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BRS/POM MOCKS > BRS HARD QUESTIONS > Flashcards

BRS HARD QUESTIONS Flashcards

1
Q

Inflammatory cells in asthma?

A

Eosinophils, Mast cells, Th2 lymphocytes.

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2
Q

Inflammatory cells in COPD?

A

Neutrophils, Macrophages, Tc1 lymphocytes.

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3
Q

Inflammatory mediators in asthma?

A

IL-4, IL5

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4
Q

Inflammatory mediators in COPD?

A

TNF alpha, IL-8

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5
Q

Asthma pathology?

A

Bronchoconstriction + mucus. Formation of mucus plug in airway lumen.

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6
Q

Types of COPD?

A

Chronic bronchitis, chronic bronchiolitis (small airways disease), emphysema.

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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.

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8
Q

Emphysema pathology?

A

Lung tissue destruction (alveoli). Disrupted alveolar attatchments which can lead to collapsing of alveolar.

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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.

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10
Q

What are the two types of emphysema?

A

Centriacinar emphysema and panacinar emphysema.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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25
Q

What are your peripheral nerves?

A

Motor and sensory nerve.

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26
Q

How do you describe in neuroanatomical terms if someone has pain and muscle weakness in buttock, down his thigh, calf and into his toes ?

A

The anterior and posterior nerve roots of lumbar spinal nerves L5 and S1.

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27
Q

Where are the descendings tracts in the medulla?

A

Medullary pyramids (anterior surface of medulla).

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28
Q

Where are the dorsal columns in the medulla?

A

Posterior surface of medulla.

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29
Q

Special somatic afferent nerve fibres function?

A

Fibres carry special senses of hearing and balance

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30
Q

Special visceral afferent nerve fibres function?

A

Fibres carry taste sensation.

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31
Q

Special visceral efferent nerve fibres function?

A

Innervate skeletal muscles of the jaw, face, larynx and pharynx.

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32
Q

What lies in the posterior cranial fossa?

A

Cerebellum.

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33
Q

What lies directly above the body of the sphenoid bone?

A

Hypothalamus.

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34
Q

What does the third ventricle supply?

A

Diencephalon.

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35
Q

What does the aqueduct supply?

A

The midbrain.

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36
Q

What does the fourth ventricle supply?

A

Pons and medulla.

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37
Q

Broca’s area function?

A

Motor speech.

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38
Q

Where is broca’s area located?

A

Left hemisphere.

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39
Q

Wernicke’s area function?

A

involved in the comprehension of speech.

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40
Q

Where is Wernicke’s area located?

A

Left hemisphere.

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41
Q

Common cause of acute pancreatitis?

A

Gallstone and alcohol.

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42
Q

Types of acute pancreatitis?

A

Oedematous pancreatitis. Haemorrhagic pancreatitis. Necrotic pancreatitis.

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43
Q

Symptoms of acute pancreatitis?

A

Epigastric pain radiating to back. Vomiting. Fever.

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44
Q

Key clinical signs of acute pancreatitis?

A

Tachycardia and hypotensive. Grey turner’s sign. Cullen’s sign.

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45
Q

What is grey turner’s sign?

A

bruising in flanks.

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46
Q

What is cullen’s sign?

A

Bruising around umbilicus.

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47
Q

What is a smooth muscle cancer called?

A

Leiomyosarcomas

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48
Q

Who is eligible for a hepatocellular cancer screen?

A

Individuals with cirrhosis.

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49
Q

What interventional radiology is done for cancer?

A

Percutaneous biopsies.

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50
Q

What cancer can you develop in lower 1/3 of the oesphagus?

A

Adenocarcinoma.

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51
Q

Oesophageal cancer late stage symptom?

A

Dysphagia - difficult swallowing.

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52
Q

What investigations are done to stage oesophageal cancer and gastric cancer?

A

CT scan, PET CT scan, laparascopy and endoscopy ultrasound.

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53
Q

Gastric cancer symptoms?

A

Dyspepsia (upper abdominal discomfort after eating). Weight loss and abdominal mass on examination.

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54
Q

What surgery is done if tumour is present at oesophago-gastric junction?

A

oesophago gastrectomy - removal of oesophagus.

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55
Q

What surgery is done if tumour is present close to the oesophago-gastric junction?

A

Total gastrectomy.

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56
Q

What surgery is done if tumour is present in the body of the stomach?

A

Subtotal gastrectomy.

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57
Q

What inherited disorder causes decreased uptake of bilirubin?

A

Gilberts syndrome.

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58
Q

What inherited disorder causes decreased conjugation of bilirubin?

A

Crigler-najar syndrome.

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59
Q

What inherited disorder causes decreased secretion of bilirubin?

A

Dublin-johnson syndrome, rotor syndrome.

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60
Q

What is fulfilmant hepatic failure?

A

It is the same as acute hepatic failure.

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61
Q

What can liver failure cause?

A

Hepatic encephalopathy, coagulopathy, ascites, hypoglycemia (due to impaired glycogen production), increased risk of infection (due to lack of globulin production).

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62
Q

What are some toxins that can cause acute liver failure?

A

Paracetamol, amanita phalloides and bacillus cereus.

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63
Q

Causes of acute liver failure?

A

Toxins, inflammation (hepatitis), disease of pregnancy, idiosyncratic drug reaction, vascular diseases and metabolic causes.

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64
Q

Causes of chronic liver failure?

A

Inflammation, alcohol abuse, side effects of drugs, reduced venous return, inherited diseases, non alcoholic steatohepatatis, autoimmune hepatitits.

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65
Q

Consequences of cholestasis?

A

Pruritus (itching), cholesterol deposition around eyes and cholangitis (inflammation of bile duct system).

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66
Q

What presinusoidal causes of portal hypertension?

