NME Flashcards
(352 cards)
1
Q
What are the boundaries of the:
- foregut
- midgut
- hindgut
and what is the blood supply to each?
A
Foregut = Distal oesophagus to proximal half of D2. Coeliac artery
Midgut = Distal half of D2 to Proximal 2/3 of transverse colon. SMA
Hindgut = Distal 1/3 of transverse colon to rectum. IMA.
2
Q
Which sphincter is responsible for the prevention of reflux?
A
Lower oesophageal sphincter
3
Q
What are the three mechanisms of control over acid protection in the stomach?
A
Direct neural = PSS fibres from vagus nerve - directly stimulate gastric parietal cells - produce H+
Paracrine - gastrin is produced by G-cells of the antrum, duodenum & pancreas when they sense peptides in the lumen - this stimulates ECL cells to produce histamine - which in turn stimulates parietal cells to produce H+
Endocrine - gastrin (from G-cells) also directly stimulates parietal cells to produce H+
4
Q
Which cells produce
1) gastrin
2) histamine (in the antrum of the stomach)
3) H+ in the stomach
A
1). G-cells
2). ECL cells
3). Parietal cells
5
Q
Name 3 causes of GORD
A
1 - failure of LOS to close fully / or it temporarily relaxes intermittently
2 - failure of diaphragmatic sphincter = hiatus hernia
3 - increased intra-abdominal pressure
6
Q
What is the biggest risk factor for GORD?
A
H-pylori
7
Q
What are the risk factors for GORD?
A
All the blue ones on this list = increased the intra-abdominal pressure.
8
Q
What is the commonest disorder of the gastrointestinal tract?
A
GORD
9
Q
What are symptoms of GORD?
A
10
Q
What methods are there for diagnosis of GORD?
A
11
Q
What does H pylori do in the stomach?
A
Secretes urease - converts urea to ammonia & CO2 - in doing so it increases the pH around it.
12
Q
Apart from GORD, what diseases are linked to H pylori?
A
13
Q
What is the most common cause of duodenal ulcers?
A
H pylori
14
Q
What is the Tx for GORD?
A
15
Q
How do PPIs work?
A
Inhibit the H+/K+ ATPase pump on parietal cells
16
Q
What are the side effects of PPIs?
A
Diarrhoea
Inc risk of C Diff
17
Q
How doe ranitidine work?
A
H2 receptor blocker - blocks the receptor on parietal cells for histamine - therefore stopping stimulation of the H+/K+ ATPase pump
18
Q
What is the surgical tx for GORD?
When is it done?
How does it work?
A
Fundoplication
When medical Tx has failed or LT medical Tx is undesirable.
Or repair of hiatal hernias.
Works by trying to inc effectiveness of LOS by wrapping fundus of stomach around it.
19
Q
What is a hernia?
A
Protusion of ALL or PART of a VISCUS through its COVERINGS into an ABNORMAL POSITION
20
Q
Name 2 types of hiatus hernia? What is the difference between them?
A
Sliding (85-95%) - GOJ mobilises upwards into the chest and some of the stomach follows it. Diaphragmatic sphincter no longer works.
Rolling (5-15%) - GOJ is fixed, gastric fundus herniates through the diaphragm. Diaphragmatic and LOS both work.
21
Q
What is the main cause of gastritis?
A
H pylori
Also - smoking, NSAIDs, alcohol, caustics, AI, infection, inflammatory conditions (Crohns, sarcoid, vasculitis)
22
Q
Why do NSAIDs cause gastric problems?
A
They inhibit COX 1 - which reduces prostaglandin production –> reduced mucous, bicarb & blood flow.
Together = reduced protection and ability to repair after injury.
23
Q
What are the two biggest causes of peptic ulceration?
A
H pylori
NSAIDs
24
Q
Why is has there been decreasing incidence of peptic ulceration in the past decades?
A
Due to improved pharmacological treatments - peptic ulceration now rare.
25
What are the less common cause of peptic ulceration?
Stress (trauma, critical illness, major surgery, med school)
Malignancy
Zollinger-Ellinson syndrome
Meds - steroids, bisphosphonates, chemo
26
What is Zollinger-Ellinson syndrome?
Rare tumour of G-cells (most commonly in pancreas)
27
Which is the most common type of peptic ulcer?
Duodenal ulcer - often in D1
28
How can you differentiate between a gastric and duodenal ulcer based on symptoms?
Gastric ulcer - get pain after eating as acid production increases
Duodenal ulcer - eating increases pancreatic juice which neutralises the acid - therefore you get less pain with eating and more pain when the stomach is empty.
29
What is the treatment for a peptic ulcer?
PPI
+/- H pylori eradication Tx
Lifestyle - stop NSAIDs, other meds if causative, smoking and decrease alcohol intake.
30
What are the two types of acute upper GI bleeds?
Variceal (11%) and non-variceal (89%)
31
What is the cause of variceal bleeding in the upper GIT? How is it treated?
Bleeding due to inc portal venous pressure (e.g. cirrhosis)
Meds - to reduce portal pressure = B blockers
Radiological intervention
Endoscopic treatment
32
What is a variceal?
An expanded blood vessel
33
How do you treat non-variceal UGI bleeding?
34
Which artery passes behind the duodenum (D1)?
What is the potential complication that can arise from this?
Gastric duodenal artery
Posterior ulcers in the D1 can erode into the GDA causing bleeding.
35
What is the difference between metaplasia or dysplasia?
Metaplasia - cell changes types from one to another but normal type
Dysplasia - cell changes into an abnormal type
36
What is Barretts oesophagus?
Why does it change?
Why is it bad?
Metaplastic change from normal oesophageal squamous epithelium to columnar epithelium
Oesophageal squamous epithelium isn't very resistant to acid whereas columnar epithelium is.
Is regarded as a premalignant condition
37
What are the RF for Barrett's oesophagus?
38
Which tumour suppressor gene mutation increases prevalence of Barrett's oesophagus?
p53 tumour suppressor gene
39
If the following changes are seen on OGD - how are they managed?
- Metaplasia without dysplasia?
- Low grade dysplasia
- High grade dysplasia
40
What is defined as diarrhoea?
Abnormal passage of loose/liquid tools > x3 / day +/- vol >200g/day
41
How long should diarrhoea persist in order for it to be
- acute
- persistent
- chronic?
