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Gastrointestinal pathophysiology > PBL 53 > Flashcards

PBL 53 Flashcards

1
Q

Where are the adrenal glands found?

A

They are retroperitoneal structures found in the posterior abdomen, immediately superior to the medial aspect of the kidneys and below the diaphragm

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2
Q

What do the adrenal glands secrete?

A

Steroid and catecholamine hormones directly into the blood

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3
Q

Which part of the adrenal glands is covered?

A

The anterior surface is covered by parietal peritoneum

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4
Q

What are the shapes of the kidneys?

A

The right kidney is pyramidal

The left kidney is semi lunar

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5
Q

What is the name of the fascia which encloses the adrenal glands and the kidneys?

A

The perinephric or renal fascia

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6
Q

What do the adrenal glands consist of?

A
  • An outer tissue capsule
  • A cortex
  • A medulla
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7
Q

What is the embryological origin of the adrenal cortex?

A

Embryonic mesoderm

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8
Q

What is the embryological origin of the adrenal medulla?

A

Ectodermal neural crest cells

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9
Q

The adrenal cortex is divided into 3 regions (superficial to deep), what are they?

A
  1. Zona glomerulosa (superficial just beneath the capsule)
  2. Zona fasciculata
  3. Zona reticularis (deepest, just above the medulla)
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10
Q

What is the role of the zona glomerulosa?

A

Produces and secretes mineralocorticoids e.g. aldosterone

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11
Q

What is the role of the zona fasciculata?

A

Produce and secrete corticosteroids such as cortisol and corticosterone
- Also secretes a small amount of androgens

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12
Q

What is the role of the zona reticularis?

A

Produces and secretes androgens such as dihydroepiandrosterone
- Also secretes a small amount of corticosteroids

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13
Q

What is the role of the adrenal medulla?

A

Contains chromaffin cells which secrete catecholamines (A/NA) into the bloodstream in response to stress

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14
Q

What makes up the vascular supply to the adrenal glands?

A
  1. Superior adrenal artery: arises from the inferior phrenic artery
  2. Middle adrenal artery: arises from the abdominal aorta
  3. Inferior adrenal artery: arises from the renal arteries
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15
Q

What is the venous drainage of the adrenal glands?

A

The right adrenal vein drains into the IVC

The left adrenal vein drains into the left renal vein

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16
Q

Which nerve innervates the adrenal glands?

A

Greater splanchnic
Coeliac plexus
- T10 to L1 spinal cord segments

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17
Q

What is the role of cortisol and corticosterone?

A

Regulate carbohydrate metabolism, particularly during times of stress (fight or flight)

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18
Q

What is the major precursor for all steroids?

A

Cholesterol

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19
Q

Which factors increase the rate of aldosterone production within the zona glomerulosa?

A
  1. Increase in plasma Ang-II concentration
  2. Increase in plasma K+ concentration
  3. Decrease in plasma pH (acidosis)
  4. Decreased blood pressure, as detected by atrial stretch receptors
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20
Q

The androgens released by the zona reticularis are converted into what?

A

They are transported to the gonads where they are converted into testosterone or oestrogen

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21
Q

Name some different pathologies associated with the adrenal gland?

A
  • Congenital adrenal hyperplasia
  • Addison’s disease
  • Cushing’s disease
  • Conn’s syndrome
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22
Q

What is congenital adrenal hyperplasia (CAH)?

A

Congenital adrenal hyperplasia (CAH) can result from one of several autosomal recessive diseases, most common cause is the lack of enzyme known as 21-hydroxylase.

There is typically a mutation in an enzyme mediating one of the steps necessary in the production of mineralocorticoids or glucocorticoids from cholesterol. This results in a lack of mineralocorticoids and glucocorticoids, as well as an excess of testosterone and its derivatives.

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23
Q

Clinical features of CAH

A 
Virilisation of female babies
Neonatal salt-losing crisis
Hypotension
Hypoglycaemia
Hyponatraemia
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24
Q

What is Cushing’s syndrome?

