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MRCS A - Dr Bishoy > 11- Physiology Explains (3) > Flashcards

11- Physiology Explains (3) Flashcards

1
Q

What are the physiological changes in the sympathetic nervous system response to surgery?

A

Blood is diverted from the skin and visceral organs, bronchodilation occurs, intestinal motility is reduced, and there is an increase in glucagon production and glycogenolysis. Insulin levels are reduced. Heart rate and myocardial contractility are increased.

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2
Q

What is the acute phase response in response to surgery?

A

In response to surgery, the release of cytokines such as TNF-α, IL-1, IL-2, IL-6, interferon, and prostaglandins occurs. Excess cytokines may cause systemic inflammatory response syndrome (SIRS). Cytokines also increase the release of acute phase proteins.

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3
Q

How does the endocrine system respond to surgery?

A

The hypothalamus-pituitary-adrenal axis is activated, leading to increased production of ACTH and cortisol. This results in increased protein breakdown, elevated blood glucose levels, increased sodium re-absorption by aldosterone, and increased water re-absorption with vasoconstriction by vasopressin.

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4
Q

What effects does the vascular endothelium have in response to surgery?

A

Nitric oxide produced by the vascular endothelium leads to vasodilation. Platelet activating factor enhances the cytokine response. Prostaglandins also contribute to vasodilation and induce platelet aggregation.

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5
Q

What is von Willebrand’s disease?

A

von Willebrand’s disease is the most common inherited bleeding disorder. It is caused by mutations in the gene for von Willebrand factor, an adhesive glycoprotein secreted by endothelium and megakaryocytes.

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6
Q

What is the role of von Willebrand factor in the body?

A

von Willebrand factor promotes platelet adhesion to damaged endothelium and other platelets. It is also involved in the transport and stabilization of factor VIII.

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7
Q

How many subtypes of von Willebrand disease are there?

A

There are seven subtypes of von Willebrand disease. The most common is type I (autosomal dominant), accounting for 80% of cases. Type 2 von Willebrand disease (autosomal dominant or recessive) accounts for 15% of cases.

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8
Q

What are the symptoms of von Willebrand disease?

A

Symptoms of von Willebrand disease vary in severity, ranging from spontaneous bleeding and epistaxis (nosebleeds) to excessive bleeding following minor procedures.

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9
Q

What is the diagnostic test for von Willebrand disease?

A

The bleeding time test is most typically diagnostic for von Willebrand disease.

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10
Q

What are the treatment options for von Willebrand disease?

A

Tranexamic acid can be administered for minor cases undergoing minor procedures. More significant bleeding or procedures respond well to DDAVP. However, DDAVP is most effective in type I, less effective in type 2, and contraindicated in type 2B. Patients with type 3 disease do not respond to DDAVP as they lack the ability to secrete von Willebrand factor.

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11
Q

What is the treatment option for individuals who cannot have DDAVP or in whom it is contraindicated?

A

For individuals who cannot have DDAVP or in whom it is contraindicated, receive factor VIII concentrates containing vWF.

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12
Q

What are the features or symptoms associated with hypomagnesemia?

A

Some features or symptoms of hypomagnesemia include paraesthesia (tingling or numbness), tetany (muscle spasms), seizures, arrhythmias (abnormal heart rhythms), and decreased parathyroid hormone (PTH) secretion leading to hypocalcemia. ECG features can also resemble those of hypokalemia. Additionally, hypomagnesemia can exacerbate digoxin toxicity.

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13
Q

What are some causes of hypomagnesemia?

A

Hypomagnesemia, or low magnesium levels, can be caused by various factors, including the use of diuretics, total parenteral nutrition, diarrhea, and alcohol consumption. It can also be associated with hypokalemia (low potassium levels) and hypocalcemia (low calcium levels).

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14
Q

What is the role of leptin in the regulation of body weight?

A

Leptin, produced by adipose tissue, plays a key role in regulating body weight. It acts on satiety centers in the hypothalamus, decreasing appetite. In obesity, where there is more adipose tissue, leptin levels are high.

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15
Q

How does leptin affect hormone release?

A

Leptin stimulates the release of melanocyte-stimulating hormone (MSH) and corticotrophin-releasing hormone (CRH). Low levels of leptin stimulate the release of neuropeptide Y (NPY).

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16
Q

What is adrenaline?

A

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

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17
Q

What is the role of ghrelin in hunger and satiety?

A

Unlike leptin, ghrelin stimulates hunger. It is mainly produced by the fundus of the stomach and the pancreas. Ghrelin levels increase before meals and decrease after meals.

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18
Q

Where is adrenaline released from?

A

Adrenaline is released by the adrenal glands.