42
When should diarrhoea be investigated?
When symptoms suggest a chronic pathology (>4w)
43
What can cause acute diarrhoea?
44
Why do infections cause diarrhoea?
45
When do you need to investigate acute diarrhoea? What would you do?
If P very unwell
Presence of blood / pus with stools
Recents ABs, hospital stay or on PPI
Recent foreign travel
IC Ps
Do stool sample for microscopy
46
What can persistent diarrhoea cause?
Dehydration
Hypokalaemia
Acidosis
47
How do we treat acute diarrhoea?
48
What are the causes of chronic diarrhoea?
49
Name 4 mechanisms of diarrhoea
50
What investigations do we do for chronic diarrhoea?
Stool microscope (infections and parasites)
Faecal calprotectin (inflammation)
qFIT (blood)
Faecal elastase
Bloods
51
When is a qFIT contraindicated?
If there is rectal bleeding
52
What do the following qFIT results indicate?
<10 micrograms Hb/g
>10
>150
53
How can we do mechanical assessment of the bowel?
54
What is the definition of IBS?
55
What is the most common age and sex for IBS?
Do we know what causes it?
Fs 20-30
No
56
How do we manage IBS?
57
What medications can be given for IBS diarrhoea?
Loperamide
Antispasmodics - hyoscine butyl bromide (buscopan)
58
How does loperamide work?
What are its side effects?
Is an agonist for opioid receptors in the bowel wall - reduces intestinal motility and secretion. (Specific to gut opioid receptors)
Commonest = constipation
Can cause cardiac arrhythmias in higher doses
59
Which laxative should be avoided in IBS?
Lactulose - as it can cause excessive bloating
60
What unusual medical Tx can be given to help with IBS symptoms?
Tricyclic antidepressants (amitriptyline ) - low dose. >90% respond to some extent.
61
What is the definition of constipation?
BO less <3 per week
62
What are the causes of acute constipation?
63
What are the causes of chronic constipation?
64
What are the potential consequences of constipation?
65
What questions should you ask a P with constipation?
66
What investigations can you do for constipation?
67
It is unusual to get constipation from IBD - why might this happen though in chronic IBD?
Chronic IBD can cause stricturing of the GIT - leading to inability to pass stools easily
68
Protrusion of mucosal pouches is known as what?
Divertular disease
69
Where in the GIT is the highest incidence of diverticular disease found? Why?
In the sigmoid colon - this is where the highest intra-luminal pressure exists in the bowel.
70
What percentage of patients with diverticular disease will be symptomatic?
10%
71
What is the greatest risk of performing a colonoscopy in a patient with diverticular disease?
Perforation - confusion in where the camera is going.
72
What is thought to be linked to diverticular disease?
Constipation (chicken and egg)
Poor dietary fibre
73
What is it important to remember about proximal bowel obstruction?
That the bowel may appear to still be working even though there is obstruction.
The more distal the obstruction - the earlier the constipation will present
74
What is a sign of distal mechanical obstruction of the colon?
Absolute constipation - no flatus or stool
75
Was percentage of adhesion small bowel obstruction will resolve without surgery?
>90%
76
What things can cause bowel obstruction?
77
What is a closed loop large bowel obstruction?
How does it present?
How is this treated?
Closed loop large bowel obstruction = when there is a competent ileocaecal valve which is preventing reflux into the ileum.
If no reflux - the bowel will get bigger until it perforates - usually in the caecum as this is has the largest diameter and thinnest wall.
Presents with right lower abdominal pain
Is surgical emergency - need to go to surgery for this.
78
How is bowel obstruction managed generally?
Resus = fluids, electrolyte replacement. Drip and suck.
79
How is chronic constipation managed generally?
80
What protein causes coeliac disease?
Gliadin - from gluten - found in wheat, barley & rye. Oats can be contaminated.
81
What is the epidemiology of coeliac disease?
1% of pop have it
F>M
Any age
Most prevalent - Western Europe and US
Some link - Downs, T1 DM, AI hepatitis, thyroid gland problems. Twin studies have shown genetic link.
82
Which genes are associated with coeliac disease?
HLA DQ2 and DQ8
83
What are the symptoms of coeliac disease?
84
How does coeliac disease affect the small bowel?
Villi get inflamed - then they shorten as a result and atrophy. Leads to malabsorption.
Get scalloping (ulceration) and smooth appearance (no villi)
85
What are the clinical signs of coeliac disease?
Dermatitis herpetiformis
Pallor (anaemia)
Angular stomatitis (Iron / B12 deficiency)
Glossitis (iron deficiency)
86
What is the difference between angular stomatitis and angular chellitis?
Angular stomatitis = inflammation of the lips
Angular chellitis = inflammation of the corners of the mouth
87
What is dermatitis herpetiformis?
88
What is the pathogenesis of coeliac disease?
Gliadin - forms a complex with tTG (transglutaminase) - binds to HLA-DQ2 on T-cells --> anti-tTG IgA ABs (3 types)
89
How can you test to see if a P has coeliac disease?
25% of Ps will be serology negative - so important to always get histopathology as well.
Endoscopy with biopsy = gold standard
90
How do we treat coeliac disease?
Also need to ensure they don't develop AI hepatitis or AI thyroid disease - AI disease can occur in more than one form.
91
Why do Ps with coeliac disease need vaccination against pneumococcus?
Ps develop functional hyposplenism - unknown why but renders the spleen inept.
92
What is the difference between Crohn's and UC?
Transmural = affects all parts of the bowel wall.
CD - get skip lesions which are separated by normal areas of mucosa.
UC - lesions start in the rectum and extend proximally with no breaks.
93
How do CD and UC look different on endoscopy?
Crohn's = cobblestone appearance - deep, patchy ulceration and inflammation.
UC = superficial continuous inflammation
94
Are granulomas seen in CD or UC?
95
What are granulomas?
Gatherings of macrophages around foreign substances they want to eliminate.
96
What are potential complications of Crohn's disease?
Strictures
Fistulas
Perianal disease
97
What is the epidemiology of CD?
Western world - high prevalence
Esp Jewish origin
Inc in Africa, South America and Asia.
Bimodal presentation - teens-20s and 60-70s.
98
What causes CD?
99
Although a cause is not yet known definitely, there is strong evidence for genetic predisposition to CD. Which gene do they think is implicated in this?
