Abdomen Flashcards
What are the branches of the abdominal aorta?
Hint: Prostitutes Cause Sagging Swollen Red Testicles [in men] Living In Sin
Inferior phrenic - T12 parietal
Coeliac (unpaired) - T12
SMA (unpaired) - L1
Middle suprarenal - L1
Renal - L1-2
Testicular - L2
Lumbar - L1-4
IMA (unpaired) - L3
Median sacral (unpaired) - L4 parietal
-> common illiac (L4)
What are the anterior relations of the abdominal aorta?
Coeliac trunk
SMA
Pancreas body
Duodenum 3rd part
Left renal vein
What are the surface markings of the transpyloric plane? What is the relevance of this?
L1
Half way between jugular notch and public symphysis
At this point you’ll find?
GB fundus
SMA coming off abdominal aorta
Duodenum 1st part
Pancreatic neck
Splenic vein + SMA -> portal vein
9th CC - hilum of spleen
What are the different types of aneurysm that can affect the abdominal aorta?
Aneurysm = abnormal dilatation of vessel wall that happen due to median cystic necrosis
Risk factors: HTN, bicuspid AV, marfans & syphilis
- Saccular: outpouching of one side
- Fusiform: outpouching of both sides
- False aneursym: extravasation of blood & connective tissue in extravascular connective tissue (post-traumatic normally)
- Dissection: extravasation of blood due to tear in intima - can propagate proximal and distal -> rupture/haemorrhage, acute MI (ascending aorta) & stroke (arch)
What are the branches of the coeliac trunk?
Hint: Left Hand Side
- Left gastric: oesophageal branches
- Common hepatic: right gastric, gastroduodenal (> R gastroepiploic + sup. pancreaticoduodenal) & L + R hepatic proper
- Splenic: left gastroepiploic, short gastrics & pancreatic
In the abdomen where do the major venous structures lie when compared to the arterial?
Venous structures are to the right of the arterial e.g. IVC to right of aorta & SMV to right of SMA
What are the branches of the SMA?
Inferior pancreaticoduodenal
Ileal
Jejunal
Ileocolic (-> appendicular)
Right colic
Middle colic
What are the branches of the IMA?
Left colic
Sigmoidal
Superior rectal
What are the tributaries of the IVC?
Hint: I Like To Rise So High
Illiacs - L5
Lumbar - L1-5
Testicular/gonadal - L2
Renal - L1
Suprarenal - L1
Hepatic - T8*
Pierces diaphragm + inf. phrenic vein
What are the anterior relations of the renal vein?
On the right: 2nd part of duodenum
On the left: SMA, pancreatic body & splenic vein
What are the lobes of the liver?
R & L
Caudate (superiorly)
Quadrate (next to GB inferiorly)
Caudate + quadrate anatomically part of right lobe but functionally part of left lobe as they recieve blood supply from left hepatic arteries/portal vein + drain into left hepatic duct
What are the structures of the porta hepatis?
Ant-post:
CBD
Portal vein
Hepatic artery
All within free edge of lesser omentum (hepatoduodenal ligament) = epiploic foramen of Winslow - communication between lesser & greater sac where pringles manouvre can be performed to stop bleeding
Borders of epiploic foramen: caudate lobe (S), D1 (I) & hepatoduodenal ligament (A)
What are the ligaments of the liver?
- Triangular ligament: connects it to diaphragm
- Coronary ligament (ant/post): connects it to diaphragm + demarcates bare area
- Falciform ligament: connects to AAW + diaphragm - free edge contains ligamentum teres (remnant of umbilical vein)
- Lesser omentum: attaches to lesser curve of stomach + 1st part of duodenum consisting of hepatogastric ligament + hepatoduodenal ligament
- Ligamentum venosum: from porta hepatic to IVC - remnant of ductus venosus (shunts umbilical vein blood to IVC directly)
Note: falciform + ligamentum venosum demarcate R + L lobe ant/post respectively - this corresponds with line from IVC to GB fossa
What are the first 2 organs injured in a stab to the epigastrium?
Liver (left lobe)
Stomach
What is the blood supply, venous drainage, nerve supply & lymph drainage of the liver?
Portal vein (75%) & hepatic artery (25%)
Venous drainage: hepatic veins -> IVC
Nerve supply: hepatic plexus containing sympathetic (coeliac) & PS (CNX) fibres entering at porta hepatis following artery/vein
Note: Glissons capsule (fibrous covering) innervated by lower IC n.’s allowing sharp localised pain on stretching
Lymphatic drainage:
Ant: hepatic -> coeliac -> cisterna chyli
Post: phrenic + post. mediastinal nodes -> R lymphatic + thoracic duct
What are the hepatic recesses?
- Subphrenic: diaphragm + liver
- Subhepatic: inferior liver + transverse colon
- Subhepatic pouch of Rutherford Morrison (R): potential space between liver + R kidney (DEEPEST PART OF PERITONEAL CAVITY WHEN SUPINE SO MOST COMMON COLLECTION POINT)
What are the surface markings of the GB?
Fundus, body, neck, Hartmans pouch + cystic duct
Fundus @ L1 transpyloric plane
At angle between 9th CC + lateral rectus sheath margin
MCL
Why does gallbladder pain refer to the shoulder tip?
Irritation of phrenic nerve with roots C3-5 which are the same dermatomes supplying shoulder via supraclavicular nerve
What is the blood supply, venous drainage, nerve supply & lymph drainage of the GB?
Cystic artery (right hepatic)
Cystic veins -> portal vein (neck)
Fundus/body venous drainage -> hepatic sinusoids
PS: CNX
Sympathetic + sensory: coeliac plexus
Contraction mediated by cholecystokinin
Lymph: cystic -> hepatic -> coeliac
What is the anatomy of the biliary tree?
Bile secreted from hepatocytes and drains from both lobes of liver via canaliculi, intralobular ducts + collecting ducts into L/R hepatic ducts -> CHD + cystic duct -> CBD + pancreatic duct -> ampulla of vater empting into major duodenal papilla (regulated by sphincter of Oddi)
What is calots triangle?
Cystohepatic triangle of safety
Borders: inferior liver (S), cystic duct (I) & CHD (M)
Contents: right hepatic artery, cystic artery, LN of lund + other lymphatics
What organs are normally palpable in abdomen?
Lower pole of right kidney
Abdominal aorta
Liver/spleen in pathologt
Liver surface anatomy?
Along nipple line to left MCL 5th ICS
Down to 10th rib inferiorly on right
What are the functions of the spleen?
HINT: FISH
Filtration of encapsulated organisms + blood cells
Immunological function
Storage of platelets
Haematopoiesis in foetus
Structures at risk in splenectomy?
Tail of pancreas
Left kidney
Diaphragm
Splenic flexure of colon
Ligaments of spleen?
Gastrosplenic: contains short gastrics + left gastroepiploic
Lienorenal: splenic vessels + tail of pancreas
What are the sites of porto-systemic anastomoses?
- Lower oesophagus: left gastric (portal) & lower oesophageal branches (azygous/hemiazygous so systemic)
- Periumbilical (caput medusae): veins of ligamentum teres (portal) + sup/inf epigastrics (systemic)
- Upper anal canal: sup. rectal (portal) + middle/inf rectal (systemic)
- Bare area of liver: portal veins + inf. phrenic
- Retroperitoneum: colonic veins (portal) + body wall veins (systemic)
Difference between jejunum & ileum?