A

Chronic hepatitis, primary biliary cirrhosis.

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67
Q

What sinusoidal causes of portal hypertension?

A

Acute hepatitis, alcohol and fatty liver.

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68
Q

What post sinusoidal causes of portal hypertension?

A

Venous occlusive diseases.

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69
Q

What does splenomegaly cause?

A

Thrombocytopenia and anaemia due to pooling and then destruction.

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70
Q

Why do varices happen in veins?

A

Thin walls.

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71
Q

What molecules are increased in the brain during liverfailure and can contribute to encephalopathy?

A

Aromatic amino acids (e.g serotin). Known as false transmitters.

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72
Q

What varices are common in liver failure?

A

Oesophageal varices and rectal varices.

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73
Q

What is used to assess severity of liver failure?

A

Child-pugh score.

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74
Q

What factors are used to assess child pugh score?

A

Total bilirubin, serum albumin, prothrombin time, ascites, hepatic encephalopathy.

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75
Q

What class of child pugh score makes them a transplant candinate?

A

Class B.

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76
Q

How to treat liver failure?

A

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.

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77
Q

What can be used to support liver for 24-48 hours?

A

Albumin exchange system such which remove albumin bound toxins from blood.

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78
Q

Biomarkers for obstructive jaundice?

A

Serum amylase and prothrombin time.

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79
Q

Radiological scans for obstructive jaundice in order of relevance?

A

Ultrasound first. MRCP. CT scan.

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80
Q

Symptoms of short bowel syndrome?

A

Diarrhoea, weight loss, dehydration.

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81
Q

What is heart failure?

A

Heart unable to maintain adequate circulation for metabolic requirements of body.

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82
Q

What can cause heart failure?

A

Cardiac damage (ischaemia), hypertension and valve disease.

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83
Q

Symptoms of Wolff-Parkinson-White syndrome?

A

Tachycardia & abnormal cardiac electrical conductance

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84
Q

Symptoms of atrial fibrilation and Wolff-Parkinson-White syndrome?

A

Palpitations & chest pain.

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85
Q

What causes QRS pre excitation in WPW syndrome?

A

Current from extra accessory pathway which causes ventricular depolarisation before you get ventricular depolarisation from AVN.

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86
Q

What causes biphasic t wave in WPW syndrome?

A

Depolarisation from extra accessory pathway when repolarisation is occuring in the ventricles.

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87
Q

What would you see on the ECG on a first degree heart block?

A

Increased P-R interval.

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88
Q

Treatment for heart blocks?

A

Discontinuation of AV-blocking drugs (e.g. beta-blockers, calcium channel blockers) or pacemaker implantation in severe cases

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89
Q

NSTEMI/STEMI symptoms?

A

chest pain, sweating, nausea & vomiting

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90
Q

ECG changes would you expect to see in hypertrophy of the left ventricle?

A

Larger QRS complex.

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91
Q

What are signs of filtration failure in kidney dysfunction?

A

Haematuria and proteinuria. Low serum albumin.

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92
Q

Urine dipstick for UTI?

A

2+ leucocytes, + nitrite, trace of blood

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93
Q

Key features of nephrotic syndrome?

A

Peripheral oedema, severe proteinuria, low serum albumin. Low blood pressure.

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94
Q

What is nephrotic syndrome associated with?

A

Hyperlipidaemia.

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95
Q

Major complication of minimal change glomerulopathy?

A

Thrombosis.

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96
Q

Presentation of kidney stones?

A

Pain in abdomen. Blood in urine.

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97
Q

How would you check for kidney stones?

A

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.

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98
Q

Treatment for kidney stones?

A

Shockwave lithotripsy, ureteroscopy, percutaneous nephrolithotomy.

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99
Q

What is the inheritance pattern of polycystic kidney disease that develops in a neonatal?

A

Autosomal recessive.

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100
Q

What is the inheritance pattern of polycystic kidney disease that develops in an adult?

A

Autosomal dominant.

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101
Q

Causes of kidney stones?

A

Prostate enlargement, gout and dehydration.

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102
Q

What does the detrusor muscle do?

A

Contracts to build pressure in urinary bladder to support urination.

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103
Q

What is a superficial nephron?

A

Loop of henle only extends into outer medulla.

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104
Q

What is a juxtamedullary nephron?

A

Loop of henle extends deep into inner medulla.

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105
Q

What is the glomerular filtration rate?

A

Amount of fluid filtered from glomeruli into bowman’s capsule per unit time. Sum of filtration rate of all functions nephrons.

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106
Q

Why is creatinine not as good as inulin?

A

Small amount of creatinine is secreted into nephron. Needs to be adjusted when calculating GFR.

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107
Q

What substances via paracellular junctions in renal tubules?

A

Water, calcium, potassium, chloride and urea.

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108
Q

What maintains sodium gradients in kidney duct cell?

A

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.

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109
Q

How does sodium and bicarbonate reabsorption occur in early proximal convoluted tube?

A

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.

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110
Q

How is glucose reabsorbed in early proximal convoluted tube?

A

Glucose enters via sodium glucose cotransporter 2. Glucose exits into blood via basolateral membrane via GLUT2.

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111
Q

What ions are reabsorbed in the thick ascending limb?

A

Sodium and chloride ions.

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112
Q

How is sodium and chloride reabsorbed in the thick ascending limb?

A

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.

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113
Q

What ions enter blodo via paracellular pathways in the thick ascending limb?

A

Na+, Ca2+, K+, Mg2+.

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114
Q

What ions get reabsorbed in the early distal convoluted tube?

A

Sodium, chloride and calcium.

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115
Q

What pumps reabsorbs chloride ions into blood in early distal convoluted tube?

A

Potassium chloride symporter.