NOD2 on Chromosome 16
100
What percentage of Ps with CD will need surgery?
50% will need surgery - 70% of these will need 2nd operation within 5 years
101
What is the epidemiology of UC?
102
What complication can arise from UC?
Causes inflammation of the mucosa. If severe - P cannot pass wind - toxic megacolon = perforation.
103
What is the lifetime risk of a colectomy with UC?
20-30%
104
What is the ladder of treatment for chronic IBD?
105
What is first line treatment for
(a) UC
(b) CD?
(a). mesalazines
(b) thiopurines
106
What type of drug are mesalazines?
5-aminosalicyclic acids (ASAs)
107
How do we treat acute CD?
NBM switches off CD - gut immediately resets.
108
How do we treat acute UC?
109
What are the functions of the kidney?
110
What is the blood supply of the kidney?
Blood (with waste) brought to the kidney by the renal artery into the afferent arteriole.
Clean blood leaves the kidney via the efferent arteriole into the renal vein.
111
What is azotaemia?
High levels of nitrogen compounds in the blood.
112
Which hormones does the kidney produce?
What will the P present with if production of each of these hormones is disrupted due to CKD?
Erythropoietin = anaemia
Renin = high BP
Prostaglandins = production may be elevated causing inc levels of inflammation and altered Na balance
Active Vit D = renal bone disease
113
At what vertebral level are the following found?
- Kidneys
- Renal hilum
Kidneys = T12 - L3
Right is slightly lower due to liver!
Hilum = L2
114
What is the term for being born with only one kidney?
Renal agenesis
115
What are the two major layers of the kidney?
Cortex and medulla
116
Name the 5 sections of the nephron
Glomerulus
PCT
Loop of Henle
DCT
Collecting duct
117
Name two types of nephrons found in the kidney.
Cortical nephrons
Juxtaglomerular nephrons
118
Which part of the kidney produces renin?
The juxtaglomerular apparatus
119
Which cells in the juxtaglomerular apparatus can sense BP changes?
Macula densa cells
120
What are the following called
- capillaries which supply the cortical parts of the tubules of the nephron
- capillaries which supply the medullary parts of the tubules of the nephron?
Peritubular capillaries
Vasa recta
121
How much of cardiac output do the kidneys receive?
20-25%
122
Which nerves provide SS and PSS innervation to the kidney?
SS = sympathetic chain & coeliac ganglion
PSS = vagus nerve
123
What is the glomerular filtration barrier?
4 layers of physical barriers between the blood and Bowman's space in the glomerulus.
---
Glycocalyx = negatively charged proteoglycans - coat luminal surface of endothelial cells - covers the opening of the fenestra. Fenestra = pores which allow passage of water and molecules through the endothelial cells of the glomerular capillaries. Permeability of endothelium is very high - allow passage of water, ions, small molecules and small proteins - does restrict movement of large proteins, platelets and other cells.
Endothelial cell BM - porous matrix of extracellular proteins. Is physiological barrier to filtration.
Podocyte foot processes enable filtration slits. Podocytes = inner layer of Bowman's capsule.
Water, ions and small proteins can pass through from capillary to be reabsorbed. If glomerulus is damaged - can get proteins into the urine (proteinuria) - can lose albumin = problems medically. Glomerular must be a strict barrier to stop loss of important proteins.
124
What size molecules can pass through the glomerular filtration barrier?
<60KDa
125
What two factors is glomerular filtration dependent upon?
Blood pressure
Renal blood flow
126
What is GFR in a normal healthy individual?
About 125ml/min
= 180L / day
127
How is renal blood flow controlled?
It is autoregulated - therefore controlled purely by local effect from myogenic stretch of the renal arterioles.
128
What happens if the afferent arteriole sense a decrease in blood flow?
Prostaglandins, ANP, dopamine, NO and kinins are released - causing the afferent arteriole to dilate and the efferent arteriole to constrict.
129
What happens if the efferent arteriole senses an increase in blood pressure?
The afferent arteriole constricts (NOR, endothelia, adenosine & ADH) and the efferent arteriole dilates (NO & A2A&B)
130
How do changes in GFR affect systemic BP?
Macula dense cells sense a change in tubular Na levels - and stimulate juxtaglomerular cells to release Renin. This increase BP via release of AGTII.
131
What is reabsorbed from the PCT?
Which is the main pump for this?
65% Water, Na, HCO3, Cl, K & Urea
Glucose
AAs
Small filtered proteins
Na/K ATPase pump is main driving force
132
How does Na reabsorption occur in the PCT?
133
How is water reabsorbed from the PCT?
134
How is glucose reabsorbed from the PCT?
135
Some substances and drugs cannot be filtered through the glomerular filtration barrier due to their size/protein binding. How can these be transported into the nephron?
In the PCT - are two specialised pumps which can transport them from the plasma in the peritubular and vasa recta into the nephron.
- Organic acid pumps (uric acid, diuretics, ABs - penicillin)
- Organic base pumps (creatinine, procainamide)
136
Which ions are left in the PCT to be expelled in the urine?
Hydrogen
Ammonium (NH4)
Urea
Creatinine
137
What happens in the
- descending; and
- ascending limbs
of the Loop of Henle?
How do these processes occur?
Descending - reabsorption of water takes place - no active transport of salts! Water permeable via AQP-1 channels.
Ascending - Na and Cl are reabsorbed - via NKCC2 (Na/K/2Cl) co-transporters using ATP.
138
What is the osmolality of fluid in the LOH
- when it enters the LOH
- when it is at the tip of the LOH
- by the end of the LOH
Entering = isotonic
Tip = hypertonic
End = hypotonic
139
What is the name for the mechanism of water absorption in the LOH. How does this work?
Countercurrent Multiplication
Solutes reabsorbed in the ascending loop are pumped into the medullary space - creating an osmotic pull on the descending loop which forces water to leave to enter the medullary space.
140
What is reabsorbed in the LOH?
What is secreted into the urine in the LOH?
Water
Na
K
Cl
HCO2
Ca
Mg
Secreted into urine = urea
141
Na and Cl are actively reabsorbed and exchanged for K+ and H+ in the late DCT / CD. How does this happen?
Na - K transported via principal cells allows Na to be reabsorbed and K+ to be excreted into the urine - controlled by aldosterone levels!