Jejunum: thicker walled, larger, valvulae convennientes larger/thicker more proximally, longer vasa recta + fewer arcades & thinner mesentery
Ileum: thinner walled, smaller, shorter vasa recta + more arcades with thicker mesentery
Difference between SI & LI?
SI: central, smaller diameter & valvulae convennientes along whole bowel
BI: peripheral, larger, haustra extending over 1/3rd way across, taenia coli & epiploic appendages (fat)
What is a meckels diverticulum?
Remnant of vitellointestinal duct (connects midgut to yolk sac)
Rule of 2s: 2% of population, 2 inches, 2 feet from ileocaecal valve & 2x as common in males
Relevance: inflammation may mimic appendicitis, may ulceration/bleeding as lined with HCL producing gastric mucosa, intussuseption & Littre’s hernia in inguinal region
What are the relations to the kidney?
Posteriorly: psoas major, 11-12th rib, diaphragm & quadratus lumborum
Anterior: suprarenal glands, colon, SI, liver/duodenum (R) & spleen/stomach/pancreas (L)
Where do adrenals lie?
Anterosuperiorly to kidneys in seperate compartment from gerotas fascia
What are the retroperitoneal organs?
HINT: SADPUCKER
Supradrenal glands
Aorta/IVC
Duodenum (2-4th part)
Pancreas (except tail)
Ureters
Colon (ascending/descending)
Kidneys
Esophagus
Rectum (except distal 1/3rd)
What is hepatitis C?
Inflammation that disrupts hepatocytes and small bile ductules due to single stranded RNA flavivirus via parenteral transmission (IVDA/sex/needle stick/medical work)
- Acute phase: jaundice, fever, malaise, N&V + elevated ALT > AST
- Chronic: >6 months of symptoms
- Cirrhosis + portal HTN
- Liver cell failure
- HCC
What are the leading causes of chronic liver failure?
Chronic hepatitis B
Chronic hepatitis C
NAFLD
ALD
What is cirrhosis?
End stage liver damage characterised by disruption of normal hepatic parenchyma by fibrotic bands & regenerative nodules of hepatocytes most often due to chronic alcoholism in UK - can happen directly or via steatosis/hepatitis
Sequelae:
1. Portal HTN: ascites, splenomegaly, varices & HRS
2. Decreased detoxification: mental status change, asterixis, jaundice & palmar erythema (hyperestrinism)
3. Decreased protein synthesis: hypoalbuminaemia, oedema & coagulopathy
4. HCC
What is necrosis? Name the 6 types.
Dysregulated cell death where cellular membranes fall apart & cellular enzymes leak out
ultimately digesting the cell
How does cirrhosis occur?
- Exposure to alcohol may cause fatty change & perivenular fibrosis = steatosis
- Persistent tissue injury due to alcohol leads to chronic inflammation + loss of tissue architecture -> hepatitis (liver cell coagulative necrosis & mallory bodies)
- PMNs secrete cytokines to stimulate migration & proliferation of fibroblasts/myofibroblasts
- Collagen deposition along with other ECM proteins
- Normal tissue replaced by fibrosis
Note: cirrhosis can just occur directly without steatosis/hepatitis but it is reversible if abstinence occurs at these earlier points
What are the different types of candida?
Most common disease forming fungus + is a normal inhabitant of oral cavity, GIT & vagina in many individuals
1. Oral (most common): grows as yeast, pseudohyphae (diagnostic clue as represent budding yeast cells joined end to end at constrictions) or true hyphae
2. Cutaneous
3. Vaginal
4. Invasive: immunocompromised patients may get systemic disease + pneumonia
Special fungal stains normally used to pick it up e.g. Gomori methanmine-silver or periodic acid-Schiff
What is the commonest type of GB cancer? What are its risk factors? How does it spread?
AdenoCa (cholangiocarcinoma) -> directly invades liver segments 4/5 -> porta hepatis LNs -> CBD, stomach & duodenum
Risk factors: PSC most common
Non-modifiable - age, female, family Hx & mexican ethnicity
Modifiable - gallstones, chronic cholecystitis, liver disease, HIV, smoking & obesity
In developing world liver flukes are common cause due to chronic inflammation
SSI with yellow smelly discharge - whats likely cause?
Actinobacillus with sulfur granules
What organisms are associated with Nec Fac? How do you diagnose it?
Usually multimicrobial with gas forming organisms that cause extensive necrosis with thrombosis of blood vessels
Causes:
GAS
C. Perfringens
S. Aureus/MRSA
Bacteroides fragilis
Diagnosed clinically via cellulitis + crepitus + LRINEC score (>6 highly indicative) taking into account CRP, WCC, Hb, Na, Cr + glucose
How to manage nec fac?
A-E CCRISP
Abx to MCS
Urgent surgical debridement
Involve ITU
Involve plastics
What is pseudomembranous colitis?
C. Difficile colonozies cut due to Abx therapy (Clindamycin/Cephalosporin) disrupting gut microflora -> toxin A/B release disrupting epithelial function -> inflammatory response characterised by volcano-like eruptions of neutrophils from colonic crypts spreading to form mucopurulent pseudomembranes
Symptoms: fever, abdominal pain & bloody green offensive diarrhoea
What are the risk factors for oesophageal cancer?
Modifiable
Chronic GERD -> Barretts (metaplasia from NKSSE to columnar) -> adenoCa
Smoking
Alcohol
Non-modifiable
Age
Family Hx
How would you work up a patient with potential oesophagus cancer?
Ix:
Endoscopy with FNAC to find stage, grade & IHC (cytokeratin staining)
Stage with TNM:
Tis = high grade dysplasia
T1 = invasion into lamina propria, muscularis mucosae or submucosa
T2 = muscularis propria
T3 = adventitia
T4a = resectable adjacent structures e.g. diaphragm
T4b = unresectable adjacent structures e.g. aorta
N1 (1-2), N2 (3-6), N3 (7 or more)
M1 = mets
Grade with G = 1 (well differentiated) & 4 (undifferentiated)
Mx: MDT approach
Surgical resection
Chemoradiotherapy
Palliation e.g. stents
Alternative feeding routes e.g. PEG
How to manage malignant pleural effusion?
Could be due to spread to pleura, lung mets & thoracic duct obstruction
Ix = cytology
Mx: thoracentesis, indwelling pleural catheters (IPCs), pleurodesis & pleuroperitoneal shunting (PPS)
What is troponin?
Complex of three regulatory proteins troponin C, I & T integral to muscle contraction in myocardium & skeletal muscle
What are the risk factors and pathogenesis of gastric cancer?
Risk factors:
Non-modifiable = age & family Hx e.g. HNPCC/FAP
Modifiable = H. Pylori, chronic gastritis & diet high in nitrosamines
Normal mucosa -> chronic gastritis -> metaplasia -> dysplasia -> intramucosal carcinoma -> invasive
What are some types of gastric cancer? What is the lauren classification? What is the Borrman classification?
Most common = adenoCa subtypes including:
1. Tubular: different sized small branching tubes
2. Papillary: outward from stomach wall with finger-like projections
3. Mucinous: mucin around cancer
4. Poorly cohesive e.g. signet ring: arranged in clumps
5. Mixed e.g. adenosquamous
Lauren classification divides adenoCa into 2 types:
1. Intestinal - well-differentiated/slow growing, form glands & >older men
2. Diffuse - poorly differentiated, aggressive + scatter, quick mets & men/women who are younger
Borrmann classification depends on macroscopic appearance of lesion: polypoid, fungating, ulcerating & linitis plastica
How would you investigate malignant ascites? How to treat?
