Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
32 Cards in this Set
- Front
- Back
|
AdrenoCorticol Hypofunction (causes and pathology)
|
Primary Hypoadrenalism: Addisons disease. Destruction of adrenal cortex. Low Gluco, Mineralocorticoids and Androgens.
Autoimmune, Tb, Surgical removal, Haemorrhage, Malignancy, Amyloid Secondary Hypoadrenalism: Hypothalamic-Pituitary disease (ACTH not produced), or Iatrogenic (HPA suppression due to chronic steroid therapy) HP disease mainly only affects Glucocorticoids. It is also usually due to Panhypopituitarism and thus patients are deficient in T3/4 also. |
|
|
Maintenance treatment of adrenal insufficiency
|
Hydrocortisone/Prednisolone: Cortisol
Fludrocortisone: Aldosterone |
|
|
Acute Adrenal Insufficiency.
|
Severe hypotension, dehydration
precipitated by Intercurrent illness, surgical stress, sepsis |
|
|
Symptoms of Addisons
|
anorexia & weight loss, weakness, depression, amenorrhoea, N&V, Postural hypotension, constipation,, myalgia, joint pain.
|
|
|
Signs of Addisons
|
Pigmentation (due to high ACTH) particularly in palmar creases, loss of body hair.
|
|
|
Emergency management of acute adrenal insufficiency.
|
Dextrose 50% -hypoglycemia.
Hydrocortisone 100 mg intravenously (IV) every 6 hours. OR Dexamethasone (4 mg IV) Fludrocortisone acetate (mineralocorticoid) 0.1 mg every day. Treat the underlying problem that precipitated the crisis. |
|
|
Electrolyte imbalances in acute adrenal insufficiency.
|
Hypoglycemia (67%)
Hyponatremia (88%) Hyperkalemia (64%) Hypercalcemia (6-33%) |
|
|
Cushings Syndrome
|
Increased Glucocorticoid.
ACTH dependent causes: cushings disease, ACTH administration ACTH independent causes: Adrenal adeno/carcinoma, Glucocorticoid admin. |
|
|
Cushings Syndrome Clinical Features
|
Central weight gain, hirsutism, hair growth, acne, moon face, buffalo hump, striae
Depression, insomnia, psychosis Ameno/oligouria, polyuria, dec libido proximal myopathy, poor wound healing, thin skin, bruising, OP HT DEATH: HT, MI, Infection, Heart Failure |
|
|
Investigations of Cushings
|
Test cortisol levels 8-9am, minimal stress.
Suppression test: Administer Dexamethasone. induces negative feedback Stimulation test: Administer synthetic ACTH. This will lead to inc cortisol. |
|
|
DD of Cushings, Investigations
|
Adrenal CT/MRI: Adenomas, carcinomas
Pituitary MRI Plasma Potassium levels: common with ectopic ACTH secretion High dose dexamethasone: failure of significant plasma cortisol suggests ectropic sourch of ACTH or adrenal tumour Plasma ACTH: low/undetectable indicate non-ACTH dependent cause Chest Xray: carcinoma of bronchus |
|
|
Causes of Hypernatraemia
|
GI: vomiting, diarrhoea
Skin: Sweating, burns Others: Tachypnoea, Diabetes insipidus, Hypertonic parenteral nutrition/saline/sodium bicarbonate |
|
|
Causes of Hyponatraemia
|
Renal: Diuretics, hypoaldosteronism, nephropathy, renal failure, Nephrotic syndrome.
