Surgery FFP Flashcards

1
Q

Fibroadenomas - presentation, examination, diagnosis, treatment

A

Aberrations of Normal Development and Involution (ANDI)
Benign breast condition
younger patients - 20s
smooth, very mobile, “breast mouse”, can be tender, firm rubbery, can change over menstruation
diagnoses using triple assessment; US, mammogram, clinically and core biopsy
left alone or removed if too big; surgery/vacuum excision

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2
Q

Breast cysts - presentation, examination, diagnosis, treatment

A

Aberrations of Normal Development and Involution (ANDI)
Benign breast condition
30-50; 50+ if on HRT
Lump +/- pain with cyclical fluctuation
Smooth, mobile lump, can be tender
Triple assessment; US, mammogram, clinically and core biopsy
Left alone if asymptomatic or simple drainage

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3
Q

Fibroadenosis presentation, examination, diagnosis, treatment

A

Aberrations of Normal Development and Involution (ANDI)
“Benign breast changes” - Benign breast condition
Lumpiness +/- pain with cyclical fluctuation
Thickening +/- tenderness

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4
Q

Fat necrosis presentation, examination, diagnosis,

A

Any age
Trauma (surgery, accident) except in older women; can be small hits
Could feel benign (solid/cystic) or malignant +/- bruise
Triple assessment

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5
Q

What tests should be done for pts less than 40 vs those older than 40 with suspected breast cancer

A

<40 => Ultrasound
40< => Ultrasound and mammogram

This is due to younger patients breasts being too dense for mammograms to be of use.

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6
Q

Types of nipple discharge and when it may be significant

A

Milky discharge or galactorrhoea is often due to hyperprolactinaemia, which may point to an underlying endocrine condition so the patient should be managed accordingly.

Pus discharging from the nipple is often part of an infection such as periductal mastitis, so should be managed accordingly.

Significant/Pathological :
Spontaneous
Persistent
Unilateral
Single-duct

Insignificant/Physiological :
Provoked
intermittent
bilateral
multi-duct

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7
Q

For unilateral and single-duct discharge, the commonest underlying pathology is …..

and treatment

A

For unilateral and single-duct discharge, the commonest underlying pathology is a duct papilloma, which is again a benign condition. However ductal carcinoma in situ (DCIS) could also present this way.

In the absence of any abnormal radiological findings (mammogram and ultrasound), if we are still worried, we will tend to operate by removing the discharging duct (a procedure called microdochectomy) for histological examination. That will also treat the symptom of discharge.

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8
Q

Breast pain - facts and questions to ask, next steps

A

Pain alone is rarely due to breast cancer

  1. Is it Disturbing vs non-disturbing life activities
  2. Cyclical vs non-cyclical

We do not normally have to carry out radiological examination except for a screening mammogram if the patient falls into the age group who will benefit from this (40 years onward).

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9
Q

Breast infections (two main ones)
History
Physical findings
Pathogens
Investigations
Management

A

Lactational mastitis/abscess
History of lactation

Found Peripherally, Deep with Acute inflammation

S. aureus

US if ?abscess

Antibiotic (flucloxacillin) +/- drainage* + C/ST

Breast feeding can continue

Periductal mastitis/abscess
20s-40s, Chronic smoker, Recurrent episodes
Found Peri-areolar, Superficial, Chronic inflammation (scarring, fistula)

Mixed, including anaerobes

US if ?abscess

Antibiotic (co-amoxiclav) +/- drainage* + C/ST
↓Smoking
?Surgery

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10
Q

Most common types of breast cancer

A

Invasive Ductal carcinoma, followed by lobular
DC in situ

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11
Q

Breast cancer risk factors

A

Female
Age
BRCA
Direct family history
Radiation
Past breast surgeries
alcohol
Combined contraceptives
increased exposure to oestrogen

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12
Q

Breast cancer presentation, examination, diagnosis

A

Hard, immobile lump, rough borders, non-tender
Triple assessment

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13
Q

At risk pathologies for breast cancer

A

At-risk pathology: Atypical Ductal hyperplasia, ALH, LCIS, papillomatosis.

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14
Q

Types of pathology tests for breast cancer

A

Pathological assessment is done by biopsy.

Fine needle aspiration (FNA) cytology - gives you cell morphology

Needle core biopsy, which is now preferred, gives you tissue architecture.

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15
Q

Angles for mammogram

A

The standard views are cranio-caudal (CC) and oblique, so you broadly cover two dimensions, but also include the axilla – pectoral muscles as shown here in an oblique view, which shows a mass with irregular border in the upper aspect of the breast near the axilla.

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16
Q

Following radiology, the results for a breast lump are defined as either (5)

A

Normal
Benign Indeterminate
Suspicious
Malignant

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17
Q

TMN Staging for breast cancer

A

T (Primary Tumor):

T0: No evidence of primary tumor.
Tis: Carcinoma in situ (non-invasive cancer).
T1: Tumor size ≤2 cm
T2: Tumor size >2 cm but ≤5 cm
T3: Tumor size >5 cm
T4: Tumor of any size invading nearby structures (e.g., chest wall or skin)

N (Regional Lymph Nodes):
NX: Regional lymph nodes cannot be assessed.
N0: No regional lymph node involvement.
N1: regional lymph node involvement.
N2: distant nodes

M (Distant Metastasis):
M0: No distant metastasis.
M1: Distant metastasis present.

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18
Q

Manchester 4 stage classification of breast cancer

A

1 - confined to breast
2 - breast and mobile axillary nodes
3 - growth beyond mammary parenchyma
4 - growth beyond breast area

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19
Q

What is the commonest first site of distant metastasis in breast cancer?

A

Bone

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20
Q

Two broad groups of inoperable breast cancers and management

A

Locally advanced primary disease – The tumour is inoperable e.g. fungating or ulcerated tumour, tumour fixed to the pectoralis major muscle or chest wall, or inflammatory cancer, but has NOT yet spread to distant sites. There are two distinct points in terms of the principles of managing this group – (i) Since the chance of asymptomatic distant metastases is higher than in early operable disease, we normally do some staging investigations like a CT scan of the chest, abdomen and pelvis, prior to starting treatment; (ii) the initial treatment tends to be systemic such as chemotherapy (or we call it neoadjuvant chemotherapy) with a view of down-staging the cancer to allow surgery.

  • Metastatic breast cancer – The disease is no longer curable so the goal of treatment is palliative aiming at improving quality of life.
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21
Q

Management of primary breast cancer - surgery

A

In general, surgery is performed as the INITIAL treatment, followed by what we call adjuvant therapies.

Locoregional control
Obtaining information&raquo_space;> Adjuvant therapies
Cosmesis

Breast - masectomy or wide local incision; if unifocal and small
Axilla - sentinel lymph node (first to spread to) biopsy; identified using radioisotopes or a dye which fails to clear and can be identified by a surgeon.
- If positive: axillary clearance

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22
Q

Management of primary breast cancer - adjuvant therapies

A

Radiotherapy to affected area if tolerated;
Reasons that they might not tolerate could be previous radiotherapy (like a previous breast cancer, radiotherapy to treat mediastinal lymphoma as a child, or some collagen vascular disease associated with increased skin toxicity eg scleroderma, or that the patient has significant shoulder restriction so the external beam radiation can’t be delivered with her arm stretched

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23
Q

Factors to consider endocrine therapy

A

The most important ones which we use clinically for making a decision about adjuvant systemic therapies are oestrogen receptor (ER) and human epidermal growth receptor 2 (HER2).

Most invasive breast carcinomas are ER+ (about one-third overall) and only about 15% are HER2+.