A
  • Pathology of the zona fasciculata
  • In a steroid-producing adrenal tumour (or anterior pituitary adenoma) large concentrations of glucocorticoids/cortisol are secreted into the body. Leading to symptoms of high glucocorticoid secretion
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25
Q

Signs of Cushing’s syndrome

A
  • Acne
  • Moon facies
  • Plethora
  • Buffalo hump
  • Hypertension
  • Proximal muscle weakness
  • Hyperpigmentation (in ACTH-dependant causes)
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26
Q

Symptoms of Cushing’s syndrome

A
  • Tiredness
  • Depression
  • Weight gain
  • Easy bruising
  • Amenorrhoea
  • Reduced libido
  • Striae
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27
Q

What is Addison’s disease?

A
  • It is opposite to Cushing’s disease

- Lack of cortisol due to autoimmune destruction or dysfunction of the adrenal cortex causing hypotension and anorexia

28
Q

What is the most common cause of adrenal insufficiency?

A

Autoimmune adrenalitis

29
Q

Why do you get hyperpigmentation in Addison’s disease?

A

The decrease in cortisol leads to an increase in ACTH via negative feedback.

ACTH stems from a precursor molecule called pro-opiomelanocortin (POMC). POMC is also a precursor to Melanocyte Stimulating Hormone (MSH), causes darkening of skin. Therefore, an increase in ACTH, leads to an increase in POMC and as a by-product, an increase in MSH and therefore leads to skin darkening.

30
Q

Signs and symptoms of Addison’s disease

A
  • In women, loss of libido and loss of hair in axillary/pubic regions
  • Muscle wasting
  • Postural hypotension
  • Hyperpigmentation
  • Dehydration
  • Nausea/vomiting
  • Abdominal pain
  • Depression
  • Psychosis
  • Fatigue
31
Q

What is an Addisonian crisis?

A

Caused by a significant deficiency in glucocorticoids and mineralocorticoids.
- It is most commonly seen in tertiary adrenal insufficiency (termed an ‘adrenal crisis’) as a result of the sudden withdrawal of exogenous steroids.

32
Q

Signs and symptoms of an Addisonian crisis

A
  • Confusion
  • Coma
  • Abdominal pain
  • Nausea/vomiting
  • Pyrexia
  • Hypotensive and shocked
  • Hyperpigmentation
33
Q

What is Conn’s syndrome?

A

Conn’s syndrome occurs when patients develop an adenoma (benign tumour) of the zona glomerulosa which secretes excess aldosterone, leading to primary hyperaldosteronism

34
Q

What can Conn’s syndrome lead to and why?

A

This condition is usually asymptomatic, however, some patients will experience muscle cramps, headaches, and lethargy due to electrolyte disturbances.

Most importantly, the increased reabsorption of sodium and water by the kidneys leads to hypertension, which increases the patient’s risk of diseases such as strokes and ischaemic heart disease

35
Q

Causes of Conn’s syndrome?

A
  1. Bilateral idiopathic hyperaldosteronism (60-70%)
  2. Aldosterone-producing adenoma (30-40%)
  3. Unilateral hyperplasia (approx. 3%)
  4. Other (familiar hyperaldosteronism, adrenal carcinoma)
36
Q

How is Conn’s syndrome treated?

A

Conn’s syndrome is usually treated by surgical removal of the tumour (adrenalectomy). The patient may also be given spironolactone (an aldosterone antagonist) to reduce their blood pressure and relieve any symptoms prior to surgery

37
Q

What is phaeochromocytoma?

A

A phaeochromocytoma is a tumour of the adrenal medulla (80-85%) or preganglionic sympathetic neurones (15-20%), especially the chromaffin cells.
- It secretes adrenaline and noradrenaline uncontrollably, leading to constant activation of the flight or fight response, causing blood pressure to greatly increase

38
Q

What may patients with phaeochromocytoma present with?

A

Patients may present with tachycardia, hypertension, anxiety, weight loss, hyperglycaemia, palpitations, headaches and diaphoresis (profuse sweating).

39
Q

What is shock?

A

A state of organ hypoperfusion with resultant cellular dysfunction and death

40
Q

What are the main categories of shock?

A
  • Hypovolaemic
  • Cardiogenic
  • Distributive
41
Q

What is hypovolaemic shock?

A

Shock induced by low fluid volume of blood

42
Q

How can hypovolaemic shock be classified?

A

Haemorrhagic or non-haemorrhagic

43
Q

What is non-haemorrhagic shock?