Na - H transported via intercalated cells - Na is reabsorbed and H+ excreted into the urine.
142
How does aldosterone affect the kidney?
Aldosterone increases the Na-K transporter in principal cells - which increases the amount of Na reabsorption. More Na reabsorption = more water reabsorption = increased fluid in BVs = increased BP.
143
How are the DCT and CD involved in acid-base regulation?
Intercalated cells =
α intercalated cells = secrete H+ into urine (via Na-H+ exchange pump) AND reabsorb HCO3.
β intercalated cells = secrete HCO3 and reabsorb H+
144
How does ADH (Vasopressin) affect the collecting duct?
ADH = allows water to diffuse into the medulla (therefore conc urine and inc BP) - does this by INC AQP2 (apical membrane) and APQ3 (basolateral membrane). Therefore water reabsorption is increased.
145
Which receptors for ADH act upon?
Vasopressin (V2) receptors --> inc activation of AQP2 channels = inc water reabsorption
146
Which disease can be caused by a lack of ADH?
Diabetes insipidus
147
Describe the RAAS system.
148
What is renal clearance?
Clearance = (Glomerular filtration + Tubular secretion) - Tubular reabsorption
Measured the volume of plasma completely cleared of a given substance in a unit time.
149
What is normal GFR?
125mls/min
150
What factors determine GFR?
Glomerular hydrostatic pressure
- Bowman's capsule pressure
- Glomerular colloid osmotic pressure
= GFR
151
At what vertebral level do the following branch off from the AA?
- Coeliac artery
- SMA
- IMA
Coeliac artery - T12
SMA - L1
IMA - L3
152
What are the three main branches of the coeliac artery?
Left gastric a.
Splenic a.
Common hepatic a.
153
154
155
At what level does the aorta bifurcate?
L4
156
What are the 5 levels of the abdominal wall?
Skin
Superficial fascia (Camper's and Scarpa's)
Rectal Sheath
Deep Fascia (Trasversali fascia)
Extraperitoneal fat and peritoneum
157
What are the muscles of the abdominal wall?
External oblique
Internal oblique
Transversus abdominus
Rectus abdominus
158
What is the name of the central tendinous insertion between the abdominal muscles?
Linea alba
159
What is the significance of the arcuate line?
The rectus sheath changes and vessels underneath (inferior epigastric a.) pass into the rectus sheath at this point.
Above arcuate line - IO aponeurosis splits into anterior laminar and posterior laminar around rectus abdominus - 3/4s of rectus sheath has this organisation. Much more supportive mechanism than below.
Below arcuate line - aponeurosis of all 3 muscles pass anterior to the rectus abdominus, with only the transversalis fascia and parietal peritoneum posterior.
160
What are the lesser and greater curvatures of the stomach connected to?
Lesser = lesser omentum - which is connected to the stomach
Greater = greater omentum - connected to rest of the abdominal cavity
161
Where does the small intestine begin and end?
Begins = pylorus of stomach
Ends = ileocaecal junction
162
163
What combines to form the hepatopancreatic ampulla?
The main pancreatic duct + common bile duct
164
What is the rectus sheath made from?
165
166
What are the two surfaces of the liver?
Diaphragmatic and visceral
167
What are the lobes of the liver?
Right
Left
Quadrate
Caudate
168
Wha is the hilum of the liver called?
What travels through this?
Porta hepatis
Portal vein
Hepatic artery proper
Common hepatic duct
169
What separates the R and L lobes of the liver?
Falciform ligament
Left sagittal fissure
Ligamentum teres hepatis (remnant of umbilical vein)
170
What is the liver contained in?
A capsule (Glisson capsule) and peritoneum - except posteriorly in the bare area where it lies in direct contact with the diaphragm
171
What anchors the liver to the stomach?
Lesser omentum - made of hepatogastric and hepatoduodenal ligaments
172
What anchors the liver to the diaphragm?
Coronary ligament
R & L Triangular ligaments
173
What is the path of bile from the liver to the duodenum?
Made by hepatocytes - drains into canaliculi.
These drain into R&L hepatic ducts -> common hepatic duct
+ cystic duct from bile duct joins = forms common bile duct
+ pancreatic duct = forms hepatopancreatic duct - opens into duodenum at D2
174
How much of CO does the liver receive?
25%
175
What is the dual blood supply to the liver?
Hepatic artery proper (provides 25%)
Portal vein (provides 75%) - brings blood for metabolism & detoxification, nutrient rich
176
177
What does the portal venous system do?
Drains blood from GI tract to the liver
178
Which veins make up the portal vein?
Superior mesenteric vein & Splenic vein
- form the portal vein
179
What are the communications between the portal veins and the systemic veins known as?
What clinical implication can these suffer?
Portosystemic anastomoses
If portal hypertension exists (e.g. liver disease) - can cause dilatations of the anastomoses = varices, caput medusa etc.
180
What are liver lobules divided into?
Couinaud segments
181
What are the three main branches of the coeliac artery?
182
What is the venous drainage of the liver?
183
Where does lymphatic drainage of the liver go?
Cisterna chyli
184
How much lymph is produced by the liver
25-50%
185
What is the liver innervated by?
SS = coeliac plexus
PSS = anterior and posterior vagal trunks
186
What is the function of bile?
Emulsifies fats
187
What is the function of the gallbladder?
188
When is the gallbladder stimulated to release bile?
When food enters the second part of the duodenum.
189
What is the blood supply to the gallbladder?
Cystic artery (which is normally a branch of the right hepatic artery)
190
191
Can you ever palpate the gallbladder?
Only if it is inflamed
192
What is the venous drainage of the gallbladder?
Lots of small veins that go directly to the liver.
193
What are the exocrine and endocrine functions of the pancreas?
194
Digestive enzymes made in the main body of the pancreas collect small ducts which join to form the main pancreatic duct which is called?
The head of the pancreas drains separately into which duct?
Duct of Wirsung
Duct of Santorini
195
Which artery runs along the superior and inferior margins of the pancreas?
What runs behind the pancreas?
Superior = splenic artery
Inferior = SMA
Posterior = Splenic vein + SMA - both drain into portal vein.
196
What is the blood and nerve supply of the pancreas?
- Arteries
- Veins
- Nerves
197
What is the spleen comprised of?
What's the function of each?
Red pulp (blood filled sinuses)
White pulp (lymphatic tissue)
198
What are the functions of the spleen?