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24
Q

Systemic therapies for breast cancer

A

Chemotherapy
Endocrine therapy (oestrogen +ve) e.g. tamoxifen pre-menopausal, aromatase inhibitors post menopausal (anastrozole, letrozole, exemestane)
Anti-HER2 targeted therapy e.g. trastuzumab (Herceptin)

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25
Reducible, irreducible, obstructed, incarcerated, strangulated hernias
Reducible Contents of the hernia can be manipulated back into its original position through the defect from which it emerges Irreducible Cannot be reduced without surgery Incarcerated Irreducible hernia, contents trapped due to adhesions Strangulated Compression of bowel -> Ischaemia as blood supply cut off -> necrosis -> sepsis Obstructed Hernias containing bowel -> contents compressed -> bowel lumen is no longer patent Presents as triad of symptoms
26
Hernia repair
Open for strangulation laparoscopic otherwise mesh repair
27
Spigelian hernia
Spigelian – through spigelian fascia (aponeurotic layer between the rectus abdominus mm medially and semilunar line laterally). Below and lateral to umbilicus. "6 pack hernia"
28
Hernia risk factors
Increased intraabdominal pressure from: lifting, chronic constipation, chronic cough, obesity Protein deficiencies and older patient: less collagen for tensile strength of gut lining
29
Inguinal canal borders
Anterior wall – aponeurosis of the external oblique, reinforced by the internal oblique muscle laterally. Posterior wall – transversalis fascia. Roof – transversalis fascia, internal oblique, and transversus abdominis. Floor – inguinal ligament (a ‘rolled up’ portion of the external oblique aponeurosis), thickened medially by the lacunar ligament.
30
Which border do inguinal hernias break through?
Posterior wall – transversalis fascia. - only has one layer
31
Indirect inguinal hernias
Indirect inguinal hernias result from bowel passing through the deep ring of the inguinal canal due to an incomplete closure of the processus vaginalis. Indirect hernias are more likely to strangulate than direct hernias. Both types of hernia can exit the superficial ring and pass into the scrotum but this is more common with indirect hernias as the path through both inguinal rings, rather than a muscle defect, has less resistance.
32
Direct inguinal hernias
Direct inguinal hernias are less common than indirect inguinal hernias. Direct inguinal hernias are where bowel enters into the inguinal canal through a weakness in the posterior wall (called Hesselbach’s triangle). Direct hernias tend to reduce easily and do not rarely strangulate. Less likely to pass through to the scrotum
33
Determining indirect vs direct inguinal hernia
Reduce the hernia Press over the deep ring (just above midpoint of the inguinal ligament) Ask the patient to cough If the hernia reappears it is… DIRECT Technically, we can only be certain that the inguinal hernia is direct or indirect via surgical exploration. Indirect inguinal hernias are lateral to the inferior epigastric vessels. Direct inguinal hernias are medial to the inferior epigastric vessels.
34
Femoral hernias
Femoral hernias occur when abdominal viscera or omentum pass through the femoral ring into the potential space of the femoral canal; lies medial to the femoral vein and it’s purpose is allow space for the vein to expand. HIGH risk of strangulation due to narrow neck of the femoral canal Relatively uncommon (5% of all hernias) Risk Factors: Female (due to wider anatomy of pelvis) Pregnancy Raised intra-abdominal pressure
35
How can you tell the difference between inguinal and femoral hernias on clinical examination?
Inguinal hernias are SUPERIOMEDIAL to the pubic tubercle Femoral hernias are INFEROLATERAL to the pubic tubercle
36
Umbilical hernia
Defect in the transversalis fascia = Umbilical ring Where the umbilical vessels passed in-utero More common in children Occur in adults due to pregnancy or gross ascites Low strangulation risk
37
Para-umbilical hernia
Occur adjacent to the umbilicus due to a weakness in the linea alba More common in 35-50yo women; Usually caused by obesity or gross ascites High risk of strangulation
38
Epigastric hernia
Herniation of fat which overlies the bowel through the linea alba above the umbilicus Usually small – 1cm diameter Usually occur in young males Can cause discomfort on exercise or eating Relieved by reclining
39
Divarication of recti
Separation of rectus abdominus due to linea alba laxity Men – weight gain (truncal obesity) Women – pregnancy Also repeated midline operations and chronically raised intra abdominal pressure Ultrasound diagnosis
40
Incisional hernia
Common risk of any abdominal surgery 5% at 1 year, 25% at 2 years Risk factors are those that affect wound healing – poor blood supply, reduced ability to produce collagen, factors relating to reduced immunity Emergency surgery is twice as likely to result in incisional hernia. Smokers are twice as likely to get a wound infection post operatively Early - midterm complication Due to risk factors, normally repair these with mesh but often these reoccur after repair. Should form part of the consent process along with a scar in abdominal surgery Do not have to intervene surgically if patient assymptomatic
41
Articular cartilage has all of the following properties except: Avascular Alymphatic Aneural Acellular
Articular cartilage is Avascular, Alymphatic and Aneural
42
Which zones of cartilage resist which direction of forces
Superficial and deep withstand horizontal intermediate withstands vertical forces
43
Hyaline cartilage composition and function
type II collagen for tensile strength proteoglycans for compressive strength chondrocytes in lacunae
44
How does synovial joint cartilage receive nutrition?
synovial fluid and subchondral bone marrow blood
45
How does cartilage repair in acute trauma?
Bleeding from subchondral bone clot fills defect becomes fibrous by 8 weeks fibrocartilage by 4 months
46
OA on xray
4 features OA: Joint space narrowing, marginal osteophytes, subchondral sclerosis, subchondral cysts. Additionally, varus/valgus deformities can develop in more severe cases.
47
OA vs RA vs psoriatic arthritis features in hand
OA: diffuse osteopenia, no erosion, osteophytes, asymmetrical joint space loss, no swelling, PIP & DIP RA: juxta-articular osteopenia, marginal erosion, no osteophytes, uniform joint space loss, swelling, PIP & MCP PA: minimal osteopenia, proliferative erosion, no osteophytes, uniform joint space loss, swelling, DIP
48
OA causes
Abnormal concentration of force on normal cartilage e.g. CAM deformity, loss of menisces Normal concentration of force on abnormal cartilage e.g. inflamm or crystal arthropathy Normal concentration of force on normal cartilage supported by stiffened subchondral bone e.g. Pagets Normal concentration of force on normal cartilage supported by weakened subchondral bone e.g. avascular necrosis
49
OA treatment
Non pharma: physio, weight loss etc. Topical NSAIDs then Oral NSAIDs then intra-articular steroids No opiates (NICE) Surgical: hip/knee/shoulder = hemi, partial, complete arthroplasty Hand = cortiva implant, trapeziotomy
50
Causes for extensive internal bleeding and what can it lead to
AAA rupture most serious cause Ruptured ectopic pregnancy Bleeding Gastric ulcer Trauma Hypovolaemic shock: Hypotension Tachycardia Pale and clammy Cool to touch
51
Peritonitis presentation
Patients lay completely still Tachycardia and potential hypotension / pyrexial Percussion / rebound tenderness Involuntary guarding Reduced or absent bowel sounds
52
Ischaemic bowel presentation
Diffuse and constant pain reported Examination may be unremarkable Acidaemia with raised lactate on blood gases
53
Colic definition
Colic is an abdominal pain that crescendos to become very severe and then goes away completely.
54
list of investigations for an acute abdomen
Bedside Basic obs – lots of information in your NEWS2 score – indication of how unwell the patient is ECG – Exclude MI, baseline ECG if surgery required Urine dip - For signs of infection or haematuria. +/- MC+S. Pregnancy test- (bHCG) Include a pregnancy test for all women of reproductive age BM – DKA can present with abdominal pain Bloods Routine bloods FBC – infection, bleeding UE – dehydration(AKI), obstructive hydroneprhosis e.g kidney stone LFT – gallbladder or liver pathology (further talk) Amylase/lipase +/- serium calcium – in suspected pancreatitis. Note amylase needs to be 3x higher than the upper limit to be diagnostic of pancreatitis. Values lower than this might be due to other pathology e.g. perforated bowel, ectopic pregnancy or DKA. CRP - inflammation G+S and co-ag – If the patient is bleeding or is likely to need surgery soon Blood cultures – if considering infection as a potential diagnosis Basic Imaging – Depends on what you think the likely cause is! Erect CXR - for evidence of bowel perforation AXR/ USS discussed on the next slide Specialist Imaging - best discussed with a senior depending on the suspected underlying diangosis