Ix
Ascitic tap + cytology
Liver biopsy for mets
FNA from any LNs
CA-72-4 marker (gastric Ca)
Mx
Opioids
Feeding jejunostomy
Palliation of ascites by repeated tapping
Palliative chemotherapy
What paraneoplastic syndromes are associated with gastric cancer?
Dermatomyositis
Acanthosis nigricans
What are the complications of a total gastrectomy?
Early
Haemorrhage
Leak
Post-op wound infection
Pancreatitis
Late
Pernicious anaemia (vit B12 deficiency due to lack of IF)
Metabolic bone disease
Recurrence
Dumping syndrome = loss of reservoir function of stomach meaning rapid transit of highly osmotically active substances into duodenum post-meals may cause this - can be:
- Early -30-60 mins after eating due to fluid shift from intravascular compartment causing small bowel distention, abdo pain, diarrhoea & vasomotor symptoms (tachy/postural hypotension)
- Late - rebound hypoglycaemia due to large insulin release after rapid transit of carbs occurring 1-3 hours following meal
How is ascites classified?
Exudative - protein content >25g/L or low serum ascites albumin gradient <11 e.g. 4Ps - peritonitis, peritoneal mets, post-radiation & pancreatitis
Transudative - protein content <25 or SAAG >11e.g. cirrhosis, RHF, nephrotic syndrome or starvation (latter due to hypoalbuminaemia, former due to portal HTN)
How to treat C. Difficile?
If mild PO metronidazole
Then PO fidaxomicin + vanc
Vanc can be given PR/NG
Faecal transplant
IV Igs
NG decompression if toxic megacolon develops with likely colonic resection
What is the difference between a mallory weis tear and boerhaaves syndrome?
Mallory-weis: tear on gastric side of GOJ which may extend to distal oesophagus just affecting the mucosa and submucosa
Boerhaaves: complete rupture of lower thoracic oesophagus causing hammans sign i.e. crunching on auscultation of heart due to pneumomediastinum - characterised by shock, chest pain + subcutaneous emphysema
How do you manage a patient with an oesophageal variceal bleed?
A-E via CCRISP
High flow O2
Blood products/IVF
D/C with haem for FFP/platelets
Invasive monitoring
Assess coagulation status via PT + platelet count
Ultimately: control bleeding with Vasopressin/Octreotide + endoscopy with banding or injection sclerotherapy OR minesota tube if uncontrolled = double balloon tamponade (4 lumens now to include esophageal content suction)
In alcoholic patients what blood abnormalities might you find and why?
Thrombocytopenia due to hypersplenism, DIC, haemodilution or chronically low platelets due to toxic effect on bone marrow + impaired haematopoeisis
Anaemia + raised MCV
Elevated liver enzymes e.g. ALT/AST/GGT/ferritin
What is the pathogenesis of portal HTN and how do you manage it?
- Alcoholism causes cirrhosis via changes in lipid metabolism, decreased lipoprotein export & cell injury by ROS/cytokines
- Liver cell damage, fibrosis + nodular regeneration obstructs portal venous return causing portal HTN
- Arteriovenous shunts also contribute to portal HTN
Mx:
1. TIPS: transjugular intrahepatic portosystemic shunt
2. Stapled oesophageal transection - gastric vein + short gastrics ligated with distal oesophagus + re-anastomosed above cardia
3. Orthoptic liver transplant: will need family counselling, discussion re options/prognosis, abstinence 6/12, ABo matching + immunosuppresion
How is alcohol normally metabolised by the body?
- Microsomal ethanol oxidizing system (MEOS)
- Alcohol dehydrogenase
- Catalase reaction
= ethyl alcohol -> acetic acid
How does ascites form in alcoholism?
Hypoalbuminaemia
Increased hepatic + sphlanchnic lymph
Retention of salt/water due to increased aldosterone + ADH
How does vitamin B12 deficiency cause macrocytic anaemia?
Vital role in DNA synthesis so when it is deficient, the cell cycle is arrested in G2 phase meaning it grows in size but does not undergo mitosis resulting in continued cell growth without division = macrocytosis
How do you insert a sengstaken blakemore tube?
- Elevate bed to 45 degrees + lubricate balloons
- Spray nostrils + posterior pharynx with topical anaesthetic
- Pass at least up to 50cm mark, suction from both ports + when gastric balloon appropriately positioned inflate with 500ml, clamp port and pull back on diaphragm
- Inflate oesophageal balloon to 30-45mmHg + clamp port
- When bleeding controlled, reduce oesophageal balloon by 5mmHg every 3h until 25 without bleeding then remove 12-24h later
Note: deflate oesophageal balloon for 5 min/6 hours to prevent oesophageal necrosis
What are the risk factors for PUD + perforation?
H. Pylori
Chronic GERD/gastritis
Steroids
Malignancy
NSAIDS -> inhibiting PG synthesis via COX reducing mucosal blood flow + interferes with superficial injury = impairment of mucosal barrier + topical irritant
How to manage a perforated PUD?
Conservative if small : Abx, NG tube + good peritoneal toileting
Surgical: omental patch repair + intra-abdominal drain - take biopsy for malignancy
Post-op: PPIs -> irreversible binding of H+/K+ ATPase of parietal cells reducing HCl production
What cells control gastric acid secretion?
Acetylcholine released from CNX PS innervation causes:
- Increased acid production by parietal cells
- Secretion of gastrin from G cells
- Histamine from enterochromaffin cells
All these also increase acid production
- Somatostatin release decreased
HCl then causes:
- Pepsinogen activated to pepsin for proteolysis
- Antimicrobial
- Stimulates intestinal mucosa to release CCK/secretin
- Absorption of Ca/iron in SI
What are the phases of gastric acid secretion?
- Cephalic: sight/taste of food -> HCl (30%) + gastrin released via vagal anticholingernic stimulation as above
- Gastric: stomach distended once food has been eaten -> 60% acid produced + peptides cause gastric release
- Intestinal: hypertonic solution in duodenum inhibits gastric acid secretion (10%) via CCK/secretin + neural reflexes
What is the NCEPOD classification?
National Confidential Enquiry into Patients Outcomes & death scored 1-4 - used to determine urgency of surgery required
1 being immediate surgery is needed to save a life or limb e.g. ruptured AAA or fasciotomy
4 being elective work
What biochemical abnormalities might you get in vomiting?
Hypochloraemic hypokalaemic metabolic alkalosis due to low of Cl in vomiting + low K+ due to increased aldosterone in response to hypovolaemia
Increase HCO3- due to more uptake in response to Cl - loss + retention of bicarb rich pancreatic secretions
Hyponatraemia due to kidneys excreting more NaHCO3 to reduce blood alkalinity -> RAAS -> Na/H2O reabsorption in exchange of H+/K+ -> paradoxical aciduria
Mx: 0.9% saline + K+ supplementation
What are the causes of hyponatraemia? How might a hyponatraemic patient present?
Causes:
1. Depletional: diarrhoea
2. Dilutional: HF
3. Endocrine: addisons
4. SIADH
Symptoms/signs:
Confused/agitated
Seizures
Reduced GCS
Why is clotting abnormal in liver disease? What is the management?
Liver synthesizes most of clotting factors -> decreased absorption of vitamin K -> 10, 9, 7 & 2 affected -> increased PT/INR
Mx: IV vitamin K, FFP, PCC & consult haem
What is bile & its function?
