BRS HARD QUESTIONS Flashcards
1
Q
Inflammatory cells in asthma?
A
Eosinophils, Mast cells, Th2 lymphocytes.
2
Q
Inflammatory cells in COPD?
A
Neutrophils, Macrophages, Tc1 lymphocytes.
3
Q
Inflammatory mediators in asthma?
A
IL-4, IL5
4
Q
Inflammatory mediators in COPD?
A
TNF alpha, IL-8
5
Q
Asthma pathology?
A
Bronchoconstriction + mucus. Formation of mucus plug in airway lumen.
6
Q
Types of COPD?
A
Chronic bronchitis, chronic bronchiolitis (small airways disease), emphysema.
7
Q
Chronic bronchitis pathology?
A
Long-term inflammation on bronchi. Mucus hypersecretion resulting in luminal obstruction. Hyperplasia of goblet cells, hypertrophy of submucosal glands.
8
Q
Emphysema pathology?
A
Lung tissue destruction (alveoli). Disrupted alveolar attatchments which can lead to collapsing of alveolar.
9
Q
What test may be done to analyse severity of emphysema?
A
High resolution CT scanning. Counting number of holes and size of holes.
10
Q
What are the two types of emphysema?
A
Centriacinar emphysema and panacinar emphysema.
11
Q
Centriacinar emphysema vs panacinar emphysema?
A
Centriacinar involves loss of the respiratory bronchioles in the proximal portion of the acinus with sparing of distal alveoli. Panacinar involves all lung fields, particularly the bases.
12
Q
How do you describe a lesion that results in loss of movement in one side of the body?
A
Verterbrae level (e.g T10) hemisection of the spinal cord on the (left/right) side.
13
Q
Explain loss of motor function and fine touch in right leg due to lesion of spinal cord on right side?
A
Interrupts right lateral corticospinal tract projecting to ipsilateral motor neurones and right ascending dorsal columns tract from ipsilateral leg. Therefore, loss of function below the injury.
14
Q
Explain loss of temperature and pain sensation in left leg due to lesion of spinal cord on the right side?
A
There is no loss of pain and temperature in the ipsilateral leg because the ascending spinothalamic tract crosses the midline within a few segments of the level of entry of the sensory information into the spinal cord. The spinothalamic tract from the contralateral leg will be interrupted by the lesion, hence the loss of pain and temperature sensation in that leg.
15
Q
What determines if someone is to recover from a lesion?
A
If some parts of the pathways have only been temporarily affected. If the tracts are completely disrupted it is very unlikely that there will be any regeneration in the CNS.
16
Q
Why may there be there may be segmental loss of pain and temperature ipsilaterally at the level of the injury?
A
Due to direct damage to the cord or nerve receiving the information.
17
Q
How do you describe the location of the infarct that affects sensation on left hand side?
A
Right parietal cortex in or close to the primary somatosensory cortex, hence disturbance of sensation in left hand.
18
Q
Why may an infarction of somatosensory cortex result in jerking movements?
A
Primary epileptic focus formed as a result of tissue damage in somatosensory cortex from stroke. Jerks caused by propagation of discharge to arm area of motor cortex in frontal lobe.
19
Q
What happens if you don’t treat jerking movements due to stroke?
A
Seizures may spread to involve whole motor cortex and even propagate to other hemisphere to produce generalised seizures.
20
Q
What would occur if there is a lesion in the dorsal root and why is this not as severe as other lesions?
A
Damage to dorsal root leads to loss of sensation in dermatome supplied by the corresponding spinal nerve. If only one root is affected its not severe lesion as there is considerable overlap of dermatome innervation by adjacent spinal nerves.
21
Q
Why would occur if there is a lesion in the ventral root and why does this not lead to paralysis?
A
Damage to ventral root leads to weakness of muscles supplied by the corresponding spinal nerve. Most limb muscles are innervated by 2 or more spinal nerves therefore paralysis is unlikely unless all spinal roots are damaged.
22
Q
What would occur if there is a lesion in the sensory nerve?
A
Leads to loss of sensation in the area of distribution of that peripheral nerve.
23
Q
What would occur if there is a lesion in the motor nerve?
A
Damage to a motor nerve leads to weakness/paralysis of the muscle supplied by that peripheral nerve.
24
Q
What is the most likely cause of spinal root and spinal nerve damage?
A
Strain injuries to the spine, e.g. prolapsed or herniated intervertebral disc.
25
What are your peripheral nerves?
Motor and sensory nerve.
26
How do you describe in neuroanatomical terms if someone has pain and muscle weakness in buttock, down his thigh, calf and into his toes ?
The anterior and posterior nerve roots of lumbar spinal nerves L5 and S1.
27
Where are the descendings tracts in the medulla?
Medullary pyramids (anterior surface of medulla).
28
Where are the dorsal columns in the medulla?
Posterior surface of medulla.
29
Special somatic afferent nerve fibres function?
Fibres carry special senses of hearing and balance
30
Special visceral afferent nerve fibres function?
Fibres carry taste sensation.
31
Special visceral efferent nerve fibres function?
Innervate skeletal muscles of the jaw, face, larynx and pharynx.
32
What lies in the posterior cranial fossa?
Cerebellum.
33
What lies directly above the body of the sphenoid bone?
Hypothalamus.
34
What does the third ventricle supply?
Diencephalon.
35
What does the aqueduct supply?
The midbrain.
36
What does the fourth ventricle supply?
Pons and medulla.
37
Broca’s area function?
Motor speech.
38
Where is broca’s area located?
Left hemisphere.
39
Wernicke’s area function?
involved in the comprehension of speech.
40
Where is Wernicke’s area located?
Left hemisphere.
41
Common cause of acute pancreatitis?
Gallstone and alcohol.
42
Types of acute pancreatitis?
Oedematous pancreatitis. Haemorrhagic pancreatitis. Necrotic pancreatitis.
43
Symptoms of acute pancreatitis?
Epigastric pain radiating to back. Vomiting. Fever.
44
Key clinical signs of acute pancreatitis?
Tachycardia and hypotensive. Grey turner’s sign. Cullen’s sign.
45
What is grey turner’s sign?
bruising in flanks.
46
What is cullen’s sign?
Bruising around umbilicus.
47
What is a smooth muscle cancer called?
Leiomyosarcomas
48
Who is eligible for a hepatocellular cancer screen?
Individuals with cirrhosis.
49
What interventional radiology is done for cancer?
