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MRCS Part A (KF edition) > Physiology > Flashcards

Physiology Flashcards

1
Q

What do the parasympathetic and sympathetic fibres that supply the heart release?

A

Parasympathetic: Acetylcholine (alpha 1)

Sympathetic: noradrenaline (B1 receptors)

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2
Q

What is Starling’s law?

A

The law governs effects on stroke volume and states that an increased preload causing increased stretch of the cardiac muscle fibres will lead to a greater stroke volume (cardiac output)

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3
Q

Where are the baroreceptors found and via which nerve are their impulses carried by?

A

Found in aortic arch and carotid sinus

Carried by vagus from aortic arch

Carried by glossopharyngeal nerve from carotid sinus

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4
Q

Which part of the JVP waveform is absent during AF?

A

A wave

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5
Q

What are the 5 waves that make up the JVP waveform and what do they each represent?

A
  • a wave: atrial contraction
  • c wave: closure of tricuspid valve + ventricular contraction
  • x wave: fall in atrial pressure during ventricular systole
  • v wave: passive filling of atrium against a closed tricuspid valve
  • y wave: opening of tricuspid valve + ventricular filling
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6
Q

What is the mechanism of the rapid depolarisation phase of the heart?

A

Rapid sodium influx

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7
Q

What is the mechanism of the early repolarisation phase of the heart?

A

Efflux of potassium

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8
Q

What occurs during the plateau phase of the myocardial action potential?

A

Slow influx of calcium

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9
Q

What occurs during the final repolarisation of the myocardial action potential?

A

Efflux of potassium

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10
Q

Which 2 receptors are found in blood vessels and cause vasoconstriction when stimulated?

A

Alpha 1
Alpha 2

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11
Q

What are the effects of binding to D1 and D2 receptors and where are they found?

A

D1: renal and spleen vasodilation

D2: Inhibits release of noradrenaline

Found in the kidneys

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12
Q

Which receptor is the main binding site for adrenaline?

A

Alpha 1

causes vasoconstriction

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13
Q

What are the preferred inotropes given during septic shock and anaphylaxis?

A

Septic shock: Noradrenaline (a1, a2, b1, b2)

Anaphylaxis: Adrenaline (a1, a2, b1, b2)

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14
Q

What is the main receptor site of noradrenaline to increase heart rate?

A

Beta 1 receptors

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15
Q

In a patient with cardiogenic shock, what is the most appropriate inotrope and why?

A

Dobutamine

Binds to B1 and B2 to increase heart and contractility of the heart

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16
Q

What is the normal pCO2 range?

A

4.7 - 6 kPa

45 - 35 mmHg

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17
Q

What is the normal range of HCO3?

A

22 - 26

<22 = acidosis
>26 = alkalosis

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18
Q

What ABG result shows T1RF?

A

Low PaO2

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19
Q

How is T2RF shown on an ABG?

A
  • Hypoxemia = low paO2
  • Hypercapnia = high pCO2
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20
Q

How long does metabolic compensation of acidosis / alkalosis take to start?

A

~2 days

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21
Q

How is the anion gap calculated and what is the normal range?

A

Normal range: 4 - 12

(Na + K) - (HCO3 + Cl)

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22
Q

What metabolic state can diarrhoea cause and why?

A

Metabolic acidosis

Due to increase excretion of HCO3

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23
Q

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

A
  • Lactate (shock, hypoxia)
  • Ketones (DKA, ETOH)
  • Urate (renal failure)
  • Acid poisoning (salicylates, methanol)
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24
Q

In a patient with excessive vomiting (i.e secondary to pyloric stenosis), what metabolic and electrolyte state are they likely to be in?

A

Hypocholeraemic Hyperkalaemic Metabolic alkalosis

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25
Q

What is the mechanism of metabolic alkalosis?

A
  • RAAS system activated secreting aldosterone
  • Aldosterone causes reabsorption of Na+ in exchange for H+ in DCT
  • H+ shifts into the cells and K+ will shift out of cells into the ECF to maintain ion neutrality
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26
Q

What would expect to see on an ABG in early salicylate poisoning?

A

Respiratory alkalosis followed later by metabolic acidosis

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27
Q

What is SIRS?