Bile is made up of water, cholesterol, lecithin, bile pigments (bilirubin) & bile salts/acids -> emulsifies fat into micelles increasing SA for lipase to act - bile salts help with this because they are hydrophilic on one side + hydrophobic on the other so they aggregate around lipid droplets forming micelles but prevents them from aggregating into larger fat particles due to negative charge
Other functions include: excretory route for harmful lipophilic substances, absorbs fat souble vits ADEK & elimination of cholesterol
Bile is released from the GB when fatty acids are in duodenum stimulating CCK release causes GB contraction + sphincter of Oddi relaxation
How is bilirubin formed then metabolised?
Formed by breakdown of RBCs -> haem -> bilverdin -> bilirubin releasing iron - transported to liver bound to albumin
- Some is free and rest is conjugated to glucoronic acid by glucoronyl transferase allowing it to be water soluble & excreted in bile
- Conjugated bilirubin goes into bile + into SI -> colonic bacteria disconjugate + metabolise it into urobilinogen
- 10% urobilinogen reabsorbed into enterohepatic circulation to be re-excreted in bile but some is processed in kidneys to go into urine as urobilin
- Some urobilinogen is oxidized to stercobilin = brown stool
- Most bile acid reabsorbed in TI to enter enterohepatic circulation (95%)
What are the 3 types of jaundice?
- Pre-hepatic: haemolytic anaemia + transfusion reasons
- Hepatic: hepatitis + HCC
- Post-hepatic: gallstones, pancreatic head tumour
Please describe the anatomy of the pancreas.
Head, uncinate process, neck, body & tail - all RP except tail which is connected to spleen via lienorenal ligament
Main pancreatic duct of Wirsung drains head/body/tail into major duodenal papilla
- Accessory pancreatic duct of santorini drains uncinate process into minor duodenal papilla
Relations (from tail to head):
A: stomach, right kidney, duodenum
P: IVC/aorta, splenic a (body), portal vein (neck), lesser sac, SMA/SMV go under and then over the top of uncinate process
Blood supply: sup. pancreaticoduodenal (from gastroduodenal) + inf pancreaticoduodenal (from SMA) supply head whilst pancreatic branches (splenic) supplies rest
Embryology: ventral bud from hepatic diverticulum gives rise to lower head/uncinate process & dorsal bud from duodenum gives rise to upper head, neck body & tail
Endocrine (A, B, D + PP cells)
Exocrine to digest fats, carbs & proteins via lipase, amylase & trypsin
Pathology of acute pancreatitis.
Pathogenesis:
1. Ductal obstruction: bile reflux into pancreatic ducts, increased pressure damages acini so enzymes leak out & further damage pancreas
2. Direct acinar damage by virus (mumps), bacteria (m. pneumoniae) or parasites (hyatid)
3. Protease causes widespread pancreatic destruction, lipase causes fat necrosis + elastase destroys blood vessels causing haemorrhage
Hypocalcaemia: saponification of omental fat which releases FFAs that chelate Ca + later sepsis will produce catelcholamines that cause IC shift of Ca
Hyperglycaemia: digestion of B islet cells of langerhans
Haemorrhage: rupture of splenic a or pseudoaneurysm
ASSCC of pancreas.
Blood tests to perform: RBs + amylase (digestive enzymes in pancreatic juice act as glycoside hydrolases to break down starch into smaller carbohydrates - returns to normal 48h after attack) OR lipase is preferable + ABG/LDH/Alb/Ca for scoring with Glasgow
Ideally CT 48h later unless clinical uncertainty + USS for gallstones
Mx:
A-E as per CCRISP
Aggressive IVF
Sepsis 6 - consider Abx
ITU involvement if Glasglow score 3 or >
Early enteral feeding with NJ tube or TPN - need MDT to d/c options depending on patients premorb status + nutritional state
IV PPIs
Octreotide
Corticosteroids to suppress inflammatory response
Pethidine is analgesia of choice
What vessels are encountered during a whipples?
SMA/SMV
Splenic a
Portal vein
Aorta
Sup/inf pancreaticoduodenals
How can IR stop bleeding?
Real time imaging
Catheter guided through artery + releases clotting agents (coils/particles/fel foam) slowing blood flow + causing internal injury to activate coagulation cascade
What is a pseudocyst?
Amylase rich fluid enclosed in wall of granulation tissue occuring 4 weeks from attack - not true cyst as not seperated by line of epithelial cells
Symptoms/signs: epigastric pain/fullness, fevers, vomiting & dyspepsia
Complications: abscess, rupture into peritoneum causing peritonitis, obstructive jaundice & erosion into vessel causing haemorrhage
Ix: USS/CT, MRCP + cyst fluid analysis (amylase high but CEA/CEA-125/fluid viscosity low - would be high in Ca)
Mx: watch/wait as may resolve but if it doesnt in 2 months, >6cm or becomes infected -> cystogastronomy
How is paracetaml detoxified in liver?
Toxic metabolite = NAPQI
Detoxified by glutathione
System overwhelmed in OD so metabolite accumulates in liver effecting vital function
What is the anatomy of the spleen?
9th-11th rib - weighs 150-200g
Blood supply: splenic a (coeliac trunk -> L above upper pancreas -> behind stomach -> lienorenal ligament -> hilum of spleen gives off terminal branches = spleen, stomach + pancreas)
Drainage: splenic v -> SMV -> portal vein
What is the anatomy of the oesophagus?
Begins at cricoid (C6) -> GOJ (T10) lined by NKSSE - constrictions at cricoid, aortic arch, L main bronchus & oesophageal hiatus - 40cm long
Arterial/venous/lymph supply:
Upper 1/3rd (striated muscle) = inf. thyroid a/v + deep cervical
Middle 1/3rd (SM + striated) = direct branches of aorta/azygous + mediastinal
Lower 1/3rd (SM) = left gastric a/v + gastric
Define achalasia.
A esophageal dysmotility disorder of SM that causes uncoordinated peristalsis & lack of relaxation of LOS/increased LES tone causing by loss of myenteric plexus causing hypertrophied musculature
What is the anatomy of the stomach?
Cardia, fundus, body, pyloric antrum & pylorus
Blood supply:
L gastric (coeliac)
Rright gastric (hepatic)
L gastroepiploic & short gastrics (splenic)
R gastroepiploic (gastroduodenal)
Venous drainage
L/R gastric -> portal vein
L gastroepiploic + short gastrics -> splenic
R gastroepliploic -> SMV
What is PUD and the pathology of H. Pylori?
Ulcer: local defect of mucous membrane/skin due to gradual disintegration of surface epithelial cells
Risk factor for PUD = H. pylori (gram negative microaerophilic spiral bacteria) - diagnosed by gastric biopsy put in urea medium + phenol red colour when urease is produced by bacteria converting urea to ammonia
Pathogenesis:
1. Urease production converting urea to ammonia elevates pH + allows survival
2. Protease/phospholipase production damage gastric mucosa + cause inflammation
3. Flagella allow motility in viscus mucus
4. Adhesins enhance bacterial adherence to surface foveolar cells
5. CagA toxin -> cancer development (adenoCa or MALT)
= imbalance between mucosal defences + damaging forces that overcome them
Mx: 7/7 CAP course
What are the actions of HCl?
Converts pepsinogen to pepsin -> proteolysis
Antimicrobial
What is the anatomy of the duodenum?