A

Loss of fluid which is NOT from bleeding

- E.g. stranded in the desert

44
Q

What is haemorrhagic shock?

A

Haemorrhagic means loss of blood volume through ruptured blood volume. Loss of about 20% of total blood volume, approximately 1L can be enough to induce hypovolaemic shock (causes decrease EDV –> decreased SV –> decreased CO –> decreased BP

45
Q

What are the compensatory mechanisms in response to hypovolaemic shock?

A
  • Catecholamine release
  • ADH secretion
  • Ang II secretion

All of these increase cause vasoconstriction of blood vessels, this will increase vascular resistance and heart rate, which increases cardiac output. These combined effects cause an increase in blood pressure.

46
Q

What is MVO2?

A

A good indicator of tissues not getting enough blood due to hypovolaemia is the decreased mixed venous oxygen saturation (MVO2), this is the amount of O2 bound to Hb in blood coming to the RA from the tissues.

This is the amount of leftover oxygen not used by the tissues. If blood volume is low, then there will be low circulating O2 and therefore less O2 left over which means MVO2 will be low in hypovolaemic shock!

47
Q

What happens to the skin temperature in hypovolaemic shock?

A

Since blood flow provides heat to the tissues as well, when it is down it makes the skin feel cold and clammy, therefore it is considered a cold shock.

48
Q

What is cardiogenic shock?

A

When something happens to the heart such that it cannot pump enough blood to the tissues, usually secondary to MI

Heart muscle cells die –> weaker contractions –> decreased SV –> decreased CO –> decreased blood pressure

49
Q

What happens to MVO2 in cardiogenic shock?

A

MVO2 will be down since there is less O2 being pumped out, so less will be left over

50
Q

What happens to skin temperature in cardiogenic shock?

A

Similarly to hypovolaemic shock, reduction in cardiac output leads to reduced blood flow, which means the skin becomes cool and clammy = cold shock

51
Q

What is distributive shock?

A

Where there is typically a leakiness of blood vessels and excessive amounts of peripheral vasodilatation

If arterioles dilate, vascular resistance to blood flow decreases, and blood pressure decreases, so there is less perfusion and distribution of blood to organs and tissues

52
Q

What is the most common form of distributive shock?

A

Septic shock due to pathogens in the blood, most commonly gram-negative ones

53
Q

What is the mechanism for septic shock/meningococcal sepsis?

A

Mechanism: endotoxins (LPS molecules) which are found in the outer membrane of gram neg bacteria causes a cascade of events that leads to lower perfusion:

  1. Directly damage endothelial cells causing them to release vasodilators such as nitric oxide
  2. Activate the complement pathway –> leads to mast cell release of histamine, another vasodilator
  3. Activate macrophages and neutrophils which help create pro-inflammatory cytokines such as TNF and IL-1, these help the immune system destroy the invading pathogens, but they also stimulate the endothelial cells to release more pro-inflammatory molecules such as platelet activating factor and reactive oxygen species
  4. All these inflammatory chemicals damage the endothelial cells, affecting their permeability, making them leaky.
    - Also, endothelial cells express a pro-coagulant called tissue factor, this, alongside a decreased amount of anti-coagulants which are used up during sepsis, causes a net increase in blood clotting in the microvasculature, this will further decrease perfusion!
    - The increased vasodilation, increased vascular permeability and increased microvascular blood clotting all contribute to decreased blood perfusion to vital organs
54
Q

What happens to MVO2 in distributive shock?

A

This widespread vasodilation will cause very vascular low resistance, meaning that blood will move too fast through the vasculature, so it will not be able to unload as much O2, so MVO2 can be normal or even increased.

55
Q

What happens to the skin temperature in septic shock?

A

Increase in flow in peripheral blood vessels causes the skin to become warm and flushed = warm shock

56
Q

What are two subtypes of distributive shock?

A
  1. Anaphylactic shock: allergic reaction leading to low BP

2. Neurogenic shock: damaged CNS which leads to low BP

57
Q

How can reperfusion of cells be damaging?

A

Reperfusion of ischaemic cells can cause further injury.

As substrate is reintroduced, neutrophil activity may increase, increasing production of damaging superoxide and hydroxyl radicals. After blood flow is restored, inflammatory mediators may be circulated to other organs.

58
Q

What is multiple organ dysfunction syndrome (MODS)?