Percutaneous biopsies.
50
What cancer can you develop in lower 1/3 of the oesphagus?
Adenocarcinoma.
51
Oesophageal cancer late stage symptom?
Dysphagia - difficult swallowing.
52
What investigations are done to stage oesophageal cancer and gastric cancer?
CT scan, PET CT scan, laparascopy and endoscopy ultrasound.
53
Gastric cancer symptoms?
Dyspepsia (upper abdominal discomfort after eating). Weight loss and abdominal mass on examination.
54
What surgery is done if tumour is present at oesophago-gastric junction?
oesophago gastrectomy - removal of oesophagus.
55
What surgery is done if tumour is present close to the oesophago-gastric junction?
Total gastrectomy.
56
What surgery is done if tumour is present in the body of the stomach?
Subtotal gastrectomy.
57
What inherited disorder causes decreased uptake of bilirubin?
Gilberts syndrome.
58
What inherited disorder causes decreased conjugation of bilirubin?
Crigler-najar syndrome.
59
What inherited disorder causes decreased secretion of bilirubin?
Dublin-johnson syndrome, rotor syndrome.
60
What is fulfilmant hepatic failure?
It is the same as acute hepatic failure.
61
What can liver failure cause?
Hepatic encephalopathy, coagulopathy, ascites, hypoglycemia (due to impaired glycogen production), increased risk of infection (due to lack of globulin production).
62
What are some toxins that can cause acute liver failure?
Paracetamol, amanita phalloides and bacillus cereus.
63
Causes of acute liver failure?
Toxins, inflammation (hepatitis), disease of pregnancy, idiosyncratic drug reaction, vascular diseases and metabolic causes.
64
Causes of chronic liver failure?
Inflammation, alcohol abuse, side effects of drugs, reduced venous return, inherited diseases, non alcoholic steatohepatatis, autoimmune hepatitits.
65
Consequences of cholestasis?
Pruritus (itching), cholesterol deposition around eyes and cholangitis (inflammation of bile duct system).
66
What presinusoidal causes of portal hypertension?
Chronic hepatitis, primary biliary cirrhosis.
67
What sinusoidal causes of portal hypertension?
Acute hepatitis, alcohol and fatty liver.
68
What post sinusoidal causes of portal hypertension?
Venous occlusive diseases.
69
What does splenomegaly cause?
Thrombocytopenia and anaemia due to pooling and then destruction.
70
Why do varices happen in veins?
Thin walls.
71
What molecules are increased in the brain during liverfailure and can contribute to encephalopathy?
Aromatic amino acids (e.g serotin). Known as false transmitters.
72
What varices are common in liver failure?
Oesophageal varices and rectal varices.
73
What is used to assess severity of liver failure?
Child-pugh score.
74
What factors are used to assess child pugh score?
Total bilirubin, serum albumin, prothrombin time, ascites, hepatic encephalopathy.
75
What class of child pugh score makes them a transplant candinate?
Class B.
76
How to treat liver failure?
Reduce protein intake and phosphate enemas (empties bowels) for encephalopathy. Dextrose and calcium gluconate for hypoglycaemia and hypocalcaemia. Haemofiltration for renal failure. Albumin and vasoconstrictors for hypotension. Vitamin K, FFP and platelets for bleeding. Antibiotics for infection.
77
What can be used to support liver for 24-48 hours?
Albumin exchange system such which remove albumin bound toxins from blood.
78
Biomarkers for obstructive jaundice?
Serum amylase and prothrombin time.
79
Radiological scans for obstructive jaundice in order of relevance?
Ultrasound first. MRCP. CT scan.
80
Symptoms of short bowel syndrome?
Diarrhoea, weight loss, dehydration.
81
What is heart failure?
Heart unable to maintain adequate circulation for metabolic requirements of body.
82
What can cause heart failure?
Cardiac damage (ischaemia), hypertension and valve disease.
83
Symptoms of Wolff-Parkinson-White syndrome?
Tachycardia & abnormal cardiac electrical conductance
84
Symptoms of atrial fibrilation and Wolff-Parkinson-White syndrome?
Palpitations & chest pain.
85
What causes QRS pre excitation in WPW syndrome?
Current from extra accessory pathway which causes ventricular depolarisation before you get ventricular depolarisation from AVN.
86
What causes biphasic t wave in WPW syndrome?
Depolarisation from extra accessory pathway when repolarisation is occuring in the ventricles.
87
What would you see on the ECG on a first degree heart block?
Increased P-R interval.
88
Treatment for heart blocks?
Discontinuation of AV-blocking drugs (e.g. beta-blockers, calcium channel blockers) or pacemaker implantation in severe cases
89
NSTEMI/STEMI symptoms?
chest pain, sweating, nausea & vomiting
90
ECG changes would you expect to see in hypertrophy of the left ventricle?
Larger QRS complex.
91
What are signs of filtration failure in kidney dysfunction?
Haematuria and proteinuria. Low serum albumin.
92
Urine dipstick for UTI?
2+ leucocytes, + nitrite, trace of blood
93
Key features of nephrotic syndrome?
Peripheral oedema, severe proteinuria, low serum albumin. Low blood pressure.
94
What is nephrotic syndrome associated with?
Hyperlipidaemia.
95
Major complication of minimal change glomerulopathy?
Thrombosis.
96
Presentation of kidney stones?
Pain in abdomen. Blood in urine.
97
How would you check for kidney stones?
Physical examination to see if there is tenderness in loin or back area. Dipstick to see if there is blood in urine. Blood tests for kidney function. X ray, ultrasound or CT scan.
98
Treatment for kidney stones?
Shockwave lithotripsy, ureteroscopy, percutaneous nephrolithotomy.
99
What is the inheritance pattern of polycystic kidney disease that develops in a neonatal?
Autosomal recessive.
100
What is the inheritance pattern of polycystic kidney disease that develops in an adult?
Autosomal dominant.
101
Causes of kidney stones?
Prostate enlargement, gout and dehydration.
102
What does the detrusor muscle do?
Contracts to build pressure in urinary bladder to support urination.
103
What is a superficial nephron?
Loop of henle only extends into outer medulla.
104
What is a juxtamedullary nephron?
Loop of henle extends deep into inner medulla.
105
What is the glomerular filtration rate?
Amount of fluid filtered from glomeruli into bowman’s capsule per unit time. Sum of filtration rate of all functions nephrons.