A

Systemic Inflammatory Response Syndrome

Parameters:
- Temp <36 / >38 degrees
- HR >90
- RR >20
- WCC >12 or <4
- Altered mental state OR hyperglycaemia (in absence of DM)

SIRS describes symptoms of SEPSIS

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28
Q

What is septic shock?

A

Sepsis with hypotension which does not respond to fluid resuscitation leading to tissue hypoperfusion

Characterised by:
- Decreased Systemic vascular resistance
- Increased HR
- Decreased cardiac output
- Normal pulmonary pressure

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29
Q

How many classes of haemorrhages shock are there?

A

4 classes

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30
Q
A
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31
Q

What is the normal rate of urine output?

A

0.5-1ml/kg/hr

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32
Q

What are the cardiovascular changes that occur in a patient with hemorrhagic/hypovolaemic shock?

A
  • Increased HR
  • Increased systemic vascular resistance
  • Decreased BP
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33
Q

What causes shock during neurogenic shock?

A

Decreased sympathetic tone / Increased parasympathetic tone

  • Decreased HR
  • Decreased BP
  • Decreased Cardiac output
  • Decreased systemic vascular resistance
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34
Q

How is neurogenic shock managed acutely?

A

Fluid resus and inotropes (Dobutamine to bind to B1 receptors)

long term is surgery to fix neuropathic damage

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35
Q

What is the most common cause of cardiogenic shock?

A

Medically: IHD

Surgically/trauma: Cardiac tamponade

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36
Q

What happens to pulmonary pressures in cardiogenic shock?

A

Pressures are high

Basis of use of venodilators in treatment of pulmonary oedema

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37
Q

What dose of adrenaline is given in anaphylaxis and how often can it be given?

A

500mcg (1:1000) IM

can be given every 5mins if needed

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38
Q

How is cerebral perfusion pressure calculated?

A

CPP = MAP - ICP

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39
Q

Which fluid compartment holds the highest percentage of total body volume?

A

Intracellular = 60 - 65%

Extracellular: 35 - 40%

60% of body weight is water. 40% intracellular and 20% extracellular

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40
Q

What components can be found in CSF?

A

Glucose 50-80mg/dL
Protein 15-40 mg/dL
RBC: NIL
WCC: NIL to very minimal

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41
Q

How is mean arterial pressure calculated?

A

Diastolic pressure + 1/3(systolic pressure - diastolic pressure)

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42
Q

What are symptoms of raised ICP?

A
  • Headaches
  • Vomitng
  • Papilloedema
  • Seizures
  • Focal neurological symptoms
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43
Q

If the raised ICP is caused by trauma, what is the medical management given initially?

A

Mannitol

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44
Q

What can low CPP lead to?

A

Secondary brain injury by hypo perfusion of brain tissue causing hypoxic brain injury

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45
Q

What is involved in the Extrinsic pathway of the coagulation cascade?

A
  • Tissue is damaged releasing tissue factor
  • Factor 7 binds to Tissue factor creating a complex
  • This complex activates Factor 9
  • Activated Factor 9 works with Factor 8 to activate Factor 10
  • Factor 10 is part of the common pathway
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46
Q

What occurs in the common pathway of the coagulation cascade?

A

Activated Factor 10 causes the conversion of prothrombin to thrombin

Thrombin hydrolyeses fibrinogen to form FIBRIN and also activates Factor 8 to form links between the fibrin molecules

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47
Q

How is the extrinsic pathway monitored?

A

PT

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48
Q

How is the intrinsic pathway monitored?

A

APTT

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49
Q

Why factors of the coagulation cascade are Vitamin K dependent?

A

Factor 10, 9, 7, 2

1972

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50
Q

What part of the coagulation cascade does Heparin have an effect on?

A

Intrinsic pathway

Prevents activation of Factors 2, 9, 10, 11

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51
Q

Which factors does warfarin disrupt in the coagulation cascade?

A

Affects synthesis of Factors 10, 9, 7, 2 (1972) - extrinsic pathway

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52
Q

In which type of thrombophilia is heparin likely to be ineffective and why?

