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MRCS- physiology + surgery > Endo Physiology > Flashcards

Endo Physiology Flashcards

1
Q

Location of the hypothalamus

A

Forebrain

Floor of third ventricle

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2
Q

Hypophyseal stalk

A

Communication between hypothalamus and pituitary gland

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3
Q

Development of anterior pituitary

A

Outpouching of tissue from oral cavity - ectoderm
rathke’s pouch

Linked to hypothalamus by hypophyseal portal circulation

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4
Q

Development of posterior pituitary

A

Dwongrowth of neural tissue

Continuous with hypothalamus

Paraventricular and supraoptic nuclei lie in hypothalamus and project neurons down to posterior pituitary

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5
Q

Production of ACTH

A

Released with MSH and B-endorphin in response to CRH

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6
Q

What is growth hormone stimulated by?

A

GHRH, inhibited by GHIH or somatostatin

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7
Q

Dopamine control of prolactin

A

Dopamine inhibits prolactin release

If dopamine levels are lowered (or it can’t access the anterior pituitary) prolactin levels will increase

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8
Q

Paraventricular nucleus

A

Produce oxytocin, stimulated by mechanoreceptors on breast and stimulates uterine contractions

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9
Q

Supraoptic nucleus

A

Produces ADH, in response to osmoreceptors and cardiac stretch receptors

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10
Q

Prolactin inibits…

A

GnRH

–> reduction in andogens and oestrogens

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11
Q

Urinary sodium in SIADH

A

ADH –> reabsorption of water in collection ducts

There is increased urinary osmolarity

Volume expansion has occured –> there will be salt wasting and hence Urinary Na >30

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12
Q

What is the main components of thyroid colloid?

A

Thyroglobulin

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13
Q

Production of triiodothyronine and thyroxine

A

Iodide ions pumped from ECM to follicular cells

Iodide ions converted to iodine

Iodine paired with tyrosine in colloid
Forms monoiodotyrosine
Diiodotyrosine

Coupled to form T3 and T4

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14
Q

Causes of Primary Hyperthyroidism

A

Graves: IgG autoantibodies binding to receptors

Plummer disease: Singular toxic adenoma / nodules

Toxic multiodular goitre

Acute phase of thyroid cell injury

Drugs e.g. amiodarone

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15
Q

Causes of secondary hyperthyroidism

A

Pituitary / Hypothalamic tumour secreting TRH / TSH

Metastatic thyroid cancer

Choriocarcinoma (can produce substance similar to TSH)

Ovarian teratoma - struma ovarii

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16
Q

Thionamides

A

Competively compete for the thyroid peroxidase enzyme that converts iodide to iodine

Also inhibits coupling of iodotyrosine molecules

Carbimazole
Propylthiourcail
- Propylthiouracil also inhibits the peripheral deiodination of T4

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17
Q

Lugol’s solution

A

Iodide

iodide is thought to work by blocking the binding of iodine with tyrosine residues

+ reduces vascularity of thyroid gland

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18
Q

Pendred syndrome

A

Hypothyroidism + Deafness

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19
Q

Causes of primary and secondary hypothyroidism

A

Autoimmune e.g. Hashimoto’s (fibrosis, atrophy and hurthle cells)

Iodine deficiency

Congenital - Pendred’s syndrome

Iatrogenic

Drugs e.g. Lithium

Neoplasmia

secondary: Hypopituitarism, TSH deficiency

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20
Q

Actions of hydroxylated Vitamin D3

A

Increase calcium and phosphate absorption from gut

Increase calcium and phosphate absorption from kidney

Activates osteoclast bone resorption

Promotes mineralisation of osteoid

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21
Q

Actions of PTH

A

Stimulates osteocyte mobilisation of Ca from bone and longer term osteoclast resorption from bone

increase in Ca resorption from kidney

increased phosphate excretion

stimulates conversion of vitamin D to active form

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22
Q

Actions of Vitamin D

A

Increases phosphate and Ca resorption from gut and kidney

Stimulates osteoclastic bone resorption

Promotes mineralization of osteoid

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23
Q

Actions of calcitonin

A

Produced by parafollicular C-cells

Decreases Ca2+ and phosphate reabsorption
from the renal tubules

Stimulates osteoblasts to mineralise bone and
thus take Ca2+ from the circulation.