106
Why is creatinine not as good as inulin?
Small amount of creatinine is secreted into nephron. Needs to be adjusted when calculating GFR.
107
What substances via paracellular junctions in renal tubules?
Water, calcium, potassium, chloride and urea.
108
What maintains sodium gradients in kidney duct cell?
Lack of sodium in duct cell created by Na+K+ATPase pump on basolateral surface that is pumping 3 sodium ions into blood for every 2 potassium ions into duct cell. This allows sodium to move from tubular fluid down a concentration gradient.
109
How does sodium and bicarbonate reabsorption occur in early proximal convoluted tube?
Carbonic acid converted to carbon dioxide and water by carbonic anhydrase in tubular fluid. CO2 enters duct cell by diffusion. Carbon dioxide and water in duct cell is converted to H+ and bicarbonate in cell by carbonic anhydrase. H+ diffuses out into tubular fluid and sodium diffuses into cell by Na+H+ antiporter. Sodium and bicarbonate enter blood by sodium bicarbonate symporter.
110
How is glucose reabsorbed in early proximal convoluted tube?
Glucose enters via sodium glucose cotransporter 2. Glucose exits into blood via basolateral membrane via GLUT2.
111
What ions are reabsorbed in the thick ascending limb?
Sodium and chloride ions.
112
How is sodium and chloride reabsorbed in the thick ascending limb?
Sodium, chloride and potassium ions enter via symporter into duct cell. Potassium and chloride exit into blood via symporter on basolateral membrane. Sodium reabsorbed into blood via sodium potassium atpase.
113
What ions enter blodo via paracellular pathways in the thick ascending limb?
Na+, Ca2+, K+, Mg2+.
114
What ions get reabsorbed in the early distal convoluted tube?
Sodium, chloride and calcium.
115
What pumps reabsorbs chloride ions into blood in early distal convoluted tube?
Potassium chloride symporter.
116
What pumps are involved in intercalated cells?
Chloride bicarbonate antiporter and H+ ATPase.
117
What part of nephron is the filtrate least concentrated?
Distal convoluted tube and collecting duct.
118
When does the amount of water and sodium in the filtrate decrease the fastest?
Proximal convoluted tube.
119
Nitrite detected in dipstick test indicate what?
Gram-negative bacteria in large number, e.g., E. Coli.
120
Ketones in dipstick test indicate what?
Starving or fasting or diabetic ketoacidosis
121
What does low specific gravity mean?
Urine is too diluted.
122
What does low specific gravity in dipstick test indicate?
Diabetes Insipidus.
123
What is diabetes insipidus?
Decreased release of AVP or decreased response to AVP.
124
Protein in dipstick indicates what?
Nephrotic syndrome
125
Blood in dipstick indicates what?
Nephritic syndrome or kidney stones or UTI
126
Bilirubin in dipstick indicates what?
Liver disease or gallstones
127
Urobilinogen in dipstick indicates what?
Liver disease or haemolysis
128
What does freely filtered mean?
Same concentration in glomerular filtrate as in plasma.
129
Why can para aminohippurate be used for renal plasma flow?
All the para aminohippurate is removed from the plasma passing through filtration and secretion and all the PAH arriving at the kidneys in the plasma appears in the urine, and virtually none leaves in the renal vein. Renal clearance of this molecule equals the renal plasma flow.
130
When can para aminohippurate not be used to calculate RPF?
If too high of a concentration has been infused. Results in some leaving in the renal vein instead of all being in the urine.
131
Arterial plasma inulin concentration were 1 mmol/L, what would be the plasma inulin concentration in the efferent arteriole if 20% of inulin was filtered??
1mmol / L
132
the arterial plasma inulin concentration were 1 mmol/L, what would be the plasma inulin concentration in the renal vein if 20% of inulin was filtered?
0.8 mmol/L
133
Why is measurement of PAH clearance rarely performed clinically when renal disease is suspected
Incomplete secretion and issues with renal plasma flow.
134
A small amount of creatinine enters the urine by secretion into the proximal tubule. Why is this not too big of a problem to use creatinine for GFR?
Creatinine measurement in plasma, measures creatinine and non-creatinine chromogens. This means the excess creatinine present in urine due to secretion and the excess creatinine in plasma due to non creatinine chromogens cancel each other out.
135
How does the gradient of Log plasma 51Cr EDTA activity change in someone with renal failure?
Less steep gradient.
136
What is a 1st degree heart block involve?
Longer PR interval as there is a delay in conduction.
137
What artery supplies the proximal transverse colon?
Middle colic artery.
138
What artery supplies the distal third of transverse colon?
Inferior mesenteric artery.
139
How is the rectum different to the colon?
Rectum has transverse rectal folds in its submucosa and doesn’t have taenia coli.
140
What contractions occur in transverse and descending colon?
Segmental contractions of circular muscle called haustral contractions.
141
What parasympathetic nerve innervates ascending colon and transverse colon.
Vagus nerve.
142
What parasympathetic nerve innervates distal colon?
Pelvic nerves.
143
What nerves control external anal sphincter?
Somatic motor fibres in the pudendal nerves.
144
What does aldosterone do to the large bowel?
Promotes sodium and water absorption (synthesis of Na+ ion channel, Na+/K+ pump).
145
How does defecation occur?
Distension of walls of rectum. Pressure receptors send signals via myenteric plexus to initiate peristaltic waves in descending, sigmoid colon and rectum. Internal anal sphincter inhibited. External anal sphincter under voluntary control.
146
Sympathetic nerves emerging from what ganglion innervate the colon?
Inferior mesenteric and pelvic ganglion.
147
What is the submucosal plexus responsible for?
Senses the gut lumen environment. Controls secretion, blow flow, epithelial and endocrine cell function.
148
What is hirschsprung’s disease? What does it result in?
Congenital absence of ganglion of myenteric and submucosal. Enlarged colon.
149
What stimulates release of gastrin?
Amino acids and peptides present in the lumen of the stomach. Gastric distention and vagus nerve.
150
What does CCK do?
Stimulates pancreatic enzyme release. Stimulates gallbladder contraction and relaxation of sphincter of oddi. Delays gastric emptying and decreases food intake.
151
What stimulates release of GIP?
All 3 macronutrients.
152
What cells secretes GIP and where are these cells located?
K cells in duodenum and jejunum.
153
What stimulates release of GLP-1?
Hexose and fat.
154
What does GLP-1 do?