A

Antithrombin deficiency (unable to inactivate thrombin)

Heparin may be ineffective as it works via antithrombin

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53
Q

Which genetic thrombophilia is the most common genetic defect causing DVT?

A

Factor V Leiden

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54
Q

How is warfarin monitored?

A

INR + PT

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55
Q

How is raised INR secondary to warfarin usage corrected?

A
  • Vit K (works over 24hrs)
  • Prothrombin complex concentrate (works within 1hr)
  • FFP
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56
Q

How long before an operation should warfarin be stopped?

A

4 days

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57
Q

How can the effects of unfractionated heparin be reversed?

A

Protamine sulfate

58
Q

When would a high CRP post-operatively suggest evolving complications?

A

a CRP >150 after 48hrs post-operatively suggest evolving complications

59
Q

What are the signs and symptoms of hypocalcaemia?

A

CATS go NUMB

  • Convulsions
  • Arrhythmia
  • Tetany
  • Spasms and stridor (Chvosteks sign; twitching of facial muscles in response to tapping over facial nerve)
  • Numbness in fingers
60
Q

What effect does PTH have on calcium and phosphate levels and what is the mechanism?

A

Increases Calcium
Decreases Phosphate

  • Directly works on osteoblasts to cause bone resorption to increase extracellular calcium levels
  • Increases synthesis of Vitamin D in kidney which increases calcium absorption from the bowel and kidney tubules

Decreases renal resorption of phosphate

61
Q

What is the function of calcitonin and where is it secreted from?

A

Secreted by C cells of thyroid

  • Inhibits intestinal calcium absorption
  • Inhibits osteoclast activity (reduces bone resorption)
  • Inhibits renal absorption of calcium
62
Q

What are causes of hypocalcaemia?

A
  • Vit D deficiency (osteomalacia)
  • Acute pancreatitis
  • Chronic renal failure
  • Hypoparathyroidism
  • Magnesium deficiency (due to end organ PTH resistance)
63
Q

What are the main 3 causes of hypercalcaemia?

A
  • Malignancy (IP pts)
  • Primary hyperparathyroidism (OP pts)
  • Sarcoidosis
64
Q

What are the clinical features of hypercalcaemia?

A

Stones, bones, abdominal grains and psychiatric moans

  • Kidneys stones
  • Weak/brittle bones
  • Constipation
  • Confusion
65
Q

What is the management of hypercalcaemia?

A
  • IVF
  • Diuretics (furosemide)
  • Calcitonin
  • Bisphosphonates
66
Q

Which bisphosphonate is used to treat hypercalcaemia associated with malignancy?

A

IV Zolindronate

67
Q

What is the effect of insulin on potassium levels?

A

Causes hypokalaemia

68
Q

What is the effect of aldosterone on potassium?

A

Increases potassium by exchanging sodium for potassium in the renal tubules

Hence why hyperkalaemia occurs in Addison’s disease

69
Q

What are ECG features of hypokalaemia?

A
  • U waves
  • small/absent T waves
  • Prolonged PR
  • ST depression
  • Long QT interval
70
Q

How is hyperkalaemia managed?

A

1- Calcium gluconate
2- Insulin/Dextrose (50 units insulin in 50mls saline given at rate of 0.1units/kg/hr)
3- IVF given alongside insulin

71
Q

What are the causes of hypomagnasaemia?

A
  • Diuretics
  • TPN
  • Alcohol
  • Diarrhoea
72
Q

A patient had a TURP. They now have hyponatraemia. What is the most likely cause of this imbalance?

A

Water excess

TURP uses saline/dextrose as part of the procedure which can cause water excess leading to a dilution effect on sodium

73
Q

If a patient with hyponatraemia has a urinary sodium <20mmol/L, where is it likely their sodium is being depleted?

A

Extra-renal loss

Causes:
- D+V
- Sweating
- Burns

74
Q

If a patient with hyponatraemia has a urinary sodium >20mmol/L, where is it likely their sodium is being depleted?

A

Renal loss

Causes:
- Hypovolaemia/euvolaemic
- Diuretics
- Addison’s
- SIADH

75
Q

What is the max rate of Na correction and why?

