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MRCS A - Dr Bishoy > 11- Physiology Explains (2) > Flashcards

11- Physiology Explains (2) Flashcards

1
Q

What is the mnemonic for the adrenal cortex layers?

A

GFR - ACD

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2
Q

What hormones are mainly produced in the zona glomerulosa of the adrenal cortex?

A

Mineralocorticoids, mainly aldosterone

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3
Q

What hormones are mainly produced in the zona fasciculata of the adrenal cortex?

A

Glucocorticoids, mainly cortisol

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4
Q

What hormones are mainly produced in the zona reticularis of the adrenal cortex?

A

Androgens, mainly dehydroepiandrosterone (DHEA)

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4
Q

What stimulates the release of renin?

A

Reduced renal perfusion and low sodium levels

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5
Q

What does renin hydrolyze to form?

A

Angiotensin I

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6
Q

What factors stimulate renin secretion?

A

Low blood pressure, hyponatremia, sympathetic nerve stimulation, catecholamines, erect posture

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7
Q

What converts angiotensin I to angiotensin II?

A

ACE (angiotensin-converting enzyme) in the lungs

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8
Q

What are the effects of angiotensin II?

A

Vasoconstriction leading to raised blood pressure, stimulation of thirst, stimulation of aldosterone and ADH release

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9
Q

What stimulates the release of aldosterone?

A

Raised angiotensin II levels, potassium levels, and ACTH levels

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10
Q

What does aldosterone cause in the distal tubule?

A

Retention of sodium in exchange for potassium and hydrogen ions

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11
Q

Where does iron absorption primarily occur?

A

Duodenum and upper jejunum

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12
Q

What percentage of dietary iron is typically absorbed?

A

About 10%

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13
Q

Which form of iron is more readily absorbed: ferrous iron or ferric iron?

A

Ferrous iron

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14
Q

What happens to ferrous iron during absorption?

A

It is oxidized to form ferric iron, which combines with apoferritin to form ferritin

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15
Q

What factors can increase iron absorption?

A

Vitamin C and gastric acid

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16
Q

How is iron transported in the plasma?

A

Bound to transferrin

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17
Q

Where is iron stored in the body?

A

Ferritin (or haemosiderin) in the bone marrow

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18
Q

How is iron excreted from the body?

A

Lost via the intestinal tract following desquamation

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19
Q

What is the typical volume of pancreatic secretions per 24 hours?

A

1000-1500ml

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19
Q

What is the distribution of iron in the body?

A

Total body iron 4g
70% in hemoglobin, 25% in ferritin and haemosiderin, 4% in myoglobin, and 0.1% in plasma iron

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20
Q

What is the pH of pancreatic secretions?

A

8

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21
Q

Which cells in the pancreas produce enzymes?

A

Acinar cells

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21
Q

Name some enzymes produced by acinar cells.

A

Trypsinogen, procarboxylase, amylase, elastase

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21
Q

What are some components found in the aqueous portion of pancreatic secretions?

A

Sodium, bicarbonate, water, potassium, chloride

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22
Q

Which cells in the pancreas produce aqueous components of pancreatic secretions?

A

Ductal and centroacinar cells

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23
Q

How are pancreatic secretions regulated?

A

Stimulation of acinar and ductal cells by CCK (cholecystokinin) and ACh (acetylcholine) released in response to digested material in the small bowel. Secretin released by S cells of the duodenum stimulates ductal cells and increases bicarbonate secretion.

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24
Q

What role does trypsin play in enzyme activation?

A

Trypsin activates other inactive enzymes in the duodenum.

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24
Q

How is trypsinogen activated in the duodenum?

A

It is converted to active trypsin via enterokinase.

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25
Q

What is collagen?

A

One of the most important structural proteins in the extracellular matrix

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26
Q

What determines the properties of tissues along with collagen?

A

Components such as elastin and glycosaminoglycans

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27
Q

How is collagen composed?

A

Three polypeptide strands woven into a helix, often with a combination of glycine and either proline or hydroxyproline plus another amino acid

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28
Q

What provides additional strength to collagen through numerous hydrogen bonds?

A

Hydrogen bonds within the collagen molecule

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29
Q

What is the most common subtype of collagen in the body?

A

Type I collagen (90% of bodily collagen)

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30
Q

What is the role of vitamin C in collagen formation?

A

It is important in establishing cross-links

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31
Q

What are some characteristics of patients with Ehlers Danlos syndrome?

A

Features of hypermobility, prone to joint dislocations and pelvic organ prolapse, and other connective tissue-related defects

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31
Q

Which cells synthesize collagen?

A

Fibroblasts

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32
Q

What are some examples of collagen diseases?

A

Osteogenesis imperfecta and Ehlers Danlos syndromes

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33
Q

What are the different etiological groups of shock?

A

Septic, haemorrhagic, neurogenic, cardiogenic, anaphylactic

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33
Q

What is the defect in osteogenesis imperfecta?

A

Deficiency or insufficient quantity of type I collagen

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34
Q

What is shock?

A

Insufficient tissue perfusion

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35
Q

What is the mortality rate for patients with severe sepsis?

A

In excess of 40%

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36
Q

What are the hallmarks of the septic process?

A

Excessive inflammation, coagulation, and fibrinolytic suppression

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37
Q

What are the diagnostic criteria for sepsis?

A

Infection triggering Systemic Inflammatory Response Syndrome (SIRS) with specific signs such as abnormal body temperature, elevated heart rate, increased respiratory rate, abnormal white blood cell count, altered mental state, or hyperglycemia

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38
Q

What are the key areas highlighted by the Surviving Sepsis Campaign for sepsis management?

A

Prompt administration of antibiotics, haemodynamic stabilisation, and modulation of the septic response

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39
Q

Which surgical patients are at risk of septic shock?

A

Those with anastomotic leaks, abscesses, and extensive superficial infections such as necrotising fasciitis

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40
Q

What is the recommended approach when performing surgery on patients with septic shock?

A

Undertake the minimum necessary to restore physiology and consider definitive surgery when physiology is restored and clotting has normalized

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41
Q

What is the average blood volume in an adult?

A

5 liters

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42
Q

What are the four major classes of haemorrhagic shock based on blood loss?

A

Class I (<750ml), Class II (750-1500ml), Class III (1500-2000ml), Class IV (>2000ml)

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43
Q

What are the physiological sequelae associated with each class of haemorrhagic shock?

A

Pulse rate, blood pressure, respiratory rate, urine output, and symptoms

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44
Q

What is the recommended level of transfusion to maintain hemoglobin (Hb) levels in trauma patients?

A

Hb of 7-8 for those with no risk factors for tissue hypoxia, and Hb of 10 for those with risk factors

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44
Q

What arterial pressure is required to generate a palpable femoral pulse in trauma patients?

A

> 65mmHg

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44
Q

What is the equation for cardiac index?

A

Cardiac index = Cardiac output / body surface area

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45
Q

What are some other possible causes or concomitant conditions in trauma patients besides haemorrhage?

A

Tension pneumothorax, spinal cord injury, myocardial contusion, cardiac tamponade

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45
Q

What is neurogenic shock?

A

A condition that occurs following spinal cord transection, resulting in decreased sympathetic tone or increased parasympathetic tone, leading to marked vasodilation and decreased peripheral vascular resistance

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46
Q

What is the difference between neurogenic shock and other types of shock?

A

Neurogenic shock requires the use of peripheral vasoconstrictors to return vascular tone to normal

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46
Q

What is the main cause of cardiogenic shock in medical patients?

A

Ischaemic heart disease

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47
Q

What is the main cause of cardiogenic shock in the traumatic setting?

A

Direct myocardial trauma or contusion

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47
Q

What diagnostic tool can be used to determine evidence of pericardial fluid or direct myocardial injury in cardiogenic shock?

A

Transthoracic echocardiography

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48
Q

Where is the most likely site of injury in blunt cardiac injury associated with cardiogenic shock?

A

Right side of the heart, with chamber and/or valve rupture

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49
Q

What is anaphylaxis?