55
When to do an abdo xray
Bowel obstruction Toxic megacolon Foreign body ingestion or insertion
56
Appendicitis presentation and signs on examination
Patients typically complain of a vague abdominal pain which intensifies and moves to the RIF in mcburneys point (1/3 of line between asis and umbilicus) There is usually associated nausea and anorexia Fever There may be some vomiting, urinary symptoms or loose stools Rovsing’s sign: RIF fossa pain on palpation of the LIF On examination, patients may be tachycardic, tachypnoeic, and pyrexial. There is likely rebound tenderness and percussion pain over McBurney’s point, as well as potential guarding (especially if perforated). An appendiceal abscess may also present with a RIF mass.
57
Mr Wright, a 67 year old gentleman, presents to A and E with a tender, swollen abdomen. He is vomiting and hasn’t opened his bowels for 6 days Differentials?
Bowel obstruction Constipation Paralytic ileus - Functional obstruction of the bowel due to temporary paralysis Usually affects the whole bowel Extremely common post-op Toxic megacolon - Acute colonic distension Acute colitis and system toxicity Secondary to IBD or colonic infections such as C.Diff
58
Symptoms of bowel obstruction differences between sbo and lbo
Vomiting Absolute constipations Abdo distension Colicky abdo pain Large bowel obstruction (LBO) - Absolute constipation and pain are more prominent early. Vomiting often late. Symptoms generally are more gradual due to the large volume of colon and caecum and its resorptive activity Small bowel obstruction (SBO) – Vomiting is the predominant early feature. Constipation often late.
59
Ileus
Functional obstruction of the bowel due to temporary paralysis Usually affects the whole bowel There is no pain and the bowel sounds are absent Extremely common post-op complication Can occur secondary to: Hypokalaemia Sepsis Intra- abdominal inflammation
60
Bowel obstruction on examination
Abdo distension Abdo tenderness Central resonance to percussion Tinkling bowel sounds Dehydration
61
Why does bowel obstruction cause dehydration
‘Third spacing’ from increased electrolyte fluid in the bowel Vomiting ++ Lack of fluid intake – patients with bowel obstruction commonly develop anorexia
62
Strangulating obstructions 
Strangulating obstructions are characterised by interruption of the intestinal blood supply with simultaneous blockage of the intestinal lumen 
63
Closed loop obstruction
Obstruction at two points which forms a loop of grossly distended bowel SURGICAL EMERGENCY Bowel will continue to distend, stretching the bowel wall until it becomes ischaemic and ultimately perforates
64
Large bowel obstruction with competent or incompetent ileo-ceocal valve
Ileocaecal valve Normally prevents backflow of bowel contents from large bowel to small bowel If ileocaecal valve is competent closed-loop obstruction forms If ileocaecal valve is incompetent bowel content flows from large to small bowel
65
Sigmoid volvulus
Twisting of bowel on itself
66
Small or large bowel obstruction more common? Causes
SBO 80% - Adhesions, hernias, crohns LBO 20% - malignancy, diverticular disease, volvulus
67
List of tests for bowel obstruction
Bedside Observations – ?dehydrated ?shocked ?infection or peritonitis Abdominal exam – signs of bowel obstruction (Abdominal distension, Abdominal tenderness, Central resonance to percussion, Tinkling bowel sounds, Dehydration). Also scars ?adhesional bowel obstruction Hernia – Examine groin. If a strangulated hernia is present may have overlying red and tender skin. More likely to cause SBO. PR – obstructing mass / faecal impaction Bloods FBC - Raised WBC count may indicate an infective or inflammatory cause O complication such as perforation or impending perforation. Microcytic (iron deficency) anaemia may be found in the presence of an underlying malignancy. U+E Colon secretes potassium and bicarbonate in exchange for sodium chloride and water absorption. If this is disrupted in the obstructed colon may have resulting hypokalaemia. An increase in the urea shows the severity of dehydration/renal failure CRP- raised in infection or perforation G+S and co-ag- pre-surgery VBG - metabolic derangement (secondary to dehydration or excessive vomiting). High lactate ?ischaemia Basic Imaging AXR – diagnosis (May have rectal gas if PR performed) Erect CXR – looking for free air under the diaphragm if ?perforation Specialist Imaging CT more sensitive than AXR Differentiate mechanical vs. pseudo-obstruction; Site and cause of obstruction can be seen on a CT which is helpful for operation planning If malignant cause for obstruction may be able to see presence of metastases on a CT
68
SBO and LBO on x ray
SBO Tends to lie centrally in the X-ray Normal diameter is <3cm ‘Conniventes are continuous’ – cross the entire diameter of the bowel LBO Tends to lie around the edge of the abdomen Normal diameter is <6cm (<9cm at caecum) May contain faeces, which has a mottled appearance Haustra go half way’ – incomplete crossing of the bowel
69
Bowel obstruction management
NBM, IVI, fluid balance and or catheter Analgesia, antiemetic's SBO: Usually Drip and Suck LBO: Surgery Volvulus: Initial management is a flatus tube Recurrent or unresolving disease may necessitate surgery
70
Gallstone risk factors
Female Forty Fat Fair Fertile Family History Increased plasma oestrogen → Obesity, pregnancy, OCP, female Depletion of the bile acid pool → Terminal ileum resection or disease Lack of stimulus to GB emptying → Fasting, TPN Haemolytic Disorders → Spherocytosis, sickle cell disease or malaria
71
Gallstone types
20% Cholesterol Often solitary Large (>2.5cm) Smooth 75% Mixed Predominantly cholesterol Multiple stones ‘Generations’ Range of colours and shapes 5% Bile pigments Multiple Small Irregular and fragile
72
Biliary colic
PATHOPHYSIOLOGY Stone impacted in neck of GB or cystic duct PAIN Sudden, sharp, stabbing, RUQ-epigastric pain. Typically radiates to right shoulder and lasts <6 hours ASSOCIATIONS Pain may be precipitated by eating, (especially fatty foods) May have associated N+V EXAMINATION Typically unremarkable. Apyrexial. INVESTIGATIONS Typically unremarkable other than presence of stones on USS MANAGEMENT Analgesia Outpatient cholecystectomy
73
Cholecystitis
PATHOPHYSIOLOGY Stone impacted in neck of the GB or CD results in super concentrate, irritant, bile +/- infection via ascending gut bacteria (Klebsiella, E.coli) PAIN Constant RUQ-epigastric pain which persists Radiates to right shoulder ASSOCIATIONS May have N+V Likely to have fever and or lethargy EXAMINATION Tender RUQ with possible guarding. Murphy’s sign INVESTIGATIONS Raised inflammatory markers Mildly deranged AST/ALT/ ALP USS shows enlarged gall bladder with stone(s) and thickened walls MANAGEMENT Analgesia, NBM, IVI, IV Abx (cef + met) Cholecystectomy within one week
74
Cholangitis
PATHOPHYSIOLOGY CBD biliary outflow obstruction and ascending infection (most common E. coli) PAIN RUQ pain, persistent, may be colicky in nature ASSOCIATIONS Patient is jaundiced, typically unwell and pyrexial with rigors May also have pruritis, pale stool and dark urine Often causes sepsis EXAMINATION Tender RUQ with possible guarding Pyrexial, jaundiced INVESTIGATIONS Raised white cell count, blood cultures Raised Bilirubin Raised ALP/ GGT > AST/ALT USS will show dilated bile ducts +/- gall bladder stones +/-ductal stones MANAGEMENT Analgesia, NBM, IVI, IV Abx May need ERCP / open or lap stone removal
75
Gallstone Ileus
Inflammation of the gallbladder can cause a fistula between the gallbladder wall and the duodenum allowing gallstones to pass into the small bowel directly If a the stone impacts at the terminal ileum this results in small bowel obstruction
76
Causes of acute pancreatitis (Drugs in particular)
I-idiopathic G-gallstones (most common cause) E-ethanol (alcohol-2nd most common cause) T-trauma (esp stabs) S-steroids M-mumps A-autoimmune (eg: Lupus, Sjogrens) S-scorpion stings H-hypercalcaemia/hypertriglyceridaemia E-ERCP D-drugs (eg: azathioprine, furosemide, immunosuppressants, thiopurines, thiazides, furosemide, sodium valproate, steroids)
77
Acute Pancreatitis- Symptoms and Signs
N+V Epigastric pain with radiation to the back, relieved by sitting forward Cullen's sign - Bruising around periumbilical region Grey-Turner's sign - Bruising around flanks Sepsis
78
Pancreatitis investigations
Bloods; Amylase -> usually elevated Lipase -> these are elevated as well and are specific for pancreatitis Bone profile-> to look at calcium levels (for hypercalcaemia) Triglycerides-> to check for elevated triglyceride levels (and do normal bloods such as FBC, U+Es, LFTs, CRP) ABG- used for checking lactate and PaO2 Abdo X-ray-> may show ileus Ultrasound-> used to confirm or exclude gallstones CT abdo-> not done routinely but can be used to confirm diagnosis when uncertainty present and also used to look for complications
