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MRSA theory > Physiology > Flashcards

Physiology Flashcards

1
Q

Causes of hypomagnesaemia?

A

Diuretics
Total parenteral nutrition
Diarrhoea
Alcohol
Hypokalaemia, hypocalcaemia

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2
Q

Feature of hypomagnesaeia?

A

Paraesthesia
Tetany
Seizures
Arrhythmias
Decreased PTH secretion → hypocalcaemia
ECG features similar to those of hypokalaemia
Exacerbates digoxin toxicity

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3
Q

CSF path of circulation?

A
  1. Lateral ventricles (via foramen of Munro)
  2. 3rd ventricle
  3. Cerebral aqueduct (aqueduct of Sylvius)
  4. 4th ventricle
  5. Subarachnoid space (via foramina of Magendie and Luschka)
  6. Reabsorbed into the venous system via arachnoid granulations into superior sagittal sinus
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4
Q

CSF composition?

A

Composition
Glucose: 50-80mg/dl
Protein: 15-40 mg/dl
Red blood cells: Nil
White blood cells: 0-3 cells/ mm3

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5
Q

What is TRALI?

A

Acute onset non cardiogenic pulmonary oedema
Leading cause of transfusion related deaths
Greatest risk posed with plasma components
Occurs as a result of leucocyte antibodies in transfused plasma
Aggregation and degranulation of leucocytes in lung tissue accounts for lung injury

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6
Q

Complications of massive transfusion?

A

Hypothermia
Hypocalcaemia
Hyperkalaemia
Delayed type transfusion reaction
TRALI
coagulopathy

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7
Q

Actions of cortisol?

A

Glycogenolysis
Gluconeogenesis
Protein catabolism
Lipolysis
Stress response
Anti-inflammatory
Decrease protein in bones
Increase gastric acid
Increases neutrophils/platelets/red blood cells
Inhibits fibroblastic activity

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8
Q

Where is Gastrin secreted?

A

G cells in antrum of the stomach

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9
Q

Stimulus for gastrin secretion?

A

Distension of stomach, extrinsic nerves
Inhibited by: low antral pH, somatostatin

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10
Q

Actions of gastrin secretion?

A

Increase HCL, pepsinogen and IF secretion, increases gastric motility, trophic effect on gastric mucosa

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11
Q

Source of CCK?

A

I cells in upper small intestine

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12
Q

Stimulus for CCK secretion?

A

Partially digested proteins and triglycerides

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13
Q

Actions of CCK?

A

Increases secretion of enzyme-rich fluid from pancreas, contraction of gallbladder and relaxation of sphincter of Oddi, decreases gastric emptying, trophic effect on pancreatic acinar cells, induces satiety

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14
Q

Source of secretin?

A

S cells in upper small intestine

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15
Q

Stimulus for secretin secretion?

A

Acidic chyme, fatty acids

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16
Q

Actions of secretin?

A

Increases secretion of bicarbonate-rich fluid from pancreas and hepatic duct cells, decreases gastric acid secretion, trophic effect on pancreatic acinar cells

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17
Q

Source of somatostatin secretion?

A

D cells in the pancreas and stomach

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18
Q

Stimulus for somatostatin secretion?

A

Fat, bile salts and glucose in the intestinal lumen

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19
Q

Actions of somatostatin?

A

Decreases acid and pepsin secretion, decreases gastrin secretion, decreases pancreatic enzyme secretion, decreases insulin and glucagon secretion
inhibits trophic effects of gastrin, stimulates gastric mucous production

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20
Q

Which clotting factors are most temperature sensitive?

A

F5 and 8

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21
Q

Typical intracellular fluid % of total volume?

A

60-65%
28L

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22
Q

Typical extracellular fluid % of total volume?

A

35-40%
14L

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23
Q

Typical plasma % of total volume?

A

5%
3L

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24
Q

Typical interstitial % of total volume?

A

24%
10L

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25
Q

Typical trans cellular % of total volume?

