
Glucose (diabetes).
Lipids.
Thrombophilia screen.
If diagnosis is in doubt, perform urgent arteriography.
Investigations to identify the source of embolus:
ECG.
Echocardiogram.
Aortic ultrasound.
Popliteal and femoral artery ultrasound.
Symptoms hypothyroidism
Symptoms that commonly occur include: tiredness, weight gain, constipation, aches, feeling cold, dry skin, lifeless hair, fluid retention, mental slowing, and depression.
Less common symptoms include: a hoarse voice, irregular or heavy menstrual periods in women, infertility, loss of sex drive, carpal tunnel syndrome (which causes pains and numbness in the hand), and memory loss or confusion in the elderly.
How is severity of pancreatitis assessed
The modified Glasgow scoring system
Pancreatitis is considered severe if at least three of the following criteria are met (remember the mnemonic ‘PANCREAS’):
PO2 55
Neutrophilia (WCC 16mmol/L
(Enzymes) lactate dehydrodgenase (LDH) >600, AST>200iU/L
Albumin 10mmol/L
Causes acute pancreatitis
Gallstones
Ethanol (alcohol)
Trauma
Scorpion venom
Mumps
Autoimmune (primary biliary cirrhosis, Sjögren’s Syndrome)
Shock
Hyperlipidemia
ERCP (endoscopic retrograde cholangiopancreatography)
Drugs (prednisolone, valproic acid, azathioprine)
Blood results in acute pancreatitis
Amylase-raised to 3x the normal level (‘normal’ varies between labs)
Lipase -raised
Albumin- reduced
Features saphena varix
Dilation of saphenous vein at saphene-femoral junction bluish tinge disappears lying venous hum on auscultation Associated with varicose veins
How is a direct inguinal hernia determined from an indirect
Indirect is controlled by direct pressure on the deep inguinal ring (midpoint inguinal ligament)
How is an inguinal hernia determined from a femoral
femoral more common in females, femoral inferolateral to Pubic Tubercle, inguinal superomedial
What structures make the superior wall of the inguinal canal
Apneurosis ext oblique, int obl, transversus abdominis and transversalis fascia
what structures make the posterior wall of the inguinal canal
Transversalis fascia, conjoint tendon inguinal ligament (med 1/3), deep inguinal ring (lat 1/3)
What structures make the anterior wall of the inguinal canal
Apneurosis ext obl, internal obl (lat 1/3), superficial inguinal ring (med 1/3)
What structures make the inferior wall of the inguinal canal
inguinal ligament
What are the contents of the spermatic cord/inguinal canal
3 arteries (artery to vas, testicular, artery to cremester) 3 nerves (illioinguinal travels alongside sc, genito-femoral, sympathetics) 3 others (vas deferens, lymphatics, pampiniform venous plexus) 3 fascia layers
What routine investigations should every surgical abdo patient generally have
Full abdo exam, listen to chest, examin ext genitalia for testicular torsion and hernia orifaces
FBC, U and E, LFT, amylase and lipase, urinalysis, HCG, clotting and G&S (if surgery possible), CXR to detect LL pneumonia/intraperitoneal gas,
plain abdo radiograph if obstruction suspected/fulminant colitis/perf
Abdo US in biliary/gynae/renal/collections/uncertain appendicitis
Abdo CT if suspect sepsis/bowel obstruction and over 50 (more chance malignancy)
What are the symptoms of biliary colic, cholecysitits,complex biliary disease (cholangitis/stone in bileduct) and gallstone pancreatitis
Biliary colic; short duration of pain, minimal systemic upset, normal LFTs, US shows no biliary dilation
Acute cholecystitis; >24hrs, systemic upset (pyrexia/tachy), raised WBC, occasionally jaundice but usually mild, thick walled odematous gallbladder on US, sometimes stone stuck in neck
Complex biliary disease; variable duration of pain, deranged LFTs (usually high ALP, possibly slightly raised ALT) and dilated bilary tree on US, gallstones in bile duct and gallbladder
Gallstone pancreatitis; High Amylase, deranged LFTs, raised inflammatory markers, dilated biliary tree
How are biliary colic, cholecystitis, complex biliary disease and gallstone pancreatitis treated
Biliary colic; pain relief, discharge if severe pain settles, OP US and elective lap chole within 6/52
Acute Cholecystitis; Fluids/analgesia/abx if infection, lap/open chole within 72 hours if symptoms not settling or 6 weeks (better outcomes in these windows)