Increases sensitivity of pancreatic beta cells to glucose. Induce satiety.
155
How is water absorbed in the GI tract?
Osmotic flow of water through tight junctions into intercellular space due to hypertonic solution present in intercellular space (high concentration of ions).
156
How is sodium absorbed in the ileum?
Secondary active transport. Co-transport with chloride ions.
157
How is chloride absorbed in the colon?
Secondary active transport. Exchanged with bicarbonate.
158
How is potassium absorbed in the small intestine?
Diffusion via paracellular junctions.
159
What ions move down concentration gradient into lateral intercellular space in small intestine?
Chloride and bicarbonate.
160
Why is ferritin binding to intracellular iron important?
Prevents iron from promoting oxidative stress.
161
What stimulates inspiration?
Apneustic centre.
162
What conditions are j receptors involved in?
Pulmonary oedema and capillary engorgement.
163
What can J receptors do if activated?
Increase breathing frequency in response to events such as pulmonary oedema which cause a decrease in oxygenation.
164
What do peripheral chemoreceptors detect?
Oxygen concentration.
165
What vessels leave the liver?
3x hepatic veins and common bile duct.
166
What makes up the portal triad?
Branch of hepatic artery. Branch of portal vein. Bile duct.
167
What cells are attached to the sinusoidal endothelial cells?
Kupffer cells.
168
How are lipoproteins synthesised in the liver?
Uptake of glucose. Glucose converted to pyruvate which is converted to acetyl CoA. Acetyl CoA converted to cholesterol and fatty acids. Fatty acids added to glycerol to produce triacylglycerol. Triacylglycerol + cholesterol + apoprotein + phospholipids = lipoprotein.
169
What is excreted in bile?
Xenobiotics, cholesterol metabolites, alkaline phosphatase.
170
What are some MDR related proteins?
MRP2,MRP3.
171
What do MDR3 channels export into bile?
Phospatidylcholine.
172
Intrahepatic jaundice causes?
Acute and chronic liver damage.
173
In a nodal cell action potential what causes the prepotential phase?
Sodium influx through funny channel.
174
Why is there a plateau phase in cardiac muscle action potential?
Maintains cell at level of depolarisation. Long, slow contraction is required to produce effective pump.
175
Where is vasomotor centre located?
Medulla and lower third of pons.
176
What is the pressor area in vasomotor centre responsible for?
Vasoconstriction.
177
What is the depressor area in vasomotor centre responsible for?
Vasodilation.
178
Lateral portions of vasomotor centre regulate what?
Heart rate and contractility.
179
Medial portion of vasomotor centre does what?
Decreases heart rate via vagus nerve.
180
How does acting on M2 receptor inhibit contractility?
Activates Gi protein which inactivates adenylate cyclase.
181
Where are pressure sensors in the cardiovascular system?
Aortic arch, carotid sinus and afferent arterioles in the kidney.
182
What does constriction of veins do to venous return?
Reduces compliance and increases venous return.
183
What increases venous pressure and hence increases venous return?
Increase in blood volume, skeletal muscle pump, respiratory movements and SNS activation of veins.
184
Local vasodilators?
Nitric oxide and prostacyclin.
185
Local vasoconstrictors?
Thromboxane A2 and endothelins.
186
When is atrial natriuretic peptide released?
Secreted from the atria in response to stretch to lower blood pressure.
187
What is atenolol?
Beta blocker. Reduces heart rate.
188
What is ramipril?
ACE Inhibitor. Causes vasodilation.
189
What does a crescendo decrescendo murmur indicate?
Aortic stenosis.
190
Key difference in flow volume loops in obstructive and restrictive?
Indented expiratory curve in obstructive. Restrictive is same shape but narrower curve.
191
Why are spirometric pulmonary function tests done?
Monitor progression of lung disease over time. Monitor effectiveness of different bronchodilators.
192
Disadvantage of spirometric pulmonary function tests?
Heavy reliance on technique and can be uncomfortable for patients reducing their motivation to apply maximum effort.
193
What reflex prevents long expiration?
Hering breuer deflation reflex
194
What is FVC on flow volume loop?
Width of loop.
195
Why is volume expired is slightly larger than volume inspired?
Inspired air is dry and at room temp. Expired air is wet and at almost 37 degrees. Volume of a gas is proportional to temperature.
196
Why does additional gas dissolve into the blood during a dive? Which law explains this?
At a constant temperature, the amount of a given gas that dissolves in a given type and volume of liquid is directly proportional to the partial pressure of that gas in equilibrium with that liquid
197
Ascending rapidly without releasing inhaled gas results in?
Pulmonary barotrauma. - Alveolar rupture.
198
Why does ascending slowly prevent DCI?
Allow N2 to be unloaded in the alveoli while keeping it dissolved in the blood.
199
How is high sodium in the blood maintained from duct cells?
Na+/K+ exchange pump driven by ATP. Potassium into duct cell while sodium pumped into blood.
200
What drives water into lumen of pancreatic duct?
Sodium moves into lumen of duct down gradient from blood via paracellular junctions and water follows.
201
What stimulates enzyme secretion in pancreatic juice?
Acetylcholine from vagus nerve and cholecystokinin from duodenal I cells.
202
What stimulates release of cholecystokinin?
CCK releasing peptide due to increase in amino acid and fatty acids in lumen of duodenum. Gastrin releasing peptide.
203
What inhibits release of CCK?
Trypsin.
204
Where is pancreatic amylase secreted?
Duodenum.
205
What does the mucosa layer of the gut wall contain?
Epithelium, lamina propria (connective tissue) and muscularis mucosae (muscle).
206
How do parietal cells secrete acid.
Bicarbonate ions pumped out into interstitial fluid and chloride ions pumped into parietal cells from interstitial fluid. Sodium pumped out into interstitial fluid and potassium from interstitial fluid pumped in to parietal cell. H+ and chloride pumped into gastric lumen.
207
What may you administer to treat gout?
Non steroidal anti inflammatory drugs. Use of glucocorticoids.
208
What joints does rheumatoid arthritis commonly affect?
Joints in hands, wrists and feet.
Metacarpophalangeal joints (MCP)
Proximal interphalangeal joints (PIP)
NOT distal interphalangeal joints
Metatarsophalangeal joints (MTP)
209
What are common extra articular features present in a rheumatoid arthritis patient?
Fever, weight loss. Subcutaneous nodules.