A

A severe, life-threatening, generalized or systemic hypersensitivity reaction

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50
Q

What is the recommended treatment for patients with blunt cardiac injury and cardiogenic shock?

A

Surgery to repair defects, cardiopulmonary bypass, and possibly intra-aortic balloon pump

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51
Q

What is the most important drug in the treatment of anaphylaxis?

A

Adrenaline

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52
Q

What are the recommended doses of adrenaline, hydrocortisone, and chlorpheniramine for anaphylaxis?

A

Doses vary based on age, ranging from 150 mcg to 500 mcg for adrenaline, 25 mg to 200 mg for hydrocortisone, and 250 mcg/kg to 10 mg for chlorpheniramine

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52
Q

Where is the best site for intramuscular injection of adrenaline in anaphylaxis?

A

Anterolateral aspect of the middle third of the thigh

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53
Q

What are some common causes of anaphylaxis?

A

Food (e.g., nuts), drugs, venom (e.g., wasp sting)

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54
Q

What are the three major classes of diuretic drugs based on their site of action in impairing sodium reabsorption?

A

Loop diuretics, thiazide type diuretics, and potassium sparing diuretics

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55
Q

Where do loop diuretics impair sodium reabsorption?

A

In the thick ascending loop of Henle

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56
Q

Where do thiazide type diuretics impair sodium reabsorption?

A

In the distal tubule and connecting segment

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56
Q

Where do potassium sparing diuretics impair sodium reabsorption?

A

In the aldosterone-sensitive principal cells in the cortical collecting tubule

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57
Q

What is the role of Na / K ATPase pumps in the kidney?

A

They return reabsorbed sodium to the circulation and maintain low intracellular sodium levels

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58
Q

Which diuretic acts on the Na /K 2Cl carrier in the ascending limb of the loop of Henle?

A

Frusemide

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59
Q

What percentage of filtered sodium can be excreted by frusemide?

A

Up to 25%

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60
Q

Which diuretic acts on the Na Cl carrier in the distal tubule and connecting segment?

A

Thiazides

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61
Q

What is the range of percentage of filtered sodium excreted by thiazides?

A

Between 3 and 5%

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62
Q

What is the range of percentage of filtered sodium excreted by spironolactone?

A

Between 1 and 2%

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62
Q

Which diuretic acts on the Na /K ATPase pump in the cortical collecting tubule?

A

Spironolactone

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63
Q

What are the functions of the stomach in relation to gastric emptying?

A

Mechanical and immunological functions

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64
Q

What happens during gastric emptying in terms of peristaltic activity and the pyloric sphincter?

A

Peristaltic activity against a closed pyloric sphincter fragments the food bolus material

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65
Q

How does contact with gastric acid contribute to gastric emptying?

A

It helps to neutralize pathogens present

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66
Q

What factors affect the amount of time material spends in the stomach?

A

Composition and volume of the material

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67
Q

What effect do amino acids and fat have on gastric emptying?

A

They both serve to delay gastric emptying

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68
Q

Which neurological system mediates neuronal stimulation of the stomach?

A

The vagus and the parasympathetic nervous system

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69
Q

Why do individuals who have undergone truncal vagotomy require pyloroplasty or gastro-enterostomy?

A

To prevent delayed gastric emptying

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70
Q

Which hormones are involved in delaying gastric emptying?

A

Gastric inhibitory, cholecystokinin, and enteroglucagon

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71
Q

Which hormone is involved in increasing gastric emptying?

A

Gastrin

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72
Q

What are some consequences of diseases affecting gastric emptying?

A

Bacterial overgrowth, retained food, formation of bezoars, dyspepsia, reflux, and foul smelling belches of gas

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72
Q

How can gastric surgery affect gastric emptying?

A

It can cause delayed emptying, especially if the vagus nerve is disrupted

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73
Q

What is the impact of vagal disruption during an oesophagectomy on gastric emptying?

A

Opinions among surgeons vary, with some routinely performing a pyloroplasty and others not

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74
Q

How does the type of anastomosis performed during a distal gastrectomy affect emptying?

A

A posterior, retrocolic gastroenterostomy will empty better than an anterior one

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75
Q

What is diabetic gastroparesis?

A

A condition characterized by poor stomach emptying due to neuropathy affecting the vagus nerve

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76
Q

How is diabetic gastroparesis diagnosed?

A

Through upper GI endoscopy, contrast studies, and in some cases, a radio nucleotide scan

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77
Q

Why are drugs like metoclopramide less effective in treating gastroparesis caused by neuropathy?

A

Because they exert their effect via the vagus nerve, which is affected by the neuropathy

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77
Q

Which prokinetic drug can be used to treat gastroparesis that does not rely on the vagus nerve?

A

The antibiotic erythromycin

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78
Q

How can distal gastric cancer and pancreatic malignancies affect gastric emptying?

A

They can obstruct the pylorus and delay emptying

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79
Q

What is the treatment for gastric emptying delays caused by malignancies?

A

Gastric decompression using a nasogastric tube, insertion of a stent, or surgical gastroenterostomy

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80
Q

What is congenital hypertrophic pyloric stenosis?

A

A disease typically occurring in infancy, characterized by projectile non-bile stained vomiting

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81
Q

How is congenital hypertrophic pyloric stenosis treated?

A

With a pyloromyotomy, either through open surgery or laparoscopy

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82
Q

Where are corticosteroids synthesized from?

A

Cholesterol within the adrenal cortex

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83
Q

Where do corticosteroids bind within cells?

A

To specific intracellular glucocorticoid receptors located on the nucleus

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84
Q

What are the metabolic effects of glucocorticoids?

A

Decreased glucose uptake and utilization, increased gluconeogenesis, and hyperglycemia; increased protein catabolism; permissive effect on lipolytic hormones

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85
Q

What is the regulatory action of glucocorticoids?

A

They have a negative feedback action on the hypothalamus, reducing the release of endogenous glucocorticoids

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86
Q

What effects do glucocorticoids have on the cardiovascular system?

A

They cause decreased vasodilation and decreased fluid exudation

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87
Q

How do glucocorticoids affect bone activity?

A

They decrease osteoblastic activity and increase osteoclastic activity

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88
Q

What are the effects of glucocorticoids on inflammation and immune response?

A

They decrease acute and chronic inflammation by reducing the influx and activity of leukocytes; they also decrease clonal expansion of B and T lymphocytes

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88
Q

How can the approximate cerebral perfusion pressure (CPP) be calculated?

A

CPP = Mean arterial pressure - Intra cranial pressure

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89
Q

What is the formula for estimating the mean arterial pressure (MAP)?

A

MAP = diastolic blood pressure + 1/3 (systolic blood pressure - diastolic blood pressure)

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90
Q

What is the cerebral perfusion pressure (CPP) defined as?

A

The net pressure gradient causing blood flow to the brain

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91
Q

What happens if there is a sharp rise in CPP?

A

It may result in a rising intra cranial pressure (ICP)

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92
Q

What happens if there is a fall in CPP?

A

It may result in cerebral ischemia

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93
Q

In what situations may invasive monitoring of ICP and MAP be required?

A

Following trauma, to carefully control the CPP

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94
Q

What are the two pathways that lead to fibrin formation in the coagulation cascade?

A

Intrinsic pathway (components already present in the blood) and extrinsic pathway (needs tissue factor released by damaged tissue)

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94
Q

What is the role of the intrinsic pathway in clotting?

A

It has a minor role in clotting and is activated by subendothelial damage, such as collagen

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95
Q

Which components are involved in the formation of the primary complex in the intrinsic pathway?

A

High-molecular-weight kininogen (HMWK), prekallikrein, and Factor 12

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96
Q

What happens in the intrinsic pathway when prekallikrein is converted to kallikrein and Factor 12 becomes activated?

A

Factor 12 activates Factor 11, which then activates Factor 9

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97
Q

What is the role of the tenase complex in the intrinsic pathway?

A

Factor 9, along with its co-factor Factor 8a, forms the tenase complex, which activates Factor 10

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98
Q

What triggers the extrinsic pathway?