79
Glasgow scoring system - acute pancreatitis
PaO2 <7.9 kPa Age >55 Neutrophils >15 Calcium <2mmol/L Renal Urea >16mmol/L ERCP Albumin <32 G/L Sugar >10mmol/L
80
Management of Acute Pancreatitis
Fluids Analgesia (IV opiates) and anti-emetics NG tube if needed O2 Antibiotics if ?infection ERCP if GS induced
81
Complications of pancreatitis
Necrosis. This happens when the inflammatory process causes blood vessels to become leaky and then rupture leading to pancreatic tissue swelling. This causes premature activation of lipases which then starts to destroy peripancreatic fat. The fat and tissues liquefy and can start necrosing (process called Liquefactive Haemorrhagic Necrosis) Pseudocyst >4 weeks This is when fibrous tissue surrounds necrotic tissues and fills with pancreatic juices. The pseudocyst can also become infected to become an abscess and presents as sepsis This may cause abdominal pain, loss of appetite and a palpable tender mass. Abdominal CT scan is best way to assess for a pseudocyst/abscess Systemic hypovolemic shock ARDS DIC
82
Pancreatic pseudocyst - time of onset and treatment
Typically after 4 weeks Conservative management and monitoring Indications for active radiological fine needle aspiration would be signs of infection, mass effect on abdominal organs or a persisting pseudocyst beyond 12 weeks from it developing
83
AKI risk factors
Age > 65 years Chronic kidney disease Cardiac failure Chronic liver disease Diabetes Sepsis Hypovolaemia
84
Pre renal causes of AKI
HYPOVOLAEMIA Haemorrhage Dehydration Third space losses Increased urinary losses Burns Gastrointestinal losses HYPOTENSION Distributive shock FLUID OVERLOAD Cardiac failure Cirrhosis Nephrotic syndrome REDUCED CARDIAC OUTPUT Cardiogenic shock Arrhythmias Myocardial infarction Congestive cardiac failure VASCULAR Renal artery stenosis/ occlusion Drug-induced (e.g. NSAIDs, ACE-inhibitors) Renal vein thrombosis Abdominal aortic aneurysm
85
Intrinsic renal causes of AKI
GLOMERULAR Glomerulonephritis Thrombosis Haemolytic ureamic syndrome Ig A nephropathy ACUTE INTERSTITIAL NEPHRITIS Drugs (NSAIDS) Infection Autoimmune nephritis Lymphoma ACUTE TUBULAR NECROSIS Prolonged ischaemia Nephrotoxins (aminoglycosides, light chains in myeloma) Rhabdomyolysis (myoglobin) Radiocontrast agents VASCULAR Vasculitis Thrombosis/ emboli from angiography
86
Post renal causes of AKI
LUMINAL Stones Clots Sloughed papillae MURAL Malignancy Benign prostatic hyperplasia Strictures EXTRINSIC COMPRESSION Pelvic malignancy Retroperitoneal fibrosis
87
Signs and symptoms of AKI
SYMPTOMS Reduced urine output Nausea & vomiting Dehydration Confusion Fatigue SIGNS Dependent on underlying cause Look for the following: Fluid overload Hypotension Palpable abdominal mass Associated features of vasculitis
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Diagnosis of AKI (NICE)
A rise of serum creatinine > 26 micromol/L in 48 hours A 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days A fall in urine output <0.5mL/kg/hour for more than 6 consecutive hours Stage 1 AKI: Creatinine increase is 1.5 to 1.9 times baseline Stage 2 AKI: Creatinine increase is 2.0 to 2.9 times baseline Stage 3 AKI: Creatinine increase is 3.0 times baseline or more
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AKI Stages
Stage 1 AKI: Creatinine increase is 1.5 to 1.9 times baseline Stage 2 AKI: Creatinine increase is 2.0 to 2.9 times baseline Stage 3 AKI: Creatinine increase is 3.0 times baseline or more
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Investigations for ? AKI
BEDSIDE TESTS Urine dip Urine culture Observations ECG BLOODS U&ES, FBCs, LFTs, Clotting, CRP ABG for acid-basis imbalance Creatine kinase if indicated Immunology if indicated IMAGING Renal USS to r/o obstruction CXR if pulmonary oedema CT KUB if obstruction
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Complications from AKI
Hyperkalaemia Electrolyte imbalances: hyperphosphatemia, hyponatraemia, hypermagnesaemia, hypocalcaemia Metabolic acidosis Volume overload Uraemia Chronic kidney disease
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Acute and chronic causes of ureteric obstruction
Acute: Stones Clots (e.g. in frank haematuria) Severe constipation Chronic: Enlarged prostate Indirect backup of urine Strictures Malignancy Pregnancy Congenital abnormalities
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Risk factors for renal stones
Anatomical abnormalities E.g. horseshoe kidney, ureteral stricture HTN Gout Hyperparathyroidism Immobilisation Dehydration Metabolic disorders
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4 types of renal stones + info
Calcium stones: Account for 80% of all renal stones 80% of these are Calcium oxalate 20% are Calcium Phosphate Risk Factors include: low urine volume hypercalciuria e.g. primary hyperparthyroidism Urate stones Account for 15% of all kidney stones These are associated with high levels of blood purines - High levels of purine  increased breakdown and increased urate formation Dietary consumption - increased red meat Haematological disorders (myeloproliferation) These are radiolucent – so will not appear on X-ray imaging Struvite stones Account for only 4% of all kidney stones Formed of magnesium, ammonium, phosphate Often form large soft stones, and are the most common cause of ‘staghorn calculi’ – see next slide Cysteine stones Associated with familial disorders – inherited hypocystinuria (citrate is a stone inhibitor) affects absorption and transport of cystine in the bowel and kidneys.
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3 common sites where stone get lodged
Pelviureteric junction – PUJ (renal pelvis  ureter) Pelvic brim (iliac vessels transverse the ureter in the pelvis at roughly the midureter point) Vesicoureteric junction – (VUJ) ureter  posterior aspect bladder
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Signs and symptoms of ureteric stone
Ureteric Colic Sudden onset, severe, ‘loin to groin’ Associated N+V Haematuria 90% of cases Typically microscopic ?Concurrent Infection Rigors, fever, lethargy
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Imaging used for renal stones and potential findings
US CT KUB - Periureteric fat stranding may indicate recent stone passage, if a ureteric calculus is not present.
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Causes of frank haematuria - apparent and true
True: Malignancy of the renal tract Stones Infection Nephritis Bleeding disorders inc over anticoagulation Trauma Apparent Menstruation Dyes Drugs e.g. rifampicin
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Management of renal stones
Pain: PR Diclofenac IV paracetamol Opiates Buscopan If in the lower ureter or <5mm in diameter Fluid resuscitation as required, if dehydrated IV Abx and urology referral – If evidence of infection Large Stone/ Hydronephrosis Extracorporal shockwave lithotripsy Endoscopic removal Percutaneous removal Open surgery
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Surgical management of renal stones
Extracorporeal Shock Wave Lithotripsy (ESWL) sonic waves are used to break up the stone, which can then be passed spontaneously. This is reserved for small stones (<2cm), and is performed with radiological guidance (either X-ray or ultrasound imaging). Contraindications include pregnancy, or stones positioned over a bony landmark (e.g. pelvis). Most simple renal calculi (80-85%) can be treated with shock wave lithotripsy. Percutaneous nephrolithotomy (PCNL) is used for renal stones only, being the preferred method for large renal stones (including staghorn calculi). Percutaneous access to the kidney is performed, with a nephroscope passed into the renal pelvis. The stones can then be fragmented using various forms of lithotripsy. This is the treatment of choice for complex renal calculi, and staghorn calculi Flexible uretero-renoscopy (URS) involves passing a scope retrograde up into the ureter, allowing stones to be fragmented through laser lithotripsy with subsequent removal of the fragments. Ureteroscopy is the preferred treatment in patients who are pregnant or morbidly obese, or in patients with coagulopathy.
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Temporary measures to relieve obstruction and avoid renal damage in obstruction
Retrograde stent insertion is the placement of a stent within the ureter, approaching from distal to proximal via cystoscopy. It allows the ureter to be kept patient and temporarily relieve the obstruction. Commonly, these stents are called “J-J stents”, as they are curled at each end to prevent damage to the kidney or the bladder, and in order to reduce the risk of them becoming dislodged. Nephrostomy is a tube placed directly through the skin on the back, into the renal pelvis and collecting system, relieving the obstruction proximally. If required, an anterograde stent can subsequently be passed via the same tract made
