Physiology Flashcards
Causes of hypomagnesaemia?
Diuretics
Total parenteral nutrition
Diarrhoea
Alcohol
Hypokalaemia, hypocalcaemia
Feature of hypomagnesaeia?
Paraesthesia
Tetany
Seizures
Arrhythmias
Decreased PTH secretion → hypocalcaemia
ECG features similar to those of hypokalaemia
Exacerbates digoxin toxicity
CSF path of circulation?
- Lateral ventricles (via foramen of Munro)
- 3rd ventricle
- Cerebral aqueduct (aqueduct of Sylvius)
- 4th ventricle
- Subarachnoid space (via foramina of Magendie and Luschka)
- Reabsorbed into the venous system via arachnoid granulations into superior sagittal sinus
CSF composition?
Composition
Glucose: 50-80mg/dl
Protein: 15-40 mg/dl
Red blood cells: Nil
White blood cells: 0-3 cells/ mm3
What is TRALI?
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
Complications of massive transfusion?
Hypothermia
Hypocalcaemia
Hyperkalaemia
Delayed type transfusion reaction
TRALI
coagulopathy
Actions of cortisol?
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
Where is Gastrin secreted?
G cells in antrum of the stomach
Stimulus for gastrin secretion?
Distension of stomach, extrinsic nerves
Inhibited by: low antral pH, somatostatin
Actions of gastrin secretion?
Increase HCL, pepsinogen and IF secretion, increases gastric motility, trophic effect on gastric mucosa
Source of CCK?
I cells in upper small intestine
Stimulus for CCK secretion?
Partially digested proteins and triglycerides
Actions of CCK?
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
Source of secretin?
S cells in upper small intestine
Stimulus for secretin secretion?
Acidic chyme, fatty acids
Actions of secretin?
Increases secretion of bicarbonate-rich fluid from pancreas and hepatic duct cells, decreases gastric acid secretion, trophic effect on pancreatic acinar cells
Source of somatostatin secretion?
D cells in the pancreas and stomach
Stimulus for somatostatin secretion?
Fat, bile salts and glucose in the intestinal lumen
Actions of somatostatin?
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
Which clotting factors are most temperature sensitive?
F5 and 8
Typical intracellular fluid % of total volume?
60-65%
28L
Typical extracellular fluid % of total volume?
35-40%
14L
Typical plasma % of total volume?
5%
3L
Typical interstitial % of total volume?
24%
10L
Typical trans cellular % of total volume?
3%
1L
What is the main component of colloid in the thyroid gland?
thyroglobulin
Synthesis and secretion of thyroid hormones?
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.
which antibodies are in graves?
IgG antibodies to the TSH receptors
2 main mechanisms of metabolic acidosis?
- Gain of strong acid (e.g. diabetic ketoacidosis)
- Loss of base (e.g. from bowel in diarrhoea)
How to calculate anion gap? and normal range
(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
Causes of metabolic acidosis raised anion gap?
Lactate: shock, hypoxia
Ketones: diabetic ketoacidosis, alcohol
Urate: renal failure
Acid poisoning: salicylates, methanol
Causes of metabolic acidosis normal anion gap?
= hyperchloraemic metabolic acidosis
Gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
Renal tubular acidosis
Drugs: e.g. acetazolamide
Ammonium chloride injection
Addison’s disease
Types of metabolic acidosis due to high lactate?
Lactic acidosis type A: (Perfusion disorders e.g.shock, hypoxia, burns)
Lactic acidosis type B: (Metabolic e.g. metformin toxicity)
Causes of metabolic alkalosis?
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
Mechanism of metabolic alkalosis?
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
Causes of respiratory acidosis?
Usually alveolar hypoventilation
COPD
Decompensation in other respiratory conditions e.g. Life-threatening asthma / pulmonary oedema
Sedative drugs: benzodiazepines, opiate overdose
Causes of respiratory alkalosis?
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
Where is onufs nucleus found?
anterior horn of S2 and is the origin of neurones to the external urethral sphincter.
Which nerves provide somatic innervation to the bladder?
pudendal, hypogastric and pelvic nerves
Hormones that are increased in the stress response?
Growth hormone
cortisol
renin
ACTH
aldosterone
prolactin
ADH
Glucagon
Hormones that are decreased in the stress response?
Insulin
Testosterone
Oestrogen
Hormones that do not change in the stress response?
TSH
LH FSH
Why is insulin release inhibited by stress?
Release inhibited by stress
Occurs via the inhibition of the beta cells in the pancreas by the α2-adrenergic inhibitory effects of catecholamines
Effects of PTH?
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.
what is septic shock?
refractory systemic arterial hypotension in spite of fluid resuscitation
Effects of α-1, α-2 receptor binding?
vasoconstriction
Effects of β-1 receptor binding?
increased cardiac contractility and HR
Effects of β-2 receptor binding?
vasodilatation
Effects of D-1 receptor binding?
renal and spleen vasodilatation
Effects of d-2 receptor binding?
inhibits release of noradrenaline
Adrenaline cardiovascular receptor action?
α-1, α-2, β-1, β-2
Noradrenaline cardiovascular receptor action?
α-1,( α-2), (β-1), (β-2)
Dobutamine cardiovascular receptor action?
β-1, (β 2)
Dopamine cardiovascular receptor action?
(α-1), (α-2), (β-1), D-1,D-2
Causes of pseudohyponatruaemia?
hyperlipidaemia (increase in serum volume) or a taking blood from a drip arm
multiple myeloma
Hyponatraemia urinary sodium >20
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
hyponatraemia urinary sodium <20
Sodium depletion, extra-renal loss
Diarrhoea, vomiting, sweating
Burns, adenoma of rectum (if villous lesion and large)
Causes of hypervolaemic hyponatraemia?
Secondary hyperaldosteronism: CCF, cirrhosis
Reduced GFR: renal failure
IV dextrose, psychogenic polydipsia
How to calculate sodium requirement?
(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
at which part of the bowel is most water absorbed?
(jejunum and ileum)
what causes raised carbon monoxide transfer factor (TLCO)?
Causes of a raised TLCO:
asthma
pulmonary haemorrhage (Wegener’s, Goodpasture’s)
left-to-right cardiac shunts
polycythaemia
hyperkinetic states
male gender, exercise
What causes a lowerTLCO?
pulmonary fibrosis
pneumonia
pulmonary emboli
pulmonary oedema
emphysema
anaemia
low cardiac output
Drugs causingSIADH?
Drugs causing SIADH: ABCD
A nalgesics: opioids, NSAIDs
B arbiturates
C yclophosphamide/ Chlorpromazine/ Carbamazepine
D iuretic (thiazides)
Which receptor does morphine and other conventional opioids attach to?
MU
Functions of insulin?
Secreted in response to hyperglycaemia
Glucose utilisation and glycogen synthesis
Inhibits lipolysis
Reduces muscle protein loss
Effect of vitamin B1 deficiency?
beriberi