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18
Q

How does adrenaline affect cardiac output and total peripheral resistance?

A

Adrenaline increases cardiac output and total peripheral resistance.

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19
Q

What are the effects of adrenaline on receptors?

A

Adrenaline has effects on α1 and α2 receptors, as well as β1 and β2 receptors.

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20
Q

What is the effect of adrenaline on β2 receptors in skeletal muscle vessels?

A

Adrenaline causes vasodilation in skeletal muscle vessels through its action on β2 receptors.

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21
Q

What is the effect of adrenaline on α adrenergic receptors?

A

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

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22
Q

What is the effect of adrenaline on β adrenergic receptors?

A

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

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23
Q

Pancreas endocrine physiology
Hormones released from the islets of Langerhans:

A

Beta cells Insulin (70% of total secretions)
Alpha cells Glucagon
Delta cells Somatostatin
F cells Pancreatic polypeptide

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24
Q

Which receptor does morphine attach to?

A

Morphine attaches to mu1 receptors.

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25
Q

Where do opioids bind in the central nervous system (CNS)?

A

Opioids combine to specific opiate receptors in the CNS, specifically in the periaqueductal grey matter, limbic system, and substantia gelatinosa.

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26
Q

How is the anion gap calculated?

A

The formula is: (sodium + potassium) - (bicarbonate + chloride).

27
Q

What is considered a normal anion gap range?

A

A normal anion gap is typically between 8-14 mmol/L.

28
Q

What are some causes of a normal anion gap or hyperchloremic metabolic acidosis?

A

Causes of a normal anion gap or hyperchloremic metabolic acidosis include gastrointestinal bicarbonate loss (e.g., diarrhea, ureterosigmoidostomy, fistula), renal tubular acidosis, drugs like acetazolamide, and ammonium chloride injection. Addison’s disease is also a potential cause.

29
Q

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

A

Causes of a raised anion gap metabolic acidosis include lactate (due to shock or hypoxia), ketones (seen in diabetic ketoacidosis or alcohol-related conditions), urate (associated with renal failure), and acid poisoning (caused by substances like salicylates or methanol).

30
Q

What happens when circulating glucose enters the cell during cellular metabolism?

A

When circulating glucose enters the cell, it undergoes glycolysis, resulting in the generation of ATP and pyruvate.

31
Q

What happens to pyruvate in the presence of oxygen?

A

In the presence of oxygen, pyruvate enters the Krebs cycle, where it undergoes further metabolism to generate additional energy.

32
Q

What happens to pyruvate in the absence of oxygen?

A

When oxygen is limited or absent, pyruvate enters an anaerobic pathway. In this pathway, pyruvate can be converted into lactic acid. This allows glycolysis to continue by keeping pyruvate concentration low and also oxidizes NADH into NAD+ needed by glycolysis.

33
Q

What happens to lactic acid produced during anaerobic respiration?

A

The lactic acid produced during anaerobic respiration diffuses into the plasma and is carried to the liver. In the liver, it can be converted back into pyruvate or glucose through a process called the Cori cycle.

33
Q

Why is anaerobic respiration important in cells?

A

Anaerobic respiration occurs in cells when oxygen is limited or mitochondria are absent or nonfunctional. It is an effective pathway for short-term ATP production, such as in erythrocytes (red blood cells) that lack mitochondria.

34
Q

What happens to pyruvate in the presence of oxygen during cellular metabolism?

A

In the presence of oxygen, pyruvate can enter the Krebs cycle. During this process, additional energy is extracted as electrons are transferred to receptors such as NAD+, GDP, and FAD. Carbon dioxide is produced as a byproduct.

35
Q

What is the role of oxygen in cellular metabolism?

A

Oxygen acts as the terminal electron acceptor in the electron transport chain, the final step of cellular metabolism. It combines with electrons and hydrogen ions to create water inside the mitochondria.

36
Q

What is the difference in ATP generation between oxidative and anaerobic pathways?

A

Oxidative pathways, which occur in the presence of oxygen, yield a total of 36 ATP molecules. This is significantly higher than what can be generated through anaerobic pathways.

37
Q

What is tranexamic acid?

A

Tranexamic acid is a synthetic derivative of lysine.

38
Q

How does tranexamic acid work?

A

Tranexamic acid functions as an antifibrinolytic by competitively inhibiting the conversion of plasminogen to plasmin. This inhibits the degradation of fibrin, thereby slowing down the process.

39
Q

What was the role of tranexamic acid investigated in?

A

Tranexamic acid’s role in trauma was investigated in the CRASH 2 trial.

40
Q

When is tranexamic acid beneficial in bleeding trauma?

A

Tranexamic acid has been shown to be beneficial when administered within the first 3 hours of bleeding trauma.