199
What can cause splenomegaly?
Diseases such as major haematological disorders and some tropical parasites can cause massive enlargement of the spleen.
200
What are the contents of the retroperitoneum?
SAD PUCKER
Suprarenal glands
Aorta & IVC
Duodenum (2nd & 3rd parts only)
Pancreas
Urter
Colon (ascending, descending only)
Kidneys
Esophagus
Rectum
201
What is important about the arteries in the kidney?
They are end arteries - therefore if one is cut there is no collateral supply and potentially a segment of kidney will die.
202
Which renal vein is longer?
Left - because the IVC lies more to the right.
203
What is the distribution of renal and uteric pain?
204
205
What are the following called:
- One or both kidneys don't form
- Additional kidney / ureter
- Kidneys joined cross the midline
- Kidney agenesis
- Supernumerary kidney / ureter
- Renal fusion / Horseshoe kidney
- Ectopic kidney
- Polycystic kidney
206
What are the three narrow areas for the ureter that can be subject to constriction?
PUJ
Crossing the iliac artery
As it inserts into the bladder
207
What is the epidemiology of bowel cancer?
208
What are the RF for bowel cancer?
209
Why does high dietary fibre reduce the risk of bowel cancer?
Inc turnover = inc clearout of damaged cells - gut bacteria are integral to this.
210
What is a polyp?
A protrusion into a holly viscus
211
What are neoplasia, dysplasia and metaplasia?
Neoplasia = new formation (any growth) - can be benign or malignant
Metaplasia: Transforms a cell from one form to another; caused by external stimulus; can be reversible; less likely to lead to cancer.
Dysplasia: Transforms a cell into an abnormal version of itself; caused by internal stimulus; is not reversible; more likely to lead to cancer.
212
What is the precursor for the majority of bowel cancers?
Polyps
213
What are the different types of polyps in the LGIT?
Hyperplastic - normally benign - don't really develop into cancer
Serrated - can develop into cancer
Adenomas - have a mixture of morphologies
Pedunculated = on stalks
Sessile = flat
Semipedunculated = wide stalk
214
Which mutation in which tumour suppressor gene that regulates cell growth can be responsible for bowel cancer?
TP53
215
What is the adenoma-carcinoma sequence?
A stepwise progression from normal bowel mucose to adenomatous polyp to bowel cancer.
216
What is the bowel screening used for?
To identify pre-malignant polyps which can be removed (polypectomy) and therefore to prevent them moving to the malignant stage.
217
What is the peak incidence age for bowel cancer and that for polyps?
Polpys = 60
BC = 71
218
Which genetic condition can predispose Ps to inc chances of developing polyps AND has almost 100% risk of BC by the time Ps reach 30?
Familial Adenomatous Polyposis (FAP)
219
What is the two hit hypothesis?
That you need to incur two mutations to a cell in order for it to mutate into a cancerous cell. Unless you already have a genetic weakness such as FAP in which case you only need one mutation.
220
Which gene is damaged by FAP?
APC gene
221
Which genetic condition causes abnormalities with the mismatch repair genes?
Lynch Syndrome
222
Which criteria is used to identify families at risk of Lynch syndrome?
Amsterdam criteria
223
How do bowel cancers present?
Most from screening or symptomatic presentation
224
What is the current bowel screening programme? When does it start?
qFIT testing
From 60-74 years (although can request after this) - done every 2 years
225
What sx can present with bowel cancer?
226
What is the gold standard test for bowel cancer?
Colonoscopy
227
What are the alternatives to colonoscopy for investigating bowel cancer?
Flexible sigmoidoscopy
Virtual colonoscopy
Plain CT
228
What are the predictors of poor outcome for bowel cancer?
229
Why do poorly differentiated cancers have worse outcomes?
Poor differentiation = sign of tumour aggression
230
If you have bowel cancer and mets in the liver = does this mean you have mets elsewhere?
No - due to the portal blood supply from the bowel - presence of liver mets does not guarantee disease elsewhere.
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232
How can bowel cancer present as an emergency?
PR bleeding
Bowel obstruction
Bowel perforation
Fistula formation
Infection / abscess
233
What is hepatitis?
Inflammation of hepatocytes (not cholangiocytes)
234
What are common causes of hepatitis?
Drugs (paracetamol)
Alcohol
Viruses
AI disease
235
How does hepatitis present in terms of Sx?
N&V
Fevers
Joint Pain
Muscle aches
Jaundice
Abdo pain
Pruritis
Pale stools
Dark urine
236
Which viruses can cause acute hepatitis?
Hepatitis A
Also Hepatitis B & E
237
Which viruses can cause chronic hepatitis?
Hepatitis C, and B & E
Also AI hepatitis can cause chronic hepatitis
238
Which LFTs are raised in hepatitis?
ALT and AST
239
What is ALT >1000 indicative of?
Acute viral cause
Ischaemia
Paracetamol OD
240
What does not markedly raise liver transaminases (ALT, AST)?
Alcohol
NAFLD
AI Hepatitis
241
How can you tell if alcohol is a cause from the LFTs?
AST > ALT
Also GGT can be raised
242
What is AST and ALT?
Liver transaminases
Enzymes found in the liver cells (hepatocytes) which leak into the blood stream when the liver cells are damaged. They indicate the degree of inflammation present in the liver.
243
Which is more specific to liver damage - AST or ALT?
The ALT is more specific to the liver than the AST value because the AST value may also be high if there is muscle damage elsewhere in the body.
244
What do ALP and GGT measure?
These are enzymes found mainly in the bile ducts of the liver. Increases in ALP and another liver enzyme called y-Glutamyltransferase (GGT) can indicate obstructive or cholestatic liver disease, where the flow of bile from the liver is blocked because of an obstruction of the bile duct.
GGT levels are also a potential indicator of how much alcohol a patient drinks and can also be higher in those with non-alcohol related fatty liver disease (NAFLD).
245
How much protein in the blood is albumin?
Approximately 60%.
Made by the liver - therefore if there are problems with the liver this value may be low.
246
Apart from AST, ALT, ALP and GGT - what other markers of liver failure can be screened in the bloods?
Bilirubin
INR (not making clotting factors)
Creatinine
Albumin
Blood glucose
247
What investigations can you do for hepatitis?