All RP except 1st part
Blood supply: sup. pancreaticoduoneal a (gastroduodenal), inf. pancreaticoduodenal (SMA) & hepatic, R gastric/gastroepiploic + supraduodenal branches
Relations:
D1 (superior): epiploic foramen (S), pancreatic head/neck (I), quadrate liver/GB (A) & portal vein/CBD (P)
D2 (descending): GB/R liver/transverse colon/SI (A), R kidney/IVC/psoas (P), pancreatic head (M) & ascending colon/R liver (L)
D3 (horizontal): pancreatic head/uncinate process (A), jejunum (I), mesentery/SM vessels/jejunum (A) & psoas/ureter/IVC/abdo aorta/R gonadal vessels (P)
D4 (ascending): transverse colon (A), L psoas/symphatic chain/gonadal/IMV (P), pancreas body (S), L kidney/ureter + R roof of mesentery
What is the anatomy of the appendix?
Commonly retrocaecal but can also be pre-ileal, post-ileal + pelvic
Blood supply: appendicular a from ileocolic a from SMA
Appendicular V to SMV
Pain referred to umbilicus because visceral nerve fibres enter spinal cord at T10 (umbilical dermatome) then parietal peritoneum localises the pain to RIF
What is the anatomy of the diaphragm?
3 openings
1. Caval: IVC + R phrenic n (T8 in central tendon)
2. Oesophageal: oesophagus & CNX (T10 in R crus)
3. Aortic hiatus: aorta, azygous vein + thoracic duct (T12 behind median arcuate ligament)
Origin:
1. Sternal part from xiphoid process
2. Costal part from lower 6 CCs
3. Vertebral part (crura/arcuate ligaments) from R crus (L1-3), L crus (L1-2), median arcuate ligament (between 2 crura), medial arcuate ligament (L1 lateral body to L2 transverse process) & lateral arcuate ligament (L1 transverse process tip to lower border of 12th rib)
Insertion: central aponeurotic tendon
Blood supply: inf. phrenic a
What is the anatomy of the abdominal wall?
- EO (ventral rami of T7-T12)
- From lowest 8 ribs -> illiac crest, linea alba, public tubercle/crest & ASIS
- Fibres run down, forward + medial (hands in pockets)
- Contains viscera, increases intra-abdominal pressure + moves trunk to one side - IO (T7-12, illiohypogastric + illioinguinal)
- From thoracolumbar fascia, illiac crest + inguinal ligament to lower 3 CCs, conjoint tendon, pubic crest + linea alba
- Fibres run perpendicular to EO so upwards
What is the anatomy of the inguinal canal?
Boundaries:
Inferiorly = inguinal ligament
Anteriorly (2As) = external + internal oblique aponeurosis
Posteriorly (2Ts): transversalis fascia + conjoint tendon
Superiorly (2 muscles): IO + TA
Medial: superficial ring
Lateral: deep ring
What is the anatomy of the bladder?
Base, trigone (ureters entering at base + corners), apex (median umbilical ligament), neck + urethra
Peritoneum covers superior and upper part of posterior surface
Arterial supply: sup/inf vesical (internal illiac)
Venous: vesical venous plexus (internal illiac)
Nerve supply: sympathetics (L1-2) & PS (S2-4)
Posterior relations:
Male - rectovesical pouch, vas deferens & ureters
Females - vesicouterine pouch (of Douglas) + ureters
What layers are encountered in SPC placement?
Skin
Subcut fascia
Scarpas fascia
Linea alba
Transversalis fascia
Preperitoneal fat
What is the anatomy of the kidneys?
Outer cortex -> inner medulla -> renal pyramids -> papilla -> minor calyx -> major calyx -> renal pelvis -> hilum -> ureter
Layers (deep to superficial): renal capsule, perirenal fat, renal fascia (gerotas) + pararenal fat
Function: filter + excrete waste products + water/electrolyte balance
L kidney higher than R - both (L1-3) but L hilum at L1 whereas R hilum at L1-2
RP so seperated from peritoneal cavity be peritoneum, gerotas fascia (derived from transversalis fascia) + perinephric fat
Relations:
Posteriorly: psoas, quadratus lumborum & diaphragm
Anteriorly: hepatic flexure/liver/adrenal gland (R) & stomach/pancreatic tail/spleen/adrenals (L)
At hilum (ant-post): vein, artery (L1-2) + ureter
R renal artery crosses posterior to IVC + L renal vein is anterior to aorta
Blood supply: renal a (abdominal aorta) -> 5x segmental -> interlobar -> arcuate -> interlobular -> afferent arterioles
Venous drainage: renal veins -> IVC
Lymph: para-aortic
Why are accessory renal arteries important?
Beware of accessory renal arteries branching outside of the kidneys as they are terminal arteries (normally there are 5) and if damaged will devascularise the kidney
Access via avascular plane - line of brodel = imaginary line along lateral + slightly posterior to kidney
What is the anatomy of the ureters?
25cm long from renal pelvis -> bladder descending along psoas major (RP) -> cross pelvic brim @ SIJ crossing common illiac bifurcation -> at ischial spines turn anteromedially towards bladder piercing it obliquely (one-way walve with high intramural pressure to prevent backflow)
Developed from mesonephric bud
Posterior to everything except the common illiacs which they pass over
Narrower points: PUJ, pelvic brim + VUJ
Blood supply:
Upper 1/2: renal/gonadal
Lower 1/2: sup/inf vesical
Nerve supply: renal/gonadal/hypogastric plexuses (T11-L2)
Vascular relations:
Females - ovarian & uterine arteries (run underneath these)
Males - vas deferens cross over ureters
What is sickle cell?
An autosomal recessive inherited haemoglobinopathy where there is a point mutation in B globin that promotes polymerisation of Hb -> red cell distortion, haemolytic anaemia, microvascular obstruction + ischaemic tissue damage
Complications:
1. Vaso-occlusive crisis: bones, lungs, stroke, retinopathy & autosplenectomy (splenomegaly in childhood due to sickled red cells being trapped causing red pulp congestion -> splenic infarction, fibrosis + progressive shrinkage) triggered by infection, dehydration + acidosis
2. Sequestration crisis: rapid splenomegaly + hypovolaemic shock due to entrapment of sickled RBCs
3. Aplastic crisis: parvovirus infection of RBCs
4. Chronic tissue hypoxia causing organ damage
5. Increased susceptibility to infection with encapsulated organisms (S. Pneumoniae, H. Influenzae & N. Meningitidis)
Surgical relevance: gallstones, avascular bone necrosis, osteomyelitis & autosplenectomy
What is the Dukes staging?
A = through mucosa, muscularis mucosa + submucosa
B1 = into muscularis propria
B2 = through muscularis propria
C1 = 1-3 LNs
C2 = >4 LNs
D = distant mets
What is the pathogenesis of haemorrhoids?
Normal anal cushions fixed by fibromuscular Treitz ligaments (remnant of longitudinal layer of muscularis propria from rectum)
With chronic increased pressure due to straining, these fragment meaning anal cushions no longer restrained from engorging excessively with blood becoming swollen/inflamed -> prolapse/bleeding
Sudden raised pressure e.g. exercise causes rupture of vascular plexus -> blood clot at anal verge = thrombosed haemorrhoid
Define melanosis coli.
Pigmentation of colon wall identified during colonoscopy - benign with no significant correlation with disease
Can be due to excessive laxative use
What is an adenoma?