41
Q

What is stroke volume?

A

Stroke volume refers to the volume of blood ejected from the ventricle during each cycle of cardiac contraction.

42
Q

What is the typical volume of stroke for both ventricles?

A

The volumes for both ventricles are typically equal and approximately 70ml for a 70Kg man.
Stroke volumes range from 55-100ml.

43
Q

How is stroke volume calculated?

A

Stroke volume is calculated by subtracting the end systolic volume from the end diastolic volume.

44
Q

What factors can affect stroke volume?

A

Several factors can influence stroke volume, including cardiac size, contractility, preload, and afterload.

45
Q

Where does potassium secretion occur in the gastrointestinal (GI) tract?

A

Potassium secretion occurs in various parts of the GI tract, including the salivary glands, stomach, bile, pancreas, small bowel, and rectum.

46
Q

What is the average potassium secretion in:
Salivary glands
Stomach
Bile
Pancreas
Small bowel
Rectum

A

Salivary glands Variable may be up to 60mmol/L
Stomach 10 mmol/L
Bile 5 mmol/L
Pancreas 4-5 mmol/L
Small bowel 10 mmol/L
Rectum 30 mmol/L

47
Q

What factors can affect the exact composition of potassium secretions in the GI tract?

A

The exact composition of potassium secretions can vary depending on factors such as the presence of disease, serum aldosterone levels, and serum pH.

48
Q

What is the cause of hypokalemia in vomiting?

A

Hypokalemia in vomiting is usually a result of renal wasting of potassium, not due to potassium loss in vomit itself.

49
Q

What is renin and where is it secreted from?

A

Renin is an enzyme that is secreted by juxtaglomerular cells.

50
Q

What is the function of renin?

A

Renin hydrolyses angiotensinogen to produce angiotensin I, which is a precursor to angiotensin II.

51
Q

What are the factors that stimulate renin secretion?

A

Renin secretion can be stimulated by factors such as hypotension causing reduced renal perfusion, hyponatremia, sympathetic nerve stimulation, catecholamines, and being in an erect posture.

52
Q

What are the factors that reduce renin secretion?

A

Renin secretion can be reduced by certain drugs, such as beta-blockers and NSAIDs.

52
Q

What factors affect free calcium levels?

A

Free calcium levels are affected by pH (increased in acidosis) and plasma albumin concentration.

53
Q

What are the ECG changes associated with hypercalcemia?

A

One of the ECG changes associated with hypercalcemia is the shortening of the QTc interval.

54
Q

When is urgent management indicated for hypercalcemia?

A

Urgent management is indicated if calcium levels are above 3.5 mmol/L, the patient has reduced consciousness, severe abdominal pain, or pre-renal failure.

55
Q

What is the initial management approach for hypercalcemia?

A

The initial management approach includes airway breathing circulation (ABC), intravenous fluid resuscitation with 3-6L of 0.9% normal saline in 24 hours, and concurrent administration of calcitonin to lower calcium levels.

56
Q

What medical therapies are used for hypercalcemia when corrected calcium is above 3.0 mmol/L?

A

Medical therapies used for hypercalcemia include bisphosphonates and analogues of pyrophosphate, which prevent osteoclast attachment to bone matrix and inhibit bone resorption.

57
Q

What are the agents used for medical therapy in hypercalcemia?

A

The agents used for medical therapy in hypercalcemia include IV pamidronate and IV zoledronate.

58
Q

What are the side effects of IV pamidronate?

A

The side effects of IV pamidronate may include pyrexia and leukopenia.

59
Q

How long does the response to IV zoledronate last?

A

The response to IV zoledronate typically lasts for 30 days and is used for malignancy-associated hypercalcemia.

60
Q

In which conditions is prednisolone given for hypercalcemia?

A

Prednisolone may be given in hypercalcemia related to sarcoidosis, myeloma, or vitamin D intoxication.

61
Q

When is calcitonin used in the management of hypercalcemia?

A

Calcitonin has the quickest onset of action but has a short duration, so it is usually given with a second agent for the management of hypercalcemia.

62
Q

What is the main function of the terminal ileum?

A

The main function of the terminal ileum is the absorption of vitamin B12 and bile salts.

63
Q

What can happen if the terminal ileum is resected in surgical patients?

A

In surgical patients, resection of the terminal ileum is common in conditions like terminal ileal Crohn’s disease. When a significant portion of the ileum is removed, patients are at an increased risk of bile salt malabsorption, leading to bile salt diarrhea and an increased risk of gallstones. Additionally, the lack of vitamin B12 absorption may predispose patients to macrocytic anemia.

MRCS A - Dr Bishoy (58 decks)

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