A
  • The combination of direct and reperfusion injury may cause MODS— the progressive dysfunction of ≥ 2 organs consequent to life-threatening illness or injury. MODS can follow any type of shock but is most common when infection is involved; organ failure is one of the defining features of septic shock.
  • MODS also occurs in > 10% of patients with severe traumatic injury and is the primary cause of death in those surviving > 24 hours.
  • Any organ system can be affected, but the most frequent target organ is the lung, in which increased membrane permeability leads to flooding of alveoli and further inflammation.
  • Progressive hypoxia may be increasingly resistant to supplemental oxygen therapy. This condition is termed acute lung injury or, if severe, acute respiratory distress syndrome (ARDS).
  • The kidneys are injured when renal perfusion is critically reduced, leading to acute tubular necrosis and renal insufficiency manifested by oliguria and progressive rise in serum creatinine.
59
Q

Signs and symptoms of hypovolaemic shock

A
  • Skin: cold, pale, slate-grey, slow CRT, ‘clammy’
  • Kidneys: oliguria, anuria
  • Brain: drowsiness, confusion and irritability
  • Tachycardia
  • Weak pulse
  • Sweating
  • Tachypnoea
  • Extreme hypovolaemia may be associated with bradycardia
60
Q

Signs and symptoms of cardiogenic shock

A
  • Skin: cold, pale, slate-grey, slow CRT, ‘clammy’
  • Kidneys: oliguria, anuria
  • Brain: drowsiness, confusion and irritability
  • Raised JVP
  • Gallop rhythm
  • Basal crackles
  • Pulmonary oedema
  • Tachycardia
  • Weak pulse
  • Sweating
  • Tachypnoea
  • Extreme hypovolaemia may be associated with bradycardia
61
Q

Signs and symptoms of distributive shock: anaphylactic

A

• Signs of profound vasodilation

  • warm peripheries
  • low blood pressure
  • tachycardia
  • Erythema, urticaria, angio-oedema, pallor, cyanosis
  • Bronchospasm, rhinitis
  • Oedema of the face, pharynx and larynx
  • Pulmonary oedema
  • Hypovolaemia due to vascular leak
  • Nausea, vomiting, abdominal cramps, diarrhoea.
62
Q

Signs and symptoms of distributive shock: septic shock

A
  • pyrexia and rigors, or hypothermia (unusual, but more common in the elderly and associated with worse prognosis)
  • nausea, vomiting
  • vasodilation, warm peripheries
  • bounding pulse
  • rapid capillary refill
  • hypotension, low diastolic pressure, widened pulse pressure
  • Occasionally, signs of cutaneous vasoconstriction

• Other signs:

  • Jaundice
  • Coma, stupor
  • Bleeding due to coagulopathy (e.g., from vascular puncture sites, gastrointestinal tract and surgical wounds)
  • Rash and meningism
  • Hyperglycaemia; in more severe cases, hypoglycaemia.
63
Q

Clues for sepsis in the elderly

A
  • Mild confusion
  • Tachycardia
  • Tachypnoea
  • Unexplained hypotension
  • Reduction in urine output
  • Risking plasma creatinine
  • Glucose intolerance
64
Q

Management/treatment of shock

A

Initial assessment/management of shock:
ABC response

A) Airway with OXYGEN therapy
- Give high flow oxygen

B) Breathing with VENTILATORY assessment/assistance
- Respiratory exam

C) Circulation with FLUID RESUSCITATION

  • Check peripheral perfusion — cool and clammy vs warm and dry
  • Pulse - volume/rate
  • IV access
  • Fluid challenge is nearly always the first ‘C’ treatment - crystalloids vs colloids

D) Disability

  • Conscious level — AVPU vs GCS
  • Pupils

E) Exposure, environment and other examination
- Causes: revealed bleeding, concealed bleeding, peripheral oedema

65
Q

What is the principal management for patients with shock from pump failure?

A

Inotropes and possibly vasodilators because these patients are very vasoconstricted

66
Q

What is the principle management for patients with distributive shock?

A

Vasopressors: noradrenaline

67
Q

What is the main treatment for sepsis?

A
  1. Antibiotics
  2. Crystalloids
  3. Vasopressors
  4. BUFALO

Gastrointestinal pathophysiology (22 decks)

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