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Physiology Flashcards

1
Q

Define a homeostatic mechanism

A

A regulating mechanism triggered by an alteration in physiological property or quantity, acting to produce a compensatory change in the opposite direction

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2
Q

What organ is responsible for the control of thermoregulation

A

Hypothalamus
Controls both heat production (shivering and increased voluntary effort) and heat loss (change to blood flow, sweating)

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3
Q

Where are temperature sensitive receptors found

A

Anterior hypothalamus

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4
Q

Below what temperature does the temperature regulatory mechanism completely fail

A

<30

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5
Q

What ECG changes can be found in hypothermia

A

J waves

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6
Q

What occurs with spinal cord injuries in regard to thermoregulation

A

Thermoregulatory mechanism lost below the level of injury
Vasoconstriction is lost therefore heat loss is increased
Patient is unable to shiver

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7
Q

What are the two types of diuresis

A

Water diuresis - where there is excess water to the bodies requirement and so water is lost
Osmotic diuresis - where there is more solute than can be absorbed, so it is lost and due to osmosis so is water

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8
Q

How is body osmolality controlled

A

Adjustments in the secretion of ADH
Thirst mediated water intake

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9
Q

Why do the osmotic receptors indicating thirst have a higher threshold than the osmotic receptors involved in ADH release

A

It ensures that thirst is not experienced until ADH release has ensured that the water ingested is retained by the kidneys

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10
Q

Where is most of the filtered sodium in the kidney reabsorbed

A

65% proximal tubule
25% loop of Henle

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11
Q

What are the two important intrarenal affects of Angiotensin II

A

Stimulates sodium reabsorption in most nephron segments
Constricts the glomerular arterioles

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12
Q

Other than increased osmolality what can stimulate thirst and ADH release

A

Reduced arterial blood pressure - signals via carotid and aortic baroceptors
Reduced central venous pressure - signals via martial low pressure receptors
Increased angiotensin II in the brain

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13
Q

What is ANP released in response to

A

Released from the cardiac atria in response to stretch

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14
Q

Briefly outline RAAS

A

Renin, Angiotensin Aldosterone System

Renin released from the juxtaglomerular apparatus in response to reduced sodium, reduced perfusion pressure, direct sympathetic stimulation

Angiotensin I produced, cleaved to produce Angiotensin II - net effect of this is to increase TPR and BP
Stimulates hypothalamus - thirst reflex and posterior pituitary - ADH release

Angiotensin II acts on adrenal cortex to release Aldosterone
Aldosterone acts on the principal cells of the collecting ducts of the nephrons

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15
Q

How does ANP increase the secretion of Na

A

Increases GFR
Inhibits sodium reabsorption on collecting ducts
Reduces the secretion of aldosterone and renin

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16
Q

Causes of hypernatraemia

A

Water depletion - reduced intake, diuretic stage of AKI, diabetes insipidus
Sodium excess - XS sodium therapy, Conn’s syndrome, Cushing’s syndrome, Steroid, CCF, Cirrhosis

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17
Q

Causes of hyperkalaemia

A

Renal failure
Haemolysis
Crush injuries
Tissue necrosis
Metabolic acidosis
Adrenal insufficiency

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18
Q

Causes of hypokalaemia

A

Reduced oral intake
Renal - diuretics, renal tubular disorders
GI - D+V, fistula, laxatives, villous adenoma
Endocrine - Cushing’s, steroids, hyperaldosternoism (Conns)

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19
Q

What are the causes of respiratory acidosis

A

CNS depression - head injury, drugs coma, CVA, encephalitis
Neuromuscular disease - Myasthenia graves, GBS
Skeletal disease - Kyphosis, Ank Spon, Flail chest
Artificial ventialtion
Impaired gaseous exchange - thoracic injury, obstructive airway disease, alveolar disease

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20
Q

What are the causes of respiratory alkalosis

A

Stimulation of respiratory centre - high altitude, pneumonia, pulmonary oedema, PE, feel, head injury
Increased alveolar gas exchange - hyperventilation, artificial ventilation

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21
Q

What are the causes of metabolic acidosis

A

DKA
Lactic acidosis
Septicaemia
Starvation
Renal failure
Diarrhoea
Intestinal, biliary and pancreatic fistulae

