Endocrinologie L4 Flashcards
(41 cards)
What is Addison’s disease?
It’s a (pathology) hypofunction of the adrenal cortex
- failure of adrenal cortex to produce adrenocortical hormones
- may involve total destruction of the gland
- mostly tuberculosis → atrophy of adrenal glands (involves adrenal medulla as well as adrenal cortex)
*Adrenocortical hormones stimulate cortisol → glucocorticoid deficiency and aldosterone → mineralocorticoid deficiency
What are the consequences of glucocorticoid deficiency? (can be caused by Addison’s disease → no adrenocortical hormones)
Decrease in blood sugar
Decrease in Lipolysis
Decrease in Gluconeogenisis
Causes:
Lack of energy, muscular weakness, inability to take stress
Traitement: Carbohydrate metabolism
What are the consequences of mineralocorticoid deficiency (can be caused by Addison’s disease → no adrenocortical hormones)
Plasma: decrease Na+ (Hyponatremia), decrease in Cl-, decrease in H2O, Lost in urine
All of this causes: decrease in extracellular fluid, decrease in plasma volume, decrease in Cardiac Output
Increase in K+ (Hyperkalemia), H+ (Acidosis) reabsorbed from Urine
*Patient dies in shock 7 days after complete absence of mineralocorticoids
Treatment: Aldosterone → control electrolyte, blood levels
What is Cushing’s Disease?
Its Diagnosis and Treatment?
Hyperfunction of the Adrenal Cortex
Increase in ACTH → Adrenal cortex → Hyperplasia
Excerssive production of glucocorticoids + increased production of mineralocorticoid
*ACTH levels undetectable so detected by high blood pressure no other reason
Increase Sex hormones + Androgens → Masculinization
Diagnosis: Puffiness of face, Masculinization, Hypertension, increase glucose, increased steroid metabolites in urine
Treatment: Surgery → subtotal removal of adrenal cortex
What are the consequences of excess glucocorticoid? (can be caused by Cushing’s disease → increased cortisol)
Increase blood glucose (Adrenal diabetes)
Increase insulin secretion (can become Diabetes Mellitus if b-cells burn out)
Decrease protein synthesis, Increase protein breakdown
Osteoporosis : loss of protein and Ca++ in bones
What are the consequences of excess mineralocorticoids? (can be caused by Cushing’s disease → increased aldosterone)
Plasma: increase Na+ (Hypernatremia), increase Cl-, increase H2O reabsorbed from urine
Causes increase extracellular fluid, plasma volume and Hypertension
Decrease K+ (Hypokalemia), H+ (Alkalosis) lost in urine
What is the composition of Pancrease?
99% exocrine → secretes digestive enzymes
within the exocrine pancreas, small endocrine structures → islets of Langerhans → compact mass of cells with good vascularization
60% cells of islet of Langerhans = beta-cells → synthesize insulin
25% = alpha-cells → synthesize glucagon
Insulin and glucagon = small protein hormones controlling glucose concentration in blood (insulin more important)
What is the importance of Insulin?
How is glucose found in our body?
Only hormone that acts primarily to decrease blood glucose
Glucose present in blood, very little free in tissues
Dosen’t diffuse into most cells, need transport
a) in the liver, muscle cells → converted to glycogen
b) in adipose tissue → converted to fat, stored for later use
c) many cells of body is oxidized → energy
Insulin receptors: membrane receptors, stimulates insertion of glucose transport proteins stored in cytoplasm → plasma membrane → increase glucose uptake
*Glucose = very hydrophilic, won’t cross membrane
What is the fasting level of glucose in the blood?
80 mg/100mL
What can happen in cases of insulin deficiency?
b-cells are destroyed → Diabetes mellitus → most tissues cannot take up glucose → accumulates in circulation
Occurs even if no glucose in diet → bc cell starving for glucose → protein breakdown to amin acids → synthesis of glucose with aa → gluconeogenesis
Free fatty Acids (FFA) → principal source of energy → increased lipolysis BUT fat inefficiently used → increase circulating acetoacetic acid + b-hydroxybutyrix acid + acetone (ketosis breath)
→ build up of fatty acids → decreased blood pH → diabetic coma → death unless treatment
What are some symptoms of diabetes mellitus?