A

Tissue damage, which leads to the release of tissue factor

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99
Q

Which factor is activated when Factor 7 binds to tissue factor in the extrinsic pathway?

A

Factor 9

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100
Q

What is the role of the common pathway in the coagulation cascade?

A

Activated Factor 10 causes the conversion of prothrombin to thrombin, which hydrolyses fibrinogen peptide bonds to form fibrin and also activates factor 13 to form links between fibrin molecules

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101
Q

What is the process of fibrinolysis?

A

Plasminogen is converted to plasmin to facilitate clot resorption

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102
Q

Which factors are affected in the intrinsic, extrinsic, and common pathways?

A

Intrinsic pathway: Factors 8, 9, 11, 12; Extrinsic pathway: Factor 7; Common pathway: Factors 2, 5, 10; Vitamin K dependent Factors: 2, 7, 9, 10

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103
Q

What is pleural pressure?

A

The pressure surrounding the lung, within the pleural space

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103
Q

What is the normal pleural pressure during quiet breathing?

A

Negative, below atmospheric pressure

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104
Q

What are the two sides of the pleura called?

A

Visceral pleura (covers the lung) and parietal pleura (covers the chest wall)

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105
Q

Where do the visceral and parietal pleura meet?

A

At the hilum of the lung

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106
Q

What determines the size of the lung?

A

The difference between alveolar pressure and pleural pressure, or the transpulmonary pressure

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107
Q

How does gravity affect pleural pressure in an upright individual?

A

Pleural pressure is greater (less negative) at the base of the lung compared to the apex

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108
Q

What happens to pleural pressure when an individual lies on their back?

A

Pleural pressure becomes greatest along the back

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108
Q

What can positive pleural pressure during active expiration cause?

A

Temporary collapse of the bronchi and limitation of air flow

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109
Q

What happens to the top and bottom of the lung in terms of transpulmonary pressure during breathing?

A

The top of the lung generally experiences greater transpulmonary pressure, resulting in more expansion and less compliance compared to the bottom of the lung

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110
Q

What is the most common surgical acid-base disorder?

A

Metabolic acidosis

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111
Q

What are the two mechanisms of metabolic acidosis?

A
  1. Gain of strong acid (e.g. diabetic ketoacidosis) 2. Loss of base (e.g. from bowel in diarrhea)
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112
Q

How is the anion gap calculated?

A

By subtracting the sum of chloride (Cl) and bicarbonate (HCO3) from the sum of sodium (Na) and potassium (K): (Na + K) - (Cl + HCO3)

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113
Q

What is a normal anion gap?

A

10-18 mmol/L

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114
Q

What are some causes of metabolic acidosis with a normal anion gap? (hyperchloraemic metabolic acidosis)

A

Gastrointestinal bicarbonate loss (diarrhea, ureterosigmoidostomy, fistula), renal tubular acidosis, drugs (e.g. acetazolamide), ammonium chloride injection, Addison’s disease

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115
Q

What are some causes of metabolic acidosis with a raised anion gap?

A

Lactate (shock, hypoxia), ketones (diabetic ketoacidosis, alcohol), urate (renal failure), acid poisoning (salicylates, methanol)

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116
Q

How is metabolic alkalosis usually caused?

A

By a rise in plasma bicarbonate levels

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117
Q

What are some causes of metabolic alkalosis?

A

Vomiting/aspiration, diuretics, liquorice/carbenoxolone, hypokalemia, primary hyperaldosteronism, Cushing’s syndrome, Bartter’s syndrome, congenital adrenal hyperplasia

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118
Q

What happens when plasma bicarbonate levels rise above 24 mmol/L in metabolic alkalosis?

A

Excess bicarbonate is typically excreted by the kidneys

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119
Q

What is the main cause of metabolic alkalosis?

A

Problems of the kidney or gastrointestinal tract resulting in a loss of hydrogen ions or a gain of bicarbonate

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120
Q

What is the key factor in the mechanism of metabolic alkalosis?

A

Activation of the renin-angiotensin II-aldosterone (RAA) system

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121
Q

What does aldosterone do in the distal convoluted tubule?

A

Causes reabsorption of sodium (Na) in exchange for hydrogen (H)

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122
Q

What can lead to the activation of the RAA system and raised aldosterone levels?

A

Extracellular fluid (ECF) depletion due to vomiting or diuretics, resulting in sodium (Na) and chloride (Cl) loss

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123
Q

What is the usual cause of respiratory acidosis?

A

Rise in carbon dioxide (CO2) levels due to alveolar hypoventilation

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124
Q

What happens in hypokalemia that causes alkalosis?

A

Potassium (K) shifts from cells to the extracellular fluid (ECF), and hydrogen (H) shifts into cells to maintain neutrality

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125
Q

When may renal compensation occur in respiratory acidosis?

A

In compensated respiratory acidosis, where the kidneys attempt to restore acid-base balance

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126
Q

What are some causes of respiratory acidosis?

A

COPD, decompensation in other respiratory conditions (e.g., life-threatening asthma, pulmonary edema), sedative drugs (benzodiazepines, opiate overdose)

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127
Q

What is the cause of respiratory alkalosis?

A

Hyperventilation resulting in excess loss of carbon dioxide (CO2)

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128
Q

What are some causes of respiratory alkalosis?

A

Psychogenic causes (anxiety leading to hyperventilation), hypoxia (pulmonary embolism, high altitude), early salicylate poisoning, CNS stimulation (stroke, subarachnoid hemorrhage, encephalitis), pregnancy

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129
Q

What is the effect of salicylate overdose on acid-base balance?

A

It leads to a mixed respiratory alkalosis and metabolic acidosis. Early stimulation of the respiratory center causes respiratory alkalosis, while later the direct acid effects of salicylates may lead to an acidosis, especially when combined with acute renal failure.

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130
Q

What do the chromaffin cells of the adrenal medulla secrete?

A

Noradrenaline and adrenaline (catecholamines)

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130
Q

How are the chromaffin cells of the adrenal medulla stimulated to secrete their contents?

A

By acetylcholine released by preganglionic sympathetic fibers of the splanchnic nerves

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131
Q

What hormone is secreted by the zona glomerulosa?

A

Aldosterone

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131
Q

What are phaeochromocytomas derived from and what do they secrete?

A

Phaeochromocytomas are derived from the chromaffin cells of the adrenal medulla and secrete both adrenaline and noradrenaline

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132
Q

What are the three histologically distinct zones of the adrenal cortex?

A

Zona glomerulosa (outer zone), zona fasciculata (middle zone), and zona reticularis (inner zone)

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133
Q

What hormones are secreted by the zona fasciculata?

A

Glucocorticoids

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133
Q

Where are glucocorticoids and aldosterone mostly bound in the circulation?

A

To plasma proteins

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133
Q

How are glucocorticoids inactivated and excreted?

A

By the liver

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134
Q

What hormones are secreted by the zona reticularis?

A

Androgens

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135
Q

What information can the jugular vein waveform provide?

A

Information on right atrial pressure and clues to underlying valvular disease

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136
Q

What does a non-pulsatile jugular venous pressure (JVP) indicate?

A

Superior vena caval obstruction

137
Q

What does the ‘a’ wave represent in the jugular vein waveform?

A

Atrial contraction

137
Q

What is Kussmaul’s sign?

A

A paradoxical rise in JVP during inspiration, seen in constrictive pericarditis

138
Q

When is the ‘a’ wave large?

A

When there is increased atrial pressure (e.g., tricuspid stenosis, pulmonary stenosis, pulmonary hypertension)

138
Q

When is the ‘a’ wave absent?

A

In atrial fibrillation

139
Q

What causes Cannon ‘a’ waves in the jugular vein waveform?

A

Atrial contractions against a closed tricuspid valve, seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm, and single chamber ventricular pacing

140
Q

What does the ‘c’ wave in the jugular vein waveform represent?

A

Closure of the tricuspid valve

140
Q

Is the ‘c’ wave normally visible in the jugular vein waveform?

A

No, it is not normally visible

141
Q

What does the ‘v’ wave in the jugular vein waveform represent?