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116
Q

What pumps are involved in intercalated cells?

A

Chloride bicarbonate antiporter and H+ ATPase.

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117
Q

What part of nephron is the filtrate least concentrated?

A

Distal convoluted tube and collecting duct.

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118
Q

When does the amount of water and sodium in the filtrate decrease the fastest?

A

Proximal convoluted tube.

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119
Q

Nitrite detected in dipstick test indicate what?

A

Gram-negative bacteria in large number, e.g., E. Coli.

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120
Q

Ketones in dipstick test indicate what?

A

Starving or fasting or diabetic ketoacidosis

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121
Q

What does low specific gravity mean?

A

Urine is too diluted.

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122
Q

What does low specific gravity in dipstick test indicate?

A

Diabetes Insipidus.

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123
Q

What is diabetes insipidus?

A

Decreased release of AVP or decreased response to AVP.

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124
Q

Protein in dipstick indicates what?

A

Nephrotic syndrome

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125
Q

Blood in dipstick indicates what?

A

Nephritic syndrome or kidney stones or UTI

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126
Q

Bilirubin in dipstick indicates what?

A

Liver disease or gallstones

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127
Q

Urobilinogen in dipstick indicates what?

A

Liver disease or haemolysis

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128
Q

What does freely filtered mean?

A

Same concentration in glomerular filtrate as in plasma.

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129
Q

Why can para aminohippurate be used for renal plasma flow?

A

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.

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130
Q

When can para aminohippurate not be used to calculate RPF?

A

If too high of a concentration has been infused. Results in some leaving in the renal vein instead of all being in the urine.

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131
Q

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??

A

1mmol / L

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132
Q

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?

A

0.8 mmol/L

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133
Q

Why is measurement of PAH clearance rarely performed clinically when renal disease is suspected

A

Incomplete secretion and issues with renal plasma flow.

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134
Q

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?

A

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.

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135
Q

How does the gradient of Log plasma 51Cr EDTA activity change in someone with renal failure?

A

Less steep gradient.

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136
Q

What is a 1st degree heart block involve?

A

Longer PR interval as there is a delay in conduction.

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137
Q

What artery supplies the proximal transverse colon?

A

Middle colic artery.

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138
Q

What artery supplies the distal third of transverse colon?

A

Inferior mesenteric artery.

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139
Q

How is the rectum different to the colon?

A

Rectum has transverse rectal folds in its submucosa and doesn’t have taenia coli.

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140
Q

What contractions occur in transverse and descending colon?

A

Segmental contractions of circular muscle called haustral contractions.

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141
Q

What parasympathetic nerve innervates ascending colon and transverse colon.

A

Vagus nerve.

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142
Q

What parasympathetic nerve innervates distal colon?

A

Pelvic nerves.

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143
Q

What nerves control external anal sphincter?

A

Somatic motor fibres in the pudendal nerves.

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144
Q

What does aldosterone do to the large bowel?

A

Promotes sodium and water absorption (synthesis of Na+ ion channel, Na+/K+ pump).

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145
Q

How does defecation occur?

A

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.

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146
Q

Sympathetic nerves emerging from what ganglion innervate the colon?

A

Inferior mesenteric and pelvic ganglion.

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147
Q

What is the submucosal plexus responsible for?

A

Senses the gut lumen environment. Controls secretion, blow flow, epithelial and endocrine cell function.

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148
Q

What is hirschsprung’s disease? What does it result in?

A

Congenital absence of ganglion of myenteric and submucosal. Enlarged colon.

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149
Q

What stimulates release of gastrin?

A

Amino acids and peptides present in the lumen of the stomach. Gastric distention and vagus nerve.

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150
Q

What does CCK do?

A

Stimulates pancreatic enzyme release. Stimulates gallbladder contraction and relaxation of sphincter of oddi. Delays gastric emptying and decreases food intake.

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151
Q

What stimulates release of GIP?

A

All 3 macronutrients.

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152
Q

What cells secretes GIP and where are these cells located?

A

K cells in duodenum and jejunum.

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153
Q

What stimulates release of GLP-1?

A

Hexose and fat.

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154
Q

What does GLP-1 do?

A

Increases sensitivity of pancreatic beta cells to glucose. Induce satiety.

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155
Q

How is water absorbed in the GI tract?

A

Osmotic flow of water through tight junctions into intercellular space due to hypertonic solution present in intercellular space (high concentration of ions).

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156
Q

How is sodium absorbed in the ileum?

A

Secondary active transport. Co-transport with chloride ions.

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157
Q

How is chloride absorbed in the colon?

A

Secondary active transport. Exchanged with bicarbonate.

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158
Q

How is potassium absorbed in the small intestine?

A

Diffusion via paracellular junctions.

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159
Q

What ions move down concentration gradient into lateral intercellular space in small intestine?

A

Chloride and bicarbonate.

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160
Q

Why is ferritin binding to intracellular iron important?

A

Prevents iron from promoting oxidative stress.

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161
Q

What stimulates inspiration?

A

Apneustic centre.

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162
Q

What conditions are j receptors involved in?

A

Pulmonary oedema and capillary engorgement.

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163
Q

What can J receptors do if activated?

A

Increase breathing frequency in response to events such as pulmonary oedema which cause a decrease in oxygenation.

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164
Q

What do peripheral chemoreceptors detect?

A

Oxygen concentration.

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165
Q

What vessels leave the liver?

A

3x hepatic veins and common bile duct.

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166
Q

What makes up the portal triad?

A

Branch of hepatic artery. Branch of portal vein. Bile duct.

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167
Q

What cells are attached to the sinusoidal endothelial cells?

A

Kupffer cells.

168
Q

How are lipoproteins synthesised in the liver?

A

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
Q

What is excreted in bile?

