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1MRCP Part 1 > Physiology > Flashcards

Physiology Flashcards

1
Q

What is the systemic response in vasculature to hypoxia?
Where is this NOT the case?

A

Hypoxia results in vasodilation in systemic arteries
e.g. brain, kidneys, gut and myocardium
Pulmonary arteries causes vasoconstriction
e.g. in lungs to allow blood to be re-directed within the lung to higher concentrations of O2: allows blood to flow to the most well ventilated parts of the lung = improve O2 delivery
Occurs via increased sympathetic tone

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2
Q

Osmolality =
- Low osmolality

A

2(Na+ + K+) + glucose + urea
Low = dilution, low solute available

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2
Q

Control of inspiration and expiration

A

Expiration = ventral medulla oblongata
Inspiration = dorsal medulla oblongata

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3
Q

Anion Gap =

A

(Na+ + K+) - (Cl- + HCO3-)
Usually 10-16

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4
Q

Causes of raised anion gap

A

MUDPILES
Methanol
Uraemia
Renal failure
DKA
Lactic Acidosis
Salicylate
Ethylene glycol

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5
Q

Where does bicarbonate buffering occur (2)

A

Proximal tubules (most)
- H+ coupled with sodium/bicarbonate reabsorption
RBC (minor role)
- bicarbonate exchanged for chloride

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6
Q

How is an acidosis compensated for? (2)

A

Acute = red blood cell buffering
Chronic = renal bicarbonate

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7
Q

Causes of respiratory alkalosis (5)

A

Raised ICP
PE
Pneumonia
Anxiety
Pulmonary oedema

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8
Q

Causes of metabolic alkalosis (4)

A

Vomiting
Hyperaldosteronism
Cushing’s syndrome
Bartter’s syndrome

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9
Q

Hyperchloraemic acidosis

A

= occurs when there is loss of bicarbonate (rather than increased acid production)
e.g. renal tubular acidosis, acetazolamide

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10
Q

Hypochloraemic Acidosis (3)

A

Loss of GI fluids
Over treatment with diuretics
Adrenal insufficiency

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11
Q

Expiratory reserve volume

A

= maximum volume of air that can be forcibly expired in a normal breath

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12
Q

Tidal volume =

A

approx. 500ml in males
= volume inspired at rest in a normal breath

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13
Q

Inspiratory reserve volume

A

= maximum volume of air that can be inspired at the end of a normal tidal respiration

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14
Q

Vital Capacity =

A

= TV + IRV + ERV

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14
Q

Inspiratory capacity =

A

= tidal volume + inspiratory reserve volume

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15
Q

VQ Ratio
- what does it mean if it is high?

A

Volume of air entering alveoli/blood flow through lungs
High = poor perfusion, wasted ventilation
Low = poor ventilation, wasted perfusion

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15
Q

Production of pulmonary surfactant

A

Type II pneumocytes

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16
Q

Types of resistance in work of breathing (2)

A

Static resistance - elastic recoil of lungs
Dynamic resistance - airways obstruction

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17
Q

Transfer factor =

A

= rate at which gas will difuse from alveoli into the blood

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18
Q

Effects of inspiration and expiration on the heart

A

Inspiration = increased RV filling and output increases
Expiration = increased LV filling and output

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19
Q

What is the most important factor in the control of breathing?

A

pCO2 due to pH effect - central chemoreceptors respond to changes in H+

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19
Q

Cardiac pacemaker potential

A

Slow Na+ in
Rapid Calcium in
Rapid K+ out

20
Q

Hering Bruer Reflex

A

= distension of lung slows rate of breathing

21
Q

Phases of Cardiac Action Potential

A

4,0,1,2,3,4
4 - plateau
0 = Na+ in, rapid depolarisation
1 = K+ out
2 = Ca2+ in/K+ out in balance
3 = K+ out

