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MRCS B > GI Pathology/Endocrine/ Critical Care > Flashcards

GI Pathology/Endocrine/ Critical Care Flashcards

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1
Q

What are the differences in surgical management between Chron’s and UC?

A

UC - surgery is potentially curative (panproctocolectomy)
In emergency - panproctocolectomy with ileostomy (can reverse at later date)

Chron’s - not curative, therefore surgery should be as minimal as possible and only when required (strictures/ perf)

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2
Q

Indications for surgery in ulcerative colitis

A

-Resistant to medical mx
-Acute/ severe flare (fulminant) resistant to medical mx
-Perforation
-Suspicion of cancer
-Uncontrolled bleeding

Also QoL concerns

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3
Q

Medical management of IBD

A

Acute flare - steroids

Maintenance:
Thiopurines - active + maintenance
MTX - active + maintenance
Biologics

5ASAs/ aminosalicilates (maintenance only)

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4
Q

Causes of post-op morbidity in IBD patients.

A

Short gut syndrome/ malabsorption/ malnutrition
Poor wound healing
Fistulation (Chron’s)

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5
Q

Differences in appearances/ histology in UC vs Chrons

A

UC:
Continuous/ circumferential mucosal
Crypt abscesses/ atrophy

Chrons:
Skin lesions
Cobblestone appearance
Fistulae, strictures
Granulomas

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6
Q

What are the endoscopic management options for vatical bleeding

A

Band ligation
Sclerotherapy

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7
Q

What is the management of non-variceal UGI bleeding?

A

IV PPI

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8
Q

What is the management of variceal UGI bleeding?

A

A-E/ stabilise
Terlipressin (vasoactive agent - or Vasopressin/ octreotide)
Prophylactic IV Abx

Surgical:
Endoscopy
Sengstaken/ Minnesota tube to tamponade if uncontrolled

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9
Q

What are the sites of porto systemic anastomoses?

A

1 - distal 1/3 oesophagus
2 - upper anal canal
3- bare area of liver
4 - retroperitoneal
5 - umbilical

6 - patent ductus venous

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10
Q

How long is a Sengstaken tube left for?

A

Deflated at 24hrs (gradually), and if bleeding stopped is removed at 48 hrs.

If bleeding ongoing, leave for another 48hrs.

If still not controlled, can inflate for another 24hrs.

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11
Q

Complications of a a Sengstaken tube

A

Ischemic necrosis of oesophageal mucosa

Oesophageal perforation
Aspiration

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12
Q

What is the function of the portal vein?

A

Collects blood from GI tract/ GB/ pancreas/ spleen to take to liver

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13
Q

Where does the portal vein begin

A

Joining of the splenic vein and SMV

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14
Q

Normal portal venous pressure

A

<10mmhg

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15
Q

Rectal arterial blood supply

A

upper 1/3: Superior rectal (IMA)

middle 1/3: Middle rectal (Internal iliac)

lower 1/3: Inf rectal (internal pudendal)

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16
Q

Rectal venous drainage

A

upper 1/3: IMV > splenic > portal

middle + lower 1/3: Iliac vein > IVC (systemic)

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17
Q

Management of persistent varices

A

TIPPS
Surgical shunt
Liver transplant

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18
Q

What routine blood findings would be found in alcoholic pts

A

FBC:
-low plts/ WCC/ Hb
(impaired bone marrow function)
-High MCV
-macrocytic anaemia

Haematinics:
-low B12
-high ferritin

LFTs:
Elevated AST/ALT/GGT/ ferritin

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19
Q

What hepatic changes are seen in alcoholism?

A

-Fatty - changed lipid metabolism
-Cirrhosis
-HCC
-Alcoholic hepatitis/ cell damage

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20
Q

What enzymes allow alcohol metabolisation in liver?

A

MEOS enzymes
Alcohol dehydrogenase

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21
Q

How does hepatic encephalopathy occur

A

Amonia build up as liver doesn’t metabolise ammonia/ neurotoxins into urea -> build up of ammonia.

Crosses BBB and interfere with neurotransmission

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22
Q

Triggers for hepatic encephalpathy

A

GI bleed
Dehydration
Infection
Electrolyte imbanalce
Constipation
Sedatives
XS protein

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23
Q

Management of hepatic encephalopathy

A

Remove precipitants/ manage liver disease

Lactulose (makes ammonia non-absorbable)
Rifaximin
Supportive measures

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24
Q

How does B12 deficiency cause macrocytosis

A

Needed for cell cycle. Low B12 -> halts at G2 (mitosis).