A

Xenobiotics, cholesterol metabolites, alkaline phosphatase.

170
Q

What are some MDR related proteins?

A

MRP2,MRP3.

171
Q

What do MDR3 channels export into bile?

A

Phospatidylcholine.

172
Q

Intrahepatic jaundice causes?

A

Acute and chronic liver damage.

173
Q

In a nodal cell action potential what causes the prepotential phase?

A

Sodium influx through funny channel.

174
Q

Why is there a plateau phase in cardiac muscle action potential?

A

Maintains cell at level of depolarisation. Long, slow contraction is required to produce effective pump.

175
Q

Where is vasomotor centre located?

A

Medulla and lower third of pons.

176
Q

What is the pressor area in vasomotor centre responsible for?

A

Vasoconstriction.

177
Q

What is the depressor area in vasomotor centre responsible for?

A

Vasodilation.

178
Q

Lateral portions of vasomotor centre regulate what?

A

Heart rate and contractility.

179
Q

Medial portion of vasomotor centre does what?

A

Decreases heart rate via vagus nerve.

180
Q

How does acting on M2 receptor inhibit contractility?

A

Activates Gi protein which inactivates adenylate cyclase.

181
Q

Where are pressure sensors in the cardiovascular system?

A

Aortic arch, carotid sinus and afferent arterioles in the kidney.

182
Q

What does constriction of veins do to venous return?

A

Reduces compliance and increases venous return.

183
Q

What increases venous pressure and hence increases venous return?

A

Increase in blood volume, skeletal muscle pump, respiratory movements and SNS activation of veins.

184
Q

Local vasodilators?

A

Nitric oxide and prostacyclin.

185
Q

Local vasoconstrictors?

A

Thromboxane A2 and endothelins.

186
Q

When is atrial natriuretic peptide released?

A

Secreted from the atria in response to stretch to lower blood pressure.

187
Q

What is atenolol?

A

Beta blocker. Reduces heart rate.

188
Q

What is ramipril?

A

ACE Inhibitor. Causes vasodilation.

189
Q

What does a crescendo decrescendo murmur indicate?

A

Aortic stenosis.

190
Q

Key difference in flow volume loops in obstructive and restrictive?

A

Indented expiratory curve in obstructive. Restrictive is same shape but narrower curve.

191
Q

Why are spirometric pulmonary function tests done?

A

Monitor progression of lung disease over time. Monitor effectiveness of different bronchodilators.

192
Q

Disadvantage of spirometric pulmonary function tests?

A

Heavy reliance on technique and can be uncomfortable for patients reducing their motivation to apply maximum effort.

193
Q

What reflex prevents long expiration?

A

Hering breuer deflation reflex

194
Q

What is FVC on flow volume loop?

A

Width of loop.

195
Q

Why is volume expired is slightly larger than volume inspired?

A

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
Q

Why does additional gas dissolve into the blood during a dive? Which law explains this?

A

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
Q

Ascending rapidly without releasing inhaled gas results in?

A

Pulmonary barotrauma. - Alveolar rupture.

198
Q

Why does ascending slowly prevent DCI?

A

Allow N2 to be unloaded in the alveoli while keeping it dissolved in the blood.

199
Q

How is high sodium in the blood maintained from duct cells?

A

Na+/K+ exchange pump driven by ATP. Potassium into duct cell while sodium pumped into blood.

200
Q

What drives water into lumen of pancreatic duct?

A

Sodium moves into lumen of duct down gradient from blood via paracellular junctions and water follows.

201
Q

What stimulates enzyme secretion in pancreatic juice?

A

Acetylcholine from vagus nerve and cholecystokinin from duodenal I cells.

202
Q

What stimulates release of cholecystokinin?

A

CCK releasing peptide due to increase in amino acid and fatty acids in lumen of duodenum. Gastrin releasing peptide.

203
Q

What inhibits release of CCK?

A

Trypsin.

204
Q

Where is pancreatic amylase secreted?

A

Duodenum.

205
Q

What does the mucosa layer of the gut wall contain?

A

Epithelium, lamina propria (connective tissue) and muscularis mucosae (muscle).

206
Q

How do parietal cells secrete acid.

A

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
Q

What may you administer to treat gout?

A

Non steroidal anti inflammatory drugs. Use of glucocorticoids.

208
Q

What joints does rheumatoid arthritis commonly affect?

A

Joints in hands, wrists and feet.

Metacarpophalangeal joints (MCP)
Proximal interphalangeal joints (PIP)
NOT distal interphalangeal joints
Metatarsophalangeal joints (MTP)

209
Q

What are common extra articular features present in a rheumatoid arthritis patient?

A

Fever, weight loss. Subcutaneous nodules.

210
Q

Presentation of psoriatic arthritis

A

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
Q

Main cytokines involved in ankylosing spondylitis?

A

TNF alpha, IL-17 and IL-23.

212
Q

What are the 3 factors that affect resistance in a vessel?

A

Vessel length, Vessel radius and blood viscosity.

213
Q

What helps regulated systemic arterial blood pressure?

A

Cardiovascular control centre in medulla via sympathetic nervous system and endocrine hormones.

214
Q

What is the blood pressure equation?

A

Blood pressure = cardiac output x total peripheral resistance

215
Q

What is bulk flow?

A

A volume of protein-free plasma filters out of the capillary, mixes with the surrounding interstitial fluid (IF) and is reabsorbed.

216
Q

Lymph vessel structure

A

Blind-ended, single-layered and contain large permeable water-filled one-way channels.

217
Q

What do the terms Hyperpnoea / Hypopnoea mean?

A

Increased depth of breathing / Decreased depth of breathing.

218
Q

What does the term apnoea mean?

A

Cessation of breathing (no air movement)

219
Q

What does the term orthopnoea mean?