A

3%
1L

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26
Q

What is the main component of colloid in the thyroid gland?

A

thyroglobulin

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27
Q

Synthesis and secretion of thyroid hormones?

A

1.Thyroid actively concentrates iodide to 25x plasma concentration.
2. Iodide oxidised peroxidase in the follicular cells to atomic iodine
3. atomic iodine iodinates tyrosine residues contained in thyroglobulin.
4. Iodinated tyrosine residues in thyroglobulin undergo coupling to either T3 or T4.

Process is stimulated by TSH, which stimulates secretion of thyroid hormones.
The normal thyroid has approximately 3 month reserves of thyroid hormones.

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28
Q

which antibodies are in graves?

A

IgG antibodies to the TSH receptors

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29
Q

2 main mechanisms of metabolic acidosis?

A
  1. Gain of strong acid (e.g. diabetic ketoacidosis)
  2. Loss of base (e.g. from bowel in diarrhoea)
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30
Q

How to calculate anion gap? and normal range

A

(Na+ + K+) - (Cl- + HCO3-).
- If a question supplies the chloride level then this is often a clue that the anion gap should be calculated.

The normal range = 10-18 mmol/L

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31
Q

Causes of metabolic acidosis raised anion gap?

A

Lactate: shock, hypoxia
Ketones: diabetic ketoacidosis, alcohol
Urate: renal failure
Acid poisoning: salicylates, methanol

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32
Q

Causes of metabolic acidosis normal anion gap?

A

= hyperchloraemic metabolic acidosis

Gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
Renal tubular acidosis
Drugs: e.g. acetazolamide
Ammonium chloride injection
Addison’s disease

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33
Q

Types of metabolic acidosis due to high lactate?

A

Lactic acidosis type A: (Perfusion disorders e.g.shock, hypoxia, burns)
Lactic acidosis type B: (Metabolic e.g. metformin toxicity)

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34
Q

Causes of metabolic alkalosis?

A

Caused by a loss of hydrogen ions or a gain of bicarbonate. It is due mainly to problems of the kidney or gastrointestinal tract:

Vomiting / aspiration (e.g. Peptic ulcer leading to pyloric stenosis, nasogastric suction)
Diuretics
Liquorice, carbenoxolone
Hypokalaemia
Primary hyperaldosteronism
Cushing’s syndrome
Bartter’s syndrome
Congenital adrenal hyperplasia

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35
Q

Mechanism of metabolic alkalosis?

A

Activation of renin-angiotensin II-aldosterone (RAA) system is a key factor
Aldosterone causes reabsorption of Na+ in exchange for H+ in the distal convoluted tubule
ECF depletion (vomiting, diuretics) → Na+ and Cl- loss → activation of RAA system → raised aldosterone levels
In hypokalaemia, K+ shift from cells → ECF, alkalosis is caused by shift of H+ into cells to maintain neutrality

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36
Q

Causes of respiratory acidosis?

A

Usually alveolar hypoventilation

COPD
Decompensation in other respiratory conditions e.g. Life-threatening asthma / pulmonary oedema
Sedative drugs: benzodiazepines, opiate overdose

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37
Q

Causes of respiratory alkalosis?

A

Hyperventilation

Psychogenic: anxiety leading to hyperventilation
Hypoxia causing a subsequent hyperventilation: pulmonary embolism, high altitude
Early salicylate poisoning*
CNS stimulation: stroke, subarachnoid haemorrhage, encephalitis
Pregnancy

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38
Q

Where is onufs nucleus found?

A

anterior horn of S2 and is the origin of neurones to the external urethral sphincter.

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39
Q

Which nerves provide somatic innervation to the bladder?

A

pudendal, hypogastric and pelvic nerves

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40
Q

Hormones that are increased in the stress response?

A

Growth hormone
cortisol
renin
ACTH
aldosterone
prolactin
ADH
Glucagon

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41
Q

Hormones that are decreased in the stress response?