GI: vomiting, diarrhoea Skin: Sweating, burns Others: Cortisol deficiency, Hypothyroidism, Pregnancy, Heart failure, Cirrhosis |
|
|
Diabetes Insipidus: Causes of Thirst and Polyuria in
|
ADH lack/insensitivity
Loss of water balance (water not reabsorbed), and thus urine is dilute. As they lose a lot of fluid, they drink to replace the fluid loss. |
|
|
Subtypes of Diabetic Insipidus
|
Neurogenic/Central: Deficiency of ADH. Malfunction in Posterior Pituitary. - injury to head, infection, tumours, surgical operations, haemorrhage
Nephrogenic: Renal insensitivity to ADH. May be due to kidney disease. |
|
|
Diabetic Insipidus Investigations
|
Water Deprivation Test:
All water intake is withheld, and urine osmolality & body weight are measured hourly. 2 urine osmalalities vary <30/ weight decreases >5%, ADH SC administered. Final urine specimin 60 mins later. Healthy: water deprivation leads to urine osmalality 2-4x greater than plasma osmolality. Giving ADH leads to 9% rise in osmolality Central DI: minimal ADH levels and activity. Urine does not become concentration. Urine osmalality inc >50% in response to ADH Nephrogenic DI: norm/elevated ADH. Kindeys fail to respond to ADH administerd during the test. |
|
|
Hypernatraemia: Treatment
|
SLOW ADMINISTRATION TO AVOID CEREBRAL OEDEMA AND SEIZURES
hypovolaemic: Isotonic saline hypervolaemic: Diuretics, 5% dextrose euvolaemic: 5% dextrose |
|
|
Hyponatraemia: Treatment
|
hypertomic 3% saline
|
|
|
Structural and Functional relationship between Hypothalamus and Pituitary Gland
|
Hypothalamus: Around the 3rd ventricle, above the pituitary stalk
Pituitary: Lies within Sella Turcica. Lies beneath the hypothalamus. Anterior Pit: Adenohypophysis Posterior Pit: Neurohypophysis. Extension of Hypothalamus. |
|
|
Hormones secreted by Pituitary
|
Anterior:
GH: TSH Prolactin ACTH Posterior: ADH/ Vasopressin Oxytocin |
|
|
Role of GH
|
Increase collagen and protein synthesis, retention of ca, Po, N for anobolism, and oppose the actions of insulin. This leads to Skeletal and Soft Tissue Growth.
In acts upon GHRH from Hypothalamus |
|
|
Role of TSH
|
Responsible the synthesis of T3,4 by the Thyrotrophs of the Thyroid gland
It acts upon TFH from the Hypothalamus |
|
|
Role of Prolactin
|
Stimulates breast milk secretion, reduces gonadal activity.
|
|
|
Role of ACTH
|
Responsible for the secretion of Cortisol by the Adrenal Gland (Zona Fasciculata).
It acts upon CRH from Hypothalamus. |
|
|
Clinical Features of Hypopitutarism
|
Isolated or multiple deficiencies:
GH and Gonadotrophins are usually affected first. Hyperprolactinaemia occurs relatively early because of loss of inhibitory Dopamine, rather than hypoprolactin. TSH and ACTH are usually last to be associated. Panhypo: Deficiency of all anterior hormones. |
|
|
Treatment of Hypopituitarism
|
Corticosteroids (hydrocortisone, prednisolone): ACTH deficiency
Levothyroxine: Replaces deficient thyroid hormones caused by deficient TSH Testosterone in M (patch, gel, injection), O or O+P in F (pills, patches) Desmopressin: Replace ADH (nasal spray, tablet, injection) GH/Somatotropin: (injection) |
|
|
Blood supply to Adrenal gland
|
Inferior Phrenic Artery --> Superior suprarenal arteries
Abdo Aorta --> Middle suprarenal arteries Renal artery --> Inferior suprarenal arteries When the blood reaches the adrenal's centre, it flows into the medullary vein --> suprarenal veins --> inferior vena cava |
|
|
Relationship between Adrenal Medulla and Nervous system
|
The adrenal medulla contains chromaffin cells which are surrounded by a meshwork of blood vessels called venous sinusoids.
The chromaffin cells are stimulated by the sympathetic NS to secrete noradrenaline and adrenaline into the sinusoids --> rest of the body |
|
|
Zones of Adrenal Cortex + Hormones
|
Zona:
Glomerulosa - Mineralocorticoid Aldosterone Fasciculata - Glucocorticoid Cortisol Reticularis - Androgen Testosterone, Oestrogen |
|
|
Endocrine Hypertension Investigations
|
Renin & Angiotensin - Renal Artery Stenosis, Tumours
Catecholamines: Pheochromocytoma GH: Acromegaly Aldosterone: Conns, Idiopathic adrenal hyperplasia, Dexamethasone hyperaldosterone Mineralocorticosteroids: Cushings |
|
|
Pheochromocytoma
|
rare, catecholamine-secreting tumor derived from chromaffin cells. Adrenaline & NA.
Headaches, palpitations, and diaphoresis in association with severe hypertension Hyperglycemia Hypercalcemia Plasma metanephrine testing 24-hour urinary collection for catecholamines and metanephrines CT, MRI, PET |
|
|
Conns syndrome
|
PRIMARY HyperAldosteronism
Adenoma/Carcinoma/Idiopathic Hyperplasia Acts on DCT for Na reasborption at the expense of K and H ion loss Serum Hypopotassium Inc urinary Potassium excretion Inc plasma Aldosterone Hypertension CT, MRI |