210
Presentation of psoriatic arthritis
Scaly red plaques on extensor surfaces (elbows and knees). Asymmetrical pattern of joint involvement. Usually affects interphalangeal joints.
Doesn’t affect MCPJ’s unlike RA.
211
Main cytokines involved in ankylosing spondylitis?
TNF alpha, IL-17 and IL-23.
212
What are the 3 factors that affect resistance in a vessel?
Vessel length, Vessel radius and blood viscosity.
213
What helps regulated systemic arterial blood pressure?
Cardiovascular control centre in medulla via sympathetic nervous system and endocrine hormones.
214
What is the blood pressure equation?
Blood pressure = cardiac output x total peripheral resistance
215
What is bulk flow?
A volume of protein-free plasma filters out of the capillary, mixes with the surrounding interstitial fluid (IF) and is reabsorbed.
216
Lymph vessel structure
Blind-ended, single-layered and contain large permeable water-filled one-way channels.
217
What do the terms Hyperpnoea / Hypopnoea mean?
Increased depth of breathing / Decreased depth of breathing.
218
What does the term apnoea mean?
Cessation of breathing (no air movement)
219
What does the term orthopnoea mean?
Positional difficulty in breathing (when lying down)
220
At functional residual capacity what are the lungs forces like?
The lung-chest forces are in equilibrium. Chest recoil = lung recoil.
221
What occurs in inspiration?
Diaphragm moves down and intercostal muscles move rib cage up and out.
222
What is henry’s law?
Solubility of gas is directly proportional to partial pressure of that gas in equilibrium with that liquid.
223
What is boyle’s law?
At constant temperature, volume of gas is inversely proportional to pressure of that gas.
224
What happens to carbonic acid in haemoglobin?
H+ ions bind to haemoglobin chain. Bicarbonate leaves red blood cell in exchange of a chloride ion via the AE1 transporter.
225
Why is the AE1 transporter on red cells important?
Allows negative chloride ions to enter the RBC to maintain resting membrane potential.
226
Why is the mean arterial pressure equation an approximation?
Assumes steady flow (which does not occur due to the intermittent pumping of the heart). Rigid vessels
Right atrial pressure is negligible.
227
What does an increase in arterial stiffness result in?
Increase in systolic blood pressure. Lower diastolic pressure as less diastolic flow.
228
Why does pressure fall slowly in aorta after aortic valve closes?
Diastolic flow in the downstream circulation.
229
When are veins the most compliant?
At low pressures.
230
What hormone results in decidualisation?
Progesterone.
231
What changes occur in the endometrium during decidualisation?
Glandular epithelial secretion. Glycogen accumulation in stromal cell cytoplasm. Growth of capillaries. Increased vascular permeability which leads to oedema.
232
What factor is involved in changes to endometrium?
IL11.
233
What does leukaemia inhibitory factor do?
Stimulates adhesion of blastocyst to endometrial cells.
234
What maternal hormones are lowered during pregnancy?
FSH and LH. GH and TSH.
235
Oxytocin effects for partruition?
Uterine contraction, cervical dilation and milk ejection.
236
What occurs in puberty?
Production of sex steroids. Development of secondary sexual characteristics. Attain capability to reproduce.
237
Describe the luteal phase
Formation of corpus luteum after ovulation. Corpus luteum secretes progesterone and oestradiol.
238
What occurs in the proliferative phase of the endometrium cycle?
Growth of epithelial cells and increase in arterioles due to high levels of oestradiol.
239
What occurs in the secretory phase of the endometrium cycle?
Endometrial glands secrete glycogen. Increase volume of stromal cells produce thick lining.
240
Menopause biomarkers?
Low oestradiol, High LH/FSH, Low inhibin, Low anti mullerian hormone.
241
Symptoms of menopause?
Skin dryness, Hot flushes, Osteoporosis, Decreased libido.
242
How does intramembrous ossification occur?
MSC’s form osteoblasts. Osteoblasts cluster together and secrete osteoid which traps osteoblasts to form osteocytes. MSC’s form periosteum and formation of trabecular matrix occurs. Crowded red blood cells condense into red bone marrow.
243
What is a volkmann’s canal and where would you find it?
Transverse canals that are inbetween haversian canals or emerge from periosteum that contain blood vessels.
244
Osteoblasts function
Forms bone by secreting osteoid and catalysing mineralisation of osteoid.
245
Can you describe the process of endochondral ossification?
Bone collar forms around diaphysis of the hyaline cartilage model. Cartilage calcifies in the center of the diaphysis and then develops cavities. Blood vessel of periosteal bud invades internal cavities and formation of cancellous bone occurs. Diaphysis elongates and medullary cavity forms. Secondary ossification center develops after birth at the epiphysis. Ossification occurs at epiphysis; cartilage is replaced by bone. Eventually only cartilage left is at epiphyseal plate and articular cartilage.
246
Where is cancellous bone located in long bone?
Epiphysis.
247
What is the epiphyseal side in interstitial growth?
Active hyaline cartilage dividing to form hyaline cartilage matrix.
248
What metastases have lytic effects on bone?
thyroid, lung and kidney
249
what metastases have both trophic and lytic effects on bone?
breast
250
what metastases have trophic effects on bone?
prostate
251
When a large fracture where bone edges are not close and there is low stability what occurs at the fracture?
Haematoma formation, release of cytokines and angiogenesis at fracture. Soft callus formation which is converted to a hard callus. Excess bone is removed.
252
What do ligaments do and how do they do it?
Provide stability by restricting joint movement. Ligaments also provide proprioception.
253
4 stages of healing of a tendon or ligament?
Bleeding, inflammation, proliferation and remodelling.
254
What are between keratinocytes?
Tight junctions, adherens junctions, demosomes, gap junctions.
255
What are adherens junctions and what do they do?
Transmembrane structures that engage with the actin skeleton.
256
Describe melanocytes
Dendritic cells that distribute melanin pigment to keratinocytes.
257
What are the most prominent types of collagen in the basement membrane?
IV, VII
258
What is the function of the basement membrane?
Cell adhesion, gate keeping functions for cell migration and diffusion of molecules. Presence of rete ridges.
259
What proteins does the dermis contain?
Collagen, fibrillin and elastin.
260
What glycoproteins does the dermis contain?
Fibronectin, fibulin and integrins.
261
What do the glycoproteins in the dermis do?
Facilitate cell adhesion and cell motility.
262
What makes up the ground substance in dermis?