Leads to continued cell growth without division

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25
How do NSAIDs cause ulceration?
Topical irritant to mucosa/impair barrier Suppress gastric prostaglandins (normally suppress acid) Reduce gastric mucosal blood flow Interfere with repair of superficial injury
26
Management of perforated peptic ulcer
Omental patch repair Peritoneal washout + drain Gastric - bx to rule out malignancy Long term - PPI
27
Factors stimulating HCl release from stomach
1)Vagus nerve: -direct - ACh to M receptors on parietal cells -indirect - stimulates gastrin release via vagal GRP 2) Gastrin (in circulation) 3) Histamine -from ECL cells in stomach
28
Describe 3 phases of gastric secretion
1)Cephalic (30%) Trigger = taste/smell Vagus - direct + indirect (gastrin) 2) Gastric (60%) Trigger = distension -Vagus - direct + indirect -Histamine - Local reflexes/ peptides -> gastrin 3) Intestinal (10%) Trigger = duod distention/ acid inhibits HCl via CCK/ secretin/ neural
29
Mechanism of action of PPI
Irreversibly binds H/K ATPase pump to block H+ ion secretion
30
Describe method of HCl secretion from parietal cells of stomach
CO2+H20 ->H & HCO3 HCO3 swapped out for Cl from blood H/K ATPase for H+ ions into lumen and K+ into cell CL- ions follow H+ by diffusion into lumen
31
Functions of gastric HCl
Antimicrobial Converts pepsinogen -> pepsin Stimulate SI secretion of CCK/ secretin Promote SI Ca/iron absorption
32
Causes of gastric outlet obstruction
Benign - pyloric stenosis (2y chronic ulceration in adults) Malignancy - gastric/ pancreatic
33
Blood gas finding for gastric outlet obstruction
Hypochloremic, hypokalemic metabolic alkalosis +hyponatremia Low Cl - due to vomiting Low K+ - due to increased aldosterone as hypovolemic from vomiting -> loss of H+ and K+ in urine in exchange for water retention Alkalosis - increased bicarb uptake in response to low Cl + reduced pancreatic juice secretion (aka retention of bicarb rich juice) Low Na - kidneys excrete more Sodium bicarb to compensate for alkalosis
34
What is paradoxical aciduria (in context of gastric outlet obstruction)
Low Na -> RAAS stimulated -> Na/H20 resorption increase in exchange for H+ and K+ Leads to loss of H+ and K+ in urine (hypokalaemia)
35
Clinical presentation of low Na
Confusion/ agitation/ fits/ reduced GCS
36
Causes of low Na
Dehydration/ depletion Dilution (HF/ XS IVF) SIADH Pseudo (multiple myeloma) Endocrine (addisons/ hypothyroid)
37
why is clotting deranged in liver disease
Reduced production clotting factors Reduced Vit K absorption - needed for factor 2 7 9 10
38
How does bilirubin circulate in plasma
Free Conjugated (to glucuronic acid)
39
What clotting test will be prolonged in liver disease
PT/INR
40
management of biliary stone disease a) colic b) cholecystitis c) cholangitis/cbd stone
a) Lap chole if recurrent b) abx + lap chole (later date) c) Abx, ERCP (?lap chole at later date)
41
What is a gallstone ileus?
Fistula between GB and duodenum - massive stone passes through causing obstruction of SI
42
What is Mirizzi's syndrome
External compression of other structures from GB stone in Hartmans pouch
43
Main side effect of cholecystectomy
severe chronic diarrhoea
44
Function of bile re fat
Emulsifies fat into smaller micelles to increase surface area for lipases to act. Bile salts are hydrophobic on one side (towards fat), and hydrophilic on other (prevent fat droplets reaggregating)
45
Constituents of bile
Water Cholesterol Bile pigments (bilirubin) Bile salts Lecithin (phospholipid)
46
What is bile conjugated to?
Glucoronic acid By enzyme - glucoronyl transferase
47
What is the fate of conjugated bilirubin?
Conj bili -> terminal ileum -> metabolised by gut flora to urobilinogen a) 10% reabsorbed into EH circulation - some reexcreted as bile by liver - some enter systemic circulation to be excreted by kidneys (yellow urine) b)90% ->oxidised to stercobilin (brown colour to stool)
48