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22
Q

What are the causes of a metabolic alkalosis

A

Vomiting
Nasogastric aspiration
Gastric fistula
Diuretic therapy
Cushing’s syndrome
Conn’s syndrome

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23
Q

What is the normal anion gap

A

Between 10-19 mmol/LH

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24
Q

How is the anion gap calculated

A

(Na+ + K+) - (HCO3 - + CL - )

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25
Q

What hormones are increased following trauma/surgery

A

ADH
Catecholamines
Cortisol
Aldosterone

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26
Q

What is the starling equilibrium

A

Capillary hydrostatic pressure + tissue oncotic pressure = interstitial fluid pressure + plasma oncotic pressure

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27
Q

What are the causes of oedema

A

Increased capillary hydrostatic pressure - CCF, venous obstruction, increased fluid volume
Decreased plasma oncotic pressure due to hypoproteinaemia - starvation, cirrhosis, nephrotic syndrome
Increased capillary permeability - inflammatory reactions, allergic reactions

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28
Q

Describe the mechanics of pulmonary ventilation

A

At the beginning of inspiration intrapleural pressure is around -4cmH20
Contraction of the respiratory muscles increases the volume of the chest - this decreases the intrapleural pressure to around -9cmH20
The change in intrapleural pressure causes the lungs to expand and thus generate a negative intra-alveolar pressure as the alveoli are pulled open
As the atmospheric pressure is higher air flows from the high pressure to the low pressure.

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29
Q

What is the function of accessory muscles during exercise

A

They can generate more intreapleural pressures - which allow inhalation of 2-3L of air

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30
Q

Is inspiration or expiration a passive process

A

Expiration - passive process due to the recoil of the chest wall

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31
Q

What are the three forces acting on the lung

A

Elastic nature of the lungs - under normal conditions the lungs are stretched
Surfactant - lines the alveoli and exerts inwards or collapsing pressure
Negative intrapleural pressure - oppose the above two forces. Negative pressure is created by the chest wall and diaphragm pulling the parietal pleura outwards. As the two layers of pleural are pulled in opposite directions they generate a negative pressure

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32
Q

What is the function of surfactant

A

Lowers surface tension, increased compliance and reduced the work of breathing
Prevents fluid accumulating in the alveoli
Reduces the tendency of alveoli to collapse

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33
Q

What is alveolar instability

A

The tendency of alveoli collapsing

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34
Q

What two factors govern compliance of breathing

A

Elasticity of the lung parenchyma
Surface tension

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35
Q

What decreases lung compliance

A

scarring/fibrosis of lung parenchyma
pulmonary oedema
deficiency of surfactant

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36
Q

What is work of breathing

A

The work required to move the lung and chest wall

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37
Q

Define tidal volume

A

The total amount of air taken in and exhaled during quiet breathing

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38
Q

Define inspiratory reserve volume

A

The maximum volume of air that can be inspired in excess of normal inspiration

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39
Q

Define expiratory reserve volume

A

The maximum amount of air that can be forcefully expired after normal expiration

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40
Q

Define functional residual capacity

A

The volume of gas left in the lungs after expiration during normal breathing

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41
Q

Define residual volume

A

The volume remaining after maximal expiration - it cannot be measured directly (RV = FRC - ERV)

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42
Q

Define total lung capacity

A

The sum of all lung volumes plus residual volume

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43
Q

Define vital capacity

A

The volume of air that is expelled from maximal inspiration to maximal expiration

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44
Q

How can FRC be determined

A

By the helium dilution method

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45
Q

What is dead space in regard to ventilation

A

The volume of air which has been ventilated but does not actually take part in gas exchange
Can be anatomical - the volume of gas that does not mix with the air in the alveoli
Physiological - the volume of gas that may reach the alveoli, but due to lack of perfusion does not take place in gas exchange

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46
Q

What is diffusion capacity

A

A test which reflects the diffusion capacity of the alveolar membrane and the pulmonary vasculature

Diffusion capacity is reduced with increased diffusion distance, loss of alveolar area

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47
Q

What determines blood flow in the lungs

A

Hydrostatic pressure in the pulmonary arteries
Pressure in the pulmonary veins
Pressure of air in the alveoli