A

Pts with Na <120, correction should be no more than 10mmol per 24hrs

To prevent Central pontine Myelinosis

76
Q

Where in the GIT is iron mostly absorbed?

A

Duodenum and upper Jejunum

77
Q

What can reduce absorption of iron in the GIT?

A
  • PPIs
  • Tannin (found in tea)
  • Tetracyclines
78
Q

How can pulmonary artery occlusion pressures differentiate between ARDS and Pulmonary oedema (overload)?

A

ARDS: low pressures with pulmonary oedema (<5mmHg)

Overload: High pressures (>18mmHg)

79
Q

What are the 3 classifications of hyponatraemia?

A

Normal osmolality: Hyperproteinaemia // hyperlipidaemia

Hypotonic hyponatraemia: further divided based on fluid status (hypovolaemic, euvolaemic, hypervolaemic)

Hypertonic hyponatraemia: Hyperglycaemia // radiocontrast agents // mannitol and sorbitol

80
Q

What are the causes of hypotonic hyponatraemia in a euvolaemic patient?

A
  • SIADH
  • Hypothyroidism
  • Endurance exercise
  • Thiazides and ACEi
  • Post-operatice hyponatraemia
81
Q

What effects on sodium does Diabetes insipidus cause?

A
  • Serum Na+ is high
  • Serum osmolality is high
  • Urine osmolality is low
82
Q

How is diabetes insipidus investigated and what can DI be further divided?

A

Vasopressin stimulation test

  • if no change after vasopressin: Nephrogenic DI. Treat underlying cause
  • if improvement after vasopressin: Cranial DI and managed with vasopressin
83
Q

What is vital capacity?

A

Inspiratory reserve volume + Tidal volume + Expiratory reserve volume

Maximal volume of air that can be forcefully exhaled after maximal inspiration

84
Q

In a patient who has post-operative oliguria, how would you initially manage them?

A

Fluid challenge

  • 500ml STAT
  • up to 4 fluid challenges
  • if no improvement, HDU + inotropes
85
Q

What fluid resuscitation fluids would you use in post-operative oliguria and trauma patients?

A

Ringer or Hartmanns

86
Q

When would you use normal saline with K+ as a resuscitation fluid?

A

Obstructive gastric outlet or repeated vomiting

To replace loss of Cl and K+ from vomiting

87
Q

What can overuse of NaCl cause when resuscitating?

A

Hypercholeraemic metabolic acidosis

88
Q

What is meant by Forced vital capacity?

A

Volume of air that can be maximally forcefully exhaled

89
Q

In the medulla, how is the respiratory centre here divided and what are their respective functions?

A

In the medulla, there is the:

  • Dorsal respiratory group: Inspiration
  • Ventral respiratory group: Forced voluntary Expiration
90
Q

Which respiratory centre is affected by opioid use?

A

Mainly medullary centres

91
Q

What is the function of the apneustic centre and where is it located?

A

Stimulates inspiration and prolongs inhalation.

Found in Lower Pons

92
Q

Where are the central and peripheral chemoreceptors found?

A

Central: Medulla

Peripheral: bifurcation of carotid arteries AND arch of aorta

93
Q
A
94
Q

In a patient with COPD, which lung volume will be increased?

A

Residual volume

95
Q

What is the significance of a right shift on the oxygen dissociation curve and what causes this shift?

A

Raised oxygen delivery

CADET face right

  • CO2 (raised)
  • Acidosis (raised H+, lactic acid)
  • 2-3 DPG
  • Exercise
  • Temp (raised temp)
96
Q

What is affected in the lung in a patient with ARDS?

A

Decreased gas diffusion

97
Q

What are causes of a reduced TLCO?

A

FIGHT EM

  • Fibrosis
  • Infection
  • Embolism
  • Emphysema
  • Anaemia
  • Emptying of heart (low CO)
98
Q

How are lung functions affected in Obstructive lung disease (e.g. COPD)?

A

FVC: normal
FEV1: Decreased
FEV1/FVC ratio: <0.8 (decreased)

99
Q

How are lung functions affected in restrictive lung diseases?