A

Insulin
Testosterone
Oestrogen

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42
Q

Hormones that do not change in the stress response?

A

TSH
LH FSH

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43
Q

Why is insulin release inhibited by stress?

A

Release inhibited by stress
Occurs via the inhibition of the beta cells in the pancreas by the α2-adrenergic inhibitory effects of catecholamines

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44
Q

Effects of PTH?

A

Bone: Binds to osteoblasts which signal to osteoclasts to cause resorption of bone and release calcium.
Kidney: Active reabsorption of calcium and magnesium from the distal convoluted tubule. Decreases reabsorption of phosphate.

Intestine (via kidney): Increases intestinal calcium absorption by increasing activated vitamin D. Activated vitamin D increases calcium absorption.

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45
Q

what is septic shock?

A

refractory systemic arterial hypotension in spite of fluid resuscitation

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46
Q

Effects of α-1, α-2 receptor binding?

A

vasoconstriction

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47
Q

Effects of β-1 receptor binding?

A

increased cardiac contractility and HR

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48
Q

Effects of β-2 receptor binding?

A

vasodilatation

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49
Q

Effects of D-1 receptor binding?

A

renal and spleen vasodilatation

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50
Q

Effects of d-2 receptor binding?

A

inhibits release of noradrenaline

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51
Q

Adrenaline cardiovascular receptor action?

A

α-1, α-2, β-1, β-2

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52
Q

Noradrenaline cardiovascular receptor action?

A

α-1,( α-2), (β-1), (β-2)

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53
Q

Dobutamine cardiovascular receptor action?

A

β-1, (β 2)

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54
Q

Dopamine cardiovascular receptor action?

A

(α-1), (α-2), (β-1), D-1,D-2

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55
Q

Causes of pseudohyponatruaemia?

A

hyperlipidaemia (increase in serum volume) or a taking blood from a drip arm
multiple myeloma

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56
Q

Hyponatraemia urinary sodium >20

A

Mnemonic: Syndrome of INAPPropriate Anti-Diuretic Hormone:
In creased
Na (sodium)
PP (urine)

Sodium depletion, renal loss
Patient often hypovolaemic
Diuretics (thiazides)
Addison’s
Diuretic stage of renal failure
SIADH (serum osmolality low, urine osmolality high, urine Na high)
Patient often euvolaemic

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57
Q

hyponatraemia urinary sodium <20

A

Sodium depletion, extra-renal loss
Diarrhoea, vomiting, sweating
Burns, adenoma of rectum (if villous lesion and large)

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58
Q

Causes of hypervolaemic hyponatraemia?

A

Secondary hyperaldosteronism: CCF, cirrhosis
Reduced GFR: renal failure
IV dextrose, psychogenic polydipsia

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59
Q

How to calculate sodium requirement?

A

(125 - serum sodium) x 0.6 x body weight = required mEq of sodium

Aim to correct until the Na is > 125 at a rate of 1 mEq/h. or central pontine myelinolysis

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60
Q

at which part of the bowel is most water absorbed?

A

(jejunum and ileum)

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61
Q

what causes raised carbon monoxide transfer factor (TLCO)?

A

Causes of a raised TLCO:
asthma
pulmonary haemorrhage (Wegener’s, Goodpasture’s)
left-to-right cardiac shunts
polycythaemia
hyperkinetic states
male gender, exercise

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62
Q

What causes a lowerTLCO?

A

pulmonary fibrosis
pneumonia
pulmonary emboli
pulmonary oedema
emphysema
anaemia
low cardiac output

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63
Q

Drugs causingSIADH?

A

Drugs causing SIADH: ABCD

A nalgesics: opioids, NSAIDs
B arbiturates
C yclophosphamide/ Chlorpromazine/ Carbamazepine
D iuretic (thiazides)

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64
Q

Which receptor does morphine and other conventional opioids attach to?

A

MU

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65
Q

Functions of insulin?