A

Positional difficulty in breathing (when lying down)

220
Q

At functional residual capacity what are the lungs forces like?

A

The lung-chest forces are in equilibrium. Chest recoil = lung recoil.

221
Q

What occurs in inspiration?

A

Diaphragm moves down and intercostal muscles move rib cage up and out.

222
Q

What is henry’s law?

A

Solubility of gas is directly proportional to partial pressure of that gas in equilibrium with that liquid.

223
Q

What is boyle’s law?

A

At constant temperature, volume of gas is inversely proportional to pressure of that gas.

224
Q

What happens to carbonic acid in haemoglobin?

A

H+ ions bind to haemoglobin chain. Bicarbonate leaves red blood cell in exchange of a chloride ion via the AE1 transporter.

225
Q

Why is the AE1 transporter on red cells important?

A

Allows negative chloride ions to enter the RBC to maintain resting membrane potential.

226
Q

Why is the mean arterial pressure equation an approximation?

A

Assumes steady flow (which does not occur due to the intermittent pumping of the heart). Rigid vessels
Right atrial pressure is negligible.

227
Q

What does an increase in arterial stiffness result in?

A

Increase in systolic blood pressure. Lower diastolic pressure as less diastolic flow.

228
Q

Why does pressure fall slowly in aorta after aortic valve closes?

A

Diastolic flow in the downstream circulation.

229
Q

When are veins the most compliant?

A

At low pressures.

230
Q

What hormone results in decidualisation?

A

Progesterone.

231
Q

What changes occur in the endometrium during decidualisation?

A

Glandular epithelial secretion. Glycogen accumulation in stromal cell cytoplasm. Growth of capillaries. Increased vascular permeability which leads to oedema.

232
Q

What factor is involved in changes to endometrium?

A

IL11.

233
Q

What does leukaemia inhibitory factor do?

A

Stimulates adhesion of blastocyst to endometrial cells.

234
Q

What maternal hormones are lowered during pregnancy?

A

FSH and LH. GH and TSH.

235
Q

Oxytocin effects for partruition?

A

Uterine contraction, cervical dilation and milk ejection.

236
Q

What occurs in puberty?

A

Production of sex steroids. Development of secondary sexual characteristics. Attain capability to reproduce.

237
Q

Describe the luteal phase

A

Formation of corpus luteum after ovulation. Corpus luteum secretes progesterone and oestradiol.

238
Q

What occurs in the proliferative phase of the endometrium cycle?

A

Growth of epithelial cells and increase in arterioles due to high levels of oestradiol.

239
Q

What occurs in the secretory phase of the endometrium cycle?

A

Endometrial glands secrete glycogen. Increase volume of stromal cells produce thick lining.

240
Q

Menopause biomarkers?

A

Low oestradiol, High LH/FSH, Low inhibin, Low anti mullerian hormone.

241
Q

Symptoms of menopause?

A

Skin dryness, Hot flushes, Osteoporosis, Decreased libido.

242
Q

How does intramembrous ossification occur?

A

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
Q

What is a volkmann’s canal and where would you find it?

A

Transverse canals that are inbetween haversian canals or emerge from periosteum that contain blood vessels.

244
Q

Osteoblasts function

A

Forms bone by secreting osteoid and catalysing mineralisation of osteoid.

245
Q

Can you describe the process of endochondral ossification?

A

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
Q

Where is cancellous bone located in long bone?

A

Epiphysis.

247
Q

What is the epiphyseal side in interstitial growth?

A

Active hyaline cartilage dividing to form hyaline cartilage matrix.

248
Q

What metastases have lytic effects on bone?

A

thyroid, lung and kidney

249
Q

what metastases have both trophic and lytic effects on bone?

A

breast

250
Q

what metastases have trophic effects on bone?

A

prostate

251
Q

When a large fracture where bone edges are not close and there is low stability what occurs at the fracture?

A

Haematoma formation, release of cytokines and angiogenesis at fracture. Soft callus formation which is converted to a hard callus. Excess bone is removed.

252
Q

What do ligaments do and how do they do it?

A

Provide stability by restricting joint movement. Ligaments also provide proprioception.

253
Q

4 stages of healing of a tendon or ligament?

A

Bleeding, inflammation, proliferation and remodelling.

254
Q

What are between keratinocytes?

A

Tight junctions, adherens junctions, demosomes, gap junctions.

255
Q

What are adherens junctions and what do they do?

A

Transmembrane structures that engage with the actin skeleton.

256
Q

Describe melanocytes

A

Dendritic cells that distribute melanin pigment to keratinocytes.

257
Q

What are the most prominent types of collagen in the basement membrane?

A

IV, VII

258
Q

What is the function of the basement membrane?

A

Cell adhesion, gate keeping functions for cell migration and diffusion of molecules. Presence of rete ridges.

259
Q

What proteins does the dermis contain?

A

Collagen, fibrillin and elastin.

260
Q

What glycoproteins does the dermis contain?

A

Fibronectin, fibulin and integrins.

261
Q

What do the glycoproteins in the dermis do?

A

Facilitate cell adhesion and cell motility.

262
Q

What makes up the ground substance in dermis?

A

Glycosaminoglycans and proteoglycans.

263
Q

What other cells apart from fibroblasts are present in the dermis?

A

Mast cells, neutrophils and lymphocytes.

264
Q

What stimulates eccrine sweat glands?

A

Cholinergic nerves and adrenergic nerves.

265
Q

What stimulates apocrine sweat glands?

A

Adrenergic nerves.

266
Q

Describe the meissner’s corpuscle?

A

Encapsulated, unmyelinated mechanoreceptor present in the superficial dermis. Most concentrated in thick hairless skin.

267
Q

What is the meissner’s corpuscle responsible for?