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48
Q

What are the physiological changes associated with a pulmonary embolism

A

Increased pulmonary vascular resistance
Pulmonary HTN
Increased right ventricle afterload, leading to RV dilatation and dysfunction
Reduced left ventricle output
Impaired gas exchange, due to shunting of blood through non-perfused segments of lung
Decreased lung compliance, due to bleeding and loss of surfactant over the area affected

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49
Q

What are the stages of pulmonary oedema

A

Interstitial oedema
Alveolar oedema
Airway oedema

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50
Q

What is the physiological effects of pulmonary oedema

A

Decreased lung compliance due to the reduction in surface tension and alveolar shrinkage
Increased airway resistance - this can occur due to the reduction in lung volume and fluid filling the airways. Resistance is due to bronchoconstriction

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51
Q

What are the causes of pulmonary oedema

A

Raised pulmonary hydrostatic pressure - 2y to left ventricular failure
Increased pulmonary capillary permeability
Blocked lymphatic drainage
High altitude
Neurogenic

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52
Q

What are the direct and indirect causes of ARDs

A

Direct - contusion, near drawing, aspiration, smoke inhalation
Indirect - Trauma, sepsis, pancreatitis

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53
Q

What is the criteria for ARDs

A

Known cause
Acute onset of symptoms
Hypoxia refractory to oxygen
New, bilateral, fluffy infiltrates on CXR
No evidence of cardiac failure (pulmonary artery wedge pressure <18mmHg)

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54
Q

What are the two phases of ARDS

A

Acute exudative
Late organisation

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55
Q

What are the three factors affect the diffusion of gases

A

Pressure gradient
Diffusion coefficient
Tissue factor

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56
Q

What does the oxygen dissociation curve show

A

The relationship between the partial pressure of oxygen and the concentration of oxygen in the blood

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57
Q

If the oxygen dissociation curve shifts to the right what happens

A

There is decreased oxygen affinity, and therefore increased oxygen unloading to tissues

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58
Q

What causes the oxygen dissociation curve to shift to the right

A

Increased hydrogen ions
Increased temperature
Increased 2,3 DPG
Increased carbon dioxide

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59
Q

If the oxygen dissociation curve shifts to the left what happens

A

There is increased oxygen affinity, and therefore decreased oxygen unloading to tissues

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60
Q

What causes the oxygen dissociation curve to shift to the left

A

Decreased hydrogen ions
Decreased temperature
Decreased 2,3 DPG
Decreased carbon dioxide

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61
Q

What is the function of myoglobin

A

Provide additional oxygen in muscles during periods of anaerobic respiration

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62
Q

What is the Bohr effect

A

Shifting of the oxygen dissociation curve to the right
Represents a method to increased oxygen extraction

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63
Q

What is the Haldane effect

A

The amount of carbon dioxide carried increased as the oxygen level falls

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64
Q

Where is the respiratory centre found and what two types of neuroses are found there

A

Medulla Oblongata

Inspiratory neurones - demonstrate rhythmical firings potentials with intervening periods of inactivity. The action potentials stimulate the diaphragm and external intercostals to contract

Expiratory neurones - inactive during quiet respiration. During periods of exercise or increased respiration - they fire action potentials which cause the internal intercostals and abdominal wall muscles to contract

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65
Q

What is the function of the apneustic centre

A

Prolongs inspiration and results in short expiratory efforts

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66
Q

What is the function of the Pneumotaxic centre

A

Inhibits inspiratory neurones and shortens respiration

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67
Q

Which chemoreceptors are the main determinant of respiration and what are they sensitive to

A

Central chemoreceptors in the medulla
Sensitive to changes in CO2

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68
Q

Where are peripheral chemoreceptors found and what do they respond to

A

In the carotid bodies, close to the bifurcation of the common carotids and in the aortic bodies
Respond to arterial pH and low levels of pO2

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69
Q

What is the pathogenesis of hypoxic drive

A

In severe long-standing lung disease with persistently elevated carbon dioxide patients will become accustomed to this and lose the controlling effect of P CO2
Therefore the low levels of oxygen (detected by peripheral chemoreceptors) are relied on to stimulate respiration