A

Secreted in response to hyperglycaemia
Glucose utilisation and glycogen synthesis
Inhibits lipolysis
Reduces muscle protein loss

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66
Q

Effect of vitamin B1 deficiency?

A

beriberi

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67
Q

Effect of vitamin B2 deficiency?

A

Dermatitis and photosensitivity

68
Q

Effect of vitamin B3 deficiency?

A

Pellagra

69
Q

Effect of vitamin C deficiency?

A

Poor wound healing
Impaired collagen synthesis

70
Q

Effect of vitamin D deficiency?

A

Rickets (Children)
Osteomalacia (Adults)

71
Q

Total CSF volume in the brain?

A

150 ml

72
Q

What produces CSF?

A

500 ml is produced by the ependymal cells in the choroid plexus (70%), or blood vessels (30%). It is reabsorbed via the arachnoid granulations which project into the venous sinuses.

73
Q

Circulation of CSF?

A
  1. Lateral ventricles (via foramen of Munro)
  2. 3rd ventricle
  3. Cerebral aqueduct (aqueduct of Sylvius)
  4. 4th ventricle
  5. Subarachnoid space (via foramina of Magendie and Luschka)
  6. Reabsorbed into the venous system via arachnoid granulations into superior sagittal sinus
74
Q

Composition of CSF?

A

Glucose: 50-80mg/dl
Protein: 15-40 mg/dl
Red blood cells: Nil
White blood cells: 0-3 cells/ mm3

75
Q

Causes of right shift of O2 dissociation curve?

A

CADET face RIGHT[reduced affinity]

C O2
A cidosis
2,3-DPG
E xercise
T emperature

[ie when there is increased O2 requirement of the tissue]

76
Q

Causes of left shift of O2 dissociation curve?

A

decreased temp
decreased2,3-dpg
co
IncreaseH+

77
Q

What is DPG and when is it released?

A

DPG is found in erythrocytes and is increased during glycolysis. It binds to the Hb molecule, thereby releasing oxygen to tissues. DPG is increased in conditions associated with poor oxygen delivery to tissues, such as anaemia and high altitude.

78
Q

How much bile enters the small bowel daily?

A

between 500 mL and 1.5 L

79
Q

What is bile composed of?

A

bile salts, bicarbonate, cholesterol, steroids and water

80
Q

Factors regulating bile flow?

A

hepatic secretion, gall bladder contraction and sphincter of oddi resistance

81
Q

What are the three phases gastric secretion?

A
  1. Cephalic phase (smell / taste of food)
    30% acid produced
    Vagal cholinergic stimulation causing secretion of HCL and gastrin release from G cells
  2. Gastric phase (distension of stomach )
    60% acid produced
    Stomach distension/low H+/peptides causes Gastrin release
  3. Intestinal phase (food in duodenum)
    10% acid produced
    High acidity/distension/hypertonic solutions in the duodenum inhibits gastric acid secretion via enterogastrones (CCK, secretin) and neural reflexes.
82
Q

Factors increasing gastric acid production?

A

Vagal nerve stimulation
Gastrin release
Histamine release (indirectly following gastrin release) from enterchromaffin like cells

83
Q

Factors decreasing gastric acid production?

A

Somatostatin (inhibits histamine release)
Cholecystokinin
Secretin

84
Q

How long will it take for the serum PTH levels to fall if the functioning adenoma has been successfully removed?

A

10 MINS
[shorthalflife]

85
Q

Actions calcitonin?

A

Secreted by C cells of thyroid
Inhibits intestinal calcium absorption
Inhibits osteoclast activity
Inhibits renal tubular absorption of calcium

86
Q

Most likely explanation for generalised oedema following burns?

A

Reduction in capillary oncotic pressure

The significant burns will result in generalised loss of high molecular weight proteins thereby reducing the capillary oncotic pressure

87
Q

What are starlings forces?

