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Satia's MRCS copied decks > 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
Q

Causes of Hyperparathyroidism

A

Primary (most common due to single adenoma) (low phosphate)

Secondary (calcium normal or low)

Tertiary (Ca, PTH and phosphate high)

26
Q

Ectopic PTH

A

SQUAMOUS CELL lung cancer

27
Q

ECG in Hypercalcaemia and Hypocalcaemia

A

Hyper: Short QT interval

Hypo: Long QT interval

28
Q

Causes of hypocalcaemia

A

HypoAlb
HypoMg
HypoPhos
Acute Pancreatitis
Rhabdomyolysis
Sepsis

29
Q

Causes of hypercalcaemia

A

Excess PTH
Excess Vit D
Sarcoidosis
Excess Calcium intake
Drugs e.g. thiazide
Malignancy

30
Q

Causes of hypophosphataemia

A

Refeeding
TPN
Diabetic ketoacidosis
Hyperparathyroidism
Paracetamol overdose
Acute liver failure

31
Q

Causes of hyperphosphataemia

A

Chronic renal failure
Tumour lysis syndrome
myeloma

32
Q

Vitmain D-resistant Rickets

A

Famlilial condition

Hypophosphataemia

Phosphoturia

Rcikets

33
Q

Adrenal medulla produces

A

Epinephrine (adrenaline)

Norepinephrine (noradrenaline)

Dopamine

β-hydroxylase (enzyme involved in catecholamine
synthesis)

ATP

Opioid peptides (metenkephalin and leuenkephalin).

34
Q

Adrenal cortex

A

Cholesterol converted to pregnenolone in mitochondria

adrenal steroids are broken down by liver and excreted via kidneys and faeces

35
Q

Aldosterone

A

Mineralocorticoid stimulated by:
RAS
Increase in potassium
ACTH

Actions:
Resorption of Na from DCT
Secretes K into DCT
Secretes H into DCT

36
Q

Protein-binding of cortisol

A

Transcortin ~ 75%

Albumin 15%

= 10% active

37
Q

Cortisol

A

Released by ZF of adrenals

Stimulated by:
ACTH
Circadian rhythm
Stress
Burns
Trauma
Infection
Exercise
Hypoglycaemia

Actions: gluconeogenesis, glycogenesis, lipolysis, Vasopressor effect, Euphoria,

38
Q

Immune effects of Cortisol

A

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
Q

Secretion of androgens in the zona reticularis

A

Stimulated by ACTH

NOT LH

40
Q

Causes of Addison’s

A

Autoimmune 80%

TB 20%

Waterhouse-Friderichsen: meningococcal septicaemia –> haemorrhage

malignant infiltration
drugs

41
Q

Effects of Addison’s disease

A

decreased blood sodium
decreased BP
metabolic acidosis

weight loss
anorexia
lethargy

42
Q

Primary causes of Conn’s

A

most commonly due to adrenal adenoma (60-70%)

BAH in 20-30%

43
Q

Secondary causes of Hyperaldosertonism

A

Due to increased renin production

Causes:
Renal artery stenosis
CCF
Cirrhosis

–> Hypokalaemia
–> Fluid overload
–> Metabolic alkalosis as H+ secretion in DCT

44
Q

Cushing’s

A

ACTH dependent: (either pituitary or ectopic secretion from tumour)

ACTH independent (Adrenal adenoma, carcinoma, exogenous steroid)

45
Q

Features of Cushing’s

A

Hyperglycaemia
muscle wasting
stretch marks
osteoporosis
moon face
buffalo hump
high BP
hirsutism and acne

46
Q

Congenital adrenal hyperplasia

A

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
Q

Phaeo rule of 10s

A

10% are malignant
10% are multiple
10% from medulla

48
Q

Growth hormone stimulators

A

GHRH
Hypoglycaemia
high during deep sleep

anxiety
pain
hypothermia
haemorrhage
fever
trauma
exercise

49
Q

Gigantism

A

GH excess in children
aided by IGF-1

stimulates mitosis in cartilage cells in epiphyseal plates at end of long bones

50
Q

Acromegaly

A

GH excess in adults

increases glycogenolysis
decreased glucose uptake by cells
promotes amino acid uptake
promotes protein synthesis
increases lipolysis
decreases ldl cholesterol

51
Q

Half life of insulin

A

10 - 15 minutes

52
Q

Stimulation of insulin

A

Most things stimulate insulin include all of the mediators released in response to food

Inhibitors:
-Sympathetic input
-Somatostatin
-Serotonin
-Dopamine
-Cortisol (reduces sensitivity)

53
Q

Effects of glucagon

A

Increases glycogenolysis
Increases gluconeogenesis
stimulates lipase

54
Q

Necrolytic migratory erythema

A

Sign of glucagonoma
-75% malugnant

55
Q

Somatostatin

A

stimulated by:
increased plasma glucose, increased amino acids, increased glycerol

effects:
inhibits glucagon and insulin, decreases GI motility secretion and absorption .

56
Q

Gastrinoma

A

seen in Zollinger-Ellinson syndrome

arise from G cells
gastric hypersecretion, diarrhoea and widespread peptic ulceration

57
Q

VIPoma

A

excess VIP

severe watery diarrhoea
decrease in potassium
Achlorhydria

58
Q

Somatostatinoma

A

from D cells

causes DM, cholelithiasis and steatorrhoea

59
Q

Platelet activating factor

A

Produced in response to IL-1 and TNF-a

Stimulates platelet aggregation and vasoconstriction

60
Q

Ebb anf Flow Phase

A

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
Q

What do norepinephrine and epinephrine bind to?

A

alpha receptors and beta receptors respectively

deactivated by COMT and MAO in liver and kidney

Satia's MRCS copied decks (32 decks)

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