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70
Q

Define hypoxia

A

A deficiency of oxygen in the tissues

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71
Q

Define hypoxaemia

A

Reduction in the concentration of oxygen in the arterial blood

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72
Q

What causes hypoxic hypoxia and give conditions in which this would be expected

A

Results from low arterial pO2

Causes: high altitude, PE, hypoventilation, lung fibrosis, pulmonary oedema

73
Q

What causes anaemic hypoxia

A

A decreased in the amount of haemoglobin and therefore a decrease in oxygen content of arterial blood

74
Q

What is histotoxic hypoxia

A

Poisoning of the enzymes involved in cellular respiration, oxygen is available but cannot be utilised.
Occurs in cyanide poisoning

75
Q

What are the causes of hypoxaemia

A

Hypoventilation
Impaired diffusion
Shunt
Ventilation and perfusion inequality
Reduction in inspired oxygen tension

76
Q

Describe type I respiratory failure

A

Hypoxaemic respiratory failure
PaCO2 <6 kPA
Due to ventilation perfusion mismatching

Causes: Pneumothorax, pneumonia, contusion, PE, ARDS

77
Q

Describe type II respiratory failure

A

Ventilatory failure
Due to the inadequate movement of air
Causes: COPD, neuromuscular disorders, airway obstruction, central respiratory depression, chest wall deformity

78
Q

What are the indications for ventilation

A

Inadequate ventilation - apnoea, RR >35, PaCO2 >8kPa
Inadequate oxygenation - PaO2 <8kPa with 60% oxygen
Surgical indications - head injury, chest injury, facial trauma, high spinal injury

79
Q

What are some complications of mechanical ventilation

A

Ventilator induced injury
Volutrauma
Barotrauma
Hypotension and reduced CO - decreased venous return due to positive intrathoracic pressure
Respiratory muscle atrophy
Nosocomial infections
Increased ICP

80
Q

What actviates the actin myosin complex and allows contraction

A

Calcium

81
Q

What is the most important factor in controlling myocardial contractility

A

Increased intracellular calcium increases the force of myocardial contraction
Decreased intracellular calcium decreases the force of myocardial contraction

82
Q

Why is conduction through the AV node slow

A

To delay transmission from atria to ventricles, ensuring that atrial contraction is finished before ventricular contraction begins

83
Q

Why does atropine not have any effect on a transplanted heart

A

Because the heart has no vagal innervation

84
Q

What happens in systole

A

Contraction
Mitral and triscupid valves close
Ejection - aortic and pulmonary valves open

85
Q

What happens in diastole

A

Relaxation
Aortic and pulmonary valves close
Filling - mitral and tricuspid valves open

86
Q

How is ejection fraction calculated

A

Stroke volume / Left ventricular end diastolic volume

87
Q

What cause the first and second heart sound

A

First - due to closure of the AV valves
Second - due to the closure of the aortic and pulmonary valves

88
Q

What is coronary blood flow at rest

A

250mL/min

89
Q

What can coronary blood flow increase to during exercise

A

up to 1L/min

90
Q

During which phase of the cardiac cycle does coronary blood flow occur

A

Diastole

91
Q

How is cardiac output calculated

A

CO = stroke volume x heart rate

92
Q

What is Starling’s Law

A

The energy contraction of a cardiac muscle fibre is a function of the initial length of the muscle fibre

The greater the stretch of the ventricle in diastole, the greater the stroke volume
Up to a point increasing the venous return will increase the force that the heart muscle can exert

93
Q

What factors modify heart rate

A

Intrinsic rhythmicity
Extrinsic factors - Sympathetic stimulation increases rate and force
Parasympathetic stimulation decreased rate

94
Q

What factors modify stroke volume

A

Contractility
Preload
Afterload

95
Q

What reduces contractility

A

Reduced filling
Hypoxia
Hypercapnia
Acidosis
Ischaemia and cardiac disease
PSNS
Electrolyte imbalances
Drugs

96
Q

How is blood pressure calculated

A

BP = CO x SVR

97
Q

What does systolic and diastolic blood pressure reflect

A

Systolic - the maximum pressure recorded during systole
Diastolic - the minimum pressure recorded during diastole

98
Q

How is pulse pressure calculated

A

Systolic pressure - diastolic pressure

99
Q

How is mean arterial pressure calculated

A

Diastolic pressure + 1/3 of the pulse pressure

100
Q

What type of receptors monitor blood pressure

A

Baroreceptors
They are stretched with increased BP, causing reflex reduction in vasoconstriction, which with a reduction heart rate leads to reduced SVR and CO and therefore BP
The opposite happens with low BP