What is the function of the enterohepatic circulation?
Reabsorption of bile salts from terminal ileum, deliver back to liver for further production of bile
49
Obstructive jaundice - is urobilinogen present in urine or not? why?
No Obstruction to bilirubin flow, therefore does not reach the colon/ reabsorbed to urine
50
Obstructive jaundice - why is urine dark/ stool light?
Light stool - bilirubin blocked so doesn't reach colon (to convert to stercobilin = brown) Dark urine - excess conj bilirubin due to build up leaks into urine via systemic circulation
51
Scoring system for acute pancreatitis
Glasgow Imrie score - 3 or more = severe, for ITU PaO2 <8 (hypoxia) Age >55 Neutrophils Calcium Renal (urea >16) Enzymes - LDH >600 Albumin <32 Sugar (glucose >10)
52
Pancreatitis blood tests
Amylase - normal after 48hrs, not indicative of severity, not specific Lipase - longer t1/2, more specific LDH
53
Why is glucose high in pancreatitis?
Pancreatic enzymes destroy islet of Langerhans -> increased glucose Also stress response
54
Why is calcium low in pancreatitis?
EARLY: 1) Pancreatitis enzymes -> fat autodigestion -> FFAs chelate Ca 2) Hypoparathyroidism 3) Hypomagnesium LATE: Sepsis -> calcium shift from serum to intracellular
55
Definition/ presentation of pancreatic pseudocyst
Collection of amylase rich fluid enclosed by fibrous/ granulation tissue >4weeks after acute attack Pain, swelling, dyspepsia, mild fever, vomit
56
Management of pancreatic pseudocyst
Most self resolving - supportive Infected/ erosion, >6cm, >2 months - surgery + drainage
57
difference between pancreatic cyst and pseudocyst
Cyst - truly walled off by epithelium Pseudo - walled off by granulation/ fibrous tissue
58
define shock
circulatory failure resulting in inadequate organ perfusion
59
define sepsis
Life-threatening organ dysfunction due to a dysregulated host response to infection Main features: Organ dysfunction Infection Dysregulated response
60
Define septic shock
Presence of sepsis (infection+ organ dysfunction) + persistent hypotension (SBP <90/ needing pressors) OR hypoperfusion (lactate >2)
61
Pros of IR vs open drainage of diverticular abscess
OPEN: -Better drainage/ washout - can make stoma IR: -No open wound for infection -Less IP stay/ morbidity -Can leave drain in situ + give abx
62
What is thumbprint sign (XR)?
Bowel wall thickening/ odema - sign of inflammation/ infection - normal haustra become thickened and look like thumbprints
63
Ddx of blood diarrhoea
IBD Diverticulitis Carcinoma Gastroenteritis- C. Diff/ campylobacter Ischaemic colitis Amoebic colitis
64
What ABG findings would be expected in small bowel obstruction
Metabolic acidosis
65
What factors affect tissue oxygenation?
O2 delivery = CaO2 (arterial O2) x CO CO = HR x SV Therefore: Cardiac output/ heart rate/ stroke volume Oxygenation of arterial blood
66
What factors affect affinity of Hb for O2
pH pCO2 2,3 DPG Temp *If Low = shift Left *If Raised = shift Right Also left in unusual versions of Hb (e.g. HbF)
67
How to investigate microcytic (aka iron deficiency) anaemia?
TIBC Serum ferritin Transferrin sats Occult stool blood test
68
Definition of enter-cutaneous fistula
Abnormal tract between GIT and skin, lined by granulation tissue
69
Factors predisposing to EC fistula
Cancer Infection Chrons Bowel anastomosis Irradiation Ischaemia
70
Complications of EC fistula?
Sepsis Malnutrition Electrolyte disturbance
71
Management of EC fistula
Stabilise with A-E Rule out abscess/ distal obstruction 60% resolve -Protect skin -Nutritional support/ dietician (?TPN) -Fluid/ electrolyte replacement Surgery only if failed cons mx/ ongoing sepsis -> excise fistula tract and bowel, + primary/ delayed anastomosis
72
What imaging for an EC fistula?
CTAP + contrast Fistulogram - locate + tract length + any distal obstruction
73
Define a steroid
Organic compound containing 4 joined cycloalkane rings
74
Layers of renal cortex and what they make