Complex biliary disease; analgesia, abx if infection, fluids, DAILY LFTs. If LFTs resolving and no biliary dilation early chole/delayed elective, slowly resolving LFTs and biliary dilation discharge when symptoms resolve with urgent OP MRCP and ERCP, persisting symptoms urgent ERCP and bile duct clearing and elective chole
Gallstone panc; determine mild/severe ranson/apache 2 score. Mild can be managed on gen ward, severe critical care, IVI, O2, analgesia, fasting. Urgent US to confirm gallstones, ERCP where existing biliary obstruction. Mild, early lap chole, severe, critical care and CT day 3-10 to review if pancreatic necrosis
How is diverticulisis managed
Bowel rest, oral fluids, abx, stool softeners and regular review, most settle in 36-72 hours, CT for severity and complications (abscess/obstruction/fistula)
Management of SBO
clinical exam for hernia/peritonism, aggressive fluid rescuss, ng tube and regular aspiration, urinary catheter, bloods inc lactate, x-ray chest/abdo
Early surgery (within 6h) and CT imaging if strangulation/ischaemia (peritonitis/pain/WBC/CRP/met acidosis)
Surgery if CT indicates none-adhesion cause
adhesions often managed conservatively up to 3 days (if no improvement best outcomes before 5 days)
Large bowel obstruction management
Continuous pain indicates ischaemia, abrupt indicates volvulus, longer plus bowel change suggests malignancy
Urgent CT (24h), If malignancy stenting buys time for LT management,
Volvulus, decompression with sigmoidoscope and flatus tube, may buy time for elective resection. Immediate resection if decompression if ischaemia/decompression fails
Symptoms of AAA
Abdo/back/flank pain, abdo distension, pulsatile abdo mass. shock
What size should an abdominal aorta measure How is an AAA monitored
Normal 3cm no followup
3-4cm monitor yearly
4-4.5cm monitor 6monthly
> 4.5 surgical evaluation and repair
what clinical exams should be done on a patient presenting with dysphagia
Gait/balance, CN V,V11 and IX TO XII), neck, lymph plus thyroid, skin changes
What condition causes an inverted champagne bottle appearance of the lower limbs
Lipodermosclerosis
What is the normal local anaesthetic used in suturing? What is the max dosage allowed
1/2% lignocaine. 3mg/kilo so in a 70kg man this is roughly 21ml (1mg in 10ml for 1%)
How long will sutures need to stay in by body part
wounds 3–5 days; scalp wound 7–10 days; limbs 10–14 days; joints 14 days; trunk of the body 7–10 days.[12]
What different suture types and size are available? When should each be used?
Absorbable none-absorbable, natural/synthetic
Monofilament/multifilament (monofilament not as smooth handling and not as much tensile strength but smaller, more cosmetically favourable and don’t aggravate infection as much)
Size 1-11, 3-4 for deep wounds, 5-7 for face, 8-10 microsurgery
What are the boundaries of the anterior triangle
Anterior Triangle
The anterior triangle is situated at the front of the neck.
It is bounded:
Superiorly – Inferior border of the mandible (jawbone)
Laterally – Medial border of the sternocleidomastoid
Medially – Imaginary sagittal line down midline of body
With respect to the vasculature, the common carotid artery passes through the anterior triangle, and bifurcates within the triangle into the external and internal carotid arteries. The internal jugular vein also can be found within this area. It drains blood from the head and neck.
Numerous cranial nerves are located in the anterior triangle. Some pass straight through, and others give off branches to innervate some of the other structures within the triangle. The cranial nerves in the anterior triangle are the facial [VII], glossopharyngeal [IX], vagus [X],accessory [XI], and hypoglossal [XII] nerves.
Carotid triangle
The carotid triangle of the neck has the following boundaries:
Superior: Posterior belly of the digastric muscle.
Lateral: Medial border of the sternocleidomastoid muscle.
Inferior: Superior belly of the omohyoid muscle.
The main contents of the carotid triangle are the common carotid artery (which bifurcates within the carotid triangle into the external and internal carotid arteries), the internal jugular vein, and the hypoglossal and vagus nerves.