A

Passive filling of blood into the atrium against a closed tricuspid valve

142
Q

When can giant ‘v’ waves be seen in the jugular vein waveform?

A

In tricuspid regurgitation

143
Q

What is the ‘x’ descent in the jugular vein waveform?

A

The fall in atrial pressure during ventricular systole

144
Q

What is the ‘y’ descent in the jugular vein waveform?

A

The opening of the tricuspid valve

145
Q

What happens during phase 0 of the myocardial action potential?

A

Rapid depolarization occurs due to a rapid influx of sodium

146
Q

What happens during phase 1 of the myocardial action potential?

A

Early repolarization occurs due to the efflux of potassium

147
Q

What happens during phase 3 of the myocardial action potential?

A

Final repolarization occurs due to the efflux of potassium

147
Q

What happens during phase 2 of the myocardial action potential?

A

A plateau phase occurs due to a slow influx of calcium

148
Q

How long does cardiac muscle remain contracted compared to skeletal muscle?

A

Cardiac muscle remains contracted 10-15 times longer than skeletal muscle

148
Q

What happens during phase 4 of the myocardial action potential?

A

Restoration of ionic concentrations and resting potential is restored by the Na/K ATPase. There is slow entry of sodium into the cell, decreasing the potential difference until the threshold potential is reached, triggering a new action potential

149
Q

What is the conduction velocity in atrial conduction?

A

Spreads along ordinary atrial myocardial fibers at a velocity of 1 m/sec

150
Q

What is the conduction velocity in AV node conduction?

A

0.05 m/sec

151
Q

What is the conduction velocity in ventricular conduction?

A

Purkinje fibers, which are of large diameter, achieve velocities of 2-4 m/sec. This allows for a rapid and coordinated contraction of the ventricles

152
Q

What is the main function of tumour necrosis factor (TNF)?

A

TNF is a pro-inflammatory cytokine with multiple roles in the immune system

153
Q

Which cells primarily secrete TNF?

A

Macrophages

154
Q

What are the effects of TNF on the immune system?

A

TNF activates macrophages and neutrophils, acts as a costimulator for T cell activation, and is a key mediator of the body’s response to Gram-negative septicaemia

155
Q

What are the receptor types for TNF-alpha?

A

TNF-alpha binds to both the p55 and p75 receptors

156
Q

What are the effects of TNF on fibroblasts?

A

TNF promotes the proliferation of fibroblasts and their production of protease and collagenase

157
Q

What are the endothelial effects of TNF?

A

TNF increases the expression of selectins and the production of platelet activating factor, IL-1, and prostaglandins

158
Q

What are the systemic effects of TNF?

A

TNF causes pyrexia (fever), increased acute phase proteins, and disordered metabolism leading to cachexia (severe weight loss and muscle wasting)

159
Q

What is the role of TNF in the pathogenesis of rheumatoid arthritis?

A

TNF is important in the pathogenesis of rheumatoid arthritis, and TNF blockers (e.g., infliximab, etanercept) are licensed for the treatment of severe rheumatoid arthritis

160
Q

What is the mechanism of action of amiloride?

A

Amiloride blocks the epithelial sodium channel in the distal convoluted tubule

161
Q

What are the two categories of potassium-sparing diuretics?

A

Epithelial sodium channel blockers (amiloride and triamterene) and aldosterone antagonists (spironolactone and eplerenone)

162
Q

What is refeeding syndrome?

A

Refeeding syndrome refers to metabolic abnormalities that occur when a person is fed after a period of starvation

162
Q

What is the mechanism of action of spironolactone?

A

Spironolactone is an aldosterone antagonist that acts in the distal convoluted tubule

162
Q

In what situations is amiloride usually given?

A

Amiloride is usually given with thiazides or loop diuretics as an alternative to potassium supplementation

163
Q

What are the indications for using spironolactone?

A

Spironolactone is used in the treatment of ascites (in patients with cirrhosis and secondary hyperaldosteronism), heart failure, nephrotic syndrome, and Conn’s syndrome

164
Q

What is the typical dosage of spironolactone for conditions like ascites?

A

Relatively large doses such as 100 or 200 mg are often used for conditions like ascites

165
Q

What are the metabolic consequences of refeeding syndrome?

A

The metabolic consequences of refeeding syndrome include hypophosphatemia, hypokalemia, hypomagnesemia, and abnormal fluid balance

165
Q

What can these abnormalities lead to?

A

These abnormalities can lead to organ failure

166
Q

What are the high-risk factors for refeeding problems?

A

High-risk factors for refeeding problems include a BMI < 16 kg/m², unintentional weight loss > 15% over 3-6 months, little nutritional intake > 10 days, and hypokalemia, hypophosphatemia, or hypomagnesemia prior to feeding (unless high)

167
Q

What are the moderate-risk factors for refeeding problems?

A

Moderate-risk factors for refeeding problems include a BMI < 18.5 kg/m², unintentional weight loss > 10% over 3-6 months, little nutritional intake > 5 days, and a history of alcohol abuse, drug therapy (including insulin, chemotherapy, diuretics, and antacids)

168
Q

What is the recommended approach for refeeding in high-risk patients?

A

For high-risk patients, refeeding should start at < 50% energy and protein levels, and the caloric intake should be increased gradually over 4-7 days

168
Q

What are the recommended supplements during refeeding?

A

During refeeding, oral thiamine (200-300mg/day), vitamin B complex, and additional K (2-4 mmol/kg/day), phosphate (0.3-0.6 mmol/kg/day), and magnesium (0.2-0.4 mmol/kg/day) should be given

169
Q

When should refeeding be initiated?

A

Refeeding should be initiated immediately before and during feeding

170
Q

What is the recommended prescription for refeeding?

A

Start at up to 10 kcal/kg/day and increase to full needs over 4-7 days

171
Q

What is the relationship between potassium and hydrogen ions?

A

Potassium and hydrogen ions can be thought of as competitors

172
Q

What is the association between hyperkalemia and acidosis?

A

Hyperkalemia tends to be associated with acidosis because as potassium levels rise, fewer hydrogen ions can enter the cells

173
Q

What are the causes of hypokalemia with alkalosis?

A

The causes of hypokalemia with alkalosis include vomiting, diuretics, Cushing’s syndrome, and Conn’s syndrome (primary hyperaldosteronism)

174
Q

What are the causes of hypokalemia with acidosis?

A

The causes of hypokalemia with acidosis include diarrhea, renal tubular acidosis, acetazolamide, and partially treated diabetic ketoacidosis

175
Q

What is the composition of plasma, commonly used intravenous fluids?

A

Plasma: Na (137-147 mmol), K (4-5.5 mmol), Cl (95-105 mmol), Bicarbonate (22-25 mmol), Lactate (-)

176
Q

What is the composition of 0.9% Saline, a commonly used intravenous fluid?

A

0.9% Saline: Na (153 mmol), K (-), Cl (153 mmol), Bicarbonate (-), Lactate (-)

177
Q

What is the composition of Hartmans, a commonly used intravenous fluid?

A

Hartmans: Na (130 mmol), K (4 mmol), Cl (110 mmol), Bicarbonate (-), Lactate (28 mmol)

177
Q

What is the composition of Dextrose/saline, a commonly used intravenous fluid?

A

Dextrose/saline: Na (30.6 mmol), K (-), Cl (30.6 mmol), Bicarbonate (-), Lactate (-)

178
Q

Why did the 2013 NICE guidelines not specifically address intraoperative fluid administration?

A

Intraoperative fluid administration does not lend itself to rigid algorithms

179
Q

What was the historical approach to perioperative fluid administration?

A

Historically, patients received large volumes of saline-rich solutions perioperatively

180
Q

What are the drawbacks of administering large volumes of saline-rich solutions?

A

Administering large volumes of saline-rich solutions can lead to sodium load clearance taking up to 36 hours or more, which can have deleterious effects on tissues, such as the development of edema, poor perfusion, increased risk of ileus, and wound breakdown

181
Q

What approach is now practiced for fluid administration in the perioperative period?