101
Q

What is a normal central venous pressure

A

5-12mmHg

102
Q

What does a low central venous pressure indicate

A

Hypovolaemia

103
Q

When is adrenaline used as a vasopressor

A

In septic shock when hypotension due to peripheral vasodilation persists despite adequate volume replacement

104
Q

Dobutamine is used in which kind of shock

A

Cardiogenic shock
Its beta -1 effect increased the heart rate and the force of contraction

First choice ionotrope in cardiogenic shock due to LVSD

105
Q

Where is the myenteric plexus found and what is it also known as

A

Found between the circular and longitudinal layers of the GI tract
It is a mainly motor function
Also known as Auerbach’s plexus

106
Q

Where is the submucosal plexus found and what is it also know as

A

Lies within the submucosa
Mainly sensory function
Also known as Meissners plexus

107
Q

What anatomical features of the oesophageal sphincter help it maintain its integrity

A

Right crus of the diaphragm compresses the oesophagus as it passes through the oesophageal hiatus
The acute angle in which the oesophagus enters the stomach acts as a valve
Mucosal folds at the end of the diaphragm act as a valve

108
Q

Hydrochloric acid is secreted from what cells

A

Parietal cells
Oxyntic cells

109
Q

What protects the stomach from digestion

A

Mucus secretion - mucus is alkaline and so helps to neutralise gastric acid
Tight epithelial junctions prevent acid reaching deeper tissues
Prostaglandin E secretion has a protective role - increased mucus layer thickness, stimulates HCO3 production, increases blood flow to the area

110
Q

What are the three phases of gastric secretion

A

Cephalic - 30% gastrin secretion, stimulates acid and Pepsin secretion, histamine secretion from mast clels
Gastric - 60% distension of stomach and chemical composition of food leads to ACh release
Intestinal - 5% stimulated by presence of food in the duodenum

111
Q

What inhibits gastrin secretion

A

pH fall to 2-3
Somatostatin
Secretin
Fatty foods - lead to the release of CCK and GIP

112
Q

What are the three muscular layers of the stomach

A

Longitudinal
Circular
Oblique

113
Q

Describe the physiology of vomiting

A

Respiration is inhibited
The larynx closes and the soft palate rises
Stomach and pyloric sphincter relax and the duodenum contracts, propelling intestinal contents into the stomach
Diaphragm and abdominal wall contracts and intragastric pressure rises
Gastro-oesophageal sphincter relaxes and the pylorus closes

114
Q

What is the plicae circulares and what is its advantage

A

The circular folds in the small intestine
Cause the chyme to to spiral round and therefore increase the time taken for absorption to take place

115
Q

Where are crypts of Lieberkuhn found

A

In the small intestine amongst the vili

116
Q

What do D cells produce

A

Somatostatin

117
Q

What do S cells produce

A

Secretin

118
Q

What to N cells produce

A

Neurotensin

119
Q

What do enterochromaffin cells produce

A

5-hydroxy-tryptamine

120
Q

In which part of the intestines are Brunner’s glands found

A

Duodenum

121
Q

What are the fat soluble vitamins

A

Vitamin A, D, E and K

122
Q

What are the water soluble vitamins

A

Vitamin C and B

123
Q

What is the site of bile salt reabsorption

A

Terminal ileum

124
Q

Why does a terminal ileum resection lead to a vitamin B12 deficiency

A

Receptor mediated reabsorption in conjunction with intrinsic factor occurs in the terminal ileum, this will result in deficiency of vitamin B12

125
Q

In what form are enzymes secreted by the pancreas

A

Proteolytic enzymes and lipolytic enzymes are secreted as pro-enzymes and require activation. The majority of them are activated by trypsin

126
Q

Which two hormones are responsible for stimulating pancreatic secretions

A

Cholecystokinin (CCK)
Secretin

127
Q

Post pancreateatectomy what physiological abnormalities remain

A

Malnutrition - inadequate digestion of protein and lipids due to loss of proteolytic and lipolytic enzymes. Absorption of fat soluble vitamins (Vit A D E K )is reduced
Loss of alkaline pancreatic secretions - reduced neutralsation of chyme and therefore loss of iron, calcium and phosphate absorption

128
Q

What are bile pigments produced by

A

The breakdown of haem unit of haemoglobin

129
Q

Describe enterohepatic circulation

A

90% of secreted bile acids are reabsorbed from the intestine and returned to the liver by the portal vein, the remaining are altered by bacterial flora and become insoluble and are therefore excreted.