Benign tumour of epithelial origin producing gland patterns or derived from glands
What is an abscess?
Localised collection of pus within a fibrous granulated wall due to seeding of pyogenic organisms
Characteristics:
Large central necrotic area
Rimmed by preserved neutrophils
Surrounding dilated vessels + fibroblast proliferation due to attempted repair
How do neutrophils migrate to inflammation?
- Roll
- Become activated
- Adhere
- Transmigrate across endothelium
- Pierce BM
- Migrate towards chemoattractant emanating from source of injury
What is a carcinoid tumour?
Slow growing neuroendocrine tumour arising from enterochromaffin cells in crypts of lieberkuhn often found in SI, appendix, stomach or rectum -> release 5HT, PGs, histamine & bradykinins
Can metastasize due to production of beta-catenin enabling tumour cell adhesion - often to liver (more symptoms at this point as liver cannot detoxify products produced by tumour)
Presentation: periodic abdo pain + flushing/diarrhoea/wheezing
Ix:
- Chromogranin A in blood
- 5HIAA in 24h urine
- IHC staining for chromogranin B
What is ulcerative colitis?
Autoimmune condition causing inflammation in the form of colitis mainly of the colon causing ulcers +/- backwash ileitis-
Causes: idiopathic
Complications: toxic megacolon, malignancy, abscess + malabsorption (ADEK vit deficiency)
Ix: stool analysis, barium follow through, PT, calcium oxalate levels + FBC
Mx: endoscopic surveillance
What are the extraintestinal manifestations of IBD?
Hint: APIESAC
Apthous ulcers
Pyoderma gangrenosum
Iritis
Erythema nodosum
Sclerosing cholangitis
Arthritis
Clubbing
Why renal stones in Crohns?
Increased intestinal fat due to malabsorption -> binds to Ca -> leaves oxalates (hyperoxaluria)
How to manage crohns?
Conservative: low residue dietary intake + gastro advice
Medical: abx, steroids, 5ASA + immunomodulators
Surgical: total colectomy in UC but in Crohns reserved for refractory disease/intestinal obstruction/toxic megacolon with emphasis on bowel reserving surgery + for complications e.g. abscess/fistula/perf/cancer/haemorrhage
What are the key differences between Crohns and UC?
Crohns: transmural inflammation in patchy skip lesions from mouth-anus
Macroscopic: cobblestone & apthous ulcers
Microscopic: non-caseating epitheloid cell aggregates with langerhan giant cells causing granulomas
Smoking worsens
UC: superficial continuous inflammation of rectum + colon
Macroscopic: pseudopolyps + ulceration
Microscopic: crypt abscesses + inflammatory cells in lamina propria
Higher risk of cancer + extraintestinal manifestations
Smoking is protective
In both: crypt abscesses (acute) or paneth cell metaplasia/hyperplasia (chronic)
What is the adenoma carcinoma sequence?
Stepwise accumulation of mutation causing oncogene activation + TSG inactivation leading to cancer via the route hyperplasia -> polyp -> dysplasia (pre-cancerous) -> adenoca (malignant)
Genes involved: APC (TSG) -> K-RAS (oncogene) -> p53 (TSG)
What are the different types of apoptosis?
Extrinsic pathway: begins outside a cell, when conditions in the extracellular environment determine that a cell must die -> inactivation of death induced signalling complex FADD
Intrinsic pathway: begins when an injury occurs within the cell and the resulting stress activates the apoptotic pathway -> p53 may cause growth arrest, DNA repair or apoptosis
What is TNF and what is its relevance in IBD?
Cytokine involved in systemic inflammation and acute phase reaction -> increases tight junction permeability increasing flux of luminal bacterial components activating innate/adaptive immunity
Drugs antagonising it include Inflixamab + Adalimumab - monoclonal IgG Abs (biologicals used in steroid refractory UC or extra-intestinal manifestations)
What is FAP What is gardner syndrome?
Familial adenomatous polyposis - autosomal dominant condition characterised by loss of APC TSG (chromosome 5) leading to hundreds of tubular adenomas + 100% risk of cancer by 40yo so colonoscopys ftrom 12yo + will need prophlactic near total colectomy by age 25 - lifestyle advice like others (fibre rich diet, limit alcohol, reduce fat + smoking)
Normally APC negatively regulates WNT pathway in colonic epithelium promoting degradation of B-catenin
Gardner syndrome is similar + mandibular osteoma, desmoid tumours + sebacous cysts + extra teeth
What are the different types of polyps?
- Non-neoplastic: haemartomatous, metaplastic
- Inflammatory: pseudopolyps or UC
- Neoplastic: villous, tubulo-villous + tubular
Malignant potential depends on type, diameter + degree of dysplasia
Define dysplasia.
Disordered cellular growth characterised by increased mitosis + pleomorphism but CANNOT invade BM
If severe -> CIS
Define endometriosis.
Condition where ectopic endometrial tissue is found in other areas of the body other than uterus -> burn powder, dark blue/black + chocolate cysts will show -> pain due to intrapelvic bleeding + adhesions -> increased risk of ovarian Ca
Uterine epithelium: simple columnar supported by thick vascular stroma (inner epithelial layer + mucous membrane, basal + functional layer which is sloughed in menstrual cycle)
What is diverticulosis? What is diverticulitis?
Congenital or acquired in age with constipation/low fibre diets reducing stool bulk -> elevated intraluminal pressure due to exaggerated peristalsis most often in sigmoid -> focal discontinuities in wall where nerves, vasa recta + connective tissue sheaths penetrate inner circular muscle (normally reinformed by external longitudinal layer of muscularis propria) -> taeniae coli -> spasmodic sequestration of bowel segments -> outpouchings form = diverticula -> diverticular disease
Obstruction of diverticula causes inflammation -> diverticulitis -> can lead to perforation as only supported by muscularis mucosa + thin subserosal adipose tissue
How is diverticulitis classified?
Hinchey classification
I = pericolic abscess
II = distant abscess
III = purulent peritonitis
IV = faeculent peritonitis
How do you manage diverticulitis?
Ix: urine, RBs, CXR/AXR, CT + rigid sigmoidoscopy when settled down
Conservative: fluids, high fibre diet
Medical: Abx - usually amoxicillin (gram +S), gentamicin (gram -s) & clindamycin (anaerobes)
Surgical: IR drainage of collection, diverting colostomy or hartmanns
What are the 4 theories of endometriosis?
- Regurgitation theory: retrograde menstruation
- Benign metastases theory: endometrial tissue spreads to distant sites via blood/lymph
- Metaplastic: endometrium arises from coelomic epithelium so mesonephric remants can undergo differentiation to ectopic endometrial tissue
- Extrautertine stem progenitor cell: stem cells from bone marrow can differentiate into endometrial tissue
What is polycystic kidney disease?
Autosomal dominant condition due to gene mutations in PKD1/2 causing enlargement of kidneys with multiple cyst formation -> renal tubule cells divide repeatedly until outpocketings of tubular wall forms saccular cyst filled with GF fluid from afferent tutuble -> expansion causes most to seperate from parent tubule leaving isolated sac filling with transepithelial secretions allowing it to expand relentlessly -> pain due to weight of organ dragging upon pedicle or stretching of renal capsule -> haematuria + abdominal mass may be present
Complications: cysts in liver/pancreas, brain aneurysm, MV prolapse, RF, infection + HTN
Other ddx: simple cyst, acquired cystic kidney disease, VHL + tuberous sclerosis
What are the types of graft rejection?