A

A tailored approach to fluid administration is now practiced, with greater usage of cardiac output monitors to provide goal-directed fluid therapy

182
Q

Vitamin deficiency

A

Vitamin deficiency
Vitamin Effect of deficiency
A: Night blindness
Epithelial atrophy
Infections
B1: Beriberi
B2: Dermatitis and photosensitivity
B3: Pellagra
B12: Pernicious anaemia
C: Poor wound healing
Impaired collagen synthesis
D: Rickets (Children)
Osteomalacia (Adults)
K: Clotting disorders

183
Q

What is packed red cells used for?

A

Packed red cells are used for transfusion in chronic anemia and cases where infusion of large volumes of fluid may result in cardiovascular compromise

183
Q

How is platelet-rich plasma prepared?

A

Platelet-rich plasma is prepared by high-speed centrifugation

184
Q

What is fresh frozen plasma?

A

Fresh frozen plasma is prepared from single units of blood and contains clotting factors, albumin, and immunoglobulin

185
Q

What is the usual dose of fresh frozen plasma?

A

The usual dose of fresh frozen plasma is 12-15ml/Kg

186
Q

What is cryoprecipitate?

A

Cryoprecipitate is formed from the supernatant of fresh frozen plasma and is a rich source of Factor VIII and fibrinogen

187
Q

What is SAG-Mannitol Blood?

A

SAG-Mannitol Blood is a blood product where all plasma is removed from a blood unit and substituted with sodium chloride, adenine, anhydrous glucose, and mannitol

188
Q

What are cell saver devices?

A

Cell saver devices collect a patient’s own blood lost during surgery and re-infuse it

189
Q

What are the two main types of cell saver devices?

A

The two main types of cell saver devices are those that wash the blood cells prior to re-infusion and those that do not wash the blood prior to re-infusion

189
Q

What is the advantage of using a cell saver device that does not wash the blood prior to re-infusion?

A

The main advantage of using a cell saver device that does not wash the blood prior to re-infusion is that it avoids the use of blood from donors and may reduce the risk of bloodborne infection

190
Q

What is the contraindication for using a cell saver device in malignant disease?

A

The contraindication for using a cell saver device in malignant disease is the risk of facilitating disease dissemination

190
Q

What is adrenaline?

A

Adrenaline is a catecholamine derived from phenylalanine and tyrosine. It functions as both a neurotransmitter and a hormone.

191
Q

What are the actions of adrenaline on α adrenergic receptors?

A

Adrenaline inhibits insulin secretion by the pancreas, stimulates glycogenolysis in the liver and muscle, and stimulates glycolysis in muscle.

192
Q

What are the actions of adrenaline on β adrenergic receptors?

A

Adrenaline stimulates glucagon secretion in the pancreas, stimulates ACTH release, and stimulates lipolysis by adipose tissue.

193
Q

Where is somatostatin produced?

A

Somatostatin is produced in the D cells of the pancreatic islets, as well as in the gut (enterochromaffin cells) and brain tissue.

194
Q

What stimulates somatostatin secretion?

A

Substances that stimulate insulin release also induce somatostatin secretion.

195
Q

What are the functions of somatostatin?

A

Somatostatin acts as an inhibitor of growth hormone, delays gastric emptying, reduces gastrin secretion, and reduces pancreatic exocrine secretions.

196
Q

How is somatostatin used therapeutically?

A

Somatostatin may be used therapeutically to treat pancreatic fistulae.

196
Q

What are the clinical manifestations associated with somatostatinomas?

A

Somatostatinomas can result in the clinical manifestations of diabetes mellitus, gallstones, and steatorrhea.

196
Q

What are somatostatinomas?

A

Somatostatinomas are rare pancreatic endocrine tumors.

197
Q

What are the main causes of hypercalcemia?

A

The main causes of hypercalcemia include malignancy (most common in hospital in-patients) and primary hyperparathyroidism (commonest in non-hospitalized patients).

198
Q

What are some less common causes of hypercalcemia?

A

Less common causes of hypercalcemia include sarcoidosis (extrarenal synthesis of calcitriol), thiazides, lithium, immobilization, Paget’s disease, vitamin A/D toxicity, thyrotoxicosis, MEN (multiple endocrine neoplasia), and milk alkali syndrome.

199
Q

What are the clinical features associated with hypercalcemia?

A

The clinical features associated with hypercalcemia are summarized as “stones, bones, abdominal groans, and psychic moans.” High serum calcium levels can lead to decreased neuronal excitability, resulting in sluggish reflexes, muscle weakness, and constipation.

200
Q

What gas is commonly used to test the rate of diffusion in the transfer factor?

A

Carbon monoxide is commonly used to test the rate of diffusion in the transfer factor.

200
Q

What does the transfer factor measure?

A

The transfer factor measures the rate at which a gas diffuses from the alveoli into the blood.

201
Q

How can the results of the transfer factor be reported?

A

The results of the transfer factor can be reported as the total gas transfer (TLCO) or as the transfer coefficient corrected for lung volume (KCO).

202
Q

What are some causes of a raised TLCO?

A

Causes of a raised TLCO include asthma, pulmonary hemorrhage (such as Wegener’s and Goodpasture’s syndrome), left-to-right cardiac shunts, polycythemia, hyperkinetic states, male gender, and exercise.

202
Q

What are some causes of a lower TLCO?

A

Causes of a lower TLCO include pulmonary fibrosis, pneumonia, pulmonary emboli, pulmonary edema, emphysema, anemia, and low cardiac output.

203
Q

What tends to happen to the KCO with age?

A

The KCO tends to increase with age.

204
Q

Which conditions may cause an increased KCO with a normal or reduced TLCO?

A

Conditions such as pneumonectomy/lobectomy, scoliosis/kyphosis, neuromuscular weakness, and ankylosis of costovertebral joints (e.g., ankylosing spondylitis) may cause an increased KCO with a normal or reduced TLCO.

204
Q

How much fluid enters the small bowel as gastrointestinal secretions in addition to oral intake?

A

In addition to oral intake, a further 8000ml of fluid enters the small bowel as gastrointestinal secretions.

205
Q

What is the process of intestinal water absorption related to?

A

Intestinal water absorption is a passive process that is related to solute load.

206
Q

How does water flow across the jejunum?

A

In the jejunum, water flows across by creating a concentration gradient through the active absorption of glucose and amino acids.

207
Q

How is most water absorbed in the ileum?

A

In the ileum, most water is absorbed through facilitated diffusion with sodium.

207
Q

How much water enters the colon daily?

A

Approximately 150ml of water enters the colon daily.

208
Q

Can the colon adapt to an increased amount of water absorption?

A

Yes, the colon can adapt to and increase the amount of water absorption following resection.

209
Q

What is the daily production rate of bile?

A

Bile is produced at a rate of between 500ml and 1500ml per day.

209
Q

What are the components of bile?

A

Bile is composed of bile salts, bicarbonate, cholesterol, steroids, and water.

210
Q

What are the three main factors regulating bile flow?

A

The three main factors regulating bile flow are hepatic secretion, gall bladder contraction, and sphincter of Oddi resistance.

211
Q

Where are bile salts absorbed and recycled?

A

Bile salts are absorbed in the terminal ileum and recycled back to the liver.

211
Q

What are the primary bile salts?

A

The primary bile salts are cholate and chenodeoxycholate.

212
Q

What is the pathophysiology of gallstones?

A

Excessive quantities of cholesterol in bile cannot be transported properly, leading to the formation of cholesterol-rich gallstones.

212
Q

What are the secondary bile salts and how are they formed?

A

The secondary bile salts, deoxycholate and lithocholate, are formed by bacterial action on primary bile salts.

213
Q

What are some factors that regulate plasma potassium levels?

A

Plasma potassium levels are regulated by factors such as aldosterone, acid-base balance, and insulin levels.

214
Q

What is the association between metabolic acidosis and hyperkalemia?

A

Metabolic acidosis is associated with hyperkalemia because hydrogen and potassium ions compete for exchange with sodium ions across cell membranes and in the distal tubule.