Glycosaminoglycans and proteoglycans.
263
What other cells apart from fibroblasts are present in the dermis?
Mast cells, neutrophils and lymphocytes.
264
What stimulates eccrine sweat glands?
Cholinergic nerves and adrenergic nerves.
265
What stimulates apocrine sweat glands?
Adrenergic nerves.
266
Describe the meissner’s corpuscle?
Encapsulated, unmyelinated mechanoreceptor present in the superficial dermis. Most concentrated in thick hairless skin.
267
What is the meissner’s corpuscle responsible for?
Light touch and slow vibration.
268
How does the skin behave as a physical barrier?
Cornified envelope prevents water and protein loss from skin. Subcutaneous fat prevents damage from trauma. Melanin produced protects DNA damage from UV.
269
How does the skin regulate temperature?
Vasodilation or vasoconstriction in deep or superficial vascular plexuses. This regulates heat loss. Eccrine sweat glands provide cooling effect.
270
What function does hair have?
Thermoregulation, source of epithelial and melanocyte stem cells, production of apocrine sweat, production of sebum.
271
Describe the isthmus part of hair?
Lower portion between sebaceous gland and arrector pili muscle
272
What does the bulge contain and why is this important?
Contains hair follicle stem cells. Can migrate downwards to form hair follicle or upwards to form sebaceous glands or heal wounds.
273
What does the outer root sheath of hair follicle contain?
Stem cells.
274
What is the nail plate firmly attached to?
Nail bed.
275
Where does the nail plate detach?
Hyponychium
276
Where does the nail plate emerge from?
Proximal nail fold.
277
What produces the nail plate?
Nail matrix.
278
What is the visible portion of the nail matrix called?
Lunula.
279
How is the nail plate produced?
Keratinocytes in the nail matrix lose their nuclei and cytoplasm and become keratin.
280
Where is the nail matrix?
Above distal bone and below proximal nail fold.
281
Psoriasis disease mechanism
Keratinocytes release DNA/RNA which form complexes with antimicrobial peptides. This activates dermal dendritic cells which migrate to lymph nodes to active th1/th17/th22 cells. This results in a chemokine release (migration of other immune cells) and cytokine release. Increased keratinocyte proliferation results in psoriatic plaque.
282
What lifestyle changes can help manage psoriasis?
Reducing alcohol consumption and smoking.
283
What is the first step management to treating psoriasis?
Topical therapies and phototherapy.
284
What topical therapies can be given for psoriasis?
Vitamin D analogues with corticosteroid. Retinoids. Tacrolimus.
285
Why can tacrolimus be a better option compared to corticosteroids?
Tacrolimus is a calcineurin inhibitor and so is not a steroid. Steroids can cause skin thinning
286
Types of phototherapy that can be used for psoriasis?
Narrowband UVB. PUVA (psoralen - makes skin sensitive to UVA. UVA is then given).
287
In severe or widespread psoriasis what treatment would you offer?
Phototherapy or systemic therapies such as methotrexate or ciclosporin.
288
What oral retinoid can you give for psoriasis?
Acitretin
289
What advanced therapies can you offer for psoriasis?
PDE4 inhibitors, biologics and JAK inhibitors.
290
Give an example for a biologic that can be used for psoriasis?
Anti TNF gamma.
291
What causes a barrier defect in atopic ecezema? How does this cause the barrier deffect?
Defect in filaggrin.
Defect in filaggrin results in increased transepidermal water loss due to loss of extracellular lipids and impaired ceramides.
This results in impaired protection against microbes and allergens.
292
What is filaggrin responsible for?
Binds and aggregates keratin bundles and intermediate filaments in stratum corneum.
293
How does dysregulation of immune system lead to atopic eczema?
S.aureus stimulates th2 response and inhibits treg cells. Presence of eosinophils as well.
294
How do you manage atopic eczema?
Use of emollients and patch testing (to test for allergens).
295
First stage treatment for atopic eczema?
Corticosteroids and tacrolimus. - topical treatment
UVB or PUVA - phototherapy
296
Steroid ladder for atopic eczema? (second stage treament)
Hydrocortisone, clobetasone, betamethasone, mometasone, clobetasol.
297
Side effects of using steroids for atopic eczema?
Folliculitis or acne.
298
Immunosuppressive drugs for atopic eczema?
Methotrexate or ciclosporin.
299
What biologics can be used for eczema?
TH2 cytokines
anti IL-4
anti IL-13
300
What stimulates alpha cells to produce glucagon?
Low blood glucose, amino acids, GI hormones, sympathetic nervous activity (via alpha adrenergic) and parasympathetic nervous system.
301
Glucagon blood glucose raising mechanisms?
Increases gluconeogenesis by increase lipolysis in adipocytes and amino acid transport to liver. Hepatic glycogenolysis takes place.
302
What does GLP-1 do?
Stimulates insulin release by increasing pancreatic beta cell sensitivity to glucose and suppresses glucagon release. Increases satiety feeling.
303
What happens when insulin binds to the insulin receptor?
Conformational change in tyrosine kinase domains of beta subunits (intracellular portion of receptor).
304
What hormones stimulate amino acid use for gluconeogenesis in liver?
Glucagon, cortisol.
305
What hormone stimulates protein breakdown in the liver?
Glucagon.
306
What does lipoprotein lipase do?
Breaks down triglycerides so glycerol and NEFA can enter adipocytes.
307
What hormones stimulate breakdown of triglycerides in adipocytes so that glycerol and fatty acids can be released into the blood?
Cortisol and growth hormone.
308
What hormones stimulates formation of ketone bodies in liver?
Glucagon.
309
What hormones stimulate conversion of glycogen to glucose-6-phosphate (glycogenolysis)?
Glucagon and adrenaline (during fight and flight).
310
What hormones inhibit uptake of glucose via GLUT4 on muscle cells?
Glucagon and growth hormone.
311
How is insulin released?
Released in 2 phases.
312
How does calcitonin lower calcium levels if calcium levels are too high?
Reduce osteoclast activity in bone and increase calcium excretion in kidney.
313
Hypercalcemia causes?
Primary hyperparathyroidism, bone metastases.
314
What is the bundling system present in muscle?
Muscle which is made up of muscle fascicle which is made up of muscle fibres which is made up of myofibrils.
315
What makes up a myofibril?
Repeating sarcomeres separated by z lines.
316
What is the structure of myosin?
Two globular heads with a single tail formed by two alpha helices.