A

Capillary pressure - forces fluid out of the capillary
Interstitial fluid pressure- which tends to force fluid inwards through the capillary membrane (when it is positive)
Plasma colloid osmotic pressure- favors influx into the capillary
Interstitial fluid osmotic pressure- favors efflux from the capillary into the interstitium

88
Q

What proportion of salivary gland secretions is contributed by the parotid gland?

A

Around25%

most from submandibular gland

89
Q

Which hormones are released from the islets of langerhans?

A

Beta cells Insulin (70% of total secretions)
Alpha cells Glucagon
Delta cells Somatostatin
F cells Pancreatic polypeptide

90
Q

How to work out GFR?

A

(Conc. of solute in urine x volume of urine produced per minute )/plasma conc

creatinine is often used as solute

plasma concentration (mmol/l)

91
Q

what is renal clearance?

A

Renal clearance = volume plasma from which a substance is removed per minute by the kidneys

92
Q

Features of substances used to measure GFR?

A
  1. Inert
  2. Free filtration from the plasma at the glomerulus (not protein bound)
  3. Not absorbed or secreted at the tubules
  4. Plasma concentration constant during urine collection
93
Q

How much water enters the descending loop of henle within24 h?

A

60L

94
Q

Metabolic consequences ofrefeeding?

A

Hypophosphataemia
Hypokalaemia
Hypomagnesaemia
Abnormal fluid balance
-> organ failure

If patient not eaten for > 5 days, aim to re-feed at < 50% energy and protein levels

95
Q

Refeeding prescription?

A

Start at up to 10 kcal/kg/day increasing to full needs over 4-7 days
Start immediately before and during feeding: oral thiamine 200-300mg/day, vitamin B co strong 1 tds and supplements
Give K+ (2-4 mmol/kg/day), phosphate (0.3-0.6 mmol/kg/day), magnesium (0.2-0.4 mmol/kg/day)

96
Q

examples of acute phase proteins?

A

CRP
procalcitonin
ferritin
fibrinogen
alpha-1 antitrypsin
caeruloplasmin
serum amyloid A
haptoglobin
complement

97
Q

proteins decreased in acute phase response? (negative acute phase proteins)

A

albumin
transthyretin (formerly known as prealbumin)
transferrin
retinol binding protein
cortisol binding protein

98
Q

What is secreted by acinar cells of the pancreas?

A

Trypsinogen
Procarboxylase
Amylase
Elastase

99
Q

What is secreted by ductal and centroacinar cells of the pancreas?

A

Sodium
Bicarbonate
Water
Potassium
Chloride
NB: Sodium and potassium reflect their plasma levels; chloride and bicarbonate vary with flow rate

100
Q

What stimulates acinar and ductal cells?

A

CCK

ductal cells potently stimulated by secretin

While secretin will typically increase electrolyte and water volume of secretions, the enzyme content is increased by cholecystokinin

101
Q

Pathological jugular venous pressure waves?

A

Absent a waves = Atrial fibrillation
Large a waves = Any cause of right ventricular hypertrophy, tricuspid stenosis
Cannon waves (extra large a waves) = Complete heart block
Prominent v waves = Tricuspid regurgitation
Slow y descent = Tricuspid stenosis, right atrial myxoma
Steep y descent = Right ventricular failure, constrictive pericarditis, tricuspid regurgitation

102
Q

Which part of the brain is most associated with thermoregulation?

A

hypothalamus
Peripheral and central thermoreceptors relay to this region.

103
Q

Deficiency of which electrolyte is likely to account for hypocalcaemia after TPN?

A

magnesium
Magnesium is required for both PTH secretion and its action on target tissues

decreased magnesium will tend to affect the permeability of cellular membranes to calcium -> hyper excitability

104
Q

what do parietal cells, chief cells and mucosal cells secrete

A

Parietal cells: secrete HCl, Ca, Na, Mg and intrinsic factor
Chief cells: secrete pepsinogen
Surface mucosal cells: secrete mucus and bicarbonate

105
Q

Which cell secretes the majority of tumour necrosis factor in humans?