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Renal cell carcinoma: Presentation Pathology Diagnosis Treatment Prognosis
Presentation 60% of patients have haematuria Other symptoms include mild loin discomfort and a loin mass Pathology Invades along the renal vein to the IVC, and spreads via haematological route Forms Parathyroid Hormone-Related Protein (PTH-rp) so patients may get pathological fractures Diagnosis Typically forms a solid mass on USS; also seen on CT scan Bloods commonly show anaemia and may show a raised ALP and ESR Treatment Radical nephrectomy No role for chemo/radiotherapy – Tyrosine Kinase Inhibitors can be useful; as can renal artery embolisation Prognosis Classically causes cannonball lung metastases Even T1 disease has only a 70% 5yr prognosis. Average survival with Metastases is <2 years
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Parasitic cause of bladder cancer
Schistosomiasis
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Bladder cancer Presentation Pathology Diagnosis Treatment Prognosis
Presentation Typically presents with painless haematuria Risk factors: Male, Smokers, Age 50+, Dyes/Rubber, Schistomiasis Pathology Due to prolonged carcinogen contact is common Initially forms carcinoma-in-situ Diagnosis Screening undertaken of those who work in at-risk industries Usually diagnosed visually (with biopsies) on flexi-cystoscopy Treatment Cystoscopic removal of the tumour +/- intravesical BCG In extensive cases radical cystectomy may be required Recurrence We need to look for parallel primaries in the entire urinary tract 50% chance of recurrence so follow-up is life-long
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Prostate cancer Presentation Pathology Diagnosis Treatment Prognosis
Presentation 2/3 men dying aged over 80 have prostate cancer! Most common presentation is raised PSA, but 20% have normal PSA Pathology Usually peripherally located Metastasise to bone and iliac/para-aortic nodes Diagnosis Trans-rectal biopsy Graded with Gleason scoring – 2 biopsies graded on malignancy 1-5 Total score is most common cell type + second most common type Staging If 7+ then we also do a staging MRI T1 = incidental, T2 = within capsule, T3 = through capsule/seminal vesicles, T4 = other Treatment Small, well differentiated disease volume = active surveillance Endocrine therapy to reduce testosterone in locally advanced/bony disease +/- Radiotherapy Surgery – TURP (usually for symptoms) or radical prostatectomy
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Types of bladder cancer
Transitional cell - most common Adenocarcinoma - glandular tissue from patent urachus/median umbilical lig. Squamous cell - when TC metaplasias to squamous due to chronic inflamm. e.g. parasitic
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UTI-Host-dependent risk factors
Female: have shorter urethra which is closer to the anal and genital regions so can have spread of bacteria from here to colonise vagina leading to ascending UTIs Pregnancy: hormonal changes leads to urinary stasis and vesicoureteric reflux Postmenopause: lower levels of oestrogen causes decreased amounts of lactobacilli which leads to increased pH therefore perfect conditions for E.coli colonisation Structural abnormality of the urinary tract: this would prevent bladder from emptying previous UTI Diabetes mellitus history of kidney surgery immunosuppression
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UTI pathogens
E. coli- most common cause (80-85%) 2. Staph. Saprophyticus- commoner in young, sexually active females (5-10%) 3. Enterococci 4. Proteus 5. Klebsiella 6. Pseudomonas- more likely from catheterisation
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Lower UTI- clinical features
Dysuria Typically “burning” in nature Haematuria Frequency/Urgency Suprapubic Pain Foul smelling/cloudy urine Confusion Lethargy Fatigue
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UTIs on dipstick
Leucocytes and nitrites
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Lower UTI-Treatment
Simple uncomplicated UTIs are treated with antibiotics: Most commonly Trimethoprim or Nitrofurantoin (though resistance is increasing, ~20% e-coli). 3 day course for women 7 day course for men
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Upper UTI-clinical features
Dysuria Typically “burning” in nature Frequency Flank Pain > Suprapubic Pain Haematuria High grade fever Nausea + Vomiting *Pyelonephritis usually has an acute onset and patient’s are usually systemically unwell
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Upper UTI-Treatment
If severe symptoms, patients will need to be admitted to hospital and have a 7 day course of IV antibiotics (Cefuroxime or Ciprofloxacin). If not severely unwell, patients can have oral antibiotics (Ciprofloxacin, Trimethoprim or Co-Amoxiclav) Drink lots of fluid to prevent dehydration May need to have imaging (USS KUB) to look for structural damage or changes
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Painless and painful scrotal lumps
Painless: Tumour cyst haem, varico,hydrocoele Painful: Torsion Epididymo-orchitis Strangulated inguinal hernia
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Varicocele
Abnormal dilatation of the testicular veins in the pampiniform plexus, caused by venous reflux More common on the left due to anatomy (90%) Presentation ‘Bag of worms’ appearance due to distended veins Presents as a lump with a dragging sensation Disappears on lying down, reappears on standing, ++ with Valsava Dull ache/ painless Associated with subfertility Management Embolisation or surgical ligation of veins only indicated in the following: Painful Oligospermia Children
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Hydrocele
Abnormal collection of peritoneal fluid between the parietal and visceral layers of the tunica vaginalis that envelopes the testis Presents as a painless fluctuant swelling that will transilluminate, either unilateral or bilateral Can be congenital Communicating: Persistence of the processus vaginalis allows peritoneal fluid to communicate freely with the scrotal portion of the processus Mostly congenital but may occur later if increased intra-abdominal pressure, peritoneal dialysis, or fluid overload Non-communicating: Due to imbalance between secretion and reabsorption of fluid Can occur secondary to minor trauma, testicular torsion, epididymitis.
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EPIDIDYMAL CYSTS/ SPERMATOCELE
Epididymal cyst= benign fluid-filled sacs arising from the epididymis Spermatocele= benign sperm-filled sacs arising from epididymis Common pathology, especially in middle-aged men Presents as painless lump(s) *superior and posterior* to the testis: Chronic onset Smooth, well-defined and fluctuant Transilluminate Separately palpable to the testes No increased risk of malignancy and generally no need for intervention Only need surgical intervention if large or painful
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EPIDIDYMO-ORCHITIS
Caused by infection that has spread from urethra or bladder In men < 35 years, STIs most common cause (chlamydia, gonorrhoea) In men > 35 years, urinary tract infections most common cause ( e.coli, pseudomonas) Mumps can cause orchitis Extrapulmonary TB Presents as unilateral scrotal pain and swelling: Onset over hours/days Tender Oedematous swelling Dysuria Fever Urethral discharge Management: Analgesia, scrotal support Abx STI screen (abstain from sexual intercourse)
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Testicular torsion
Spermatic cord twists within the tunica vaginalis  occlusion of testicular blood vessels  compromised blood supply  ischaemia Emergency BELL CLAPPER DEFORMITY Lack of normal fixation of the posterior lateral aspect of the testes to the tunica vaginalis BELL CLAPPER TESTIS Horizontal lie of the testis rather than vertical Presentation Sudden onset pain in one testis, which makes walking uncomfortable Can be intermittent Can come on during physical activity Nausea and vomiting Abdominal pain Signs Younger patient Inflammation- red, hot, tender and swollen testis Testis may be high lying and transverse Lifting testis up worsens pain Absent cremasteric reflex 4-6 hour window to salvage the testis Treatment is the untwisting of the cord and the testis and bilateral orchidoplexy +/- orchidectomy
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Testicular cancer