317
What is the structure of actin?
Filament has a helix structure. Has a myosin binding site and contains troponin and tropomyosin.
318
Explain the steps in the initial muscle contraction after an action potential has arrived
Action potential propagates across surface of muscle membrane and T tubules. DHP receptor detects voltage and results in a change in the shape of the protein linked to the ryanodine receptor. This opens the ryanodine receptor and results in calcium leaving the sarcoplasmic reticulum and traveling deep into the muscle fiber where it binds to troponin. This causes tropomyosin to move and expose myosin binding sites. Myosin head forms a cross bridge with actin. Release of ADP and phosphate allows myosin to produce power stroke and pull actin towards centre of sarcomere. ATP binding releases myosin head from actin chain and ATP hydrolysis recharges myosin head. Calcium is actively transported back into SR while action potential continues.
319
Structure of a slow motor unit?
Small cell bodies. Small dendritic trees. Thin axons.
320
What early changes in cartilage would be present in early osteoarthritis?
Loss of proteoglycan in superficial zone leads to fibrilation.
321
Where does hand osteoarthritis occur?
Distal interphalangeal joint, proximal interphalangeal joint and trapeziometacarpal joint (base of thumb OA).
322
How to manage OA?
Exercise, weight management, non steroidal anti inflammatory drug.
323
OA treatment?
Total joint replacement. Trapeziectomy
324
Describe the structure and function of type 2 alveolar cells?
Granular and cuboidal. Replicate to replace type 1 alveolar cells. Secrete pulmonary surfactant. Secrete antiproteases. Have a role in xenobiotic metabolism.
325
What cause airway relaxation?
Release of adrenaline from adrenal gland and release of nitric oxide from nerves from spinal cord.
326
What cause the P wave in ECG?
Electrical signals transmitting across the myocardium of atrium along the internodal tracts.
327
Cardiac vs skeletal muscle stretching ability?
Cardiac muscle is more resistant to stretching. Cardiac muscle therefore produces more passive force and so more overall force.
328
When is preload increased in the heart?
Hypervolemia, regurgitation of aortic and pulmonary valve (leaky heart valves - don’t close fully), heart failure.
329
Why is high afterload in a heart bad?
Reduced stroke volume. More cardiac workload.
330
How does the left ventricle walls experience similar tension to right ventricles?
Left ventricles have a low radius of curvature (radius) and a higher pressure. Allows left ventricle to generate higher pressures with similar wall stress.
331
When would you have a 4th heart sound?
During atrial systole. In patients with congestive heart failure, pulmonary embolism or tricuspid incompetence (regurgitation).
332
When is QRS complex?
Isovolumetric contraction
333
When it T wave produced?
Reduced ejection.
334
When is dichrotic notch present?
Isovolumetric relaxation.
335
What is dichrotic notch?
Caused by closure of the aortic valve. Rebound pressure as distended aortic wall relaxes.
336
Change in pressure volume loop when afterload is increased?
Extended upwards and decreased in width from the left inwards.
337
Why does an increase in afterload extended pressure volume loop upwards?
Greater pressure required to open aortic valve.
338
Change in pressure volume loop during exercise?
Extended to the left and right. Extended upwards.
339
Longest phase of cardiac cycle?
Reduced passive filling.
340
What makes up the adrenal cortex?
Zona glomerulosa, zona fasciculata and zona reticularis
341
Series of enzymes that convert progesterone to aldosterone?
21,11,18 hydroxylase.
342
Series of enzymes that convert progesterone to cortisol?
17,21,11 hydroxylase.
343
Cushing syndrome symptoms
Depression, easy bruising, red stretch marks, poor wound healing, immunosuppression.
344
What does thyroid hormone do?
Results in fetal growth and development especially in regards to the CNS. Increases basal metabolic rate. Increases catecholamine effect resulting in tachycardia and lipolysis. Increases heat production.
345
How is gestational age calculated?
Fertilisation date + 14 days. Early obstetric ultrasound and compare to embryo size charts.
346
What happens during embryogenic stage?
Development of early embryo from fertilised oocyte. Formation of two population of cells. Pluripotent embryonic cells and extraembryonic cells.
347
When does the embryogenic stage take place?
14-16 days post fertilisation.
348
How does the blastocyst implant in the uterine endometrium?
Fusion of trophoblasts with uterine endometrium to form syncitiotrophoblasts. Forms interface between embryo and maternal blood supply.
349
What is the amnion of the amniotic cavity?
Epiblast cells migrate to form a thin membrane called the amnion that surrounds the amniotic cavity, separating it from the cytotrophoblast.
350
What happens at the cranial end of the primitive streak?
Expands to form primitive node.
351
What is the primitive groove?
Depression along primitive streak.
352
How does formation of the neural tube happen?
Notochord signals direct the neural plate ectoderm to invaginate to form the neural groove. This create two neural folds that run along cranial caudal axis. Neural folds move together over neural groove and fuse forming a hollow tube. Migration of neural crest cells to other tissues.
353
What is the neural plate?
Portion of ectoderm that is specified to become the neural ectoderm.
354
What is the connecting stalk?
Links developing embryo unit to chorion.
355
What forms the chorion?
Yolk sac and trophoblast.
356
Tertiary phase of chorionic villi development
Growth of umbilical artery and vein into the villus mesoderm providing vascalature.
357
Maternal blood vessel branching before reaching endometrium
Uterine artery branches to give arcuate arteries. Arcuate arteries branch to give radial arteries. Radial arteries branch to give basal arteries. Basal arteries branch to give spiral arteries. Spiral arteries invade endometrium.
358
What is the cervix made out of?
Collagen fibres embedded in proteoglycan matrix.
359
What hormone initiates labour?
Corticotrophin releasing hormone. Rises exponentially towards end of pregnancy.
360
What stimulates oxytocin release in labour?
Stretch receptors and rising oestrogen levels.
361
What is PGE2 involved in?
Cervix remodelling. Promotes leukocyte infiltration into the cervix, IL8 release and collagen remodelling.
362
What occurs after fetal delivery?
Shrinkage of uterus. This results in folding of fetal membranes and area of contact of placenta with endometrium to shrink. Clamping of umbilical cord stops fetal blood flow to placenta which results in collapsing of villi and haematoma formation between decidua and placenta. Contractions expel placenta and fetal tissues.
363
Risk factors for pre eclampsia?