A

Light touch and slow vibration.

268
Q

How does the skin behave as a physical barrier?

A

Cornified envelope prevents water and protein loss from skin. Subcutaneous fat prevents damage from trauma. Melanin produced protects DNA damage from UV.

269
Q

How does the skin regulate temperature?

A

Vasodilation or vasoconstriction in deep or superficial vascular plexuses. This regulates heat loss. Eccrine sweat glands provide cooling effect.

270
Q

What function does hair have?

A

Thermoregulation, source of epithelial and melanocyte stem cells, production of apocrine sweat, production of sebum.

271
Q

Describe the isthmus part of hair?

A

Lower portion between sebaceous gland and arrector pili muscle

272
Q

What does the bulge contain and why is this important?

A

Contains hair follicle stem cells. Can migrate downwards to form hair follicle or upwards to form sebaceous glands or heal wounds.

273
Q

What does the outer root sheath of hair follicle contain?

A

Stem cells.

274
Q

What is the nail plate firmly attached to?

A

Nail bed.

275
Q

Where does the nail plate detach?

A

Hyponychium

276
Q

Where does the nail plate emerge from?

A

Proximal nail fold.

277
Q

What produces the nail plate?

A

Nail matrix.

278
Q

What is the visible portion of the nail matrix called?

A

Lunula.

279
Q

How is the nail plate produced?

A

Keratinocytes in the nail matrix lose their nuclei and cytoplasm and become keratin.

280
Q

Where is the nail matrix?

A

Above distal bone and below proximal nail fold.

281
Q

Psoriasis disease mechanism

A

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
Q

What lifestyle changes can help manage psoriasis?

A

Reducing alcohol consumption and smoking.

283
Q

What is the first step management to treating psoriasis?

A

Topical therapies and phototherapy.

284
Q

What topical therapies can be given for psoriasis?

A

Vitamin D analogues with corticosteroid. Retinoids. Tacrolimus.

285
Q

Why can tacrolimus be a better option compared to corticosteroids?

A

Tacrolimus is a calcineurin inhibitor and so is not a steroid. Steroids can cause skin thinning

286
Q

Types of phototherapy that can be used for psoriasis?

A

Narrowband UVB. PUVA (psoralen - makes skin sensitive to UVA. UVA is then given).

287
Q

In severe or widespread psoriasis what treatment would you offer?

A

Phototherapy or systemic therapies such as methotrexate or ciclosporin.

288
Q

What oral retinoid can you give for psoriasis?

A

Acitretin

289
Q

What advanced therapies can you offer for psoriasis?

A

PDE4 inhibitors, biologics and JAK inhibitors.

290
Q

Give an example for a biologic that can be used for psoriasis?

A

Anti TNF gamma.

291
Q

What causes a barrier defect in atopic ecezema? How does this cause the barrier deffect?

A

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
Q

What is filaggrin responsible for?

A

Binds and aggregates keratin bundles and intermediate filaments in stratum corneum.

293
Q

How does dysregulation of immune system lead to atopic eczema?

A

S.aureus stimulates th2 response and inhibits treg cells. Presence of eosinophils as well.

294
Q

How do you manage atopic eczema?

A

Use of emollients and patch testing (to test for allergens).

295
Q

First stage treatment for atopic eczema?

A

Corticosteroids and tacrolimus. - topical treatment

UVB or PUVA - phototherapy

296
Q

Steroid ladder for atopic eczema? (second stage treament)

A

Hydrocortisone, clobetasone, betamethasone, mometasone, clobetasol.

297
Q

Side effects of using steroids for atopic eczema?

A

Folliculitis or acne.

298
Q

Immunosuppressive drugs for atopic eczema?

A

Methotrexate or ciclosporin.

299
Q

What biologics can be used for eczema?

A

TH2 cytokines

anti IL-4
anti IL-13

300
Q

What stimulates alpha cells to produce glucagon?

A

Low blood glucose, amino acids, GI hormones, sympathetic nervous activity (via alpha adrenergic) and parasympathetic nervous system.

301
Q

Glucagon blood glucose raising mechanisms?

A

Increases gluconeogenesis by increase lipolysis in adipocytes and amino acid transport to liver. Hepatic glycogenolysis takes place.

302
Q

What does GLP-1 do?

A

Stimulates insulin release by increasing pancreatic beta cell sensitivity to glucose and suppresses glucagon release. Increases satiety feeling.

303
Q

What happens when insulin binds to the insulin receptor?

A

Conformational change in tyrosine kinase domains of beta subunits (intracellular portion of receptor).

304
Q

What hormones stimulate amino acid use for gluconeogenesis in liver?

A

Glucagon, cortisol.

305
Q

What hormone stimulates protein breakdown in the liver?

A

Glucagon.

306
Q

What does lipoprotein lipase do?

A

Breaks down triglycerides so glycerol and NEFA can enter adipocytes.

307
Q

What hormones stimulate breakdown of triglycerides in adipocytes so that glycerol and fatty acids can be released into the blood?

A

Cortisol and growth hormone.

308
Q

What hormones stimulates formation of ketone bodies in liver?

A

Glucagon.

309
Q

What hormones stimulate conversion of glycogen to glucose-6-phosphate (glycogenolysis)?

A

Glucagon and adrenaline (during fight and flight).

310
Q

What hormones inhibit uptake of glucose via GLUT4 on muscle cells?

A

Glucagon and growth hormone.

311
Q

How is insulin released?

A

Released in 2 phases.

312
Q

How does calcitonin lower calcium levels if calcium levels are too high?

A

Reduce osteoclast activity in bone and increase calcium excretion in kidney.

313
Q

Hypercalcemia causes?

A

Primary hyperparathyroidism, bone metastases.