Bloods
USS
Liver biopsy
Fibroscan - non-invasive assessment of fibrosis
248
What are the stages of liver damage?
Normal liver
Fatty liver
Liver fibrosis
Liver cirrhosis
249
What viruses cause hepatitis?
Hep A-E
CMV
EBV
HIV
250
How is Hep A transmitted?
Faecal to oral route - contaminated water, food (oral sex?)
251
Which hepatitis viruses have vaccines available for them?
A, B
252
How is Hep A diagnosed?
Presence of IgM anti-HAV AB in serum
253
What is the prognosis of Hep A?
Doesn't cause chronic hepatitis
Acute liver failure is rare - often seen in older Ps if at all
Usually self-limiting illness - have jaundice, fever, lethargy
254
Where is Hep A most prevalent?
Africa, Asia and South America
255
How is Hep E transmitted?
Same as HepA - faecal oral route or through blood products
256
What is the most common cause of liver failure in pregnancy?
Hep E
257
How is Hep E detected?
Presence of anti-HEV IgM AB
258
What are the complications of Hep E?
Can cause chronic hepatitis - esp in immunosuppressed.
Does not cause cirrhosis.
Most remain asymptomatic
259
Where is Hep B found?
Sub Saharan Africa
SE Asia
260
How are most cases of Hep B acquired?
Vertical transmission (M to baby)
Sex transmission
IVDU
When transmitted through sex or IVDU - tends to present acutely rather than chronically
261
What does Hep B cause?
Cirrhosis
Hepatocellular cancer
Significant cause of both of these in the UK
262
What are the 4 states of chronic hepatitis B infection?
Immune tolerant
Immune reactive
Inactive
Immune active
Born - and contract Hep B during delivery - have the virus until 25-30 - high viral load but liver doesn’t care = immunotolerant phase. Really high viral load but liver handles it ok.
Liver decides it doesn’t like it and tries to get rid of it - attacks the E antigen which makes it from positive to negative - viral load drops, liver function tests get raised and then normalise = inactive state - low viral load and normal LFTs. Around 30.
Cycle of viral load starts creeping up - liver gets angry - LFTs go up, viral load goes down again - cycle of inflammation and calming causes liver scarring - 10-30 years - develops into cirrhosis. 4 phases.
263
How do Ps with acute Hep B present?
Jaundice and fever
Although can be asymptomatic
264
What is the prognosis for Acute Hep B?
95% of adults seroconvert (get rid of Hep B completely)
5% will progress to chronic hepatitis
265
What is the Rx for Hep B?
Lifelong antivirals for chronic - started when Ps are fibrotic.
Treat in 3rd trimester to prevent transmission
Treat immunosuppressed Ps
266
Which Hepatitis viruses has to piggyback on a pre-existing Hep B infection?
Hepatitis D
267
How is Hep C transmitted?
Blood
Sex intercourse
IVDU
268
How can you detect Hep C?
HCV AB
HCV RNA
in blood
269
What Sx does Hep C present with?
Most Ps are asymptomatic
Fatigue however is common
Jaundice is rare
270
What percentage of Ps with Hep C will develop Hepatocellular carcinoma?
1-3%
271
Which Hepatitis is a DNA virus?
Hep B - remainder are RNA viruses
272
Which hepatitis does not cause chronic viral hepatitis?
Hepatitis A - self limiting
273
Apart from hepatitis viruses, which other viruses can cause hepatitis?
274
Which hepatitis always needs antiviral medication?
Hepatitis C
275
What infections can cause hepatitis?
276
How is alcohol metabolised in the body?
277
What are the end products of alcohol metabolism in the body?
Cholesterol
FAs
Ketones
CO2
278
Which enzyme is important for alcohol metabolism?
Alcohol Dehydrogenase
279
Where is the highest amount of alcohol dehydrogenase found?
In the liver
280
Why is methanol dangerous?
It metabolises to formaldehyde and then to formic acid - both of which are toxic to cells.
281
Why does methanol cause blindness?
Optic nerve cells are v sensitive to formic acid - easily destroyed by it.
282
What is the treatment for methanol poisioning?
Folate - can reduce the reaction and breaks up formic acid
Ethanol - alcohol dehydrogenase will bind more readily to this - this displaces the binding of the methanol and slows down the reaction.
283
Why is ethylene glycol posionous?
Breaks down into glycolic acid = metabolic acidosis
Also metabolises further to oxalic acid - can deposit as crystals in the kidney -> kidney failure
284
What are the metabolic effects of alcohol?
It produces lots of NADH during its metabolism - this disturbs the usual NAD:NADH ration.
This affects metabolic pathways and key liver processes. The body believes it is in an energy rick environment - therefore slows down glycolysis and citric acid cycle etc - suppresses these processes.
285
Why does excess alcohol consumption lead to fatty liver?
Excess ACoA and NADH - stimulates fatty acid synthesis over β oxidation. 3Gs are made which are deposited in hepatocytes as lipid droplets.
286
Why do chronic alcohol users get hypoglycaemia?
Fasting + low NAD:NADH ratio = gluconeogenesis inhibition & inhibited conversion of lactate to pyruvate.
Therefore BG levels drops.
287
288
289
290
How can we tell from liver screens that the cause of deranged LFTs is likely to be alcohol related?
AST derangement > ALT derangement
Raised MCV (toxic effect on bone marrow + poor nutritional intake => inc MCV)
Raised IgA
291
What calculator is used to approximate a P's fibrosis stage?
FIB-4 Calculator
292
What are the specific clinical features of alcoholic liver disease?
Dupuytren's contractures
Parotid swelling
293
Why do you get portal hypertension with cirrhosis?
Liver is supplied by portal vein and hepatic artery (2/3rds of blood supply comes from the portal vein).
When the liver is cirrhoses - it is scarred - so the blood can't flow through the liver = back flow = inc pressure = portal hypertension = pressure on all the organs which drain to the liver.
294
Where can you get varices from alcohol excess?
Oesophagus
Stomach
295
How can you treat oesophageal and gastric varices?
Endoscopic banding
Terlipressin
β blockers (dec HR - dec BP - dec pressure in portal system)
Can get TIPPS (Trans intrahepatic portosystemic shunt) - connects shunt from portal veins to adjacent BVs
Venous shunt
296
What is decompensated cirrhosis?
Ps have developed cirrhosis - liver is now failing to do its job.