A

macrophage

106
Q

Effects of TNF?

A

activates macrophages and neutrophils
acts as costimulator for T cell activation
key mediator of body’s response to Gram negative septicaemia
similar properties to IL-1
anti-tumour effect (e.g. phospholipase activation)

107
Q

What is glucagon?

A

Glucagon is a protein comprised of a single polypeptide chain.
Produced by alpha cells of pancreatic islets of Langerhans in response to hypoglycaemia and amino acids.
It increases plasma glucose and ketones.

108
Q

What causes stimulation of glucagon?

A

decreased plasma glucose
increased catecholamines
increased plasma amino acids
sympathetic nervous system
acetylcholine
cholecystokinin

109
Q

What causes inhibition of glucagon?

A

somatostatin
insulin
increased free fatty acids and kept acids
urea

110
Q

What is the most common cause of high output diarrhoea following terminal ileal resection?

A

malabsorption of bile salts. The administration of cholestyramine (bile salt binding agent) will counter this

111
Q

Where are the reticulo-endothelial cells concentrated within the spleen?

A

white pulp
(lymphoid follicles also present)

112
Q

What is found in the red pulp of the spleen?

A

blood filled venous sinuses

113
Q

What is the action of vasopressin release from pituitary?

A

ADH (vasopressin) results in the insertion of aquaporin channels in apical membrane of the distal tubule and collecting ducts.

114
Q

What is tidal volume and what is the normal range?

A

The volume of air inspired and expired during each ventilatory cycle at rest.
It is normally 500mls in males and 340mls in females.

115
Q

What is the inspiratory reserve volume?

A

Is the maximum volume of air that can be forcibly inhaled following a normal inspiration. 3000mls.

116
Q

What is the expiratory reserve volume?

A

Is the maximum volume of air that can be forcibly exhaled following a normal expiration. 1000mls.

117
Q

What is the residual volume?

A

Is that volume of air remaining in the lungs after a maximal expiration.
RV = FRC - ERV. 1500mls.

118
Q

What is functional residual capacity?

A

Is the volume of air remaining in the lungs at the end of a normal expiration.
FRC = RV + ERV. 2500mls.

119
Q

What is vital capacity?

A

Is the maximal volume of air that can be forcibly exhaled after a maximal inspiration.
VC = TV + IRV + ERV. 4500mls in males, 3500mls in females.

120
Q

What is total lung capacity?

A

Is the volume of air in the lungs at the end of a maximal inspiration.
TLC = FRC + TV + IRV = VC + RV. 5500-6000mls.

121
Q

wHAT IS forced vital capacity

A

The volume of air that can be maximally forcefully exhaled.

122
Q

How to work out fractional sodium and urea excretion?

A

ractional sodium excretion = (urine sodium/plasma sodium) / (urine creatinine/plasma creatinine) x 100

**fractional urea excretion = (urine urea /blood urea ) / (urine creatinine/plasma creatinine) x 100

123
Q

Drugs causing hyperuricaemia?

A

C iclosporin
A lcohol
N icotinic acid
T hiazides

L oop diuretics
E thambutol
A spirin
P yrazinamide

124
Q

What causes hyperuricaemia?

A

increased cell turnover or reduced renal excretion of uric acid

Increased synthesis:
Lesch-Nyhan disease
Myeloproliferative disorders
Diet rich in purines
Exercise
Psoriasis
Cytotoxics

Decreased secretion:
Drugs: low-dose aspirin, diuretics, pyrazinamide
Pre-eclampsia
Alcohol
Renal failure
Lead

125
Q

In restrictive lung disease how is the FEV1/FVC affected?

A

normal or >80%

ratio reduced in obstructive

126
Q

What modulates prolactin release?

A

+ TRH
- dopamine

127
Q

Common causes of hypercalcaemia?