Risk factors include: White ethnicity Family history Undescended testes (even if fixed) Infertility Infant hernia Klinefelters Painless testicular lump Mass tends to be irregular, fixed and firm Does not transilluminate Signs of metastases include weight loss, back pain or dyspnoea Secondary hydrocele Effects of secreted hormones - gynaecomastia Elevation of tumour markers support diagnosis (normal levels do not exclude) Alpha-fetoprotein is produced in yolk sac tumours B-hCG produced in teratomas and seminomas USS Excision biopsy Can be staged via CT CAP
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Types of testicular cancers and markers and prognosis
Germ cell (95%) Seminomas - better prognosis, B-HCG Non-seminoma - teratomas (Alpha-feto protein AFP), embryonal, yolk sac, choriocarcinoma (more likely to spread) Non germ cell 5%
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PHIMOSIS
Inability to retract the foreskin back Can be: Physiological (only retractable from > 2 years old) Pathological Caused by chronic infection (balanitis) caused by poor hygiene or trauma from forcible retraction Clinical presentation: Dribbling on micturition, weak stream, haematuria Painful erections Recurrent UTI Management options include good hygiene, steroid cream or circumcision
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PARAPHIMOSIS
Result of tight foreskin being retracted and then unable to be replaced -> acts as a constricting band causing oedema UROLOGICAL EMERGENCY Clinical Features: Swelling after the constriction Painful erection May progress to necrotic glans Management Analgesia Manual reduction Swelling reduction: Compression, Ice, Swab soaked in 50% dextrose, ‘Puncture’ technique Surgical reduction and circumcision
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PRIAPISM
Continued erection > 4 hours Does not subside with ejaculation Risk Factors: Sickle cell disease, sildenafil, antidepressants, cannabis, cocaine, leukaemia, pelvic tumours Low flow / Ischaemic Blood does not drain Most common, intermittent Painful Nerve block + needle aspiration Shunt surgery High flow Increased arterial flow Rarer, usually due to trauma Less painful Cold packs and compression wee, walk, drink, shower)
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Penile cancer
Squamous cell carcinoma, originating in the glans/prepuce Rare in developed countries and circumcised males Risk factors: Phimosis HPV – particularly 16, 18 Presentation: Burning sensation, itch, ulceration which progresses to a mass Mets to liver or lung Management Partial/total penectomy Limited response to chemo/radiotherapy
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LUTS in BPH
Voiding symptoms: hesitancy, poor stream, dribble due to obstruction LEADS TO Storage symptoms: frequency, urgency, incontinence, nocturia due to bladder dysfunction Which leads to chronic retention
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BPH management
Alpha blockers: relax smooth muscle in prostate + bladder neck; side fx - hypotension, ED, retrograde ejaculation, headache, nasal congestion 5AR inhibitors: inhibit DHT production; side fx - decreased libido, ED, teratogenicity TAKE 6MONTHS to work ISC/LTC Surgical: TURP Urolift, HoLEP, PVP, PAE, Rezum, Aqua-ablation
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Prostate cancer treatment
LHRH agonists [AKA GnRH agonists] e.g. triptorelin [Decapeptyl], goserelin [Zoladex] Prevent pituitary gland from secreting LH Risk of androgen flare: given alongside anti-androgen therapy initially LHRH antagonists [AKA GnRH antagonists] e.g. degarelix [Firmagon] Prevent LHRH from binding to its receptors in the pituitary gland Do not cause androgen flare Surgical castration Bilateral orchidectomy Androgen-receptor blockers e.g. bicalutamide [Casodex], enzalutamide [Xtandi] Compete for binding to the androgen receptor Androgen synthesis inhibitors e.g. abiraterone Prevent production of androgens by all tissues that produce them CYP17 enzyme inhibitor External beam radiotherapy (EBRT): Radiation from external source Brachytherapy: Implantation of radioactive pellets LDR vs HDR brachytherapy Radium-223 [Xogifo]: For advanced metastatic Ca prostate
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Management for: Scenario 1: 56yo M, PSA 11, otherwise fit + well DRE: firm R lobe MRI: PIRADS 4 lesion R peripheral zone (T2a) LA TP bx: Gleason 3+3 = 6, low volume Scenario II: 68yo M, PSA 21, PMHx HTN, diet controlled DM DRE: nodular L lobe MRI: PIRADS 4 lesion abutting L capsule (T2c) LA TP bx: Gleason 4+4 = 8 Scenario III: 89yo M, PSA 740, ALP 300, PMHx COPD, IHD, OA Bone scan: widespread metastatic disease
I - Active surveillance II - Radical prostatectomy vs Radiotherapy + hormone treatment III - Palliation
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Gleason scoring
Low (≤ 6) vs intermediate (7) vs high risk (8-10)
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Age specific PSA referral thresholds for suspected prostate cancer [updated Dec 2021]:
40-49yrs: >2.5mcg/l 50-59yrs: >3.5mcg/l 60-69yrs: >4.5mcg/l 70-79yrs: >6.5mcg/l
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prostatitis
E coli, enterobacter, proteus, Neisseria gon, Chlamydia 14 days quinalone e.g. Cipro
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Aneurysm clinical definition
a localised dilatation of an artery with a permanent diametre that is >1.5x its usual size
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True vs false aneurysms
True aneurysms are where the wall of the artery forms the aneurysm False aneurysms (aka pseudoaneurysm) are where other surrounding tissues form the wall of the aneurysm; These are aneurysms that are caused by a small hole in the blood vessel wall which allows blood to leak out and pool around the vessel
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2 types of true aneurysms
Fusiform: where artery wall balloons out symmetrically Saccular (aka Berry aneurysms): where artery wall only balloons out on one side of the artery (possibly due to weakening of that artery wall)
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Where are abdo aneurysms most commonly located?
40% occur in Thoracic aortic section 60% occur in Abdominal aortic section (AAA) 95% of AAA occur below the point where the renal arteries branch out of the abdominal aorta
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RF for AAA
CVD as always Marfan’s syndrome--fibrillin and other elastic properties are impaired therefore causing weak blood vessel walls -Ehlers-Danlos syndrome--ability to form collagen properties are disrupted Coarctation of aorta Pregnancy
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Complications of an aortic aneurysm near the heart
A thoracic aneurysm near the aortic valve prevents the valve from shutting properly, meaning backflow of blood into the left ventricle during diastole (aka Aortic Insufficiency)
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AAA investigations
Abdominal Ultrasound scans-to stage aneurysm. It shows location of the aneurysm and to follow up cases to assess development CT Angiography-to create highly detailed image of aneurysm and surrounding structures
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Surgical Management of aneurysm - when and what
If ruptured orIf aneurysm is Unruptured, but: Symptomatic OR asymptomatic and > 5.5 cm OR asymptomatic, larger than 4.0 cm and has grown by more than 1 cm in 1 year Endovascular Aneurysm repair - an aortic graft is transmitted through the femoral artery into abdominal aorta. a catheter is used to guide the graft to its location. this is inflated at the site of the aneurysm and its ‘arms’ are pulled into the branches of the femoral artery. blood flows smoothly through the graft or open surgery - recommended if pt suitable
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abdo Aneurysm-Surveillance who and what
All men >66 Chronic obstructive pulmonary disease (COPD) Coronary, cerebrovascular or peripheral arterial disease European family origin family history of AAA Hyperlipidaemia Hypertension Smoking history (including ex- and current smokers) offer yearly surveillance if AAA = 3.0-4.4cm offer 3 monthly surveillance if AAA = 4.5-5.4cm
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Popliteal aneurysm: Management
Conservatively: if aneurysm <2cm, continue with duplex surveillance 2. Surgical: same approach as with AAA -EVAR -Open
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Aortic Dissection - what and usual location
the inner layer (intima) of the aorta tears. This causes blood to surge through the tear causing the inner and middle layers (media) to separate Dissection usually occurs at the first 10 cm of Thoracic aorta
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Aortic Dissections are classified into either DeBakey or Stanford classification