297
What are the Sx of decompensated cirrhosis?
Encephalopathy
Variceal bleeding
Ascites
298
What can cause decompensated cirrhosis?
Progression of disease
Hepatocellular cancer
Alcohol binge
GI bleeding
Sepsis
Electrolyte abnormalities
299
Why can you get sepsis from decompensated liver disease?
Can get spontaneous bacterial peritonitis => sepsis.
Bacteria that normally live in the intestine enter the abdominal cavity and the ascites becomes infected. This happens in advanced liver disease because the immune system response weakens and the bacterial environment in the gut changes.
300
What are the features of alcoholic hepatitis?
Jaundice - due to acute inflammation of the liver from excess alcohol
Steatohepatitis
301
302
303
304
How can you tell if a P has steatohepatitis?
Get ballooning of hepatocytes + Mallory-Denk bodies (change in keratin - inside the cell is more hairy) + infiltrating immune cells and fibrosis.
305
What is the consequence of steatohepatitis on a cellular level?
XS alcohol - makes macrophages become proinflammatory - release inflammatory cytokines into the area = stress.
Also release ROS into the area - exacerbating cellular stress.
Both cause liver inflammation
306
What is cirrhosis of the liver?
Chronic inflammation + fibrogenesis -> extensive scarring
Liver parenchyma is replaced and vascular architecture is severely compromised.
307
What is the difference between compensated and decompensated liver disease?
Compensated = part of the liver remains undamaged and compensates for the damaged regions
Decompensated = scar tissue fully envelops the organ - causing portal hypertension and/or liver failure.
308
Which cells in the liver are the major contributor to cirrhosis?
Hepatic stellate cells
309
Which quick screening tool can be used when taking a Hx to ask Ps about whether they use alcohol to excess?
CAGE Screen
310
How long after alcohol cessation can withdrawal occur?
6 - 72 hours
311
What are the Sx of alcohol withdrawal?
HITS
Hallucinations
Insomnia
Increased Vital Signs
Tremens delirium
Shakes, Sweats, Seizures
312
What is the mortality rate from alcohol withdrawal?
15%
313
Which drug can be prescribed to help with alcohol withdrawal?
Chordiazepoxide
314
Which score can be used to assess withdrawal severity?
CIWA score
Mild = <15
Mod = 16-20
Severe = >20
315
What is Wernicke's encephalopathy?
Neurological Sx (CAN - Confusion, Ataxia, Nystagmus)
Due to B1 depletion (Thiamine)
316
How is Wernicke's encephalopathy prevented?
By giving thiamine IV for 48 hours followed by oral thiamine.
317
318
What are the commonest causes of liver cirrhosis in the UK?
Alcohol
Obesity
Hep B & C
319
320
How can you determine between acute and chronic liver disease?
Chronic - more likely to have stigmata of disease - e.g. gynaecomastia, spider naevi, ascites, caput medusae
321
Why does cirrhosis cause low platelet count?
Cirrhosis = inc portal hypotension
This causes sluggish progression through the spleen - congestion in spleen causes splenomegaly. Spleen likes to remove platelets - so the bigger it gets with the slower BF running through it = decreased platelet count.
Therefore - splenomegaly is a sign of portal hypertension.
322
What are the acute causes of liver disease?
Drugs (paracetamol, herbal, penicillins, thiopurines)
Alcohol
Viruses
Vascular - hepatic vein thrombosis
Ischaemic liver disease
Wilson's disease
323
What is Budd Chiari disease?
Budd-Chiari disease is a rare condition characterized by the obstruction or blockage of the hepatic veins, which are the blood vessels that drain the liver. This obstruction prevents blood from flowing out of the liver and back to the heart. As a result, blood backs up in the liver, leading to liver damage and dysfunction.
There are several potential causes of Budd-Chiari disease, including blood clot formation within the hepatic veins, compression of the veins by nearby structures (such as tumors), or diseases that affect the walls of the hepatic veins.
The symptoms of Budd-Chiari disease can vary depending on the severity of the obstruction and the extent of liver damage. Common symptoms may include:
Abdominal pain, typically in the upper right quadrant
Enlargement of the liver (hepatomegaly)
Ascites (accumulation of fluid in the abdominal cavity)
Jaundice (yellowing of the skin and eyes)
Fatigue
Portal hypertension-related complications, such as esophageal varices, splenomegaly, and ascites
324
What are the causes of chronic liver disease?
Alcohol
Fatty Liver Disease
AI Disease - AI hepatitis, primary biliary cirrhosis
Primary sclerosing cholangitis
Viruses - Hep B & C
Inherited - Haemochromatosis
Wilsons disease, A1AT deficiency
325
What is Wilson's disease?
Rare genetic disorder characterized by the abnormal accumulation of copper in various tissues of the body, particularly in the liver, brain, and corneas of the eyes. This excess copper buildup is due to a defect in the ATP7B gene, which encodes a protein involved in copper transport and metabolism.
Wilson's disease, the defective ATP7B protein impairs the liver's ability to excrete copper into bile, leading to its accumulation in liver cells.
Liver-related symptoms: Hepatitis, jaundice (yellowing of the skin and eyes), abdominal pain, hepatomegaly (enlargement of the liver), and cirrhosis (scarring of the liver).
Neurological symptoms: Tremors, difficulty with speech, abnormal gait, muscle stiffness, dystonia (involuntary muscle contractions), and cognitive impairments.
Psychiatric symptoms: Behavioral changes, depression, anxiety, and psychosis.
Ocular symptoms: Kayser-Fleischer rings, which are golden-brown rings around the cornea due to copper deposition.
326
What is haemochromomatosis?
Hemochromatosis is a hereditary disorder characterized by excessive absorption and accumulation of iron in the body. Normally, the body tightly regulates the amount of iron absorbed from food to maintain appropriate levels in tissues and organs. However, in individuals with hemochromatosis, this regulatory mechanism is impaired, leading to the gradual buildup of iron in various organs, particularly the liver, pancreas, heart, and joints.
Common symptoms may include:
Fatigue
Joint pain, especially in the hands
Abdominal pain
Weakness
Weight loss
Loss of libido
Impotence in men
Darkening of the skin, particularly in areas exposed to the sun
Enlargement of the liver or spleen
If left untreated, hemochromatosis can lead to serious complications, including liver cirrhosis, liver cancer, diabetes, heart problems, and arthritis.