215
Q

What ECG changes can be seen in hyperkalemia?

A

ECG changes in hyperkalemia include tall-tented T waves, small P waves, widened QRS complex leading to a sinusoidal pattern, and asystole.

216
Q

What are some causes of hyperkalemia?

A

Causes of hyperkalemia include acute renal failure, certain drugs (such as potassium-sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, and heparin), metabolic acidosis, Addison’s disease, tissue necrosis/rhabdomyolysis (due to burns or trauma), and massive blood transfusion.

217
Q

Which foods are high in potassium?

A

Foods that are high in potassium include salt substitutes (which contain potassium instead of sodium), bananas, oranges, kiwi fruit, avocado, spinach, and tomatoes.

218
Q

How can beta-blockers potentially cause hyperkalemia in renal failure patients?

A

Beta-blockers can interfere with potassium transport into cells and potentially cause hyperkalemia in renal failure patients. It is important to remember that beta-agonists, such as Salbutamol, are sometimes used as emergency treatment.

219
Q

Can both unfractionated and low-molecular weight heparin cause hyperkalemia?

A

Yes, both unfractionated and low-molecular weight heparin can cause hyperkalemia. This is thought to be caused by the inhibition of aldosterone secretion.

220
Q

What are some neurological conditions that can cause SIADH?

A

Neurological conditions that can cause SIADH include stroke, subarachnoid hemorrhage, subdural hemorrhage, and infections such as meningitis, encephalitis, or abscess.

220
Q

What are some malignancies associated with syndrome of inappropriate antidiuretic hormone (SIADH)?

A

Malignancies associated with SIADH include small cell lung cancer, as well as cancers of the pancreas and prostate.

221
Q

Which infections can be associated with SIADH?

A

Infections such as tuberculosis and pneumonia can be associated with SIADH.

221
Q

What is another cause of SIADH?

A

Positive end-expiratory pressure (PEEP) and porphyrias can also cause SIADH.

222
Q

Which drugs can cause SIADH?

A

Drugs such as sulfonylureas, SSRIs, tricyclic antidepressants, carbamazepine, vincristine, and cyclophosphamide can cause SIADH.

223
Q

What is the principle behind the regulation of pressure within the cranium?

A

The pressure within the cranium is governed by the Monroe-Kelly doctrine, which considers the skull as a closed box.

224
Q

How does the body compensate for increases in mass within the skull?

A

Increases in mass within the skull can be accommodated by the loss of cerebrospinal fluid (CSF).

225
Q

What happens once a critical point is reached in terms of CSF loss?

A

Once a critical point is reached (usually 100-120ml of CSF lost), there can be no further compensation and intracranial pressure (ICP) rises sharply.

226
Q

What occurs when pressure within the cranium equates with mean arterial pressure (MAP)?

A

When pressure within the cranium equates with MAP, neuronal death occurs, and herniation may also accompany this process.

226
Q

How does the central nervous system (CNS) regulate its own blood supply?

A

The CNS can autoregulate its own blood supply through vasoconstriction and vasodilation of the cerebral blood vessels.

227
Q

What can happen if blood pressure exceeds the capacity of autoregulation?

A

If blood pressure exceeds the capacity of autoregulation, there is an increased risk of stroke.

228
Q

How is a normal flow volume loop often described?

A

A normal flow volume loop is often described as a ‘triangle on top of a semi circle.’

229
Q

What is the most suitable way of assessing compression of the upper airway?

A

Flow volume loops are the most suitable way of assessing compression of the upper airway.

230
Q

Which drugs can cause tubular necrosis or interstitial nephritis, leading to haematuria?

A

Drugs such as aminoglycosides and chemotherapy can cause tubular necrosis, while penicillin, sulphonamides, and NSAIDs can cause interstitial nephritis, both of which can result in haematuria.
Anticoagulants
Rifampicin, phenytoin, levodopa, methyldopa, and quinine
*Consumption of beetroot

231
Q

What is an extradural haematoma?

A

An extradural haematoma is bleeding into the space between the dura mater and the skull. It often results from acceleration-deceleration trauma or a blow to the side of the head. The majority of extradural haematomas occur in the temporal region where skull fractures cause a rupture of the middle meningeal artery.

232
Q

How do the symptoms of a subdural haematoma differ from an extradural haematoma?

A

The onset of symptoms is slower in a subdural haematoma compared to an extradural haematoma.

232
Q

What are the features of an extradural haematoma?

A

Extradural haematomas can cause raised intracranial pressure, and some patients may exhibit a lucid interval.

233
Q

What is a subdural haematoma?

A

A subdural haematoma is bleeding into the outermost meningeal layer. It most commonly occurs around the frontal and parietal lobes and may be either acute or chronic. Risk factors include old age and alcoholism.

233
Q

What is a subarachnoid haemorrhage?

A

A subarachnoid haemorrhage usually occurs spontaneously in the context of a ruptured cerebral aneurysm but may also be seen in association with other injuries in cases of traumatic brain injury.

234
Q

What are the types of primary brain injury?

A

Primary brain injury can be focal, such as contusion or haematoma, or diffuse, such as diffuse axonal injury.

234
Q

How does diffuse axonal injury occur?

A

Diffuse axonal injury occurs as a result of mechanical shearing following deceleration, causing disruption and tearing of axons.

235
Q

What are some examples of intra-cranial haematomas?

A

Intra-cranial haematomas can be extradural, subdural, or intracerebral.

236
Q

What occurs in a coup-contrecoup injury?

A

In coup-contrecoup injury, contusions may occur adjacent to the side of impact (coup) or contralateral to the side of impact (contrecoup).

237
Q

What is secondary brain injury?

A

Secondary brain injury occurs when cerebral edema, ischemia, infection, tonsillar or tentorial herniation exacerbates the original injury. The normal cerebral autoregulatory processes are disrupted following trauma, rendering the brain more susceptible to blood flow changes and hypoxia.

238
Q

What is the Cushings reflex?

A

The Cushings reflex, characterized by hypertension and bradycardia, often occurs late and is usually a preterminal event in head injury patients.

239
Q

What is the management approach for life-threatening rising intracranial pressure, such as in extradural haematoma?

A

IV mannitol/frusemide may be required while the theatre is prepared or transfer is arranged.

239
Q

What may be required for diffuse cerebral edema?

A

Decompressive craniotomy may be required for diffuse cerebral edema.

240
Q

What is the role of exploratory burr holes in modern practice?

A

In modern practice, exploratory burr holes have little management use, except in situations where scanning may be unavailable and to facilitate the creation of a formal craniotomy flap.

240
Q

How should open depressed skull fractures be managed?

A

Open depressed skull fractures require formal surgical reduction and debridement.

241
Q

How can closed depressed skull fractures be managed?

A

Closed depressed skull fractures may be managed non-operatively if there is minimal displacement.

241
Q

When is ICP monitoring appropriate?

A

ICP monitoring is appropriate in patients with a Glasgow Coma Scale (GCS) score of 3-8 and a normal CT scan.

242
Q

When is ICP monitoring mandatory?

A

ICP monitoring is mandatory in patients with a GCS score of 3-8 and an abnormal CT scan.

243
Q

What is the most likely cause of hyponatremia in head injury patients?

A

Hyponatremia is most likely due to the syndrome of inappropriate ADH secretion.

244
Q

What is the minimum cerebral perfusion pressure in adults?

A

The minimum cerebral perfusion pressure in adults should be at least 70 mmHg.

245
Q

What is the interpretation of bilaterally dilated pupils with sluggish or fixed light response?

A

Bilaterally dilated pupils with sluggish or fixed light response indicate poor CNS perfusion.

245
Q

What is the minimum cerebral perfusion pressure in children?

A

The minimum cerebral perfusion pressure in children should be between 40 and 70 mmHg.

246
Q

What is the interpretation of unilaterally dilated pupil with sluggish or fixed light response?

A

Unilaterally dilated pupil with sluggish or fixed light response indicates 3rd nerve compression secondary to tentorial herniation.

247
Q

What does bilateral 3rd nerve palsy indicate?