Before transplant need ABO blood matching + HLA tissue mstching (A, B + DR important on WBC)
- Hyperacute: within mins of clamp release due to preformed Abs e.g. ABO or IgG HLA class I
- Accelerated acute: occurs in few days due to cellular/ab-mediated immunity due to pre-sensitisation to donor
- Acute: most common occuring at days-weeks predominantly cell-mediated by lymphocytes causing apoptosis
- Chronic: graft atrophy + atherosclerosis -> fibrosis
What malignancies are associated with immunosuppression?
Kaposis
Lymphoma
BCC
Skin
What is cryptorchidism?
Complete/partial failure of intra-abdominal testes to descend into scrotal sac -> testicular dysfunction e.g. infertility, torsion or inguinal hernia and increased cancer risk due to intratubular germ cell neoplasia (precusor of seminoma) within atrophic tubules
Risk factors: family Hx, LBW/prematurity, gastroschisis (because of high abdominal pressure) & down syndrome
Mx: orchidopexy to reduce risk of infertility + cancer whilst allowing testis to be checked in new location
What are the different typs of testicular cancer and how do you manage this?
- Seminomatous (30-40)
- Non-seminomatous (20-30) e.g. choricarcinoma (highly malignant - syncytiotrophoblast + cytotrophoblast - producing BHCG) or yolk sac
- Teratoma (3 germ cell lines mesoderm, endoderm + ectoderm) -> para-aortic nodes + locoregional spread
- Sex cord stromal tumours e.g. leydig (testosterone producing) or sertoli cell
- Lymphoma >60yo
Work up:
Markers: B-HCG, AFP & LDH (evaluate/assess mass/tumour burden, persistent elevation after orchidectomy indicates stage 2 disease even if LNs seem fine & monitors response to therapy)
USS of lump
CT-TAP for staging
MDT discussion
Orchidectomy + chemotherapy +/- retroperitoneal LN dissection
What are stages of haematoma resolution?
- Clot formation immediately by platelets + fibrin
- Inflammation 1-3 days
- Granulation 3-7 days
- Lysis of clot by macrophages 1 week
- Growth of fibroblasts into haematoma weeks 1-4 to cause fibrosis
- Remodelling weeks-months
Define metastasis.
Survival + growth of tumour cells at a site distant from that of the origin
What is virchows triad?
Endothelial injury
Hypercoagulable state e.g. in cancer tumour cells produce + secrete procoagulant/fibrinolytic substances which activate the coagulation cascade via stimulation of tissue factor production
What are the zones and lobes of the prostate? What is most affected by BPH vs cancer?
Zones:
Central
Peripheral (prostate Ca)
Transitional (BPH)
Lobes:
Ant
Post
2x lateral
Median (BPH)
What is BPH and why does it happen? How to investigate/treat?
Benign hyperplasia of prostate due to SM + epithelial proliferation in transitional zone due to high androgen levels - occurs commonly in older age but can be influenced by diet, physical activity, DM & inflammation
Ix: MSU, PSA + U&Es, IPSS, bladder diary, bladder scan + urodynamics
How do you take a prostate biopsy? How is it graded?
TRUS guided from mid lobe parasagittal plane at apex, mid gland + base B/L
Can be focal so need multiple samples from different sites as only small amount of tissue and malignant gland may be mixed with benign tissue - findings may also be subtle + there are benign mimickers of cancer leading to misdiagnosis
Gleason score = 2-10 (least to most abnormal) - pathologist allocates number 1-5 to most common histological pattern then does same for 2nd most common + adds them up
What genes are involved in prostate cancer?
TPRSS2-ETS fusion gene mutations -> activate PI3/AKT signalling pathway
After radical prostatectomy when should PSA levels fall?
4-6 weeks
If not recurrence or incomplete removal to be considered
Organ specific so only produced by prostate but not cancer specific as may also be raised after activity, ejaculation + instrumentation
How to work up prostate cancer?
RBs, PSA + ALP
TRUS guided biopsy
MRI of prostate
CT-TAP + bone scan for mets*
MDT
Radical prostatectomy +/- LN dissection
B/L orchidectomy causes androgen deprivation
*sclerotic in this cancer due to increased bone deposition due to increase osteoblastic activity
What are the types of diabetes?
Type 1: autoimmune condition where there is destruction of islet cell of langerhan B cell that produce insulin causing a deficiency and hyperglycaemia
Type 2: peripheral resistance to insulin + inadequate compensatory response of insulin secretion (most common)
What are the actions of insulin? What hormones oppose insulin?
- Increase rate of glucose transport into cells of body
- Glycogenosis in liver
- Hepatic generation of G6P from glucose
- Enhances AA uptake into peripheral tissues
- Stimulates protein synthesis (GH)
- Stimulates lipid uptake into cells then enhances oxidation
- Lipogenesis in adipocytes + liver enhancing fat deposition
Overall aims to reduce glucose and fat in blood + acts as GH
Hormones that increase glucose include: glucagon, catelcholamines, glucocorticoids + somatotrophin
What are some precautions to put in place for diabetics undergoing surgery and what can go wrong?
Should be prioritized so they are not starved more than one meal
Analgesia/antiemetics to enable early return to diet + usual regime
Insulin infusion if missing >1 meal
BMs measured hourly with target between 4-12
Post-op complications:
Immediate - hyper/hypo-glycaemia, dehydration + electrolyte imbalance, HHS + DKA
Late - infection, sepsis + impaired wound healing
If concerned involve endocrinologist
Why does polyuria occur after obstructive uropathy?
Glomeruli recover first with no improvement in distal tubules leading to increased GFR = increased UOP + dehydration
Why do uraemic patients develop anaemia?
EPO deficiency
Circulating bone marrow toxins
Bone marrow fibrosis during osteitis fibrosa cystica
Increased red cell fragility caused by uraemic toxins
What is the function of K+ and how is homeostasis maintained?
Maintains proper fluid balance, nerve impulse function, muscle function + cardiac function
Homeostasis due to:
1. GI = diet 20-100mmol/day
2. Endocrine: aldosterone stimulates Na reabsorption via active echange with potassium promoting excretion
3. Renal: acid-base balance (reciprocal changes e.g. acidosis leads to hyperkalamia + vice versa) + tubular flow rate (increased flow promotes K+ secretion)
What happens in hyperkalaemia? How do you manage it?
Heart dilates, is flaccid + HR decreases blocking conduction of cardiac impulse because resting membrane potential is depolarised causing it to be less negative decreasing intensity of AP making contraction weaker (used in cardiac surgery once bypass has been established to arrest heart in diastole)
Symptoms/signs:
- Muscular weakness/cramps
- Lethargy/confusion
- Arrythmias - peaked T waves, wide QRS, hypotension + death
- Paralytic ileus, diarrhoea, N+V + abdo pain
Mx: A-E via CCRISP + cardiac monitoring
Stop K+ fluids/drugs
Calcium gluconate 10ml of 10% over 10min
5-10U of insulin in 50ml 50% dextrose over 30 mins
Salbutamol 5-10g nebs
Calcium arsonium
Sodium bicarb
Haemodilaysis (if cant consent - best interest with 2 consultant signatures + involve family/nursing staff)
Define shock. What is septic shock?
Circulatory failure resulting in inadequate organ perfusion that cannot meet metabolic demands
Septic shock is the addition of hypotension (systolic <90) causing organ DYSFUNCTION despite adequate fluid resus
What are the basic principles of managing septic shock?