22
Q

Cardiac output =

A

= heart rate x stroke volume

23
Q

Cardiac contractility
- term
- positive
- negative

A

= inotropy
Positive inotropes = sympathetics, decrease in intracellular Na+, digoxin
Negative inotropes = B-blockers, heart failure, hypoxia, acidosis

23
Q

Preload =

A

= ventricular end diastolic volume, increased with increased venous return

24
Q

Afterload =

A

= total peripheral resistance
Altered by increasing/altering vessel calibre

24
Q

Blood pressure =

A

= cardiac output x peripheral resistance

25
Q

Trigger for release of insulin by vesicles

A

= influx of calcium

26
Q

Inhibition of insulin secretion (3)

A

Sympathetics
A-blockers
B-blockers

27
Q

Gastrin
- where released
- action

A

G cells in antrum of stomach
= increased gastric acid production and emptying

27
Q

Secretin
- where released
- action

A

S cells of duodenum/jejunum
Action = inhibits gastric acid

28
Q

CCK
- where released
- action

A

I cells of duodenum/jejunum
Actions = gallbladder contraction, sphincter of oddi relaxation, satiety

29
Q

Somatostatin
- where released
- action

A

D cells of pancreas/stomach
Action = decreases acid secretion, decreases gastrin, insulin and glucagon secretion

30
Q

VIP
- where released
- action

A

Small intestine
Action = stimulates pancreatic secretions, inhibits acid secretion

30
Q

What do parietal cells produce (2)?

A

HCl
Intrinsic Factor

31
Q

What do chief cells produce?

A

Pepsinogen (precursor of pepsin)

32
Q

Pancreatic acinar cells produce…

A

Enzymes

33
Q

What do the parafollicular cells produce?

A

Calcitonin

34
Q

What does calcitonin do?

A

Reduces blood calcium levels

34
Q

What does the zona glomerulosa produce?

A

Mineralocorticoids

35
Q

Anterior Pituitary
- hormones secreted from basophils

A

LH and FSH
TSH
ACTH
MSH

35
Q

Anterior Pituitary
- hormones secreted from acidophils

A

GH
Prolactin

36
Q

Where is ADH synthesised?
Where is ADH released from?

A

Synthesis = supraoptic and paraventricular nuclei of hypothalamus
Release from posterior pituitary

36
Q

Causes of SIADH (8)

A

Vincristine
TB
Ectopic focus e.g. small cell lung cancer
Pleural effusion
Stroke
Head Injury
Carbamazepine
Encephalitis

37
Q

Where is most sodium and potassium reabsorbed?

A

Proximal tubule

37
Q

Distal tubule
- secretion
- reabsorption

A

Secretion = H+ and K+ under influence of aldosterone
Reabsorption = Na+ and bicarbonate

37
Q

Carbonic anhydrase inhibitors act on…

A

Na+/H+ channel in proximal tubule of kidney

38
Q

Loop Diuretics act on…

A

Na+/Cl-/2K+ channel in ascending loop
= NKCC2 channel

39
Q

Where is BNP released from?

A

Ventricular myocytes = natriuresis

40
Q

Hypervolaemic Hyponatraemia
- causes (3)
- biochemical findings

A

Low serum osmolality = dilution

  1. Cirrhosis
  2. Heart Failure
    Low urine sodium
    (kidney trying to reabsorb sodium to try and increase sodium levels)
  3. Nephrotic Syndrome
    High urine sodium - unable to reabsorb
41
Q

Euvolaemic Hyponatraemia
- cause
- biochemical findings

A

Usually SIADH
= increased ADH, promotes water retention (lower levels of aldosterone/RAAS as increased ANP/BNP to try and counter water retention)

Low serum osmolality
High urine sodium
(less reabsorption of sodium mediated by aldosterone)

42
Q

Hypovolaemic Hyponatraemia
- causes (4)
- biochemical findings

A
  1. Diuretics
  2. Vomiting
  3. Adrenal Insufficiency
    High urine Na+ - less reabsorption by aldosterone
  4. Burns

1MRCP Part 1 (20 decks)

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