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MRCS Physiology > General Physiology > Flashcards

General Physiology Flashcards

1
Q

Reflex vasoconstriction: afferent, centre and efferent.
Which limbs?

A

Afferent: cutaneous nerve
Centre: hypothalamus and spinal cord
Efferent: sympathetic neurones

Bilateral limbs effected (ie cold stimulus R leg causes R+L)

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2
Q

Reflex vasodilatation: afferent, centre and efferent

A

Afferent: cutaneous nerve
Centre: above C5 of spinal cord
Efferent: sympathetic nerves (inhibition, reduce activity)

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3
Q

Which internal surfaces have thermoreceptors?

A

Resp & GI tracts

Inhalation of cold air causes shivering during inspiration
Hot food causes

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4
Q

Difference between core and mouth/axillary temp?
Variation throughout day?
Change throughout menstrual cycle?

A

0.5 C
Higher in evening
0.5 C higher latter half

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5
Q

7 causes of pyrexia?

A

Illness
Exercise
Heatstroke
Anterior hypothalamic lesion (neoplasm/surgery/ischamia)
Hyperthyroidism
Malignant Hyperpyrexia (anaesthesia)
Failure of heat-loss mechanism (e.g. dehydration)

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6
Q

3 methods of heat loss from body?

A

Conduction/evaporation from skin

Convection due to air movement (e.g. from lungs via convection of tidal air flow)

Radiation from naked skin

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7
Q

Heatstroke:
- above which temperature?
- 4 Potential complications?

A

41 C

Circulatory failure, cerebral oedema, hepatic failure, renal failure

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8
Q

Regulatory systems fail below which temp in hypothermia?

A

30 C (often fatal <32 C)

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9
Q

Symptoms of hypothermia?
What causes death?

A

Shivery
Bradycardia/Hypotension
Resp depression
Muscle stiffness
Metabolic abnormalities

Arrhythmias, esp VF

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10
Q

How anaesthesia affects temp?

A

Depresses hypothalamic function
Vasodilatation with increased heat loss
Lack of shivering

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11
Q

How circulatory shock affects temp?

A

Reduced tissue perfusion
Reduced cellular metabolism

Compensation:
Vasoconstriction piloerection, secretion of catecholamines

(exception is endotoxic (septic) shock - skin feels hot)

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12
Q

How spinal injuries affect temperature?

A

Thermoregulation lost below level of injury

  • Cannot vasoconstrict/shiver
  • Cannot sweat
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13
Q

Approximate fluid compartment volumes in 70kg man?

A

60% of weight

25L intracellular

19L extracellular:
- 3L plasma
- 15L interstitial fluid
- 1L transcellular (CSF, peritoneal, intraocular)

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14
Q

What is water diuresis?

A

Excess water ingested
ADH secretion suppressed, collecting ducts relatively impermeable, excrete more water without affecting solutes

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15
Q

What is osmotic diuresis?

A

More solute presented to tubule than can reabsorb (e.g. glucose in diabetes)
Water stays with the solutes
Or in diuretics which block rebasorption of NaCl in tubule

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16
Q

Approx water loss routes and volumes daily?

A

Evaporation (respiratory) 500ml

Skin (insensible) 400ml

Faeces 100ml

Urine (obligatory) 500ml

Total 1.5L
(in practice 1.5L urine daily from drinking water to maintain fluid balance)

17
Q

Normal serum osmolality?
What regulates this?
Normal solute excretion daily in urine?

A

285-296 mosmol/L

Adjustments in ADH secretion and thirst-mediated water intake

600 mosmol

18
Q

Relationship between osmolality, ADH release and thirst?

A

Thirst and ADH release determined by osmolality of plasma-perfusing nuclei in hypothalamus

Receptors indicating thirst have an osmotic threshold of 10mosmol higher than osmoreceptors in ADH release

Therefore, thirst not experience until ADH release has ensured water retention from kidneys

19
Q

Apart from osmolality, 2 other mechanisms for thirst and ADH release?

A

Reduced arterial BP (signals via carotid and aortic baroreceptors)

Reduced central venous pressure (signals via ATRIAL low pressure receptors)

Increased angiotensin II in brain

All indicate reduced circulating blood volume

20
Q

Sodium urine concentration in dehydration?

A

LOW despite hypernatraemia (retaining sodium to retain fluid)

21
Q

Clinical manifestations of hypernatraemia?

A

Occur >160mmol/L

CNS depression, lethargy, coma

22
Q

Max water excretion volume per hour in healthy adults?

A

750ml/hr

23
Q

Causes of water intoxication?

A

-Renal failure with excessive fluid intake
-Cardiac failure
-Liver disease
-Hypoalbuminaemia
-ADH secreting tumours
-Excessive administration of 5% dextrose in post-op period when ADH secretion is high

24
Q

Renal regulation of Na+?

A
  • 99% filtered is reabsorbed (65% PCT, 25% LoH, 10% distal)
  • Determined by GFR, RAAS and several prostaglandins
  • Angiotensin II stimulates Na+ reabsorption throughout nephron and constricts arterioles
25
Q

Extrarenal regulation of Na+?

A
  • RAAS: angiotensin II releases aldosterone from zona glomerulosa which promotes Na+ reabsorption in distal tubule and collecting ducts, as well as colon epithelium, salivary ducts and sweat glands
  • ANP released from atria in response to stretch. This increases excretion of Na+ by increasing GFR, inhibiting reabsorption in ducts and reducing RAAS
26
Q

Causes of sodium excess leading to hypernatraemia?

A
  • Excessive IV infusion (e.g. post-op)
  • Conn’s (hyperaldosterone)
  • Cushing’s
  • Steroid therapy
  • Chronic CCF
  • Cirrhosis
27
Q

Causes of water depletion leading to hypernatraemia?

A
  • Reduced intake (coma/confusion)
  • Renal (osmotic diuresis, diuretic phase acute renal failure, post-relief obstructive uropathy, diabetes insipidus)
  • Fever, burns, diarrhoea, fistulae
28
Q

Causes of Na+ deficiency?

A
  • Low intake (coma/dysphagia/dextrose)
  • GI loss (diarrhoea obstruction, fistulae, ileus)
  • Excessive sweating (eg fever)
  • Burns
  • Drainage of ascites
  • Addison’s disease
  • Diuretics
  • SIADH (meds, lung Ca, head injury etc)
29
Q

What regulates K+ levels?

A

Aldosterone - increases excretion in distal tubule

Insulin - promotes K+ entry into cells

Acid-base - acidosis results in reduced K+ entry into cells and reduced urinary excretion (alkalosis opposite)

  • Hydration - K+ lost from cells when dehydrated
  • Catabolic states (trauma, surgery, infection) K+ lost from cells
30
Q

Causes of hyperkalaemia?

A
  • Excess administration
  • Renal failure
  • Haemolysis
  • Crush injuries
  • Tissue necrosis (burns, ischaemia)
  • Metabolic acidosis
  • Adrenal insufficiency (addison’s)
31
Q

ECG changes hyperkalaemia?

A

Peaked T waves
Loss of P waves
Wide QRS complex

32
Q

Hypokalaemia ECG changes?

A

Low, broad T waves
Presence of U waves

33
Q

Causes of hypokalaemia?

A

Inadequate intake (dextrose/saline, coma, dysphagia)

Excessive loss:
- Renal (diuretucs, renal tubular disorders)
- GI (D&V, fistulae, laxatives, villous adenoma)
- Endocrine (Cushing’s, steroid, hyperaldosteronism prim and sec)

34
Q
A

MRCS Physiology (1 decks)

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