A

Main causes
-Malignancy (most common cause in hospital in-patients)
-Primary hyperparathyroidism (commonest cause in non hospitalised patients)

Less common
-Sarcoidosis (extrarenal synthesis of calcitriol )
-Thiazides, lithium
-Immobilisation
-Pagets disease
-Vitamin A/D toxicity
-Thyrotoxicosis
-MEN
-Milk alkali syndrome

128
Q

What are the 4 types of opioid receptor?

A

1.δ (located in CNS)- Accounts for analgesic and antidepressant effects
2.k (mainly CNS)- analgesic and dissociative effects
3.µ (central and peripheral) - causes analgesia, miosis, decreased gut motility
4.Nociceptin receptor (CNS)- Affect of appetite and tolerance to µ agonists.

129
Q

Causes of hyperkalaemia?

A

‘Machine’ - Causes of Increased Serum K+

M - Medications - ACE inhibitors, NSAIDS
A - Acidosis - Metabolic and respiratory
C - Cellular destruction - Burns, traumatic injury
H - Hypoaldosteronism, haemolysis
I - Intake - Excessive
N - Nephrons, renal failure
E - Excretion - Impaired

130
Q

Causes of oxygen curve left shift [haldane effect]?

A

HbF, methaemoglobin, carboxyhaemoglobin
low [H+] (alkali)
low pCO2
low 2,3-DPG
low temperature

131
Q

Causes of bohr effect (right shift)?

A

raised [H+] (acidic)
raised pCO2
raised 2,3-DPG*
raised temperature

132
Q

What are the actions of somatostatin?

A

an inhibitor of growth hormone
delays gastric emptying reduces gastrin secretion
reduces pancreatic exocrine function

133
Q

What are some factors stimulating renin secretion?

A

Low BP
Hyponatraemia
Sympathetic nerve stimulation
Catecholamines
Erect posture

134
Q

What do A γ nervous fibres transmit?

A

information relating to motor proprioception

135
Q

what do A β nervous fibres transmit?

A

touch and pressure

136
Q

What do B nervous fibres transmit?

A

autonomic fibres

137
Q

Whatdo C fibres transmit?

A

high intensity mechanothermal stimuli

138
Q

What are peripheral nociceptors innervated by?

A

small myelinated fibres (A-delta) fibres or by unmyelinated C fibres.

139
Q

At whoich site is most dietary iron absorbed?

A

duodenum (and upper jejunum)

140
Q

What increases absorption of iron?

A

vitamin C
gastric acid

141
Q

What do central chemoreceptors do?

A

Respond to increased H+ in BRAIN INTERSTITIAL FLUID to increase ventilation.

142
Q

Where are peripheral chemoreceptors located?

A

bifurcation of carotid arterie and arch of aorta

143
Q

What is control of respiration coordinated by?

A

respiratory centres, chemoreceptors, lung receptors and muscles.

144
Q

What do the medulla and pons control? (respiratory)

A

Automatic, involuntary control of respiration

145
Q

what does the respiratory centre control?

A

respiratory rate and the depth of respiration

146
Q

What is the most important urinary acid base buffer?

A

phosphate

147
Q

What electrolyte abnormality may result from large villous adenomas of rectum?

A

marked secretory activity and result in the development of hypokalaemia as rectal secretions are rich in potassium

148
Q

What is the same as end diastolic volume?

A

PRELOAD

149
Q

What is after load the same as?

A

aortic pressure

150
Q

Where are baroreceptors located and what are they stimulated by?

A

aortic arch and carotid sinus
arterial stretch

151
Q

what does increase in baroreceptor stretch cause?

A

Aortic baroreceptor impulses travel via the vagus and from the carotid via the glossopharyngeal nerve.

Increased parasympathetic discharge to the SA node.
*Decreased sympathetic discharge to ventricular muscle causing decreased contractility and fall in stroke volume.
*Decreased sympathetic discharge to venous system causing increased compliance.
*Decreased peripheral arterial vascular resistance

152
Q

MOA of tranexamic acid?