Outer > Inner: Glomerulosa - aldosterone (mineralocorticoids) Fasiculata - cortisol (glucocorticoids) Reticularis - sex hormones Medulla - catecholamines
75
Actions of aldosterone
Salt/Water balance - Reabsorbs Na and excretes K+ (in DCT/collecting ducts) Can cause metabolic acidosis (by K+ excretion)
76
Actions of cortisol
Anti-inflammatory + immunosuppressive Glucose: - stimulate gluconeogenesis - anti-insulin effect (inc blood glucose conc) Protein: -stimulate protein synthesis in liver/plasma -protein depletion elsewhere Fat: lipolysis
77
What 2 hormones are released by the posterior pituitary
ADH (vasopressin) Oxytocin
78
Steroid side effects
Mood/behaviour change Infection/ immnunocompromise Hyperglycemia Peptic ulcers - don't take NSAIDs Addisonian crisis - don't stop suddenly Osteoporosis Reduced wound healing Muscle weakness
79
What is an Addisonian crisis/ addisons disease
Addisons disease - primary adrenal insufficiency Addisonian crisis = acute reduction in body's circulating steroids - 2y causes = infection, surgery, trauma, stopping steroids rather than weaning **deficiency of all 3 steroids**
80
Sx of Addisonian crisis
N/V Abdo pain Unexplained shock Low Na, High K+ - mineralocorticoid function
81
Management of Addisonian crisis
CCRISP/ A-E IV steroids - bolus of hydrocortisone -> infusion over 24h IVF correct metabolic disturbance
82
How to avoid addisonian crisis in surgery
Increase steroid dose + convert to IN
83
Effect of PTH on calcium + how
Increases serum ca Bone: increase osteoclast activity/ bone resorption to release ca Kidney: increase ca resorption + Vit D3 synthesis
84
Effect of Vit D on calcium + how
GI: Increase intestinal absorption of Ca/PO4 Kidney: Increase reabsorption of Ca/PO4 Bone: ? increase osteoblasts?
85
Effect of calcitonin on calcium + how
Bone: increase osteoblast activity to reduce bon resorption Kidney: increased excretion of Ca/Cl/Na/PO4
86
Hypocalcemia signs
Coma/ seizure/ irritability Arrhythmia Tetany/ spasm/ stridor (most concerning in laryngeal muscles > airway obstruction) Cramps Numbness Chvostek's sign - facial twitching when tapping facial nerve Trousseu's sign - median nerve spasm with BP cuff (arm ischaemia)
87
Treatment of hypocalcemia
Cardiac monitoring Ca gluconate bolus (10ml) + infusion
88
Acidosis effect on serum calcium
Decreased (hypocalcemia) due to increased binding of ionised (free) calcium
89
Summary of steps in thyroid hormone synthesis
1) Iodide ion trapping (into cell by Na/I symporter) - absorbed from diet 2) Oxidation of Iodide > Iodine (by TPO) 3) Iodination of thyroglobulin -> MIT/DIT 4) Coupling: MIT + DIT = T3, DIT + DIT = T4 -(by TPO) 5) Excretion (via lysosomes) 6)Peripheral conversion of T4-T3 -T3 more active, T4 better bound in plasma
90
Hashimotos Abs
Anti TPO Abs - affect Oxidation of iodide and coupling of MIT/DIT
91
Bloods in sick euthyroid syndrome/ non-thyroidal illness
High T4, Low/ normal TSH
92
Risks of hypothyroidism in surgery
Preop: Anaemia IHD Intra-op: Bradycardia Hypotensions Hypothermia - > coagulopathy/ airway compromise Post-op: Myxedema coma Confusion Delayed recovery/ wound healing
93
T1 vs T2 diabetes pathogenesis
T1 - absolute insulin deficiency due to beta cell destruction, usually autoimmune T2 - peripheral insulin resistance+ some receded production
94
Main functions of insulin
Carbs (reduce circulating glucose): -Increase glucose cell uptake -Glycogen synthesis (mainly in liver) -Reduce gluconeogenesis in liver Protein (increase - acts as growth hormone): -Amino acid uptake into cells -Protein synthesis Fat (reduce): -Increase lipid uptake into cells -Oxidation of lipids in cells -Lipogenesis + fat deposition
95
Hormones affecting blood glucose level
Insulin Glucacon Cortisol Catecholamines Somatotrophin
96
Diabetes surgical complications
Early: Hypo/ hyper DKA HHS Dehydration + electrolyte abnormality Late: Poor wound healing Sepsis/ infection

MRCS B (10 decks)

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