A

FVC: Decreased
FEV1: decreased
FEV1/FVC ratio: Normal (as both FEV1 and FVC both decreased)

100
Q

What is the mechanism of RAAS in maintaining blood pressure?

A
  • Renin converts Angiotensinogen (made by liver) into Angiotensin 1

-Angiotensin 1 is converted into Angiotensin 2 by ACE (made by lungs and kidneys)

  • Angiotensin 2 increases sympathetic activity causing vasoconstriction of arterioles
  • Angiotensin 2 also increases ADH for water retention and causes increased excretion of sodium and retention of K+ by stimulating the adrenal cortex to secrete aldosterone
101
Q

In which part of the kidney is glucose reabsorbed?

A

In PCT

In PCT, also absorbed is:
- 65% of water
- Glucose
- A.A
- Phosphate

102
Q

On which part of the kidney does Furosemide work?

A

Loop of Henle (thick ascending limb)

103
Q

What is the descending limb of the loop of Henle permeable and impermeable to?

A

Permeable to water

Impermeable to solutes

104
Q

Which part of renal physiology does thiazide affect?

A

DCT

105
Q

Where are the Na+/K+ pumps found in the kidney?

A

Collecting Duct andDCT

106
Q

What factors stimulate renin secretion?

A
  • Hypotension
  • Hyponatraemia
  • Catecholamines (Adrenaline)
  • Erect posture
107
Q

What drugs reduces renin secretion?

A

Beta blockers
NSAIDS

108
Q

What are the 4 phases of wound healing?

A

1- Haemostasis
2- Inflammation
3- Regeneration
4- Remodelling

109
Q

What occurs in each stage of wound healing and what is their respective durations?

A

1- Haemostasis

Vasospasm in adjacent vessels + Platelet plug formation. Lasts from SECONDS TO MINUTES

2- Inflammation

Neutrophils migrate into the wound (impaired in DM). Growth factors are released. Macrophages and fibroblasts couple matrix regeneration and clot substitution. Lasts for DAYS

3- Regeneration

Platelet derived growth factors stimulate fibroblasts and epithelial cells which produce a collagen network. Angiogenesis occurs and wound resembles granulation tissue now. Takes WEEKS.

4- Remodelling

Longest phase. Fibroblasts become differentiated and facilitate wound contraction. Collagen fibres are remodelled and micro vessels regress leaving a pale scar. Last 6 WEEKS TO A YEAR

110
Q

What is the most important cell involved in acute and chronic inflammation?

A

Acute: Neutrophils

Chronic: Macrophages

111
Q

What hormones are increased in response to surgery?

A
  • GH
  • Cortisol
  • Renin
  • ACTH
  • Aldosterone
  • ADH
  • Glucagon
112
Q

What 3 hormones are decreased in response to surgery (stress)?

A

Insulin
Testosterone
Oestrogen

113
Q

What is the mechanism of the HPA in relation to cortisol production?

A
  • Hypothalamus releases CRH
  • CRH stimulates Anterior pituitary gland to secrete ACTH
  • ACTH stimulates adrenal cortex to secrete cortisol

This is controlled by a negative feedback system

114
Q

What are the effects of cortisol on the body?

A
  • breakdown of skeletal muscle proteins to provide gluconeogenic precursors
  • Stimulates lipolysis
  • Anti-insulin effect
  • Anti-inflammatory effects
115
Q

What are the symptoms and findings in a patient with an Addisonian crisis and what can precipitate this?

A
  • Abdominal pain
  • Hyperkalaemia
  • Unexplained shock
  • Hyponatraemia

Patient on steroids prior to surgery is at risk of Addisonian crisis

116
Q

If a patient is on a regular dose on prednisolone above 15mg daily prior to surgery and they are due for a major operation, what steroid regimen should they receive after surgery?

A

> 15mg + major surgery requires IV hydrocortisone 100mg for 3 days before tapering down to normal dose

117
Q

Which hormones are secreted from the anterior pituitary gland?

A
  • TSH
  • Prolactin
  • FSH
  • LH
  • GH
118
Q

Which 2 hormones are secreted from the posterior pituitary gland?

A
  • Oxytocin
  • ADH
119
Q

What drugs classes inhibit release of insulin?