130
Q

What controls the release of bile from the bile duct into the duodenum

A

CCK stimulates the GB to contract and release bile into the duodenum

131
Q

Summarise bilirubin metabolism

A

RBC are broken down in the spleen and release bilirubin, a breakdown product of the porphyrin ring of haemoglobin. Bilirubin is unconjugated at this point.
Unconjugated bilirubin is not water soluble and binds to albumin, in the liver the bilirubin is conjugated to glucuronide. This is then conjugated bilirubin.
Bilirubin is converted to urobilinogen in the bowel.

132
Q

Prehepatic causes of jaundice

A

Inherited - red cell membrane defects, haemoglobin abnormalities, metabolic defects.
Acquired - Immune, mechanical, acquired membrane defects, infections, drugs, burn

133
Q

In summary what causes of preheptaic jaundice

A

Disorders that result in excessive destruction of RBCs

134
Q

What are the causes of hepatic jaundice

A

Viruses - hepatitis A,B, C and E and EBV,
Autoimmune disorders - chronic hepatitis
Drugs - POD
Cirrhosis
Liver tumours/Mets

135
Q

In summary what causes of choelstatic jaundice

A

Obstruction of biliary system

136
Q

Which anal sphincter is under involuntary control

A

Internal sphincter

137
Q

Which anal sphincter is under voluntary control

A

External sphincter

138
Q

Describe the reflex arc of defecation

A

Rectal distension - when faecal material enters the rectum and causes distension, impulses from stretch receptors fire
Conscious awareness - as a result of rectal distension there is activation of receptors which allows differentiation between faeces and flatus. External spinchter contracts
Parasympathetic impulse - increase in tone of colon and relaxation of the external sphincter
Depending on the convenience of defecation at that point the external sphincter either relaxes or contract

139
Q

Describe the microscopic features of the glomerulus which allows filtration

A

Capillary endothelium is fenestrated - permitting free passage of water and electrolytes
Negatively charged glycopretoiens
Podocytes with foot processes through which filtration can occur

140
Q

What do the actions of ADH include

A

Increased water permeability of the distal tubule and collecting ducts
Increased arterial blood pressure by vasoconstriction
Secretion of ADH leads to the production of concentrated low volume urine

141
Q

What are juxtaglomerular cells and what do they secrete

A

Specialised smooth muscle cells that lie in the wall of the afferent arteriole and secrete renin

142
Q

What stimulates the release of renin

A

Decreased in afferent arteriole pressure
Reduction in sodium, detected by the macula dense which monitors sodium load in the distal tubule
Stimulation by renal sympathetic nerves

143
Q

What are the actions of angiotensin II

A

Stimulates arterial vasoconstriction
Stimulates the release of ADH
Stimulates drinking
Stimulates the release of aldosterone

144
Q

What are the actions of ANP

A

Increases glomerular filtration
Inhibits the reabsorption of sodium

145
Q

What is ANP released in response to

A

In response to an increased volume - via the atrial stretch receptors

146
Q

What volume of urine is in the bladder before there is a desire to micturate

A

200-300mL

147
Q

Describe the parasympathetic nervous system in urination

A

Increase detrusor muscle contraction, and decreasing the contraction of the internal sphincter

148
Q

In what injury is an atonic bladder found

A

Following a spinal injury in spinal shock

149
Q

What is the function of erythropoietin and where is it produced from

A

Action - accelerates the differentiation of marrow stem cells into erythrocytes
Mainly secreted in the Kidney, but also from the spleen

150
Q

1 alpha hydroxyls catalyse what reaction

A

25-hydroxycholecalciferol to 1,25- hydroxycholecalciferol

151
Q

What hormones are produced from the anterior pituitary

A

Adrenocorticotrophic hormone (ACTH)
Thyroid stimulating hormone (TSH)
Follicule stimulating hormone (FSH)
Lutenizing hormone (LH)
Prolactin
Growth hormone