- Respiratory support: non-invasive or invasive in ARDS/resp failure
- Circulatory support to maintain cardiac index + O2 delivery to tissues using IVF e.g. crystalloids/colloids + inotropes
- Renal support to ensure UO >0.5ml/kg/hr via dopamine/furosemide to maintain renal perfusion pressure + RRT
- Nutrition: enteral/parenteral - enteral prefered as it maintains mucosal integrity + reduces bacterial translocation
- Antimicrobials: broad spectrum -> targeted to cultures
What are the advantages and disadvantages of open vs image guided aspiration of a diverticular abcess?
Open:
Adv - proper drainage + peritoneal toilet & can make stoma if needed
Disadv - wound infection risk + increased morbidity
Image-guided
Adv - no wound infection, reduced hospital stay + can leave peg tail catheter for repeat drainage/abx administration
Disadv - less adequate drainage + cant form stoma
What factors affect tissue oxygenation?
CO x CaO2 (arterial O2 content) x 10
What factors influence haemaglobins affinity for O2?
HINT: CADET FACE RIGHT
Oxygen dissociation curve
All causes increase affinity shifting curve to Right so Raised O2 delivery:
CO2
Acidosis
2-3-DPG
Exercise
Temperature
What is the CCRISP protocol?
A-E to stabilise
Full patient assessment + chart review + history/exam -> decide/plan if patient is stable or unstable
If the patient is stable daily management plan aiming to prepare for discharge e.g. nutritional planning, removing drains/tubes, optimising meds/stepping them down + PT/OT
If the patient is unstable, a diagnosis is required so specific investigations + definitive care to be arranged
What blood tests to do in iron deficiency anaemia?
Total iron binding capacity
Serum ferritin
Stool sample for occult blood
What is a fistula? How are they classified?
An abnormal connection lined by granulation tissue between 2 epithelial surfaces e.g. in enterocutaneous fistula the surfaces are skin + GIT - IBD, infection, cancer + intestinal anastomosis predipose you to getting them -> can be complicated by sepsis, fluid/electrolyte imbalances + malnutrition
Can be classified according to:
- Congenital vs acquired
- Internal/external
- Simple/complex
- Anatomically
- Physiology i.e. high/low output
How do you manage an enterocutaneous fistula?
HINT: SNAAPP
If unstable A-E as per CCRISP
MDT approach
- Sepsis control
- Nutritional support (parenteral nutrition may be required if high output) - 25-30kcal/kg/day for normal person or 45-55kcal/kg/day following extensive trauma
- Anatomical assessment e.g. with imaging e.g. CTAP+contrast, MRI + fistulogram
- Adequate fluid + electrolyte replacement
- Protect skin to prevent excoriation
- Planned surgery
60% close spontaneously with conservative management - if there is no infection, distal obstruction, malnutrition or high output
To operation within 24h if there is intra-abdominal sepsis or distal obstruction to excise tract + resect bowel involved +/- anastomosis/stoma
How to confirm correct placement of NGT?
Measuring pH of aspirate <5.5
CXR:
Bisecting carina
Remaining in midline to diaphragm
Tip visible below diaphragm 10cm from GOJ
What are some examples of enteral feeding? What are some complications?
Oral
NGT
NJT
PEG
Complications:
Tube related - kinking, misplacement, blockage + infection
Feed-related - diarrhoea, N&V, refeeding syndrome + fluid/electrolyte imbalances
Refeeding syndrome: metabolic disturbance occuring on feeding someone following period of starvation characterised by low levels of Ph, K, Mg + abnormal fluid balance - more at risk if BMI <16, unintentional weight loss >15% over 3-6 months, little intake for >10 days + electrolytes low prior to feeding -> prevent by starting at 10kcal/kg/day increasing to full over 4-7 days, thiamine, vitamin B, K+/Ph & Mg replacement
What are some advantages and disadvantages of NJ tube?
Adv: bypass stomach so less liable to aspiration pneumonia, avoids gastric phase of stimulation, doesn’t stimulate pancreatic enzymes (so used in pancreatitis!) & feed delivered directly to intestine maintaing mucosal integrity
Disadv: needs endoscopic guidance for placement + smaller in diameter so more prone to kinking/blockage
What are signs of malnourishment vs patients identified at being at risk of malnourishment?
Malnourished: BMI <18.5, unintentional weight loss >10% over 3-6/12 + BMI <20 AND unintetional weight loss >5% over same time frame
At risk: eaten nothing/little for 5/7 + likely to remain that way for 5 more days, poor absorptive capacity, high nutrient losses + high metabolism
What is TPN and what are the indications for giving it? What are some complications of it?
Water, carbs, lipids, proteins, vitamins, nitrogen + trace elements given IV via CVC/PICC due to high osmolarity: contains NaCl, CaCl, KCl + MgCl
Given in general critical illness e.g. severe malnutrition, trauma, sepsis, MOF + burns
OR
Gut problems e.g. short gut, ECF, BO, ICD + radiation enteritis
Complications:
Line related - infection/sepsis, thrombophlebitis, pneumothorax + thrombosis
Feed related - fluid overload, refeeding syndrome, hyperlipidaemia + high/low glucose
How should you monitor nutrition?
Daily weights
BMI
Daily electrolytes
If long term will need other bloods at monthly weekly or 3-6 monthly intervals e.g. Fe/vitamin D + bone densitometry 2 yearly
What is do fats, glucose + protein provide in terms of energy?
Fats = 9.3kcal/g
Glucose = 4.1kcal/g
Protein = 4.1kcal/g
What are the disadvantages of using glucose as main energy source?
- Glucose intolerance: in acute stress response, patients in state of hyperglycaemia + glucose intolerance so these patients wont get their requirement due to poor utilisation
- Fatty liver: excess glucose is converted to lipid in liver causing fatty change & deranged LFTs
- Resp. failure: extra CO2 released upon glucose oxidation can lead to this + increased ventilatory requirements
- Deficiency of essential fatty acids
At least 50% must be from fat
What is TURP syndrome? How to manage?
Dilutional hyponatraemic hypervolaemia post-TURP due to use of glycine rich hypotonic irrigation solution (saline limits diathermy use as its isotonic) which will be absorbed/metabolised -> confusion (cerebral oedema, hypoxia + high ammonia as glycine breakdown toxic byproduct), agitation, hypoxia, HTN then hypotensive, blurred vision, HF + pulmonary oedema -> arrhythmia due to acute osmolarity/Na change, seizures due to low Na + cerebral oedema & glycine toxicity
Mx: A-E as per CCRISP
- Stop op + prevent further irrigation
- ABG + electrolytes
- Bair hugger + warmed fluids to correct hypothermia
- Diuretics: mannitol (removes water + conserves Na) or furosemide (inhibits Na/K pump preventing NaCl absorption in thick ascending LoH so Na+ preserved and K+ lost)
- Colloids or isotonic crystalloids
- Na replacement at 10mmol/day
- HDU Mx - may need intubation depending on conciousness
Name some other diuretics and their mechanism of action.
Osmotic e.g. mannitol - large molecules which increase osmotic pressure in tubules resulting in water secretion
Thiazides e.g Bendroflumethiazide inhibit Na reabsorption in DCT
K+ sparing e.g. spironolactone - aldosterone antagonist acting on Na/K pumps in CCT
Amiloride - binds to Na channels at DCT