327
What is primary sclerosing cholangitis?
Primary sclerosing cholangitis (PSC) is a chronic liver disease characterized by inflammation and scarring (fibrosis) of the bile ducts inside and outside the liver. Over time, the inflammation and scarring can lead to narrowing and obstruction of the bile ducts, impairing the flow of bile from the liver to the small intestine. The exact cause of PSC is unknown, but it is believed to involve a combination of genetic, immune, and environmental factors.
As the disease progresses, the bile ducts become increasingly narrowed and scarred, leading to bile stasis, liver damage, and eventually cirrhosis (scarring of the liver).
In some cases, PSC can also lead to complications such as liver failure, cholangiocarcinoma (bile duct cancer), and bacterial infections of the bile ducts (cholangitis).
328
What is the difference between primary sclerosing cholangitis and primary biliary cholangitis?
PBC is an autoimmune disease characterized by the progressive destruction of the small bile ducts within the liver due to immune-mediated inflammation.
PSC is also a chronic liver disease characterized by inflammation and scarring of the bile ducts, leading to narrowing and obstruction of the bile ducts. Unlike PBC, the exact cause of PSC is not well understood, but it is believed to involve a combination of genetic, immune, and environmental factors.
PBC primarily affects the intrahepatic bile ducts (bile ducts within the liver). The progressive destruction of these bile ducts leads to impaired bile flow, liver damage, and ultimately cirrhosis.
PSC: PSC affects both intrahepatic and extrahepatic bile ducts (bile ducts within and outside the liver). The inflammation and scarring of the bile ducts lead to narrowing and obstruction of the bile ducts, impairing bile flow and causing liver damage.
329
What causes ascites?
Leakage of fluid from the portal blood vessels into the peritoneal cavity
330
Why can portal hypertension cause hepatorenal failure?
Kidneys dont receive as much blood as they should due to construction of renal vessels => kidney failure.
331
Which liver enzyme goes up in obstruction?
ALP
332
What can cause extremely high ALT levels?
Drug induced hepatitis - acute (paracetamol)
Viral hepatitis - E, A
Ischaemic injury - severe infection, lost BP - lost supply to liver - developed acute ischaemic injury
333
Which two drugs can cause chronic liver disease?
Methotrexate
Amiodorone
334
Which clotting factors are failed to be produced by the liver in liver failure?
2, 7, 9 & 10
335
How is bilirubin made?
How is it excreted?
Old RBCs are broken down (in spleen and lymph nodes) by macrophages. Haem broken into iron and unconjugated bilirubin (UCB).
Unconjugated bilirubin = lipid soluble, not water soluble. It binds to albumin - taken to the liver - hepatocytes conjugate it (using UGT) making it water soluble.
Conjugated bilirubin is secreted into bile canaliculi - drain into bile ducts and sent to gallbladder when it is stored as bile.
Eventually secreted into duodenum - is converted to urobilinogen by microbes. Some is reduced to stercobilin = brown colour of faeces. Rest - reabsorbed into blood - oxidised into urobilin - some to liver and rest to kidneys (yellow wee).
336
What are the three types of cause of jaundice?
Pre-hepatic
Intra hepatic
Post hepatic
337
What are the prehepatic reasons for jaundice?
Pre-hepatic = nothing to do with the liver - more of a problem with haemolysis of RBCs (e.g. sickle cell).
Can also be Gilberts syndrome (UDPGT deficiency) - means RBCs are not broken down properly.
338
What are intrahepatic causes of jaundice?
2 reasons
- hepatocellular (viruses, fat, alcohol, drugs, ischaemia, congenital)
- cholestatic (PBC, PSC, drugs - flucox, sarcoidosis)
339
How can you differentiate between hepatocellular and cholestatic causes of jaundice?
Hepatocellular - will have raised ALT & AST (these are liver enzymes that help with metabolic processes)
Cholestatic - will have raised ALP and GGT (these are enzymes found in the bile ducts in the liver)
In any liver problem all 4 will be raised - but in hepatocellualr ALT & AST will be more greatly deranged, and in cholestatic - ALP and GGT will be more greatly deranged.
340
Where are cholangiocytes found in the liver?
Lining the bile ducts
341
What are post hepatic causes of jaundice (obstructive jaundice)?
Stones
Strictures (e.g. PSC)
Worms
Pancreatic Cancer
Gall bladder Cancer
Cholangiocarcinomas
342
What is bile duct cancer called?
Cholangiocarcinoma
343
What is primary sclerosing cholangitis?
Inflammation of the bile duct -> narrowing of the bile duct.
If bile cannot pass = creates jaundice. Will cause cirrhosis as bile kills hepatocytes.
344
What is primary sclerosing cholangitis linked to?
Ulcerative colitis
- 80% of Ps with PSC will have UC
- 5% of UC Ps will develop PSC
If you have a P with PSC - do a colonoscopy to rule out UC
345
What is the upper limit of normal for
- ALT
- ALP
- AST
ALT = 56
ALP = 129
AST = 40
346
What does an isolated raised ALP indicate?
Bone problems as the cause or pregnancy.
Do bone profile and Vit D levels to check the bone.
347
What is Gilbert's syndrome?
Gilbert syndrome (GS) is a syndrome in which the liver of affected individuals processes bilirubin more slowly than the majority.
Many people never have symptoms. Occasionally jaundice (a slight yellowish color of the skin or whites of the eyes) may occur.
Gilbert syndrome is due to a genetic variant in the UGT1A1 gene which results in decreased activity of the bilirubin uridine diphosphate glucuronosyltransferase enzyme. It is typically inherited in an autosomal recessive pattern and occasionally in an autosomal dominant pattern depending on the type of variant. Episodes of jaundice may be triggered by stress such as exercise, menstruation, or not eating Diagnosis is based on higher levels of unconjugated bilirubin in the blood without either signs of other liver problems or red blood cell breakdown.
348
What does isolated raised bilirubin indicate?
Gilbert's syndrome
Haemolysis (Sickle cell)
349
What tests are done in a full liver screen?
350
4 - Jaundice
351
Cholestatic cause - possibly gallstones
Histology shows brown = bile
Send for ERCP
352
What joins to drain fluid into the duodenum at the sphincter of ampulla?
CBD and pancreatic duct