DeBakey Classification I- intimal tear is in ascending aorta and descending aorta is also involved II- only ascending aorta is involved III- only the descending aorta is involved -Stanford Classification A- ascending aorta is involved (same as DeBakey I & II) B- descending aorta is involved (same as DeBakey III)
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Aortic Dissection complications (3)
1. Blood from the false lumen can flow up the aorta back into the heart and into the pericardial sac leading to a pericardial tamponade 2. Blood flowing through the false lumen could puncture the tunica media and externa leading to a rupture 3. The false lumen can also cause compression of nearby vasculature such as subclavian or renal artery leading to hypoxia of upper limbs or kidneys respectively.
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Aortic dissection Investigations
1. CXR- Would show a widened mediastinum due to widened aorta 2. Transoesophageal Echo (TOE)- more sensitive 3. CT Angio- will give a more detailed picture of the blood vessels and tear in the vessels
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Management of aortic dissections; stable and unstable/complicated
if stable, chronic aortic dissection: Main aim of treatment is to reduce BP using antihypertensives and B-blockers Type A - surgery + i.v. labetalol Type B - medical (i.v. labetalol) Emergency surgical repair is done if there is Increasing aortic diameter Compromise of major branches of aorta Impending rupture Bleeding into thoracic cavity -Surgical management involves resecting and replacing the area of the aorta with intimal tear
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ATHEROSCLEROSIS: COMMON SITES
Circle of Willis Carotid arteries Popliteal arteries Coronary arteries Abdominal aorta
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Intermittent claudication Critical limb ischaemia Acute limb ischaemia
Intermittent claudication - diminished circulation leads to pain in the lower limb on walking or exercise that is relieved by rest Critical limb ischaemia - where circulation is so severely impaired that there is an imminent risk of limb loss Acute limb ischaemia - sudden decrease in arterial limb perfusion, due to thrombotic or embolic causes
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Chronic peripheral arterial disease causes
Atherosclerosis Vasculitis Fibromuscular dysplasia
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Intermittent claudication symptoms
Gripping, cramp-like pain typically in the calves Induced by exercise Typically relieved by rest Usually predominates in one leg Reproducible
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Cauda equina vs intermittent claudication
Cauda equina: Variable claudication distance Pain often better when walking uphill but worse downhill Pain disappears after 15-30 mins typically Examination findings: LMN findings such as reduced reflexes but pulses present as normal Spinal claudication is typically relieved by flexing lumbar spine. Arterial insufficiency: Fixed claudication distance Pain exacerbated by walking uphill, better downhill Pain disappears after 1-2 mins of rest typically Examination findings: Absent peripheral pulses and reduced ABPI but no evidence of neurological findings
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Progression of intermittent claudication
At first, exercise induced intermittent claudication then the claudication distance may reduce then pain even at rest then finally symptoms of critical limb ischaemia such as gangrene.
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Clinical signs of ischaemic limb
Pale, cold and hairless legs Reduced CRT Arterial ulceration Arterial bruits Weak or absent pulses
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Arterial ulcers
Deep Punched out Painful Small Present over toe joints, heel and lateral aspect of leg (malleolus commonly
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Infected necrotic tissue =
gangrene
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Investigations for critical limb ischaemia
BEDSIDE TESTS Observations ECG - 60% of patients will intermittent claudication have evidence of CVS disease on their ECG BLOODS FBCs - Anaemia and polycythaemia will aggravate PAD ESR Thrombophilia screen Lipid levels Blood glucose SCANS ABPI Duplex USS to determine the site of the disease and indicate the degree of stenosis and length of the occlusion. MRI / CT angiography offered prior to revascularisation via angioplasty (stenting) or reconstructive surgery.
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ABPI readings
>1.2 = abnormally hard vessel => do a TBPI 1-1.2 = normal 0.8-0.9 = mild arterial disease/claudication => manage RF 0.5-0.79 = moderate arterial disease/severe claudication = routine referral <0.5 = severe arterial disease/pain at rest = urgent referral
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Acute limb ischaemia causes (2), severity, RF
Thrombotic (85%) acute on chronic less severe peripheral vascular disease, Ischaemic heart disease, cardiovascular disease, Presence of graft, Blood disorders Embolic (15%) very sudden very severe; no collaterals AF, endocarditis, mitral stenosis, aneurysms, grafts, atherosclerotic disease
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Conservative treatment for peripheral arterial disease
Supervised exercise programme to develop sufficient collateral circulation/vessels. Statins Antiplatelet therapy - clopidogrel Peripheral vasodilators
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Classical presentation of acute limb ischaemia
Pain — constantly present and persistent. Pulseless — ankle pulses are always absent. Pallor (or cyanosis or mottling). Power loss or paralysis due to nerve ischaemia Paraesthesia or reduced sensation or numbness. Perishing with cold.
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Management of acute limb ischaemia
Urgent admission required- only 6 hours to save limb First step is heparinisation If embolus, treatment is surgical embolectomy or intra-arterial thrombolysis If thrombus, treatment is angioplasty, bypass surgery or intra-arterial thrombolysis
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Signs of Irreversible limb ischaemia and management
mottled non-blanching appearance with hard woody muscles requires urgent amputation or taking a palliative approach
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acrocyanosis
Persistent cyanosis of peripheries due to spasm of cutaneous vessels
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livedo reticularis
Mottled reticular pattern, purple discolouration, decreased flow through arterioles.
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Raynaud's disease primary vs secondary
paroxysmal vasospastic and subsequent vasodilatory chain of events affecting small peripheral arterioles Pale -> Blue -> Red (reactive hyperaemia) Primary is more likely to present as a younger patient, female with a genetic component with no features of underlying disease Secondary is more likely to present as a older patient, with more severe symptoms (digital scars, ulceration or gangrene and nail changes) Secondary causes include: Autoimmune diseases- Scleroderma, SLE, rheumatoid arthritis Environmental- smoking, trauma, chronic vibration, chemical exposure Endocrine- diabetes, hypothyroidism Arterial- Buerger’s disease Blood- lymphoma, polycythaemia Drugs- B-blockers, COC, cytotoxic agents
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Selection of amputation site
Proximal sites more likely to heal than distal Likelihood of successful rehabilitation AKA requires 100% more energy to walk BKA requires 25% more energy to walk Wheelchair requires 8% more energy on a flat surface
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Compare lower limb amputation sites
Above knee Advantages Likely to heal Suitable if patient has fixed flexion deformity of knee Disadvantages Prosthesis more difficult to fit Uses 100% more energy to walk Heavier prosthesis Need to incorporate knee into prosthesis <50% patient achieve meaningful ambulation Through Knee Advantages Useful to provide a long lever when patient is bed or chair bound Disadvantages Difficult to fit a prosthesis so use AKA if patient is likely to be able to use a prosthesis Below knee Advantages High chance ( c 80%) of successful rehabilitation in motivated individuals Likely to heal if palpable femoral pulse Disadvantages Prone to develop fixed flexion contracture if no prosthesis used.
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Varicose veins: Clinical Features
Enlarged, tortuous veins in leg Pruritus Oedema Yellow or Red-Brown skin pigmentation; Due to RBC breakdown causing haemosiderin release Pain; Worse on standing, better when walking
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Complications of Varicose veins/venous ulcer:venous insufficiency