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24
Q

Causes of Hypoparathyroidism

A

Congenital e.g. DiGeorge

Autoimmune

Iatrogenic

HypoMag

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25
Causes of Hyperparathyroidism
Primary (most common due to single adenoma) (low phosphate) Secondary (calcium normal or low) Tertiary (Ca, PTH and phosphate high)
26
Ectopic PTH
SQUAMOUS CELL lung cancer
27
ECG in Hypercalcaemia and Hypocalcaemia
Hyper: Short QT interval Hypo: Long QT interval
28
Causes of hypocalcaemia
HypoAlb HypoMg HypoPhos Acute Pancreatitis Rhabdomyolysis Sepsis
29
Causes of hypercalcaemia
Excess PTH Excess Vit D Sarcoidosis Excess Calcium intake Drugs e.g. thiazide Malignancy
30
Causes of hypophosphataemia
Refeeding TPN Diabetic ketoacidosis Hyperparathyroidism Paracetamol overdose Acute liver failure
31
Causes of hyperphosphataemia
Chronic renal failure Tumour lysis syndrome myeloma
32
Vitmain D-resistant Rickets
Famlilial condition Hypophosphataemia Phosphoturia Rcikets
33
Adrenal medulla produces
Epinephrine (adrenaline) Norepinephrine (noradrenaline) Dopamine β-hydroxylase (enzyme involved in catecholamine synthesis) ATP Opioid peptides (metenkephalin and leuenkephalin).
34
Adrenal cortex
Cholesterol converted to pregnenolone in mitochondria adrenal steroids are broken down by liver and excreted via kidneys and faeces
35
Aldosterone
Mineralocorticoid stimulated by: RAS Increase in potassium ACTH Actions: Resorption of Na from DCT Secretes K into DCT Secretes H into DCT
36
Protein-binding of cortisol
Transcortin ~ 75% Albumin 15% = 10% active
37
Cortisol
Released by ZF of adrenals Stimulated by: ACTH Circadian rhythm Stress Burns Trauma Infection Exercise Hypoglycaemia Actions: gluconeogenesis, glycogenesis, lipolysis, Vasopressor effect, Euphoria,
38
Immune effects of Cortisol
Anti-inflammatory: lowers immunocompetent cells and macrophages Stimulates the synthesis of lipocortin in leukocytes (inhibits phospholipase A2 and prevents the formation of inflammatory mediators such as prostaglandins, leukotrienes and platelet activating factor) Immunosuppressive effects: decreases t cell number and function decreases b cel clonal expansion decreases basophils and eosinophils inhibits complement
39
Secretion of androgens in the zona reticularis
Stimulated by ACTH NOT LH
40
Causes of Addison's
Autoimmune 80% TB 20% Waterhouse-Friderichsen: meningococcal septicaemia --> haemorrhage malignant infiltration drugs
41
Effects of Addison's disease
decreased blood sodium decreased BP metabolic acidosis weight loss anorexia lethargy
42
Primary causes of Conn's
most commonly due to adrenal adenoma (60-70%) BAH in 20-30%
43
Secondary causes of Hyperaldosertonism
Due to increased renin production Causes: Renal artery stenosis CCF Cirrhosis --> Hypokalaemia --> Fluid overload --> Metabolic alkalosis as H+ secretion in DCT
44
Cushing's
ACTH dependent: (either pituitary or ectopic secretion from tumour) ACTH independent (Adrenal adenoma, carcinoma, exogenous steroid)
45
Features of Cushing's
Hyperglycaemia muscle wasting stretch marks osteoporosis moon face buffalo hump high BP hirsutism and acne
46
Congenital adrenal hyperplasia
Commonest deficiency: 21-Hydroxylase --> decreased cortisol production --> Increased ACTH Vast steroid pre-cursors converted to androgens which causes: Male - rapid growth and early development of sexual characteristics Female- Masculinisation of external genitalia + male body shape
47
Phaeo rule of 10s
10% are malignant 10% are multiple 10% from medulla
48
Growth hormone stimulators
GHRH Hypoglycaemia high during deep sleep anxiety pain hypothermia haemorrhage fever trauma exercise
49
Gigantism
GH excess in children aided by IGF-1 stimulates mitosis in cartilage cells in epiphyseal plates at end of long bones
50
Acromegaly
GH excess in adults increases glycogenolysis decreased glucose uptake by cells promotes amino acid uptake promotes protein synthesis increases lipolysis decreases ldl cholesterol
51
Half life of insulin
10 - 15 minutes
52
Stimulation of insulin
Most things stimulate insulin include all of the mediators released in response to food Inhibitors: -Sympathetic input -Somatostatin -Serotonin -Dopamine -Cortisol (reduces sensitivity)
53
Effects of glucagon
Increases glycogenolysis Increases gluconeogenesis stimulates lipase
54
Necrolytic migratory erythema
Sign of glucagonoma -75% malugnant
55
Somatostatin
stimulated by: increased plasma glucose, increased amino acids, increased glycerol effects: inhibits glucagon and insulin, decreases GI motility secretion and absorption .
56
Gastrinoma
seen in Zollinger-Ellinson syndrome arise from G cells gastric hypersecretion, diarrhoea and widespread peptic ulceration
57
VIPoma
excess VIP severe watery diarrhoea decrease in potassium Achlorhydria
58
Somatostatinoma
from D cells causes DM, cholelithiasis and steatorrhoea
59
Platelet activating factor
Produced in response to IL-1 and TNF-a Stimulates platelet aggregation and vasoconstriction
60
Ebb anf Flow Phase
Ebb phase -Initial response to injury -Phase of reduced energy expenditure and metabolic rate that lasts for approximately 24 h Flow phase -Follows = catabolic phase -Increased metabolic rate, hyperglycaemia, -Negative nitrogen balance -Increased O2 consumption. The flow phase has significant
61
What do norepinephrine and epinephrine bind to?
alpha receptors and beta receptors respectively deactivated by COMT and MAO in liver and kidney

MRCS- physiology + surgery (32 decks)

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