A

Alpha adrenergic drugs
Beta blockers

120
Q

What is mechanism by which T3 and T4 are formed in the thyroid?

A
  • Iodide is actively pumped into the follicular cells
  • Iodide + TPO = Iodine
  • Iodine + thyroxine = MIT and DIT
  • Mono-IT + Di-IT = T3
  • DIT + DIT = T4
121
Q

What is stress incontinence and how is it managed?

A

Caused by urethral hyper mobility or intrinsic sphincter deficiency. Brought on by increases in intra-abdominal pressures (sneezing, lifting etc.)

Managed by pelvic floor muscle strengthening and weight loss

122
Q

What causes urge incontinence and how is it treated?

A

Caused by overactivity of detrusor muscle. Presents as a leak with urge to void

Managed by bladder training and/or antimuscarinics (e.g. Oxybutinin)

123
Q

What is beriberi caused by?

A

Vit B1 (thiamine) deficiency

124
Q

What is ascorbic acid (Vit C) responsible for?

A

Wound healing and collagen synthesis

125
Q

What are the causes of Vitamin B12 deficiency?

A
  • Pernicious anaemia
  • Post-gastrectomy
  • Poor diet
  • Disorders of terminal ileum (site of absorption) e.g. Crohn’s
126
Q

What are the signs and symptoms of Vit B12 deficiency?

A
  • Macrocytic anaemia
  • Sore tongue and mouth
  • Neurology (e.g. Ataxia)
  • Psychiatric symptoms (e.g. mood disturbances)
127
Q

What is the mechanism of excretion of bilirubin?

A
  • breakdown of RBCs to form unconjugated bilirubin (not water soluble)
  • Unconjugated bilirubin travels to the liver where it is conjugated to glucuronic acid (now water soluble)
  • Conjugated bilirubin is transported through the biliary system to the duodenum
  • Conjugated bilirubin in the duodenum is converted to Urobilinogen by bacterial proteases
  • Urobilinogen (90%) is oxidised to form Stercobilinogen which is excreted in the faeces
128
Q

What are the 3 phases of gastric secretion and what occurs during each phase?

A

1) Cephalic phase:
- Sight, smell, taste, thought of food
- Mediated by parasympathetic (vagus)

2) Gastric phase (60%):
- Stretch receptors detect distention of stomach when eating
- Chemoreceptors detect rise in pH stimulating increase in gastric juice, increased gastric peristalsis and increased gastric emptying

3) Intestinal phase:
- Receptors detect distention of duodenum
- Chemoreceptors detect increased fatty acids and glucose causing CCK, secreting secretion and enterogastric reflex

129
Q

How much bile is secreted in a 24hr period?

A

500ml

130
Q

What volume is secreted by the pancreas in a 24hr period?

A

1L

131
Q

What is the total 24hr volume of intestinal secretions by the stomach and duodenum?

A

1.5L

132
Q

What are 3 factors that increase production of gastric juices?

A
  • Vagal nerve stimulation
  • Gastrin release
  • Histamine release
133
Q

What is secreted by chief cells?

A

Pepsinogen

134
Q

Where is gastrin secrete from?

A

G cells in antrum of stomach

135
Q

Where is somatostatin secrete from?

A

D cells in the pancreas nd stomach

136
Q

What is the most specific enzyme to diagnose pancreatitis?

A

Lipase

137
Q

What is responsible for auto digestion of the pancreas?

A

Trypsin

138
Q

What is the usual cause of primary hyperparathyroidism?

A

Hyperplasia, adenoma or carcinoma of the parathyroid

Managed usually by surgery

139
Q

What are the causes of secondary parathyroidism and how does it present biochemically?

A

Caused by Chronic renal failure or Vit D deficiency

Low/normal Calcium
High Phosphate

140
Q

What is the pH of stomach acid?

A

pH 2 - 5

141
Q

What is the most common cause of high output diarrhoea in a patient who has had an ileocaecal resection and how is it managed?

A

Malabsorption of bile salts causes high output diarrhoea

Managed with oral cholestyramine

142
Q

Which factor does von Willebrand factor stabilise?

A

Factor VIII (8)

MRCS Part A (KF edition) (18 decks)

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