Submandibular
Superiorly: Body of the mandible.
Anteriorly: Anterior belly of the digastric muscle.
Posteriorly: Posterior belly of the digastric muscle.
Fig 1.2 – The submental triangle
Submandibular Triangle
The submandibular triangle is located underneath the body of the mandible. It contains the submandibular gland (salivary), and lymph nodes. The facial artery and vein also pass through this area.
The boundaries of the submandibular triangle are:
Superiorly: Body of the mandible.
Anteriorly: Anterior belly of the digastric muscle.
Posteriorly: Posterior belly of the digastric muscle.
Muscular Triangle
This anatomical area is situated more inferior than the triangular sub-divisions. It is a slightly dubious triangle, in reality having four boundaries. The muscular triangle is also unique in containing no vessels of note. It does however contain some muscles – the infrahyoid muscles, the pharynx, and the thyroid, parathyroid glands.
The boundaries of the muscular triangle are:
What skin changes occur with venous dysfunction
Oedema (-typically pitting in the early stages).
o Haemosiderin deposits (brown staining-iron deposits, due to chronic leakage of blood into the tissues due to increased hydrostatic venous pressure).
o Lipodermatosclerosis: “beer bottle legs” due to the progressive sclerosis of skin and fat secondary to fibrin deposition, tissue death and scarring.
o Venous eczema: dry, flaky sometimes erythematos skin which can lead to ulceration.
o Ulcers
How do arterial venous and neuropathic ulcers
Below the knee - primarily found on the inner part of the leg, just above the ankle. Ulcers may affect one or both legs.
Appearance Base: Red in color and may be covered with yellow fibrous tissue. There may be a green or yellow discharge if the ulcer is infected. Fluid drainage can be significant.
Borders: Usually irregularly shaped. The surrounding skin is often discolored and swollen. It may even feel warm or hot. The skin may appear shiny and tight, depending on the amount of edema (swelling).
Who is affected Venous stasis ulcers are common in patients who have a history of leg swelling, varicose veins, or a history of blood clots in either the superficial or the deep veins of the legs. Venous ulcers affect 500,000 to 600,000 people in the United States every year and account for 80 to 90 percent of all leg ulcers.
Neurotrophic (diabetic) Ulcers
Location on body Usually located at increased pressure points on the bottom of the feet. However, neurotrophic ulcers related to trauma can occur anywhere on the foot.
Appearance Base: Variable, depending on the patient’s circulation. It may appear pink/red or brown/ black.
Borders: Punched out, while the surrounding skin is often calloused.
Who is affected Neurotrophic ulcers occur primarily in people with diabetes, although they can affect anyone who has an impaired sensation of the feet.
Neuropathy and peripheral artery disease often occur together in people who have diabetes. Nerve damage (neuropathy) in the feet can result in a loss of foot sensation and changes in the sweat-producing glands, increasing the risk of being unaware of foot calluses or cracks, injury or risk of infection. Symptoms of neuropathy include tingling, numbness, burning or pain.
It is easy to understand why people with diabetes are more prone to foot ulcers than other patients. This is why people with diabetes need to inspect their feet daily and wear appropriate footwear. People with diabetes should never walk barefoot. (See Foot Care Guidelines Box).
Arterial (ischemic) Ulcers
Location on body On the feet - often on the heels, tips of toes, between the toes where the toes rub against one another or anywhere the bones may protrude and rub against bed sheets, socks or shoes. They also occur commonly in the nail bed if the toenail cuts into the skin or if the patient has had recent aggressive toe nail trimming or an ingrown toenail removed.
Appearance Base: Has a yellow, brown, grey or black color and usually does not bleed.
Borders: The borders and surrounding skin usually appear punched out. If irritation or infection are present, there may or may not be swelling and redness around the ulcer base.
There may also be redness on the entire foot when the leg is dangled; this redness often turns to a pale white/yellow color when the leg is elevated.
Arterial ulcers are typically very painful, especially at night. The patient may instinctively dangle his/her foot over the side of the bed to get pain relief.
Who is affected The patient usually has prior knowledge of poor circulation in the legs and may have an accompanying disorder, such as those listed in the section, “What causes leg ulcers?”