- At 180mg% glucose → into urine → glucosurea
- Loss of water in urine → polyurea → dehydration + increased thirst (polydipsia)
Untreated → ketosis + metabolic acidosis
- Administration of insulin needed to restore levels
- In diabetic comas, acidosis additionally treated → electrolyte imbalance
What can be the causes of diabetes mellitus?
Funfact: Diabetes = “running through”
Mellitus = “sweet” (urine polyurea bc glucose coming out of urine)
In adults:
→ deficiency of insulin (type 1 insuline-dependant)
→ hyporesponsiveness to insulin (type 2 insulin-independent)
What characterizes Type 1/ Insulin-dependent diabetes mellitus?
Destruction of b-cells of pancreas → NO synthesis of insulin → Treatment = admin of insulin + proper diet
Defective insulin release → Treatment = drugs stimulating insulin release + proper diet + exercise
Have to control administration dose of insulin very carefully bc too much = important decrease in blood glucose → 20-30mg/100mL → not enough glucose for brain → coma → Insulin shock or hypoglycemic coma
*must be treated or else death of permanent brain damage
What characterizes Type 2/ Insulin-independent diabetes mellitus?
Insulin levels normal or abnormally high
Problem in hyporesponsivness of traget cells to insulin/ insulin resistance bc less insulin receptors on target cells
Associated with obesity (overeating) → prolonged high insulin levels decrease number of receptor → downregulation
Treatment: Proper diet (decreased caloric intake → less insulin → upregulation of insulin receptors) + exercise (insulin receptors increase)
*independent of body weight
What is juvenile diabetes mellitus?
Appears in childhood, insulin dependent!
b-cells of pancrease NOT produce insulin
Treatment = administration of insulin
What is the glucose tolerance test?
Body doesn’t evacuate/use glucose
Taken after overnight fast, eat and measure glucose 30 min, 60 min, 3-4hrs
In diabetic → increase blood glucose is greater directly after + return to normal more slowly (normal is back after 2-3 hrs)
How is insulin secretion controlled?
Feedback mechanisms control to avoid hypoglycemia
mosgt important: beta cells respond to levels blood glucose → secreting very little/no insulin when blood glucose is low and invertly
Release pof gastrin and vagal impulses to the beta-cells → insulin release → insulin leaves pancreas even before blood glucose begins to rise during meals
What is glucagon?
*Opposit effect than insulin
- Peptide hormone
- Synthesized + released by a-cells of pancreas
- Raises blood sugar → promoting glycogenolysis (break down of glycogen) + gluconeogenesis (synthesis of glucose) in the liver
- Adipose tissue → glucagon increases rate of lipolysis → increase concentration of free fatty acids in circulation
Gucagon release controlled by concentration of glucose concentration: Low blood glucose → stimulate pancreatic a-cells → more glucagon
*Not as important as insulin, other hormones increase blood glucose content → cortisol (glucocorticoid), epinephrine, nor-epinephrine, etc.
What is the growth hormone?
- Single chain polypeptide produces by anterior lobe of pituitary
- Responible for growth
- Called Somatotropin (STH)
- Increases protein synthesis in bones, muscle, kidney, liver → enhancing amino acid uptake by cells + accelerating transcription and translation of mRNA
What are somatomedins?
- Produced in liver
- Stimulated by GH/Somatomedins
- Structurally similar to insulin, named insulin-like growth factors (IGF-I and IGF-II)
- May bind to insulin receptors and invertly bc very alike
- Increase protein synthesis and stimulate growth
How does the control of GH release work?
Feedback mechanism mediated by 2 hypothalamic neurohormones:
1. Growth hormone releasing hormone (GRH) aka somatoliberin → stimulates growth hormone release
- Somatostatin (growth hormone inhibiting hormone) → inhibits GH release
*GH in Anterior Pituitary → plasma → liver → somatomedins → negative feedback loop (on hypothalamus and anterior pituitary)
GRH + somatostatin thightly regulated by integrated system of neural, metabolic, hormonal factors
What factors reduce growth? How?
Exercise, sleep, stress, low blood sugar
By increasing somatostatins → inhibit GH synthesis
What are the possible pathologies of Growth Hormone?
GH deficiency: in young, absence of GH → decrease physical growth
Excess of GH: in young → gigantism
Excess GH later in life → acromegaly → many bones (mostly at cartilaginous regions of bones) get longer and heavier
*Enlargement of face
What are the primary reproductive organs?
Gonads
Testes in the male
Ovaries in the female