A

Bilateral 3rd nerve palsy can be observed in head injuries.

248
Q

What is the interpretation of unilaterally dilated or equal pupils with cross-reactive (Marcus-Gunn) response?

A

Unilaterally dilated or equal pupils with cross-reactive (Marcus-Gunn) response suggest optic nerve injury.

249
Q

What does bilaterally constricted pupils indicate?

A

Bilaterally constricted pupils may be difficult to assess, but they can be observed in cases of opiate use, pontine lesions, or metabolic encephalopathy.

249
Q

What is the interpretation of unilaterally constricted pupils with preserved light response?

A

Unilaterally constricted pupils with preserved light response suggest sympathetic pathway disruption.

250
Q

What can hypomagnesemia cause and affect in patients?

A

Hypomagnesemia can both cause hypocalcemia and render patients unresponsive to treatment with calcium and vitamin D supplementation.

250
Q

What is the role of magnesium in relation to PTH secretion and its action on target tissues?

A

Magnesium is required for both PTH secretion and its action on target tissues.

250
Q

What is the abundance of magnesium in the body?

A

Magnesium is the fourth most abundant cation in the body, with a total of 1000 mmol.

251
Q

How is magnesium regulated in the body?

A

There is no one specific hormonal control of magnesium, but various hormones including PTH and aldosterone affect the renal handling of magnesium.

251
Q

How do magnesium and calcium interact at a cellular level?

A

Magnesium and calcium interact at a cellular level, and decreased magnesium levels can affect the permeability of cellular membranes to calcium, resulting in hyperexcitability.

252
Q

What percentage of cortisol is protein bound?

A

90% of cortisol is protein bound.

253
Q

Where is magnesium primarily distributed in the body?

A

Half of the magnesium is contained in bone, while the remainder is distributed in muscle, soft tissues, and extracellular fluid.

254
Q

What is the pattern of cortisol release throughout the day?

A

Cortisol follows a circadian rhythm, with higher levels in the mornings.

255
Q

What percentage of cortisol is active?

A

10% of cortisol is active.

256
Q

How does cortisol regulate its own production?

A

Cortisol exerts negative feedback on ACTH (adrenocorticotropic hormone) to regulate its own production.

257
Q

What are the actions of cortisol?

A

Cortisol has several actions, including glycogenolysis, gluconeogenesis, protein catabolism, lipolysis, stress response, anti-inflammatory effects, decrease in protein in bones, increase in gastric acid, increase in neutrophils/platelets/red blood cells, and inhibition of fibroblastic activity.

258
Q

Where does pancreatic cancer mainly occur?

A

Pancreatic cancer mainly occurs in the head of the pancreas (70%).

258
Q

What are the risk factors for pancreatic cancer?

A

The risk factors for pancreatic cancer include smoking, diabetes, adenoma, and familial adenomatous polyposis.

259
Q

How does pancreatic cancer spread?

A

Pancreatic cancer spreads locally and metastasizes to the liver.

260
Q

What are the clinical features of pancreatic cancer?

A

Clinical features of pancreatic cancer include weight loss, painless jaundice, epigastric discomfort (late feature due to invasion of the coeliac plexus), pancreatitis, and Trousseau’s sign (migratory superficial thrombophlebitis).

261
Q

What is the management approach for pancreatic cancer in the head of the pancreas?

A

Whipple’s resection is the main surgical approach for pancreatic cancer in the head of the pancreas. Newer techniques include pylorus preservation and SMA/SMV resection.

261
Q

What are the recommended investigations for pancreatic cancer?

A

Recommended investigations for pancreatic cancer include USS (may miss small lesions), CT scanning (pancreatic protocol), PET/CT for operable disease, ERCP/MRI for bile duct assessment, and staging laparoscopy to exclude peritoneal disease.

262
Q

What is the management approach for pancreatic cancer in the body and tail?

A

Pancreatic cancer in the body and tail has a poor prognosis. If operable, distal pancreatectomy is performed.

263
Q

What is the usual treatment for resectable pancreatic cancer?

A

Resectable pancreatic cancer usually requires adjuvant chemotherapy.

263
Q

How can jaundice be managed in pancreatic cancer?

A

ERCP and stent placement can be used for jaundice management and palliation.

264
Q

When is surgical bypass needed for pancreatic cancer?

A

Surgical bypass may be needed for duodenal obstruction in pancreatic cancer cases.

265
Q

How is lung compliance defined?

A

Lung compliance is defined as the change in lung volume per unit change in airway pressure.

266
Q

What are the causes of increased lung compliance?

A

The causes of increased lung compliance include age and emphysema, which is due to the loss of alveolar walls and associated elastic tissue.

267
Q

What are the causes of decreased lung compliance?

A

The causes of decreased lung compliance include pulmonary edema, pulmonary fibrosis, pneumonectomy (removal of a lung), and kyphosis (abnormal curvature of the spine).

267
Q

Which part of the brain is the main center for thermoregulation?

A

The hypothalamus is the main center for thermoregulation.

268
Q

What role do central thermoreceptors play in maintaining core temperature?

A

Central thermoreceptors play the main role in maintaining core temperature.

268
Q

What involuntary motor responses can the hypothalamus initiate to raise body temperature?

A

The hypothalamus can initiate involuntary motor responses, such as shivering, to raise body temperature.

269
Q

What other responses does the hypothalamus stimulate to raise body temperature?

A

The hypothalamus also stimulates the sympathetic nervous system to produce peripheral vasoconstriction and the release of adrenaline from the adrenal medulla.

270
Q

What is the range of the thermoneutral zone?

A

The thermoneutral zone ranges from 25 to 30 degrees, although the absolute value depends on atmospheric humidity.

270
Q

How is heat loss controlled in thermoregulation?

A

Heat loss is governed by behavioral responses and autonomic responses, including peripheral vasodilation.

271
Q

What happens during sepsis in relation to thermoregulation?

A

During sepsis, the release of cytokines resets the thermoregulatory center, resulting in fever.

272
Q

Where is the spleen located in the abdomen?

A

The spleen is located in the left upper quadrant of the abdomen.

272
Q

What is the typical size of an adult spleen?

A

The typical adult spleen is 12.5cm long and 7.5cm wide, weighing around 150g.

273
Q

Is the normal spleen palpable?

A

No, the normal spleen is not palpable.

274
Q

What structures separate the spleen from the 9th, 10th, and 11th ribs?

A

The spleen is separated from the ribs by both the diaphragm and pleural cavity.

274
Q

How does the shape of the spleen change with gastric and colonic distension?

A

Gastric distension causes the spleen to resemble the shape of an orange segment, while colonic distension makes it more tetrahedral.

275
Q

What ligaments connect the spleen to the posterior abdominal wall and stomach?

A

The spleen is connected to the posterior abdominal wall and stomach by the lienorenal ligament and gastrosplenic ligament.

276
Q

What structures are found within the lienorenal ligament?

A

The splenic vessels lie within the layers of the lienorenal ligament.

277
Q

What structures pass within the layers of the gastrosplenic ligament?

A

The short gastric and left gastroepiploic branches of the splenic artery pass within the layers of the gastrosplenic ligament.

278
Q

What structures are in contact with the lateral side of the spleen?

A

The spleen is in contact with the phrenicocolic ligament laterally.

279
Q

What structures are found at the hilum of the spleen?

A

At the hilum, you can find the tail of the pancreas and the splenic vessels. The splenic artery divides at this point, with its branches passing to the white pulp to transport plasma.

279
Q

What are the functions of the spleen?

A

The functions of the spleen include filtration of abnormal blood cells and foreign bodies, immunity through the production of IgM, properdin, and tuftsin, haematopoiesis during gestation or in haematological disorders, storage of 40% platelets, iron reutilization, and storage of monocytes.

279
Q

What is the function of the white pulp in the spleen?

A

The white pulp in the spleen is responsible for immune function. It contains a central trabecular artery and germinal centers supplied by penicilliary radicles.

280
Q

What is the function of the red pulp in the spleen?

A

The red pulp in the spleen filters abnormal red blood cells.