314
Q

What is the bundling system present in muscle?

A

Muscle which is made up of muscle fascicle which is made up of muscle fibres which is made up of myofibrils.

315
Q

What makes up a myofibril?

A

Repeating sarcomeres separated by z lines.

316
Q

What is the structure of myosin?

A

Two globular heads with a single tail formed by two alpha helices.

317
Q

What is the structure of actin?

A

Filament has a helix structure. Has a myosin binding site and contains troponin and tropomyosin.

318
Q

Explain the steps in the initial muscle contraction after an action potential has arrived

A

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
Q

Structure of a slow motor unit?

A

Small cell bodies. Small dendritic trees. Thin axons.

320
Q

What early changes in cartilage would be present in early osteoarthritis?

A

Loss of proteoglycan in superficial zone leads to fibrilation.

321
Q

Where does hand osteoarthritis occur?

A

Distal interphalangeal joint, proximal interphalangeal joint and trapeziometacarpal joint (base of thumb OA).

322
Q

How to manage OA?

A

Exercise, weight management, non steroidal anti inflammatory drug.

323
Q

OA treatment?

A

Total joint replacement. Trapeziectomy

324
Q

Describe the structure and function of type 2 alveolar cells?

A

Granular and cuboidal. Replicate to replace type 1 alveolar cells. Secrete pulmonary surfactant. Secrete antiproteases. Have a role in xenobiotic metabolism.

325
Q

What cause airway relaxation?

A

Release of adrenaline from adrenal gland and release of nitric oxide from nerves from spinal cord.

326
Q

What cause the P wave in ECG?

A

Electrical signals transmitting across the myocardium of atrium along the internodal tracts.

327
Q

Cardiac vs skeletal muscle stretching ability?

A

Cardiac muscle is more resistant to stretching. Cardiac muscle therefore produces more passive force and so more overall force.

328
Q

When is preload increased in the heart?

A

Hypervolemia, regurgitation of aortic and pulmonary valve (leaky heart valves - don’t close fully), heart failure.

329
Q

Why is high afterload in a heart bad?

A

Reduced stroke volume. More cardiac workload.

330
Q

How does the left ventricle walls experience similar tension to right ventricles?

A

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
Q

When would you have a 4th heart sound?

A

During atrial systole. In patients with congestive heart failure, pulmonary embolism or tricuspid incompetence (regurgitation).

332
Q

When is QRS complex?

A

Isovolumetric contraction

333
Q

When it T wave produced?

A

Reduced ejection.

334
Q

When is dichrotic notch present?

A

Isovolumetric relaxation.

335
Q

What is dichrotic notch?

A

Caused by closure of the aortic valve. Rebound pressure as distended aortic wall relaxes.

336
Q

Change in pressure volume loop when afterload is increased?

A

Extended upwards and decreased in width from the left inwards.

337
Q

Why does an increase in afterload extended pressure volume loop upwards?

A

Greater pressure required to open aortic valve.

338
Q

Change in pressure volume loop during exercise?

A

Extended to the left and right. Extended upwards.

339
Q

Longest phase of cardiac cycle?

A

Reduced passive filling.

340
Q

What makes up the adrenal cortex?

A

Zona glomerulosa, zona fasciculata and zona reticularis

341
Q

Series of enzymes that convert progesterone to aldosterone?

A

21,11,18 hydroxylase.

342
Q

Series of enzymes that convert progesterone to cortisol?

A

17,21,11 hydroxylase.

343
Q

Cushing syndrome symptoms

A

Depression, easy bruising, red stretch marks, poor wound healing, immunosuppression.

344
Q

What does thyroid hormone do?

A

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
Q

How is gestational age calculated?

A

Fertilisation date + 14 days. Early obstetric ultrasound and compare to embryo size charts.

346
Q

What happens during embryogenic stage?

A

Development of early embryo from fertilised oocyte. Formation of two population of cells. Pluripotent embryonic cells and extraembryonic cells.

347
Q

When does the embryogenic stage take place?

A

14-16 days post fertilisation.

348
Q

How does the blastocyst implant in the uterine endometrium?

A

Fusion of trophoblasts with uterine endometrium to form syncitiotrophoblasts. Forms interface between embryo and maternal blood supply.

349
Q

What is the amnion of the amniotic cavity?

A

Epiblast cells migrate to form a thin membrane called the amnion that surrounds the amniotic cavity, separating it from the cytotrophoblast.

350
Q

What happens at the cranial end of the primitive streak?

A

Expands to form primitive node.

351
Q

What is the primitive groove?

A

Depression along primitive streak.

352
Q

How does formation of the neural tube happen?

A

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
Q

What is the neural plate?

A

Portion of ectoderm that is specified to become the neural ectoderm.

354
Q

What is the connecting stalk?

A

Links developing embryo unit to chorion.

355
Q

What forms the chorion?

A

Yolk sac and trophoblast.

356
Q

Tertiary phase of chorionic villi development

A

Growth of umbilical artery and vein into the villus mesoderm providing vascalature.

357
Q

Maternal blood vessel branching before reaching endometrium

A

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
Q

What is the cervix made out of?

A

Collagen fibres embedded in proteoglycan matrix.

359
Q

What hormone initiates labour?

A

Corticotrophin releasing hormone. Rises exponentially towards end of pregnancy.

360
Q

What stimulates oxytocin release in labour?

A

Stretch receptors and rising oestrogen levels.

361
Q

What is PGE2 involved in?

A

Cervix remodelling. Promotes leukocyte infiltration into the cervix, IL8 release and collagen remodelling.

362
Q

What occurs after fetal delivery?

A

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
Q

Risk factors for pre eclampsia?

A

Previous pregnancy with pre-eclampsia
BMI >30
Family history
Increased maternal age

364
Q

How do endovascular cytotrophoblasts contribute to development of pre eclampsia?