Previous pregnancy with pre-eclampsia
BMI >30
Family history
Increased maternal age
364
How do endovascular cytotrophoblasts contribute to development of pre eclampsia?
Endovascular cytotrophoblast invasion of maternal spiral arteries is limited to decidual layer. Spiral arteries are not extensively remodelled, thus placental perfusion is restricted.
365
What results in endothelial dysfunction in pre eclampsia?
Excess production of Flt-1 by distressed placenta leads to reduction of available pro-angiogenic factors in maternal circulation, resulting in endothelial dysfuction.
366
What is Flt-1 (Vascular Endothelial Growth Factor Receptor-1)?
Soluble receptor for VEGF (Vascular endothelial growth factor) which binds soluble angiogenic factors to limit their bioavailabliltiy.
367
What tests can be used to determine risk of developing pre eclampsia?
sFlt-1/PlGF ratio or PlGF alone.
368
physiological action of arginine vasopressin?
Anti-diuretic hormone, vasoconstrictor and stimulates ACTH release from anterior pituitary.
369
What nuclei is AVP produced in?
Supraoptic nucleus.
370
What nuclei is oxytocin produced in?
Paraventricular nucleus.
371
OCD symptoms?
Ego-dystonic thoughts
Repetitive, circular ruminations
Compulsions
372
symptoms of depression other than core symptoms?
Weight loss, poor sleep, feeling of guilt and suicidal ideation.
373
Psychosis key symptoms
Hallucinations,
Delusions
Thought Disorder
374
Schizophrenia disorganised symptoms?
Thought disorder
Disorganised speech
375
Non-suicidal self-injury typically occurs in the context of?
Low self-worth and persistent distress. injury reduces distress.
376
What is the frontal lobe involved in?
Motor function, language and cognitive function.
377
What is the parietal lobe involved in?
Sensation, management of 5 senses, spatial orientation.
378
What is the limbic lobe involved in?
Learning, memory, emotion, motivation and reward.
379
What is the insular lobe involved in?
Visceral sensations, autonomic control and interoception.
380
Where are the two spinal cord enlargements?
Cervical and lumbar (C5 and L2).
381
What is the dorsal column pathway responsible for?
Fine touch, pressure, vibration and proprioception from skin and joints.
382
Function of vestibulospinal tract?
Head movement and position and mediates postural adjustment.
383
Function of tectospinal tract?
Orientation of the head and neck during eye movements.
384
Function of reticulospinal tract?
Movement and postural control.
385
Function of rubrospinal tract?
Upper limb control.
386
What do pain and temperature sensations ascend within?
Lateral spinothalamic tract
387
What do crude touch sensations ascend within?
Anterior spinothalamic tract
388
Explain dorsal column pathway?
Fibres enter via the dorsal horn and enter the ascending
dorsal column pathways. Information conveyed from lower limbs and upper limbs travels ipsilaterally. First synapse in medulla. Second order axons decussate in the caudal medulla. Form the contralateral medial lemniscus tract. Second order neurones synapse in the thalamus. 3rd order neurons from the thalamus project to the somatosensory cortex.
389
Explain spinothalamic tract?
Primary afferent axons terminate upon entering the spinal cord. Second order neurons decussate immediately in the spinal cord and form the spinothalamic tract. 2nd order neurons terminate in the thalamus. 3rd order neurons from the thalamus project to the somatosensory cortex.
390
How do drugs binding to GABA receptor reduce seizures?
Increases effectives of gaba activation of gaba receptor. This increases chloride influx which results in hyperpolarisation. Less action potentials. Inhibitory effect on post synaptic neurone.
391
How do drugs binding to vesicle transporter proteins reduce seizures?
Drug interferes with vesicle fusion and therefore reduces exocytosis of glutamate thus decreasing the excitatory activation of the post-synaptic neurone.
392
Where are visceral motor nuclei located?
Hypothalamus.
393
What converts noradrenaline converted to adrenaline?
Phenylethanol methyl transferase.
394
How does botulinum toxin act as a neurotoxin?
Inhibits vesicle exocytosis. Paralysis, no muscle contraction.
395
How is GABA synthesised?
GABA synthesised by decarboxylation of glutamate by glutamic acid decarboxylase (GAD).
396
How are peripheral nerves classified?
Based on conduction velocity and axonal diameter.
397
Where do sympathetic nerves emerge from in spinal cord?
T1 to L2.
398
Visceral motor nerves?
Thoracolumbar (T1-L2) and craniosacral outflow (cranial nerves III, VII, IX, X)
399
Explain sympathetic innervation of heart?
Sympathetic innervation of the heart originates from T1 to T4 of the spinal cord. These presynaptic fibers first travel to either the cervical or the thoracic ganglia of the sympathetic chain, where they synapse and form the sympathetic cardiac nerves that innervate the heart.
400
Explain sympathetic innervation of the abdominal and pelvic viscera?
Sympathetic innervation of the viscera originates from T5 - L2 of the spinal cord. Nerve fibres synapse in pre-aortic ganglia and go on to innervate the abdominal and pelvic organs.
401
How does myasthenia gravis disrupt neuromuscular junction?
Antibodies disrupt acetyl choline receptor on post synaptic terminal.
402
How does lambert eaton myasthenic syndrome disrupt neuromuscular junction?
Antibodies directed at voltage gated calcium ion channels.
403
What do schwann cells do?
Myelinate axons of PNS
404
What cells prodcues FGF23?
Osteocytes
405
What is the name given to the sign observed in hypocalcaemia whereby a patient's facial muscles twitch upon their facial nerve being tapped just below the zygomatic arch?
Chvostek's sign
406
What cell forms blood brain barrier?
Astrocyte.
407
Identify the most common genus of bacteria which makes up the gut flora?
Bacteroides.
408
What are intervertebral discs made up of?
Fibrocartilage
409
In which phase of the cardiac cycle would a pathological heart sound be heard in a patient with chronic mitral incompetance?
Rapid passive filling
410
Give one reason why slow type muscle fibres may shift into fast type muscle fibres
Spinal cord injury
411
first key step/process in fracture management?
Reduction
412
What hormone does NOT have a negative feedback mechanism?
Oxytocin
413
Which of the following pathways is responsible for transmitting sensory impulses of crude touch?
Anterior spinothalamic tract
414
Which part of a vasomotor cortex (VMC) is responsible for influencing heart rate and contractility?
Lateral
415
Acute pancreatitis biomarkers?
Raised amylase and lipase