281
Q

Why do most adult patients with sickle-cell disease have an atrophied spleen?

A

Most adult patients with sickle-cell disease have an atrophied spleen due to repeated infarction.

281
Q

What are some disorders of the spleen?

A

Some disorders of the spleen include massive splenomegaly, myelofibrosis, chronic myeloid leukemia, visceral leishmaniasis (kala-azar), malaria, Gaucher’s syndrome, portal hypertension (secondary to cirrhosis), lymphoproliferative diseases (such as CLL and Hodgkin’s), haemolytic anaemia, infections (such as hepatitis and glandular fever), infective endocarditis, sickle-cell disease, and thalassemia.
Rheumatoid arthritis (Felty’s syndrome)

282
Q

Where is prolactin released from?

A

Prolactin is released from the anterior pituitary.

283
Q

Which hormone has a stimulatory effect on the release of prolactin?

A

Thyrotropin releasing hormone has a stimulatory effect on the release of prolactin.

284
Q

Besides stimulating milk production, what other effect does prolactin have on the body?

A

Prolactin reduces gonadal activity.

284
Q

What hormone inhibits the release of prolactin?

A

Prolactin is under tonic dopamine inhibition.

285
Q

How does prolactin reduce gonadal activity?

A

Prolactin decreases GnRH pulsatility at the hypothalamic level and, to a lesser extent, blocks the action of LH on the ovary or testis.

286
Q

Where is renin secreted from?

A

Renin is secreted by juxtaglomerular cells.

287
Q

What does renin hydrolyze to produce?

A

Renin hydrolyzes angiotensinogen to produce angiotensin I.

288
Q

What are some factors that stimulate renin secretion?

A

Factors that stimulate renin secretion include hypotension causing reduced renal perfusion, hyponatremia, sympathetic nerve stimulation, catecholamines, and assuming an erect posture.

289
Q

What are some factors that reduce renin secretion?

A

Drugs such as beta-blockers and NSAIDs can reduce renin secretion.

289
Q

How does morphine exert its effects?

A

Morphine exerts its effects by binding to the 4 types of opioid receptors within the CNS and gastrointestinal tract.

290
Q

How can morphine be administered?

A

Morphine can be administered orally or intravenously.

290
Q

What are some unwanted side effects of morphine?

A

Unwanted side effects of morphine include nausea, constipation, respiratory depression, and the potential for addiction if used long-term.

291
Q

What are the ECG features of hypokalemia?

A

The ECG features of hypokalemia include U waves, small or absent T waves (occasionally inversion), prolonged PR interval, ST depression, and long QT interval.

291
Q

What is used to reverse the effects of morphine?

A

The effects of morphine can be reversed with naloxone.

292
Q

Can you provide a helpful mnemonic for remembering the ECG features of hypokalemia?

A

Certainly! A helpful mnemonic is: “In Hypokalaemia, U have no Pot and no T, but a long PR and a long QT!”

293
Q

What does the P wave represent?

A

The wave of depolarization that spreads from the SA node throughout the atria.

294
Q

What does the isoelectric period after the P wave represent?

A

The time in which the impulse is traveling within the AV node.

294
Q

How long does the P wave typically last?

A

0.08 to 0.1 seconds (80-100 ms)

295
Q

What is the P-R interval?

A

The time from the onset of the P wave to the beginning of the QRS complex.

296
Q

How long is the normal P-R interval?

A

Ranges from 0.12 to 0.20 seconds in duration.

297
Q

What does the P-R interval represent?

A

The time between the onset of atrial depolarization and the onset of ventricular depolarization.

298
Q

What does the QRS complex represent?

A

Ventricular depolarization.

299
Q

What is the normal duration of the QRS complex?

A

0.06 to 0.1 seconds.

299
Q

What does the ST segment represent?

A

The isoelectric period following the QRS complex.

299
Q

What does the ST segment correspond to?

A

The period in which the entire ventricle is depolarized and corresponds to the plateau phase of the ventricular action potential.

300
Q

What does the T wave represent?

A

Ventricular repolarization and is longer in duration than depolarization.

300
Q

What may follow the T wave?

A

A small positive U wave, which represents the last remnants of ventricular repolarization.

301
Q

What does the Q-T interval represent?

A

The time for both ventricular depolarization and repolarization to occur, roughly estimating the duration of an average ventricular action potential.

301
Q

What is the interval range for the Q-T interval?

A

0.2 to 0.4 seconds, depending on heart rate.

302
Q

How is the Q-T interval corrected for heart rate?

A

By dividing the Q-T interval by the square root of the R-R interval (interval between ventricular depolarizations) to obtain the corrected Q-T (QTc) interval.

303
Q

What is considered a normal corrected Q-Tc interval?

A

Less than 0.44 seconds.

304
Q

What proteins are considered negative acute phase proteins?

A

Albumin, transthyretin (formerly known as prealbumin), transferrin, retinol binding protein, cortisol binding protein.

304
Q

Name some acute phase proteins.

A

CRP, procalcitonin, ferritin, fibrinogen, alpha-1 antitrypsin, caeruloplasmin, serum amyloid A, haptoglobin, complement.

305
Q

Why are CRP levels commonly measured in acutely unwell patients?

A

CRP levels can indicate inflammation or infection in the body.

306
Q

What is the function of CRP?

A

CRP is a protein synthesized in the liver that binds to phosphocholine in bacterial cells and cells undergoing apoptosis. It can activate the complement system.

307
Q

What is the significance of CRP levels greater than 150 at 48 hours postoperatively?

A

Levels above 150 suggest evolving complications following surgery.

308
Q

How is fractional sodium excretion calculated?

A

Fractional sodium excretion = (urine sodium/plasma sodium) / (urine creatinine/plasma creatinine) x 100

309
Q

What are the differences between pre-renal failure and acute tubular necrosis ?

A

Pre-renal uraemia, Acute tubular necrosis:
Urine sodium: < 20 mmol/L, > 30 mmol/L
Fractional sodium excretion:* < 1%, > 1%
Fractional urea excretion:** < 35%, >35%
Urine:plasma osmolality: > 1.5, < 1.1
Urine:plasma urea: > 10:1, < 8:1
Specific gravity: > 1020, < 1010
Urine: ‘bland’ sediment, brown granular casts
Response to fluid challenge: Yes, No

310
Q

What is peristalsis?

A

Peristalsis is the coordinated contraction and relaxation of smooth muscles in the digestive tract that propels food through the digestive system.

310
Q

How is fractional urea excretion calculated?

A

Fractional urea excretion = (urine urea / blood urea) / (urine creatinine / plasma creatinine) x 100

311
Q

What is primary peristalsis?

A

Primary peristalsis is the spontaneous movement of food from the esophagus into the stomach. It takes about 9 seconds.

311
Q

What muscles are involved in peristalsis in the esophagus?

A

Circular smooth muscle contracts behind the food bolus, while longitudinal smooth muscle propels the food through the esophagus.

312
Q

When does secondary peristalsis occur?

A

Secondary peristalsis occurs when food, which doesn’t enter the stomach, stimulates stretch receptors to trigger peristalsis.

313
Q

What happens during peristalsis in the small intestine?

A

In the small intestine, peristalsis waves slow down to a few seconds and help mix the chyme, which is the partially digested food.

314
Q

What are the three main types of peristaltic activity in the colon?

A

The three main types of peristaltic activity in the colon are: segmentation contractions, antiperistaltic contractions towards the ileum, and mass movements.

314
Q

What are segmentation contractions in the colon?

A

Segmentation contractions are localized contractions that exert forces on the bolus to maximize absorption of nutrients by the mucosal lining.

315
Q

What are antiperistaltic contractions towards the ileum in the colon?

A

Antiperistaltic contractions are localized reverse peristaltic waves that slow down the entry of food into the colon. They help maximize absorption in the small intestine.

316
Q

What are mass movements in the colon?

A

Mass movements are migratory peristaltic waves that travel along the entire colon to empty the organ prior to the next ingestion of a food bolus.

MRCS A - Dr Bishoy (58 decks)

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