A

Tranexamic acid inhibits plasmin and this prevents fibrin degradation.

153
Q

Procedure for immediate reversal of warfarin in patients undergoing surgery

A
  1. Stop warfarin
  2. Vitamin K (reversal within 4-24 hours)
    -IV takes 4-6h to work (at least 5mg)
    -Oral can take 24 hours to be clinically effective
  3. Fresh frozen plasma
    Used less commonly now as 1st line warfarin reversal
    -30ml/kg-1
    -Need to give at least 1L fluid in 70kg person (therefore not appropriate in fluid overload)
    -Need blood group
    -Only use if human prothrombin complex is not available
  4. Human Prothrombin Complex (reversal within 1 hour)
    -Bereplex 50 u/kg
    -Rapid action but factor 6 short half life, therefore give with vitamin K
154
Q

Action of gastrin?

A

From G cells: stimulates gastric acid production

155
Q

Action of pepsin?

A

Digestion of protein, secretion occurs simultaneously with gastrin

156
Q

Action of secretin?

A

From mucosal cells in the duodenum and jejunum: inhibits gastric acid, stimulates bile and pancreatic juice production

157
Q

Action of gastric inhibitory peptide?

A

(produced in response to fatty acids) inhibits gastrin release and acid secretion from parietal cells

158
Q

Action of histamine on gastric?

A

Histamine released from enterochromaffin like cells then stimulates the acid-making cells (parietal cells) in a paracrine manner to increase gastric acid production.

159
Q

What is hypokalaemia commonly associated with?

A

metabolic alkalosis
1) the common causes of metabolic alkalosis (vomiting, diuretics) directly induce H+ and K loss (via aldosterone)

  1. transcellular shift in which K leaves and H+ enters the cells, thereby raising the extracellular pH
  2. transcellular shift in the cells of the proximal tubules resulting in an intracellular acidosis, which promotes ammonium production and excretion
  3. n the presence of hypokalemia, hydrogen secretion in the proximal and distal tubules increases. further reabsorption of HCO3- [net effect acid excretion]
160
Q

Causes of hypokalaemia with alkalosis?

A

Vomiting
Diuretics
Cushing’s syndrome
Conn’s syndrome (primary hyperaldosteronism)

161
Q

Causes of hypokalaemia with acidosis?

A

Diarrhoea
Renal tubular acidosis
Acetazolamide
Partially treated diabetic ketoacidosis

162
Q

How to calculate cerebral perfusion pressure

A

Cerebral perfusion pressure= Mean arterial pressure - intra cranial pressure

163
Q

Causes of normal anion gap acidosis?

A

Normal Gap Acidosis: HARDUP
H - Hyperalimentation/hyperventilation
A - Acetazolamide
R - Renal tubular acidosis
D - Diarrhoea
U - Ureteral diversion
P - Pancreatic fistula/parenteral saline

164
Q

Causes of normal anion gap acidosis?

A

Normal Gap Acidosis: HARDUP
H - Hyperalimentation/hyperventilation
A - Acetazolamide
R - Renal tubular acidosis
D - Diarrhoea
U - Ureteral diversion
P - Pancreatic fistula/parenteral saline

165
Q

Causes of increased functional residual capacity?

A

Erect position
Emphysema
Asthma

166
Q

Causes of decreased functional residual capacity?

A

Pulmonary fibrosis
Laparoscopic surgery
Obesity
Abdominal swelling
Muscle relaxants

167
Q

Causes of SIADH?

A

Malignancy
especially small cell lung cancer
also: pancreas, prostate

Neurological
stroke
subarachnoid haemorrhage
subdural haemorrhage
meningitis/encephalitis/abscess

Infections
tuberculosis
pneumonia

Drugs
sulfonylureas
SSRIs, tricyclics
carbamazepine
vincristine
cyclophosphamide

Other causes
positive end-expiratory pressure (PEEP)
porphyrias

MRSA theory (20 decks)

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