A

Endovascular cytotrophoblast invasion of maternal spiral arteries is limited to decidual layer. Spiral arteries are not extensively remodelled, thus placental perfusion is restricted.

365
Q

What results in endothelial dysfunction in pre eclampsia?

A

Excess production of Flt-1 by distressed placenta leads to reduction of available pro-angiogenic factors in maternal circulation, resulting in endothelial dysfuction.

366
Q

What is Flt-1 (Vascular Endothelial Growth Factor Receptor-1)?

A

Soluble receptor for VEGF (Vascular endothelial growth factor) which binds soluble angiogenic factors to limit their bioavailabliltiy.

367
Q

What tests can be used to determine risk of developing pre eclampsia?

A

sFlt-1/PlGF ratio or PlGF alone.

368
Q

physiological action of arginine vasopressin?

A

Anti-diuretic hormone, vasoconstrictor and stimulates ACTH release from anterior pituitary.

369
Q

What nuclei is AVP produced in?

A

Supraoptic nucleus.

370
Q

What nuclei is oxytocin produced in?

A

Paraventricular nucleus.

371
Q

OCD symptoms?

A

Ego-dystonic thoughts
Repetitive, circular ruminations
Compulsions

372
Q

symptoms of depression other than core symptoms?

A

Weight loss, poor sleep, feeling of guilt and suicidal ideation.

373
Q

Psychosis key symptoms

A

Hallucinations,
Delusions
Thought Disorder

374
Q

Schizophrenia disorganised symptoms?

A

Thought disorder
Disorganised speech

375
Q

Non-suicidal self-injury typically occurs in the context of?

A

Low self-worth and persistent distress. injury reduces distress.

376
Q

What is the frontal lobe involved in?

A

Motor function, language and cognitive function.

377
Q

What is the parietal lobe involved in?

A

Sensation, management of 5 senses, spatial orientation.

378
Q

What is the limbic lobe involved in?

A

Learning, memory, emotion, motivation and reward.

379
Q

What is the insular lobe involved in?

A

Visceral sensations, autonomic control and interoception.

380
Q

Where are the two spinal cord enlargements?

A

Cervical and lumbar (C5 and L2).

381
Q

What is the dorsal column pathway responsible for?

A

Fine touch, pressure, vibration and proprioception from skin and joints.

382
Q

Function of vestibulospinal tract?

A

Head movement and position and mediates postural adjustment.

383
Q

Function of tectospinal tract?

A

Orientation of the head and neck during eye movements.

384
Q

Function of reticulospinal tract?

A

Movement and postural control.

385
Q

Function of rubrospinal tract?

A

Upper limb control.

386
Q

What do pain and temperature sensations ascend within?

A

Lateral spinothalamic tract

387
Q

What do crude touch sensations ascend within?

A

Anterior spinothalamic tract

388
Q

Explain dorsal column pathway?

A

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
Q

Explain spinothalamic tract?

A

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
Q

How do drugs binding to GABA receptor reduce seizures?

A

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
Q

How do drugs binding to vesicle transporter proteins reduce seizures?

A

Drug interferes with vesicle fusion and therefore reduces exocytosis of glutamate thus decreasing the excitatory activation of the post-synaptic neurone.

392
Q

Where are visceral motor nuclei located?

A

Hypothalamus.

393
Q

What converts noradrenaline converted to adrenaline?

A

Phenylethanol methyl transferase.

394
Q

How does botulinum toxin act as a neurotoxin?

A

Inhibits vesicle exocytosis. Paralysis, no muscle contraction.

395
Q

How is GABA synthesised?

A

GABA synthesised by decarboxylation of glutamate by glutamic acid decarboxylase (GAD).

396
Q

How are peripheral nerves classified?

A

Based on conduction velocity and axonal diameter.

397
Q

Where do sympathetic nerves emerge from in spinal cord?

A

T1 to L2.

398
Q

Visceral motor nerves?

A

Thoracolumbar (T1-L2) and craniosacral outflow (cranial nerves III, VII, IX, X)

399
Q

Explain sympathetic innervation of heart?

A

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
Q

Explain sympathetic innervation of the abdominal and pelvic viscera?

A

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
Q

How does myasthenia gravis disrupt neuromuscular junction?

A

Antibodies disrupt acetyl choline receptor on post synaptic terminal.

402
Q

How does lambert eaton myasthenic syndrome disrupt neuromuscular junction?

A

Antibodies directed at voltage gated calcium ion channels.

403
Q

What do schwann cells do?

A

Myelinate axons of PNS

404
Q

What cells prodcues FGF23?

A

Osteocytes

405
Q

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?

A

Chvostek’s sign

406
Q

What cell forms blood brain barrier?

A

Astrocyte.

407
Q

Identify the most common genus of bacteria which makes up the gut flora?

A

Bacteroides.

408
Q

What are intervertebral discs made up of?

A

Fibrocartilage

409
Q

In which phase of the cardiac cycle would a pathological heart sound be heard in a patient with chronic mitral incompetance?

A

Rapid passive filling

410
Q

Give one reason why slow type muscle fibres may shift into fast type muscle fibres

A

Spinal cord injury

411
Q

first key step/process in fracture management?

A

Reduction

412
Q

What hormone does NOT have a negative feedback mechanism?

A

Oxytocin

413
Q

Which of the following pathways is responsible for transmitting sensory impulses of crude touch?

A

Anterior spinothalamic tract

414
Q

Which part of a vasomotor cortex (VMC) is responsible for influencing heart rate and contractility?

A

Lateral

415
Q

Acute pancreatitis biomarkers?

A

Raised amylase and lipase

BRS/POM MOCKS (23 decks)

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