Ulcers Thrombophlebitis Bleeding from minor trauma Venous eczema Lipodermatosclerosis(upside down champagne bottle appearance) Atrophie Blanche
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Venous Ulcers
Shallow Sloping, gradual outline Generally minimal pain Often fairly large Very wet, lots of exudate Usually present at medial malleolus
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Thrombophlebitis
This is inflammation and thrombosis of a superficial vein. Painful and red veins Compression stockings
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Management of varicose veins
Conservative; compression stockings Surgical; vein ablation, vein removal
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Lymphoedema and types
Lymphoedema is a chronic swelling resulting from failure of lymphatic drainage. There are 2 types of lymphoedema: Primary- occurs due to intrinsic genetic abnormality of lymphatic system Secondary- occurs when there is damage to otherwise normally functioning lymphatic system
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Causes of secondary lymphoedema:
Cancer treatment, infection, trauma Venous oedema Oedema assoc. with immobility Obesity Heart Failure Oedema of advanced cancer or other advanced condition (e.g liver disease)
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Complications of colorectal cancer
Bowel Obstruction Bowel Perforation Iron Deficiency Anaemia Hepatic and Peritoneal Metastasis Bone and Lung Metastases Colo-vesical fistula
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Symptoms from colorectal metastatic spread
Jaundice, RUQ pain, early satiety due to hepatic metastases Ascites or pain, from peritoneal metastases Pneumaturia or recurrent UTI, due to a colo-vesical fistula Weight loss
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Most common symptoms of left sided, right sided and rectal colorectal cancers
Right: pain, change in bowel habits, mass, weight loss Left: obstruction, pain, change in bowel habits, mass Rectal: bleeding, change in bowel habits
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Colorectal cancer screening
Nationally in the UK, FIT screening is done every 2 years between the ages of 50 and 74.
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Stage I-II colorectal cancer and treatmenr
Local spread only Elective Surgery– segmental resection and primary anastomosis or permanent stoma Meso-colic or meso-rectal excision Robotic, laparoscopic or open Total colectomy for - FAP, HNPCC or synchronous cancers Achieve clear margins in locally invasive cases
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Stage III colorectal cancer treatment
Colon cancer: surgery followed by adjuvant chemotherapy 6 months of oxaliplatin-based chemotherapy e.g. oxaliplatin plus 5-FU, or oxaliplatin plus capecitabine Rectal cancer: neoadjuvant chemoradiotherapy for rectal cancer followed by surgery or watch and wait
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Stage IV colorectal cancer treatment
Liver or Lung resection for resectable metastases Chemotherapy for palliative management:
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Diverticulum Diverticulosis Diverticular Disease
Diverticulum= an outpouching of the bowel wall. Diverticulosis = presence of diverticula Diverticular Disease = Presence of diverticula + symptomatic
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True vs false diverticulum
True (involving all layers of the intestine - serosa, muscle, submucosa, mucosa) OR False (does not contain all layers- often mucosa pushed through muscle defect)
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Colorectal cancer locations and indicated surgery Caecal Ascending Proximal transverse Distal transverse Descending Low sigmoid high rectal rectal Anal verge bowel obstruction/perf
Caecal, ascending or proximal transverse colon - Right hemicolectomy Distal transverse, descending colon Left hemicolectomy Sigmoid colon High anterior resection Upper rectum Anterior resection (TME) Low rectum Anterior resection (Low TME) Anal verge Abdomino-perineal excision of rectum
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Meckels diverticulum
An outpouching in the lower part of the small intestine. It is a congenital abnormality - a leftover of the umbilical cord with incomplete closure of the omphalomesenteric duct. Affects 2% of population 2 years old 2:1 M:F ratio 2 inches long 2 feet proximal to ileocaecal valve 2 types of ectopic tissue (Gastric/Pancreatic)
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Marker of bowel inflammation blood test
foecal calprotectin
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Specific investigations for diverticular disease
Routine flexible sigmoidoscopy or colonoscopy or if not fit CT colonogram
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Specific investigations for diverticulitis
VBG/ABG- ↑ lactate Blood cultures Erect CXR-for pneumoperitoneum indicating perforation AXR- to look for bowel obstruction USS abdomen/pelvis CT abdomen/pelvis; may show thickening of the colonic wall, pericolonic fat stranding, abscesses, localised air bubbles, or free air. AVOID ENDOSCOPIC PROCEDURES DUE TO RISK OF PERFORATION – plan for after acute episode
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Specific investigations for diverticular bleed
Group & Save and Crossmatch – for blood transfusion Urgent colonoscopy to find source of bleeding and treat it if indicated
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Management of diverticulitis with perforation
For acute complicated diverticulitis (perforation), surgical management may be indicated. Hartmann's procedure or sigmoid resection with primary anastomoses are most likely.
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Complications from diverticulitis
Pericolic abscess: Collection of pus within the large bowel wall Presents with swinging fevers, mass on examination and generally unwell If small, can be treated with antibiotics Normally need USS or CT-guided percutaneous drainage Fistula: Abnormal connection between two epithelialized surfaces. Colovesical Fistula = abnormal connection between the colon and the bladder, present with pneumoturia (bubbles in urine), faecal matter in urine and recurrent UTIs. Colovaginal fistula= abnormal connection between the colon and the vagina, present with faecal matter in vagina and recurrent vaginal infections. Surgical intervention is usually indicated. Perforation Bowel obstruction
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Position of anal vascular cushions
3, 7 and 11 o clock
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Perianal abscess - what can form
cryptoglandular infection fistula in ano
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management of fistula in ano
Seton fistulotomy Oral metronidazole
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Anal fissure management
Dietary Laxatives Diltiazem/gtn spray to reduce spasms Botox /lidocaine if less than one week Sphincterotomy
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Adenoma surveillance programme i.e. how many adenomas to how often colonoscopy
low risk (1-2 adenomas < 10 mm, colonoscopy at five years), intermediate risk (3-4 adenomas < 10 mm or 1-2 adenomas with one ≥ 10 mm, colonoscopy at three years), high risk (≥ 5 adenomas < 10 mm or ≥ 3 adenomas with one ≥ 10 mm, colonoscopy at one year).
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Epididymo-orchitis investigations
sexually active younger adults: NAAT for STIs older adults with a low-risk sexual history: MSSU
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If a diagnosis of acute cholecystitis remains uncertain after ultrasonography, what can be done if clinical suspicion is still high ?
Technetium-labelled HIDA scan
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Investigation for ?chronic pancreatitis
CT is more sensitive at detecting pancreatic calcification. Sensitivity is 80%, specificity is 85% functional tests: faecal elastase may be used to assess exocrine function if imaging inconclusive
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Haemorrhoids treatment
Acute pain - ice, analgesia, instillagel, laxatives, increase fibre intake. Banding, ligation, haemorrhoidectomy
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Haemorrhoids treatment
Acute pain - ice, analgesia, instillagel, laxatives, increase fibre intake. Banding, ligation, haemorrhoidectomy
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NICE advise that, as PSA levels may be increased, testing should not be done within at least:
6 weeks of a prostate biopsy 4 weeks following a proven urinary infection 1 week of digital rectal examination 48 hours of vigorous exercise 48 hours of ejaculation