152
Q

What hormones are produced from the posterior pituitary

A

Oxytocin
Antidiuretic hormone

153
Q

What are the symptoms of a prolactinoma

A

Galactorrhoea
Amenorrhoea
Impotence
Headaches
Visual field defects

154
Q

What does increase ADH lead to and what are the features

A

Syndrome of inappropriate antidiuretic hormone
Hyponatraemia, decreased plasma osmolality, increased urine osmolality, urinary sodium >30

155
Q

What are the causes of pituitary deficiency

A

Rare congenital deficiency - Kallman’s syndrome (LH and FSH deficiency)
Infection - meningitis/encephalitis
Pituitary apoplexy
Sheehans syndrome
Cerebral tumours
Radiation
Trauma
Sarcoidosis

156
Q

What is pituitary apoplexy

A

Pituitary deficiency following bleeding into the pituitary gland

157
Q

What is Sheehan’s Syndrome

A

Pituitary deficiency cause by infarction of the pituitary following postpartum haemorrhage

158
Q

Which cells secrete calcitonin

A

Parafollicular cells

159
Q

Thyrotrophin releasing hormone is released from where

A

Hypothalamus

160
Q

Describe the production of thyroid hormones

A

Hypothalamus secretes thyrotrophin releasing hormone, this then stimulates the release of thyroid stimulating hormone.
TSH stimulates the production of T3 and T4 - these then have a negative feedback on TRH and TSH

161
Q

What are the causes of primary hyperthryoidism

A

Graves disease
Solitary toxic adenoma/nodule
Toxic multinodular goitre
Acute phase of thyroiditis
Drugs - Amiodarone

162
Q

What are the causes of secondary hyperthryoidism

A

Pituitary/hypothalamic tumour
Metastatic c thyroid carcinoma
Choriocarcinoma
Ovarian teratoma

163
Q

What are the cause of primary hypothyroidism

A

Autoimmune
Hashimoto’s thyroiditis
Iodine deficiency
Genetic defects
Iatrogenic - post thyroidectomy/radiotherapy
Drugs - lithium
Neoplasia

164
Q

What is chovsteks sign

A

Twitching of muscles supplied by the facial nerve due to decreased calcium

165
Q

What is Troussea’s sign

A

The sign is observable as a carpopedal spasm induced by ischemia secondary to the inflation of a sphygmomanometer cuff,

166
Q

What are the causes of hypocalcaemia

A

Hypoalbuminaemia
Hypomagnesaemia
Hypophosphataemia
Hypoparathryodism
Acute pancreatitis
Massive transfusion
Post thyroid surgery
Vitamin D deficiency
Drugs
Hypoventilation

167
Q

What are the causes of hypercalcaemia

A

Excess PTH
Excess vitamin D
Milk -alkali syndrome
Malignancy
Drugs

168
Q

Why is measuring phosphate in ventilated patients important

A

Acute hypophosphataemia can lead to significant diaphragmatic weakness and delay weaning from a ventilator in patients in the intensive care unit.

169
Q

What are the three sections of the adrenal cortex

A

Zona glomerulosa
Zona fasciculata
Zona reticularis

170
Q

What is secreted from the zona glomerulosa

A

Mineralcorticoids

171
Q

What is secreted from the Zona fasciculata

A

Glucocorticoids

172
Q

What is secreted from the Zona reticularis

A

Sex steroids

173
Q

What are the cause of hypophosphataemia

A

Hyperparathyroidism
Vitamin D deficiency
TPN
DKA
Acute liver failure
Paracetamol overdose

174
Q

What is produced from the adrenal medulla

A

Adrenaline
Noradrenaline
Dopamine
Beta-hydroxylase
ATP
Opioid peptides

175
Q

Give an example of a Mineralcorticoid

A

Aldosterone

176
Q

Give an example of a glucocorticoid

A

Cortisol
Hydrocortisone

177
Q

Describe the anti-inflammatory and immunosuppressive action of glucocorticoids

A

Decreased the number of immunocompetent cells and macrophages
Reduces teh number to T cells and their function
Reduction B cell clonal expansion
Reduces basophils and eosinophils
Inhibits the compliment pathway

178
Q
A

MRCS (17 decks)

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